Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-52411010EnglishN2018May30HealthcareBody Mass Index, Blood Pressure and Lipid profile in type 2 diabetes-Review English0109Chitra R. HingeEnglish Sachin B. IngleEnglish Baban D. AdgaonkarEnglishDiabetes mellitus type II (formerly noninsulin-dependent diabetes mellitus (NIDDM) or adult-onset diabetes) is a metabolic disorder that is characterized by hyperglycemia (high blood sugar) in the context of insulin resistance and relative lack of insulin. Obesity is thought to be the primary cause of type 2 diabetes in people who are genetically predisposed to the disease (although this is not the case in people of East-Asian ancestry). EnglishType 2 diabetes, Obesity, Anthropometry, Lipid profileINTRODUCTION Diabetes mellitus (DM) is a syndrome of impaired carbohydrate, fat and protein metabolism caused by either lack of insulin secretion or decreased sensitivity of the tissues to insulin. Type I DM is also called as insulin dependent diabetes mellitus (IDDM) is caused by lack of insulin secretion. Type II DM is also called as non insulin dependent diabetes mellitus (NIDDM) is initially caused decreased sensitivity of target tissues to metabolic effects of insulin. This reduced insulin sensitivity of insulin is often called as Insulin resistance1. Type II DM is the most common type of diabetes and usually associated with obesity. It usually develops after the age 402. The incidence of type II diabetes mellitus (Type II DM) is rapidly increasing worldwide and it constitutes a major health problem in both developed and developing countries3. There is a great deal of evidence that both genetic and environmental factors are of importance in the pathogenesis of Type II DM. Obesity, in particular the central obesity, physical inactivity, and a diet rich in saturated fatty acids increases the risk of type II DM4.          Cardiovascular disease (CVD) is a major cause of morbidity and mortality in patients with type II DM having 2 to 4 times higher risk of developing CVD when compared to non diabetics. In diabetics cardiovascular complication occurs at an earlier age and often results in premature deaths5. Patients with type II DM are frequently affected by atherosclerotic vascular disease. Multiple factors contribute to this accelerated atherosclerosis in type II DM. These factors include dyslipidemia, obesity, hypertension, and insulin resistance6-9.          Lipid abnormalities are more common in type II DM and are aggravated with poor glycaemic control. The classical dyslipidemia in type II DM is so called atherogenic dyslipidemia. This is a constellation of lipid abnormalities which includes increased serum triglycerides (TG), increased low-density lipoprotein cholesterol (LDL-C), and decreased high-density lipoprotein cholesterol (HDL-C) also known as “lipid triad” 10. Lipid abnormalities play an important role in the causation of diabetic atherosclerosis. Elevated levels of TG, cholesterol, and LDL-C increases the risk of atherogenesis and high levels of HDL-C in contrast bear an inverse relationship to the risk of atherosclerosis and coronary heart disease (CHD) 11-12 Type II DM is associated with centralized and disharmonious distribution of fat. There is a significant association between regional fat distribution and CVD risk factors. Abdominal or central adiposity is considered the most important determinant of CVD and Type II DM13. Although imaging techniques can accurately determine total body fat and its distribution in human but are not suitable for use in large population studies because of cost, irradiation exposure, and limited availability14. The use of simple anthropometric measurements seems to diagnose obesity in early stages due to its benefits in routine monitoring and assessment in patients. Some of the simple anthropometric measures used routinely includes Body mass index (BMI), Waist circumference (WC), Waist to hip ratio (WHR) 15‚16. BMI is widely used for classification of obesity, but it does not account for the variations of fat distributions. Waist circumference is the best simple anthropometric index of abdominal visceral adipose tissue and also the best index for predicting CVD risks17.         In India 50% of diabetics has hypertension (HTN). The frequency of hypertension in diabetic population is almost twice as compared to non-diabetic general population7. In hypertensive patient with DM, atherosclerosis gets accelerated and its consequences get manifested earlier18. Both HTN and type II DM are recognised as independent CVD risk factors19.          These risk factors have a great potential for prevention through modification of life style and dietary changes. REVIEW OF LITERATURE  Type II DM is due to insulin resistance or reduced insulin sensitivity, combined with relatively reduced insulin secretion. There is a great deal of evidence that both genetic and environmental factors are of importance in the pathogenesis of Type II DM. Whereas the genetic factors are still poorly understood, numerous studies have shown that obesity (in particular, abdominal obesity), physical inactivity, a high-fat diet, and a diet rich in saturated fatty acids increases the risk of diabetes4. It is a chronic disease that requires long-term medical attention both to limit the development of its devastating complications and to manage them when they do occur. Insulin resistance associated with obesity is induced by adipokinase, free fatty acids and chronic inflammation in adipose tissue. The pancreatic beta cells compensate for insulin resistance by hypersecretion of insulin. However, at some point beta cell compensation is followed by beta cell failure and diabetes ensues20 (Fig1). The classic symptoms of diabetes are polyuria (frequent urination), polydipsia (increased thirst), polyphagia (increased hunger), and weight loss. Other symptoms that are commonly present at diagnosis include a history of blurred vision, itchiness, peripheral neuropathy, recurrent vaginal infections, and fatigue. Many people, however, have no symptoms during the first few years and are diagnosed on routine testing. People with type II diabetes mellitus may rarely present with hyperosmolar hyperglycaemic state (a condition of very high blood sugar associated with a decreased level of consciousness and there is a great low blood pressure) (Fig 2)4. World health organization (WHO) has predicted that India would experience the largest increase (48% increase in total population and 168% increase in population with >65 years of age) in type II DM and would have the greatest number of diabetic individuals in the world by the year 2030 (31.7 million in 2000 to 79.4 million in 2030) 21, 22.                          CVD is the most prevalent complication of DM23. The age-adjusted cardiovascular mortality is at least 2-fold higher in diabetic men than in non-diabetic subjects in the presence of many numbers of major risk factors24. The survival after myocardial infarction is worse in diabetic men and women25.  In general population, women experiences relative protection from myocardial infarction and usually develop coronary artery disease (CAD) approximately 10 years later than men but diabetes blunts the cardiovascular benefits of female gender26. The incidence of death from cardiovascular causes in diabetic subjects without a history of myocardial infarction during a 7-year follow-up was similar to the incidence observed in non-diabetic subjects with a history of myocardial infarction 27. Coronary angiography is one of the most reliable procedures adopted to diagnose CAD and angiographic data on Indian patients with suspected CAD had revealed that triple vessel disease (TVD) was much higher in diabetes as compared to non-diabetics 28. These observations highlight the high prevalence of undiagnosed CVD in type II DM and the gravity of cardiovascular events in this population. The problem of undiagnosed disease is the result of lack of awareness by the patients of the strong association between diabetes and CVD. Multiple factors contribute to the accelerated atherosclerosis in diabetes. These factors include excess prevalence of risks such as dyslipidemia and advanced glycosylated end products, obesity, hypertension, and, the state of insulin resistance29 (Fig. 3). In type II DM there is a global dysfunction of lipoprotein metabolism. There is increased delivery of free fatty acids (FFA) to liver due to excess adipose efflux and impaired skeletal muscle uptake increases hepatic production of very low density lipoprotein (VLDL) and cholesterol ester synthesis. Over production of triglyceride-rich lipoproteins and impaired clearance by lipoprotein lipase leads to hypertriglyceridemia in diabetes30. Triglyceride level tends to vary inversely with HDL levels as cholesterol ester transfer protein mediates exchange of cholesterol from HDL to VLDL. The combination of elevated triglycerides and low HDL is more common than elevated total and LDL cholesterol in diabetic patients with CAD. Increased concentration of small, dense LDL in diabetic person results from abnormal cholesterol and triglyceride transfer between VLDL, and LDL and depends on increased levels of  VLDL, particularly when triglyceride concentration are higher than 130mg/dl31. Small dense LDL-C is proatherogenic, first LDL-C moves into sub endothelium and is oxidized by macrophages and smooth muscle cells (stage 1 and 2). Release of growth factors cytokines attracts additional monocytes (stage 3 and 4). Foam cell accumulation and  proliferation results in growth of the plaque (stage 6, 7, and 8) 20, 32 (Fig.4).   Atherosclerosis is the process underlying CVD, which includes coronary heart disease (CHD), myocardial infarction (MI), ischemic stroke, and peripheral vascular disease (PVD) 34. Atherosclerosis is the primary cause of death in patients with type II DM and it seems to be closely related to a specific cluster of lipid abnormalities, including low levels of HDL-C, increased numbers of small dense LDL-C, and elevated triglyceride levels11. The classical dyslipidemia in type II DM is so called atherogenic dyslipidemia. This is a constellation of lipid abnormalities also known as “lipid triad” 10. This risk is even greater when the lipid triad is accompanied by insulin resistance, a procoagulant state, and hypertension–a condition known as the cardiovascular dysmetabolic syndrome. Each of these abnormalities is associated with an increased risk for cardiovascular morbidity and mortality.            Majority of Indian type II DM are dyslipidemic at baseline. The most common pattern of dyslipidemia is high LDL-C and low HDL-C among both males and females contributing to 22.7% and 33% patients of diabetic dyslipidemia, respectively35, 36. The most prevalent problem among males is high LDL –C while among females low HDL –C emerged as a bigger threat. In Indian subjects with DM the lipid profile and pattern is greatly influenced by the ethnic origin, food habit, nutritional status and lifestyle influences. There has been a quantum increase in the incidence of CAD amongst urbanites while the picture in rural India has changed very little, suggesting the major impact of lifestyle modifications on lipid profiles and the deleterious effect of the latter in causing accelerated and more extensive CAD as evident angiographically37.           Hypercholesterolemia, hypertriglyceridemia, elevated LDL-C, and low HDL-C are generally accepted as strong risk factors for cardiovascular disease (CVD) and mortality38-40.             Several evidence has contributed to our current understanding of the relationship between increase in plasma cholesterol and development of CHD. Premature atherosclerosis results from high cholesterol levels, even in the absence of other cardiovascular risk factors. Large population surveys have shown that plasma cholesterol level is predictive of CHD41. In the Framingham study individuals below 50 years, cholesterol level was directly related to cardiovascular mortality. The study highlights the profound effects of lipoprotein abnormalities on incidence of CAD in diabetics compared to non diabetics42. In a large prospective study, over 350,000 men aged 35 to 57 years were followed for 6 years. A curvilinear relationship between plasma cholesterol and coronary death rate was observed. If a risk ratio of 1 is assigned for a cholesterol level of 200 mg/dl, then at 250 mg/dl, the risk is doubled. This relation between cholesterol and CHD is not lost in the presence of other risk factors such as diabetes. The presence of diabetes further increased the risk of a given cholesterol level43. Because most cholesterol in plasma is transported in LDL and this is responsible for the correlation between plasma cholesterol and CHD. On the contrary some studies showed no significant difference in the lipids and lipoprotein profiles of diabetics and that of control5.             High-density lipoprotein cholesterol has been repeatedly shown to be an independent inverse predictor of CVD risk in epidemiological and observational studies, and patients with low HDL-C levels have been suggested to have a comparable CVD risk as those with high LDL-C levels44-45. The distribution of HDL-C levels varies with age, sex, race, and education. Women have higher levels of HDL-C than men. Alcohol consumption is directly related to HDL-C levels and an inverse relation between smoking and HDL-C levels has been reported. Low HDL-C represents a highly prevalent and potentially modifiable risk factor for CVD prevention in type II DM46-47. The rise in triglyceride rich lipoprotein concentrations which normally occur after a fat containing meal is found to be greater in type II DM patients than in people without diabetes48. Exaggerated postprandial spikes in glucose and lipid levels can lead to an excess of free radicals and trigger a cascade of endothelial dysfunction and sympathetic hyperactivity- this state is known as postprandial dysmetabolism, is an Englishhttp://ijcrr.com/abstract.php?article_id=2485http://ijcrr.com/article_html.php?did=2485   Chitra R Hinge (Ingle), Baban D Adgaonkar and Sachin B Ingle, Study of waist circumference and lipid profile in type 2 diabetes as compared to healthy individuals Biomedicine 2016;36(3):82-89 Ganong’s Review of medical physiology. 24th edition; 2012:449-450. Paul Z and Robert JS. Diabetes- A world wide problem. In: Kahn CR, Weis GC, George LK, Jacobson AM, Mose AC, and Smith JR, editors. Joslin’s Diabetes Mellitus. 14th ed. 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Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-52411010EnglishN2018May30HealthcareMorphology and Morphometry of Venous Drainage System of Heart: A Retrospective Cadaveric Study English1018Mahesh K. SharmaEnglish Jyotsna SinghEnglish Arun SharmaEnglish Kanchan KapoorEnglish DevinderEnglish Introduction: In recent times the veins of the heart have gained importance as a treatment modality for the ischaemic myocardium and carry great importance in cardiac surgery. This treatment is possible because of the presence of intramyocardial collateral venous circulation Anatomic mapping of the cardiac veins is important to guide transvenous procedures such as biventricular pacing. A detailed knowledge of cardiac venous anatomy is necessary for successful catheterization of the coronary sinus and cardiac veins. Material and Methods: The dissection of the cardiac veins was carried out on 30 preparations of formalin fixed hearts obtained from cadavers during routine undergraduate teaching. About 10 ml of CAB solution (Cellulose Acetate Butyrite crystals in acetone) was injected into the coronary sinus. The specimens were left overnight and then placed into the 5% formalin solution. The specimen was dissected to expose coronary sinus with its tributaries. Various parameters including length, diameter of coronary sinus and its tributaries and presence of muscle bridges were noted. Observations: CS was present in all 30 (100%) cases. The mean diameter of CS was calculated as 8.87±1.48mm. The great cardiac vein (GCV) normally drains the left atrium and both ventricles. This pattern was seen in 20 cases (66.6%). Arteriovenous anastomosis between GCV and the right coronary artery and anterior interventricular branch of left coronary artery were observed in 13.3% cases respectively. The present findings are discussed in light of available literature. EnglishArteriovenous anastomosis, Coronary sinus, Great cardiac veinsIntroduction Variations pertaining to the coronary arterial system have been described throughout the literature. The therapeutic modalities for Coronary Artery Disease (CAD) have also been described vastly. The coronary venous system, by comparison, has been largely neglected1. The venous system does, however, have key importance in the application of new technologies and techniques designed for the treatment of cardiovascular disease. Tori 2 was the first to outline some of the larger veins by retrograde injection of contrast material into the catheterized coronary sinus.  Recently the veins of the heart have gained importance as a treatment modality for the ischaemic myocardium3. The coronary sinus can be used for retrograde perfusion of the myocardium4-8. Presence of intramyocardial collateral venous circulation is the key to this treatment. Projects to protect the myocardium by means of reperfusion were reported to be highly successful in some centers while in others the results were reported to be inconsistent because of the great variability of the cardiac venous system. Apart from this, lack of uniform terminology/classification and incomparability in categorizing the variations of cardiac venous system exists. This process of venous reperfusion can be managed with arterial blood or nutritive solutions 9-12. The important function of the venous drainage of the heart is “venous-unity” and a great compensating capacity13.                         There are three main domains in which a thorough understanding of the venous system may lead to potentially useful clinical interventions. First is the use of percutaneous techniques to allow retroinfusion of arterialized blood into the coronary veins in patients deemed unsuitable for conventional revascularization. Second, the regional delivery of therapeutic agents such as cardioprotective drugs, cells or gene vectors, is possible14. And finally, the use of the coronary venous system as a route of access to the myocardium by the cardiac electrophysiologist15. Variability in terms of valves, diameter, angulation, extent of muscular sleeves, proximity to other cardiac structures, and cross-over spatial relationship with branches of coronary arteries have implications for practitioners seeking to make use of the system 16. Anatomic mapping of the cardiac veins is important to guide transvenous procedure such as biventricular pacing and for deployment of cardiac devices15-16. In the current scenario, there are therapeutic options for arrhythmias and for heart failure that use the coronary venous system to access target areas1. The epicardial coronary venous system has become the subject of renewed interest in recent years16. Coronary sinus cannulation has allowed access to the left atrial and left ventricular (LV) epicardium, enabling a spectrum of diagnostic and mapping maneuvers to aid in the determination of the type of arrhythmia as well as permit the delivery of ablative energy. More recently, the coronary sinus has become the gateway to LV epicardial lead placement to achieve biventricular pacing15. Retrograde cardioplegia is done in cardiac surgeries like valve replacement/repair, severe coronary lesions/ occlusion, aortic incompetence, coronary reoperations, coronary grafts and pediatric cardiac surgeries19. It is achieved by introducing the cardioplegic drug, potassium chloride through the coronary sinus after passing the catheter beyond the ostium of the coronary sinus. Hence any variation in the veins of the heart is significant1. Therefore, an attempt is made to discuss the anatomy and variations of cardiac venous system so that it may help in forming a basis for the treatment of Ischaemic Heart Disease (IHD) and CAD. Material and Methods The cross sectional study of anatomical variations in the venous drainage of heart was conducted on 30  adult cadaveric hearts obtained from the department of Anatomy, Govt. Medical College and Hospital, Chandigarh. The study was conducted by following the ethical guidelines for biomedical research on human subject as given in “Declaration of Helsinki” and by Central Ethics Committee on Human Research (CECHR) of ICMR, New Delhi. The opening of coronary sinus was approached through the opening of inferior vena cava and a 18G veinflow was introduced into it. About 10ml of 10% mixture of coloured CAB (Cellulose Acetate Butyrite) crystals in acetone was injected into the coronary sinus. Specimens were left overnight and then placed into 5% formalin solution. The specimens were dissected for the coronary sinus and its tributaries. Length and diameter of coronary sinus were measured. Tributaries of coronary sinus along with their diameter were penned down. The observations were recorded on a Performa (appended). The results were tabulated and analysed statistically using appropriate statistical tests. Observations The coronary sinus (CS) was present in all 30 (100%) cases. The mean diameter of CS was calculated as 8.87±1.48mm. The range of the diameter varied from 5.0 to 12mm. In majority of cases (63.3%), the range of the diameter was calculated as 9.0 to 12mm whereas in 36.7% cases, the range was 5.0 to 8.0mm. The most frequent shape of CS was “cylindrical” (93.3%) followed by “flattened” in 6.67% cases. The mean length of the CS was calculated as 33.76±5.36mm. The minimum length of the coronary sinus was observed as 26.0mm while the maximum was 48.0mm. In 30% cases, the range was calculated as 36 to 40mm; in 23.3% cases, the range was 32 to 34mm and in 10% cases, the range of length was 42 to 48mm as shown in Table 1. Great cardiac vein (GCV)   The great cardiac vein starts at the apex of heart and runs in the anterior interventricular sulcus (AIS) along with anterior interventricular branch of the Left Coronary Artery (LCA) (Fig.2). This pattern was observed in 25 cases (83.3%) in the present study.  In some specimens, variations were observed in the beginning of the GCV. In one case (3.3%), the GCV started at the junction of upper 2/3rd and lower 1/3rd  of AIS. In three cases (10%), it started at the middle of AIS and in only one case (Fig 1), the beginning of GCV was at the junction of upper 1/3rd  and lower 2/3rd of AIS. Superficial veno-venous anastomosis were observed in 13(42.9%) of hearts in the present study. In these cases, there was a communication seen between the GCV and the left marginal vein LMV, between the GCV, LMV and middle cardiac vein (MCV ; between the left marginal vein (LMV) and the uppermost tributary of the GCV ; between the GCV, middle cardiac vein (MCV) and posterior vein of left ventricle (PVLV)  (Fig.2) ; between the GCV and the PVLV.  The GCV, normally, drains the left atrium and both ventricles. This pattern was seen in 20 cases (66.6%). However, in the remaining 10 cases (33.3%), this normal pattern of drainage was not seen and the GCV received most of the tributaries from the left side of the heart as compared to right side. In one case (3.3%), the GCV passed superficial to one of the branches of LCA. Arterio-venous anastomosis  In four cases (13.3%)  ‘Arterio-venous’ anastomosis were observed  between the tributaries of great cardiac vein and branches right coronary artery (RCA); between the GCV and the anterior interventricular branch of the LCA at the upper end of AIS ; between the GCV and the anterior interventricular branch of the LCA at the junction of upper2/3rd  and lower1/3rd  of AIS  and also at the apex of heart. At the upper end of AIS, arteriovenous anastomosis was observed between GCV and one of the branches of LCA in a single case (Fig 3). Muscle Bridges were observed in four cases. In one case, muscle bridge was seen crossing over the major tributary of GCV from its left side; in the other, the muscle bridges were seen over the GCV and the anterior interventricular branch of the LCA in the upper part of AIS. In another heart, the MCV was covered by a muscle bridge at the middle of posterior interventricular sulcus (Fig.4). In another heart, the CS was covered by a muscle bridge at the site of termination of GCV into the CS. The mean diameter of GCV was calculated as 3.31±0.72mm. The range of diameter varied from 1.8 to 4.8mm. In majority of cases (53.3%), the range of the diameter varied from 2.8 to 3.4mm, whereas in 36.7% cases, the range of the diameter was 3.8 to 4.8mm and in 10% cases, the range was 1.8 to 2.4mm. Middle cardiac vein (MCV)  The middle cardiac vein normally starts at the apex of heart and runs in the posterior interventricular sulcus along with posterior interventricular branch of the RCA (Fig 5). This kind of normal pattern was present in 25 cases (83.3%). In others, the beginning of the middle cardiac vein varied. In one case (3.3%), the MCV started at the junction of upper 2/3rd and lower 1/3rd  of AIS. In three cases (10%), it started at the middle of AIS and in only one case at the junction of upper 1/3rd  and lower 2/3rd  of AIS. In these cases, communication was seen between the MCV, LMV and the PVLV ; between the tributaries of MCV, LMV and PVLV ; between the MCV and LMV  ; between the MCV and right marginal vein (RMV) through a communicating vein ; between the MCV, GCV and PVLV (Fig.2). In one case (3.3%), the MCV received tributaries only from its right side.  Normally, it drains the diaphragmatic surface of both ventricles. This pattern was seen in 26 cases. However, in the remaining 4 cases, this normal pattern of drainage was not seen and the MCV was also receiving tributaries from the anterior surface of ventricles.  The mean diameter of the MCV was calculated as 3.79±1.10mm. The range of diameter varied from 2.0 to 6.0mm. In majority of cases (56.7%), the range of diameter was calculated as 2.0 to 3.0mm. However, in 40% cases, the range of diameter was 4.0 to 5.0mm and 6 mm in 3.3% cases.   The middle cardiac vein diameter is greater than great cardiac vein. Small cardiac vein (SCV) The small cardiac vein normally lies posterior in the coronary sulcus between the right atrium and right ventricle and opens into the coronary sinus at its termination into the right atrium. In our study of 30 hearts, the small cardiac vein was present only in 18 cases (60%) and absent in remaining 12 cases (40%). In all the 18 cases (60%), where the small cardiac vein was present, its location was seen to be normal as described above. In one heart, there was also an “AV anastomosis” seen between the small cardiac vein and the right coronary artery. In another heart, the SCV was receiving the RMV. The mean diameter of SCV was 1.81±0.54mm. The range of the diameter varied from 1.0 to 3.0mm. In majority of cases (23.3%), the range of the diameter was calculated as 1.6 to 2.0mm. In 20% cases, the range of the diameter was calculated as 1.0 to 1.4mm; in 10% cases, the range was 2.2 to 2.4mm and in 6.6% cases, the range was 2.6 to 3.0mm. Posterior vein of the left ventricle (PVLV) The posterior vein of the left ventricle is normally found on the diaphragmatic surface of the left ventricle and a little to the left of the middle cardiac vein (Fig 2). It usually opens into the centre of the coronary sinus but sometimes into the great cardiac vein. The former kind of normal pattern was seen in 27 cases (90%). In the remaining 3 cases (10%), the PVLV joined the left end of CS (near the termination of GCV into the CS). In three cases, there was a communication seen between the PVLV and the tributaries of LMV. In two cases (6.67%), there was a communication seen between PVLV and the tributaries of MCV. In one case (3.3%), there were number of communicating veins seen between the tributaries of PVLV, LMV and MCV. The PVLV was accompanied by a vein on its left side in three cases (10%); accompanied by a vein on its right side in two cases (6.67%) and accompanied by a vein on its either side in three cases (10%). The mean diameter of PVLV was calculated as 2.84±0.97mm. The range of diameter varied from 1.0 to 2.6mm. In majority of cases (46.7%), the range of diameter was calculated as 2.1 to 3.0 mm. Out of the remaining cases (53.4%), 50% cases were in the range of 1.0 to 2.0mm and the remaining 50% cases were in the range of 3.2 to 5.6mm. Oblique vein of left atrium (OVLA) The oblique vein of left atrium descends obliquely on the back of the left atrium and drains into the CS near its atrial end (Fig 6). In our study of 30 hearts, the OVLA was present only in 9 cases (30, and not observed in the remaining 21 cases (70%). The above described normal pattern was seen in all the 9 cases (30%). The mean diameter of OVLA was 1.0±0.41mm. The range of the diameter varied from 0.4 to 1.6mm. In majority of the cases (13.3%), the range of the diameter was calculated as 1.0 to 1.2mm. In 10% cases, the range of the diameter was 0.4 to 0.8mm and 6.6% cases were in the range of 1.4 to 1.6mm. The Right Marginal Vein opened directly into the right atrium in 11 cases (36.3%) while in two cases (6.67%), it joined the small cardiac vein. In the remaining 13 cases (where it was present), it was difficult to appreciate its termination. Discussion Coronary Sinus (CS) is a major vessel which is about 2 to 3 cm long, lying posteriorly in the coronary sulcus (atrioventricular groove) between the left atrium and left ventricle (Fig.2). The sinus opens into the right atrium between the opening of the inferior vena cava (IVC) and the right atrioventricular orifice, and its opening is guarded by an endocardial fold. The incidence of presence of CS was observed by various authors 15,20-28,30. In the present study, the incidence was 100% which was similar to that observed by various authors15,20-28,30. Variations pertaining to the absence of the coronary sinus had been reported Bergman et al, 198830 and Kawashima et al, 200331. According to them in such cases, the great cardiac vein drained into the superior vena cava or the left brachiocephalic vein. Several veins, including the middle cardiac converge to empty into the right atrium directly or may reach the right atrium by passing successively into the left superior vena cava, left brachiocephalic vein and the right superior vena cava. Sahinoglu et al,1994 32 reported a case of persistent left superior vena cava with a double coronary sinus, one superior and one inferior, both emptying into the right atrium. No such anomaly was observed in the present study. In the present study, the mean diameter of the CS was 8.87±1.48 mm with a range of 5.0 mm-12 mm. None of the other studies15,21 have mentioned the mean diameter; however the range of the diameter reported by them is almost similar to the present observations. The measurement of the length shows great variability when compared to existing literature. The mean length of the CS was 33.76±5.3mm with range of the diameter varied from 26 to 48 mm in the present study. Whereas Plass et al, 200824 and Sun et al, 201226 measured the mean length as high as 108.9mm, followed Lee MS as 86.5mm. Some other authors including Ballestros LE et.al, 201025 reported it as less as 25.96±6.34 mm. Probably the points to measure the total length varied in different studies. The most common shape of coronary sinus was cylindrical (93.33%) and flattened in 6.67% in the present study (Fig.2), in accordance with other studies22,25 except Ominde BS et.al, 201528 have reported “wind-sock” shape in 100% of cases . 85% of the venous drainage of heart occurs through great, middle, small cardiac veins through coronary sinus to the right atrium. The right marginal vein may join the small cardiac vein or may open in to right atrium directly. Oblique vein of left atrium descends obliquely on the back of left atrium to join CS.15 (Fig 6). Variations regarding venous drainage were observed similar to other authors20,21,31,33,34.  The GCV had many variations due to its long course before draining into the right atrium31. In the present study, the mean diameter of the GCV was calculated as 3.31±0.72mm which was less than that observed by Ortale et.al,199421 (3.9±1.1mm). The great cardiac vein originated at the apex of heart in 25 cases (80%) which was considerably higher than that reported by Ortale et.al, 199421 (27%). In one case (3.3%), the origin was at the junction of upper1/3rd and lower 2/3rd  of AIS while the origin of GCV was absent in the upper1/3rd  as reported by Ortale et.al,199421. In three cases (10%), the origin was at the middle of AIS which was less as reported by 21(16%). In one case (3.3%), the origin of GCV was at the junction of upper 2/3rd  and lower 1/3rd  of AIS while Ortale.et.al,199421 reported 57% cases in which the origin of GCV was in the lower 1/3rd . The heart is one of the sites in which arteriovenous anastomosis are common feature21. Connection between CS and RCA have been described at the crux of the heart. 21,53 . Hadziniselimovic and Secerov, D 1974 33 observed a higher incidence (39%) and Pejkovic and Krajnc,2004 34 (6%) of arteriovenous anastomosis. In the present study the AV anastomosis were present in 36.6% cases. In four (13.3%) cases AV anastomosis existed between GCV and RCA; whereas similar frequency was observed between GCA and LCA. It is assumed that these anastomosis prevent coagulation of blood in small veins. In cases of arterial occlusion; myocardium can be supplied by retrograde vascularisation. Cardiologists who interpret imaging of the cardiac veins and cardiac surgeons who operate close to the GCV should be aware of such a variation. Venovenous anastomosis are seen at the apex, anterior and posterior aspects similar to other studies.16,33 communication between GCV, MCV and PVLV have been observed in the present study (Fig.2). There are not much variations seen in the MCV due to its short course before draining into the right atrium31. In the present study, the mean diameter of the MCV was calculated as 3.79±1.10 which was slightly greater than that observed by Ortale21 (3.6±0.8). The MCV originated at the apex of heart (Fig.5) in 25 cases (80%) as compared to 73% reported by Ortale21. In one case (3.3%), the origin was at the junction of upper 1/3rd and lower 2/3rd of AIS while the origin of MCV was absent in the upper 1/3rd of PIS as reported by Ortale21. In three cases (10%), the origin was at the middle of AIS while Ortale21 reported 5% cases in which the origin of MCV was in the middle 1/3rd of posterior interventricular sulcus. In one case (3.3%), the origin of MCV was at the junction of upper 2/3rd and lower 1/3rd of AIS while it was 22% reported by Ortale 21 in the PIS. The mean diameter of middle cardiac vein is greater than great cardiac vein thus its adequate size is useful for inserting a pacing lead 16. Venovenous anastomosis are seen at the apex, anterior and posterior aspects similar to other studies.16,33. Superficial veno-venous anastomosis were observed in 13(42.9%) of hearts in the present study. Hadziselimovich and SecerovD, 1979 33 observed such anastomosis in 49% hearts. In the present study, the small cardiac vein was present in 60% cases while its presence was reported in 54% cases by Ortale21 and 46% cases by Mochizuki20. The mean diameter of the SCV was calculated as 1.81±0.54 which was almost similar to that recorded by Ortale21 (1.8±0.8). The SCV received the RMV in two cases (6.67%). The PVLV was present in 100% cases. The mean diameter of PVLV was calculated as 2.84±0.97 which was slightly greater than that observed by Ortale21 (2.4±1.1). In majority of cases, the range of diameter was calculated as 2.1 to 3.0mm while it was 3.0 to 4.0 mm as observed by Mozhizuki22. The OVLA was present in only 30% cases while Ortale21 reported its presence in 43% cases. The mean diameter of OVLA was calculated as 1.0±0.41 which was absolutely same as that observed by Ortale21. The left marginal vein was present in 100% cases while Ortale21 reported it in 97% cases. The mean diameter was calculated as 2.81±0.99 which was greater than that observed by Ortale 21(2.3±0.8). The right marginal vein was present in 26 cases (86.7%) and Ortale21 reported its presence in 92% cases. The mean diameter was calculated as 1.71±0.71 which was slightly less as recorded by Ortale21 (1.8±0.6). The RMV opened directly into the RA in 11 cases (36.3%) while in 2 cases (6.67%), it joined the SCV. In the remaining cases, it was difficult to appreciate its termination. A study 24 has reported right marginal vein draining directly into the right atrium in 51% of cases. Table 5 shows the number and diameter of the tributary veins of the coronary sinus, while Table 6 summarizes the origin of the anterior and posterior interventricular veins. Muscle bridges play a role in sclerotic process since intimal hyperplasia of blood vessels is observed proximal to the muscle bridges. Presence of myocardial bridges results in misinterpretation of vessels in coronary angiographic studies.35,36 Angiographic studies have demonstrated muscle bridges exclusively over anterior interventricular artery.33 Whereas dissection study conducted by Reyman HC, 200836 have demonstrated myocardial bridges both over anterior interventricular artery and great cardiac vein. In the present study muscle bridges were observed not only over anterior interventricular artery and great cardiac vein, but over coronary sinus and middle cardiac vein as well (Fig.4). Conclusion The length and diameter of coronary sinus is helpful in selecting devices of appropriate length for cannulation procedures to protect the ischemic myocardium by perfusion of coronary sinus. Myocardial bridges covering coronary sinus increase chance of development of cardiac arrhythmias. The study provides a baseline data which will be helpful in conventional and interventional studies. Acknowledgement Authors acknowledge the immense help received from the scholars whose articles are cited and included in references of this manuscript. The authors are also grateful to authors/ editors/publishers of all those articles, journals and books from where the literature for this article has been reviewed and discussed. Conflict of interest: None Englishhttp://ijcrr.com/abstract.php?article_id=2486http://ijcrr.com/article_html.php?did=2486 Iyer PB. Great Cardiac Vein draining directly into the Right Atrium. A Case Report. Journal of the Anatomical Society of India ; Vol. SS, No.2 (2006-07-2006-12). Tori G. Radiological visualization of the coronary sinus and coronary veins. Acta Radiologica 1951;36:405-10. Ludinghausen MV. Clinical anatomy of cardiac veins, Vv Cardiacae. Surg Radiol Anat 1987 ; 9:159-168. Gregg DE, Dewald D (1938). The intermediate effects of the occlusion of the coronary veins on the dynamics of the coronary circulation. Amer J Physiol 122: 444-456. Cited by Ludinghausen M.V. Clinical anatomy of cardiac veins, V.V. Cardiacae. Surgical Radiologic Anatomy. 1987; 9 : 159-168. Beck CS (1948). Revascularisation of the heart. Ann Surg 128: 854-864. Cited by Ludinghausen M.V. Clinical anatomy of cardiac veins, V.V. Cardiacae. Surgical Radiologic Anatomy. 1987; 9 : 159-168. Beck CS, E. Stanton, W. Batiuchok, E. Leiter (1948) Revascularisation of the heart by a graft of systematic artery into the coronary sinus. JAMA 137: 436-442. Cited by Ludinghausen M.V. Clinical anatomy of cardiac veins, V.V. Cardiacae. Surgical Radiologic Anatomy. 1987; 9 : 159-168.  Beck C.S. Leighninger DS (1954) Operations for coronary artery disease, JAMA 156: 1226-1233. Cited by Ludinghausen M.V. Clinical anatomy of cardiac veins, V.V. Cardiacae. Surgical Radiologic Anatomy. 1987; 9 : 159-168. Sallam IA, Kolff WJ (1973). A new surgical approach to myocardial   revascularization – internal mammary artery to coronary vein anastomosis. Thorax 28 : 613-619. Cited by Ludinghausen M.V. Clinical anatomy of cardiac veins, V.V. Cardiacae. Surgical Radiologic Anatomy. 1987; 9 : 159-168. Meerbaum S (1984) The Beck Era: A springboard for renewed reserach of coronary venous retroperfusion aimed at treatment of myocardial ischemia. In : Mohl W, Wolner E, Gloger D (eds) The coronary sinus. Steinkopff Darmstadt : 320-327. Cited by Ludinghausen M.V. Clinical anatomy of cardiac veins, V.V. Cardiacae. Surgical Radiologic Anatomy. 1987; 9 : 159-168.  Bretschneider HJ (1980) Myocardial protection. Thorac Cardiovasc Surgeon 28 : 295-302. Cited by Ludinghausen M.V. Clinical anatomy of cardiac veins, V.V. Cardiacae. Surgical Radiologic Anatomy. 1987; 9 : 159-168.  Hochberg MS, Austen WG (1980) Selective retrograde coronary venousperfusion. Ann Thorac Surg 29, 6 : 578-588. Cited by Ludinghausen M.V. Clinical anatomy of cardiac veins, V.V. Cardiacae. Surgical Radiologic Anatomy. 1987; 9 : 159-168. 12.  Mohl W (1984) The development  and rationale of pressure-controlled intermittent coronary sinus occlusion – a new approach to protect ischemic myocardium. Wien Klin Wschr 96: 20-25. Cited by Ludinghausen M.V. Clinical anatomy of cardiac veins, V.V. Cardiacae. Surgical Radiologic Anatomy. 1987; 9 : 159-168. 13. Abrego FR. 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Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-52411010EnglishN2018May30HealthcareDemographic, Clinical and Etiological Profile of Young Dystonia Less Than Forty Years of Age – A Hospital Based Study English1926S. Bashir AhmadEnglish Bashir Z.English Tak S.English Goyal V.English Behari M.EnglishObjective: To study the demographic, clinical and etiological profile of dystonia in patients less than forty years of age. Material and Methods: In this study two hundred and nineteen patients with different dystonia were included. Data on demographic profile, clinical and etiological profile was recorded and statistical analysis was done by using descriptive analysis (frequency distribution). Results: Out of two hundred and nineteen patients, one hundred thirteen (51.7%) were 26 years of age of onset with mean age of onset 22.3 years, one hundred seventy six were males and forty four females. Mean duration of illness was 4.4 years. Frequency of different dystonia was focal dystonia 57.72%, multifocal 1.36%, segmental 10%, generalized 29.09%, hemidystonia 3.63% and paroxysmal kinesigenic dystonia 2.72%. Among focal dystoniaWriter’s cramp was most common (63%) followed by cervical dystonia (17.32%), and blepharospasm (7%). Among generalized dystonia Wilson’s disease was most common etiological factor in 31.25% cases. Primary generalized dystonia was seen in 17.2% cases. MRI was abnormal in all eight cases of hemidystonia. SPECT brain was abnormal in 1 out of four cases of paroxysmal kinesigenic dystonia. DYT1 was positive in four out of eleven patients of primary generalized dystonia. Conclusion: Present study showed that focal dystonia were more common even in younger age group with Writers cramp most common among all dystonia followed by cervical dystonia. In hemidystonia structural lesion should always be ruled out. EnglishDystonia, Paroxysmal kinesigenic dystonia, Writer’s crampINTRODUCTION           There have been only few studies on demographic, clinical and etiological profile of young dystonia in less than forty years of age group from India in English literature. Dystonia is defined as a syndrome of sustained muscle contraction, frequently causing twisting and repetitive movements or abnormal postures. It can be jerky, rhythmic or tremulous1.           In 1911, Oppenheim introduced term dystonia and used two different names for this syndrome, dysbasialordotica progressive and dystonia muscularamdeformens1. Flater and Sterlig emphasized its organicity and likely to be hereditary2. Since dystonia can have so many etiologies, the true prevalence is unknown.           Epidemiological survey of dystonia has shown that it is the third most prevalent movement disorder after Parkinson's disease and essential tremor3. Marsden estimated that one fourth of patients have a secondary dystonia and rest are primary or idiopathic4.           Due to clinical and etiological heterogeneity of dystonia and in recent years their classification has been reviewed leading to an etiological approach where they are classified on the basis of age of onset, by distribution, temporal pattern, associated features and cause5. Clues to secondary dystonia are, associated features, begin suddenly, occur at rest, environmental causes, cranial onset in young and lower limb onset in adults, drug or toxin exposure, past history of encephalitis, trauma, cerebral palsy, meningitis and abnormal cranial imaging6. Primary dystonia is a complex network disorder arising from the dysfunction of one or more parts of the brain including the basal ganglia, thalami, cortex, cerebellum, pons and dentate nuclei. Distorted proprioceptive propricephic feedback from muscle spindle to central process of structures7. This was confirmed by Magayar-Lehman et al on PET studies8. Fahn et al found that the yield of investigate in childhood, adolescent and adult onset dystonia was 41%, 32% and 13% respectively9. Majority of hemidystonia has secondary cause10. Clinical presentation, demographic and etiological profile is different in younger age group patients as compared to adults11. OBJECTIVES           Objectives of the present study was to study the demographic, etiological and clinical profile in different dystonia and in patients of Englishhttp://ijcrr.com/abstract.php?article_id=2487http://ijcrr.com/article_html.php?did=2487 Fahn S. Concept and classification of dystonia. Advances Neurol 1988; 50: 1-8. Flatau S, Sterling W. Progressiver Torsconsparrybie Kundera Zeilschriftgesante fur Neurologic und Psychiatrie 1981; 7: 586-612. Marsden CD. Investigation of dystonia. Advances Neurol 1988; 50:35-44. Butter AG. An epidemiological survey of dystonia with the entire population of North East England over the past 9 years. Fourth International Dystonia Symposium 2002, Atlanta, Georgia, USA. Fahn S, Bressman SB, Marsden CD. Classification of dystonia. Advances Neurol 1998; 78:1-10. Calne DB, Lang AE. Secondary dystonia. Advances Neurol 1988; 50: 9-33. Ceballos-Bauman AO, Sheean G, Passingham RE, Marsden CD, Brooks DJ. Botulinum toxin does not reverse the cortical dysfunction associated with writer’s cramp. A PET study. Brain 1997; 120: 571-582. Magyar-Lehman S, Antonini A, Roelcke U, Maguire R, Missimer J, Meyer M, Leenders KL. Cerebral glucose metabolism in patients with apasmodictorticllies. Mov Disorder 1997; 12 (5): 704- 708. Fahn S, Marsden CD, Calne DB. Classification and investigation of dystonia. In: Marsden CD, fahn S (eds.): Movement disorders, 2 london, Butter University pp 332-353. Susan B. Bressman. Dystonia current opinion. Neurology 1998; 363-372. Friedman J, Standaert DG. Dystonia and its disorders. Neurol Clin 2001;19: 681-705. Fahn S. Assessment of primary dystonia. In:Munset TL, ed. Quantification of Neurologic deficit. Boston, MA: Butterworth, 1989; 241-270. Nutt JF, Muenter MD, Aronson A, Kurland LT, Melton LJ III. Epidemiology of focal and generalized dystonia in Rochesters Minnesota. Mov Disorder 1988; 3; 188-194. Bressman SB, de Leon D, Raymond D, et al. clinical genetic spectrum of primary dystonia. Advances Neurology 1988;78:79. Ozelius LJ, Hewett JW, Page CE, et al. the early-onset torsion dystonia gene (DYT1) encodes an ATP binding protein. Nat Genet 1997; 17; 40. Chuang C, Fahn S, Frucht S. The natural history and treatment of acquired hemidystonia: report of 33 cases and review of lecture. J Neurosurg psychiatry ; 72:59-67. Defazio G, Berardelli A, Abbruzzese G, et al. possible risk factors for primary adult onset dystonia: a case-control investigation by the Italian movement disorders study group. J Neurosurgeon Psychiatry 1998; 64:25-32. Pettigrew L, Jankovic J. Hemidystonia: report of 22 patients and a review of the literature. Journal of Neurology, Neurosurgery and Psychiatry. 1985;48: 650-657. Bressman SB, Leon D,Raymud D, et al. Secondary dystonia and the DYT1 gene. Neurology 1997; 48:1571-1577. Maniak S, Sieberer M, Hagenath J, et al. Focal and segmental pimary dystonia in North and Western Germany – a clinico –genetic study. Acta Neurol Scand 2003; 107: 228-232. Benecke R,  Strumper P, Weiss H. Electron transfer complex-1 defects in idiopathic dystonia. Ann Neurol 1992;32:686. Behari M, Saha P, Prasad K, Ahuja G. Choreoacanthocytosis with marked dysphagia and laryngeal dystonia. JAPI 1991; 39(12): 967-968. Nemeth A, Mills K, Elston J, et al. Do the same genes predispose to Gillis de la Touette syndrome and dystonia? Report of a new family and review of the literature. Movement Disorders 1999; 14 (5): 826- 831. Sinngh S, Goyal V, Prasad K,  Behari M. Cervical dystonia responsive to levodopa. Neurology India 2004; 52(2): 276-277. Goyal V, Behari M. Dystonia as presenting manifestation of ataxia telangiectasia: A case report. Neurology India 2002; 50: 187-189. Behari M, Sharma A, Sharma N, et al. Case-control study of Meige’s syndrome. Result of pilot study. Neuroepidemiology 2000;19:275-280. Shyamal Kumar Das, Bhaskar Ghosh, Gautami Das, Arindam Biswas, Jharna Ray. Movement disorders - Indian scenario: A clinic-genetic review. Neurology India 2013; 61(5)(: 457-466). Kalita J, Misra UK, Pradhan PK. Oromandibular dystonia in encephalitis. J Neurol Sci 2011 May; 304: 107-110. Tufan Naiya, Amar K. Misra, Arindam Biswas, Shyamel K Das, Kunal Ray, Jharna Ray. Journal of Neural Transmission Nov. 2012; 119(11): 1343-1350. Koukouni V, Markand D, Arabia G, Quinn NP, Bhatia KP. The entity of young onset primary cercical dystonia. Mov Disorder 2007 April; 22(6):843-7. Skogseid IM. Dystonia – New advances in classification, genetics, pathophysiology and treatment. Acta Neurological Scandinavica April 2014; Vol. 129 (Suppl. 98): 13-19. Brian D. Berman, HA Jinnah. Dystonia – Five new things. Neurology Clinical Practice June 2015; Vol. 5(3): 232-240. Fung VS, Jinnah HA, Bhatia K et al. Assessment of the patient with isolated or combined dystonia: An update in dystonia syndrome. Mov Disorder 2013; 28: 889-98.

Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-52411010EnglishN2018May30HealthcareClinico-hematological Pattern of Thalassemias and Hemoglobinopathies in Children Presenting with Microcytic Anemia: An Outdoor-based Study at Burdwan, West Bengal English2734Karabi Konar (Sanyal)English Arindam KarmakarEnglish Badal Chandra MondalEnglish Objectives: Thalassemia and hemoglobinopathies are major causes of microcytic anemia in pediatric age group. The present study was done to calculate the proportion of children suffering from thalassemias and hemoglobinopathies amongst the patients of microcytic anemia and assessment of the clinical and hematological parameters of selected patients. Materials and Methods: Children of the age group 0-12 years attending the pediatrics outpatient department of Burdwan Medical College who showed microcytic anemia (i.e. MCV less than 80 fl) were included in the study. Among them, those showing features of thalassemia or hemoglobinopathy on HPLC underwent detailed clinical examination and history taking. Results: 64 (22%) children out of the total 292 patients had thalassemia or hemoglobinopathies. Rest 228 had microcytic anemia due to other causes. Hemoglobin disorders found, in decreasing order of occurrence, were E Beta-thalassemia (45%), Beta thalassemia major (26%), Beta thalassemia trait (17%) and E trait (8%). E homozygous and Beta thalassemia-HPFH had one case each. 42 children had history of blood transfusion. The average age of first transfusion was 14 months for Beta thalassemia major patients and 3 years for E Beta thalassemia patients. The age of first transfusion is highly variable in case of E Beta thalassemia. Hepatomegaly, splenomegaly and skeletal changes were almost exclusively found in transfused children. 56.3 % children suffering from hemoglobin disorders were malnourished; most of them having beta thalassemia major and E beta thalassemia. Beta thalassemia major and E beta thalassemia patients had more severe anemia and anisocytosis than the other hemoglobin disorders which were milder in nature. Conclusion: Hemoglobin disorders happen to be the cause of ailment in a considerable proportion of children suffering from microcytic anemia. So hemoglobin analysis, preferably by HPLC is very much helpful for early diagnosis and treatment.. EnglishChildren, Hemoglobinopathies, Microcytic anemia, Thalassemia, West bengalINTRODUCTION It has been estimated that approximately 7% of the world population are carriers of thalassemia and hemoglobinopathies and that 3, 00,000 –4, 00,000 babies with severe forms of these diseases are born each year 1. With a population of 1000 million at the millennium year 2000 and approximately 27 million born with pathological hemoglobinopathies each year, India is among the countries worst hit by thalassemia and hemoglobinopathies 2, 3. The frequency of carriers of hemoglobinopathies varies from 3 to 17% in different population groups of India 4. The cumulative gene frequency of the three most predominant abnormal hemoglobins, i.e. sickle cell, hemoglobin D and hemoglobin E has been estimated to be 5.35% in India 5. The abnormal hemoglobins so far detected in India include Hb D, E, H, J, K, L, M, Q, S, Lepore, Norfolk, Koya Dora, Chandigarh and the hereditary persistence of HbF. The distribution of different thalassemias and hemoglobinopathies show remarkable variation in different parts of the country and in different ethnic and tribal population 6. The most commonly found abnormal hemoglobins in India are sickle cell hemoglobin (S), hemoglobin-E and hemoglobin-D. In the very few studies done in West Bengal, mainly in adult population- based study or prevalence based study during pre-marital screening, β-thalassemia was found to be most prevalent Hb disorder with β-thalassemia carriers in the range 3.5% to 10% 7, 8. HbE comes second with carrier about 4.5% 7.      Most thalassemias and hemoglobinopathies produce anemia with smaller i.e. microcytic RBCs (red blood cells) and thus are grouped together with other causes of microcytic anemia, notably iron deficiency anemia, anemia of chronic disorders and sideroblastic anemia. Microcytic hypochromic anemia is fairly common and significant microcytosis is detected in nearly 3% of all patients who require admission to the hospital 9. While similar in many respects, the management of these different conditions is also very different. There are very few studies in pediatric population regarding microcytic hypochromic anemia and there are not much studies in Indian population.  This study was undertaken to quantify the proportion of patients coming to the pediatric outpatient department suffering from one or the other form of thalassemia or hemoglobinopathies and to assess their clinico- hematological status.  MATERIAL AND METHODS This study was conducted at the Outpatient department, Burdwan Medical College and Hospital and at the Department of Pathology, Burdwan Medical College for a period of one year (February, 2010 to January, 2011). Convenience sampling was done amongst the patients suffering from anemia in the age group 0-12 years from a rural area around Burdwan. The patients who showed microcytic RBCs i.e. Mean red cell volume (MCV) less than 80 fl on analysis by automated cell counter were included in the study. First of all, history regarding age, sex, religion, address, family history of any illness was taken. They were inquired for onset of symptoms, weakness or lethargy, poor feeding, jaundice, recurrent fever, cough and cold, diarrhea, painful crises and ulcers. History of blood transfusion and splenectomy also were taken. Height and weight of the patients were measured and plotted in the IAP growth chart for assessment of status of growth 10. Clinical examination was done regarding; pallor, jaundice, facies, skin and systemic examination with special emphasis to liver and spleen enlargement. 3 ml of EDTA blood and 2 ml of unanticoagulated blood was collected from each patient. From the EDTA blood Hemoglobin level was estimated by cyanmethemoglobin method. Total count of RBC, Red cell indices i.e. Hematocrit (Hct), Mean corpuscular volume (MCV), Mean corpuscular hemoglobin (MCH), Mean corpuscular hemoglobin concentration (MCHC), Red cell distribution width (RDW), Total count of WBC and platelet count was measured using SYSMEX KX21 automated blood cell counter. A Leishman stained peripheral blood smear was prepared for differential leukocyte count and corroboration of findings of automated counter. Reticulocyte count was done after supravital staining using new methylene blue stain. High performance liquid chromatography (HPLC) for Hemoglobin variants was done using BIORAD variant hemoglobin testing system. Manufacturer guidelines were followed for interpretation of HPLC. As per ICMR guidelines, the cut-off for HbA2 value for detection of heterozygous β-thalassemia was kept at 4.0% RESULTS Of the total 292 patients having microcytic anemia included in the study, 64 (22%) had thalassemia or hemoglobinopathies. Rest 228 had microcytic anemia due to other causes. In the thalassemia or hemoglobinopathy group, 35 (54.7%) were male and 29 (45.3%) were female. All patients included in the study were of the age 1 year or above with median of 4 yrs 8 months; the youngest 13 months old and the oldest 11 years old. (Table 1) Children even with a single transfusion were included in the “Transfused” group and others were termed as “Untransfused”. From table 3 it is seen that all the Beta thalassemia major patients and most of the E Beta thalassemia patients required blood transfusion. All the other patients did not require blood transfusion. Clinically detectable pallor was present in all of the children having blood transfusion and majority of the children not having transfusion. Most of the children with Beta thalassemia trait had pallor but most of the E trait children showed no pallor. Only mild icterus was noticeable if at all present and all icteric children were on blood transfusion. Clinically detectable enlargement of liver and spleen was mostly a monopoly of the children on blood transfusion; only one child without transfusion (diagnosed Beta thalassemia trait) showed mild splenomegaly. 82% Beta thalassemia major patients and 66% E Beta thalassemia patients had hepatomegaly. 59% Beta thalassemia major patients and 76% E Beta thalassemia patients had splenomegaly. Splenectomy was done in one patient each with Beta thalassemia major and E Beta thalassemia. Skeletal changes characteristic of hemoglobin disorders i.e. frontal bossing, undue prominence of malar eminence and dental malocclusion were observed in about one in three children on blood transfusion; no children without transfusion showed these changes. 35% Beta thalassemia major patients and 38% of E Beta thalassemia major patients showed prominent skeletal changes. Nutritional status of thalassemic patients Nutritional status was assessed according to the Harvard standard, expressed as percentiles with respect to height (or length as applicable) and weight. A children having body weight less than 80% of the 50th percentile was termed “malnourished”. Most of the Beta thalassemia major and E Beta thalassemia patients were malnourished. Only 18.2% of Beta thalassemia trait patients were malnourished. E trait and E homozygous patients did not have malnutrition. The Beta thal-HPFH patient was malnourished. Evaluation of laboratory parameters For the purpose of brevity some parameters will have to be mentioned in abbreviated form as follows: Hb – Hemoglobin concentration in g/dl TCRBC – Total count of RBC in 1x106/μl PCV – Packed cell volume in percentage. MCV – Mean red cell volume in femtolitre (fl) i.e. 1x 10-15litre MCH – Mean corpuscular hemoglobin in pictogram (pg) i.e. 1x10-12litre MCHC – Mean corpuscular hemoglobin concentration in g/dl RDW (CV) – Red cell distribution width coefficient of variation) in percentage TLC – Total leukocyte count/ μl NRBC – Number of nucleated red cells expressed in percentage of total nucleated cells in peripheral blood smear Retic (corrected) – Reticulocyte count expressed in percentage of all red cells in peripheral blood corrected for degree of anemia. HbF – Fetal hemoglobin expressed in percentage of total hemoglobin HbA – Normal adult hemoglobin expressed in percentage of total hemoglobin HbA2 – Hemoglobin A2 expressed in percentage of total hemoglobin HbE – Hemoglobin E expressed in percentage of total hemoglobin Overall the patients were grossly anemic with reduced TCRBC, hematocrit, mean cell volume, mean cell hemoglobin, mean cell hemoglobin concentration and very high RDW (CV). Beta thalassemia major and E Beta thalassemia patients showed severe degree of microcytic anemia with marked anisocytosis. Numerous nucleated red cells were seen. Beta thalassemia trait subjects had mild to moderate anemia with severe microcytosis but mild anisocytosis. E trait subjects had mild anemia with unremarkable associated features. E homozygous patient had mild anemia with slightly raised RDW (CV). Beta thal –HPFH double heterozygous patient showed moderate anemia with other parameters consistent with the degree of anemia. RDW (CV) was slightly higher than normal. A few nucleated red cells were seen. Corrected reticulocyte count was within normal range. Beta thalassemia trait, E trait and E homozygous patients did not have nucleated red cells in peripheral smear. Interestingly, corrected reticulocyte count was within normal range in all the patients. All the thalassemic and hemoglobinopathic children showed usual features on HPLC for hemoglobin variants. Notably all Beta thalassemia trait subjects had HbF in the normal range and HbA2 well above the cut-off of 4%. There was extreme elevation of HbF with HbA2 lying in the normal range in the Beta thalassemia – HPFH double heterozygous patient. He was diagnosed on clinical grounds with the aid of parental screening which showed one parent having beta thalassemia trait and the other with HPFH heterozygous. All of these children had HPLC showing normal hemoglobin analysis with Fetal Hemoglobin and HbA2 in the normal range. HbA2 values were in the range 1.8% to 3.2%. The children with hemoglobin disorders showed significantly more severe degree of anemia and higher degree of anisocytosis than the non-thalassemic children. The non-thalassemic children show higher leukocyte counts than the thalassemic children.  Both the mean values are within normal range. DISCUSSION The present study included total 292 children of the age group 0-12 years. Hemoglobin disorders constituted 22% of the cases. In earlier studies by Derkjen van Zeben et al 11 among patients of all age groups and by Martín Núñez G et al 12 among school children, the proportion of microcytic anemia was about 10%. In their studies they did not include the patients on regular blood transfusion or on iron supplementation. The difference in inclusion criteria may be the cause of increased proportion of hemoglobin disorders in the present study. Manna AK et al 7 in 2009 and Basu et al 13 in 2002 observed incidence of thalassemia and hemoglobinopathies in to be 25.15% and 20.42% respectively during clinic based screening in and around Kolkata, West Bengal, India for these disorders in all age groups. However they did not mention the exact proportion among patients with microcytic anemia. In this study E Beta-thalassemia (45%) was found to be the most frequent among the hemoglobin disorders (Table 2) followed by Beta thalassemia major (26%), Beta thalassemia trait (17%) and E trait (8%) whereas Basu et al 13, in their study in Kolkata and adjoining suburbs in 2002, observed Beta thalassemia trait (68%) as the most commonly occurring hemoglobin disorder followed in order by HbE heterozygous (25%), E Beta-thalassemia (18%) and Beta thalassemia major (6%). Manna AK et al 7 reported Beta-thalassemia minor (44%) as the single-most abnormal population around Kolkata followed by E Beta-thalassemia (22%), HbE-heterozygous (18%), Beta-thalassemia major (12%).  The present study show fewer number of Beta thalassemia trait patients than in the previous studies probably because it did not include the adult patients coming for voluntary premarital screening which comprises of a major portion of people opting for hemoglobin analysis. In both past studies E-Beta thalassemia emerged as a greater threat than other symptomatic hemoglobin disorders which is in strong agreement with the present study.  When analyzing the age of first blood transfusion and interval between successive transfusions (Table 4), it was found that Beta thalassemia major patients were transfused from a mean age of 6-24 months (mean 13.6 months) at an interval of 1-2 months (mean 1.4 months) and the transfusion dependent E Beta thalassemia patients were transfused from age of 3months to 8 years (mean 37.9 months) at an interval of 15 days to 6 months (mean 2.1 months). In an ethnically composite population of transfusion-dependent Beta thalassemia patients diagnosed in the United Kingdom, the mean age at presentation was reported to be 6 months; in a study from Greece, the age was 13.1 months, ranging from 2 months to 3years 14, 15. The present study is consistent with these reports as far as age of first transfusion is concerned. Our study also reflects the high degree of clinical variability of E Beta thalassemia ranging from severe transfusion dependent anemia to milder forms and thus conforms to earlier studies by Fucharoen, S et al 16. A brief assessment of growth status of the children with hemoglobin disorders with respect to height and weight was done in the present study (Table 5) which showed that malnutrition was present in 76.5% of Beta thalassemia major patients and 69.0% E Beta thalassemia patients. On the contrary, only 18.2% of Beta thalassemia trait patients were malnourished while E trait and E homozygous patients were well-nourished. From this observation it follows that patients with severe transfusion dependent anemia were more often malnourished than the non-transfusion dependent children. The more elaborate evaluation using growth charts also reflects that height and weight of E Beta thalassemia patients were dispersed more heterogeneously than the Beta thalassemia major patients further confirming the great clinical variability of E Beta thalassemia. The retardation of growth occurs as a consequence of anemia responsible for tissue hypoxia. Tissue hypoxia stimulates secretion of Erythropoietin which in turn causes expansion of the dyserythropoietic marrow. This causes diversion of calories required for normal development to the ineffective red cell precursors. So severely affected patients show poor development and wasting 17. On comparing the two groups of children having microcytic anemia i.e. the children having   hemoglobin disorders and children without it, it has been observed that the thalassemic children had more severe degree of anemia. The presence of patients with severe transfusion-dependent anemia in the first group explains this difference with the latter. The degree of anisocytosis was also higher in the thalassemic children. As mentioned earlier, the transfusion dependent disease conditions namely the Beta thalassemia major and E Beta thalassemia showed very high degree of anisocytosis reflected by the high values of RDW (CV). No literature expressing definitive opinions regarding degree of anisocytosis in Beta thalassemia major and E Beta thalassemia patients could be found, but it appears that it may be due to the presence of multiple populations of red cells in the transfusion dependent patients that aggravates the dispersion of red cell volume. Detailed study incorporating more number of patients is required to investigate the source of variation of red cell size in these disorders. The significantly higher value of leukocyte count of the non-thalassemic children is probably incidental or may be due to the patients with microcytic anemia associated with inflammation. CONCLUSION A significant part of the children presenting with microcytic anemia in the outpatient department are suffering from thalassemia or hemoglobinopathy. So hemoglobin analysis, preferably by HPLC is very much helpful when clinical features of hemoglobin disorders are not apparent.  E beta thalassemia and beta thalassemia major were found to be the prominent culprits in this study. It is evident from the present study and many previous studies that thalassemia and hemoglobinopathies need greater focus in terms of population based studies, mass education, premarital counseling, early diagnosis and nutritional interventions. Englishhttp://ijcrr.com/abstract.php?article_id=2488http://ijcrr.com/article_html.php?did=2488 Guidelines for the control of haemoglobin disorders. In Report of the VIth Annual Meeting of the WHO Working Group on Haemoglobinopathies, Cagliari, Sardinia, 8–9 April, 1989. Geneva: World Health Organization; 1989. Christianson A, Howson C, Modell B. March of Dimes global report on birth defects. March of Dimes Birth Defects Foundation; 2006. World population data sheet. Washington DC: Population Reference Bureau; 2009. Balgir RS. Control and prevention of the genetic load of haemoglobinopathies in India. The National Medical Journal of India. 1999 September-October; 12(5):234-238. Balgir RS. Genetic epidemiology of the three predominant abnormal hemoglobins in India. Journal of Association of Physicians of India. 1996 january; 44(1):25-28. Balgir RS. The burden of haemoglobinopathies in India and the challenges ahead. CURRENT SCIENCE. 2000 December; 79(11):1536-1547. Manna AK, Dutta SK, Chatterjee A. Relative incidence of different thalassaemias and haemoglobinopathies in South Bengal. Journal of Indian Medical Association. 2009 June; 107(6):347-349. Sur D, Mukhopadhyay SP. Prevalence of thalassaemia trait in the state of West Bengal. Journal of Indian Medical Association. 2006 January;104(1):11-15. Greer JP, Foerster J, Lukens JN, editors. Wintrobe's Clinical Hematology, 11th Ed. In.: Lippincott Williams and Wilkins Publishers; 2003.959. Khadilkar V, Khadilkar A, Choudhury P, Agarwal K, Ugra D, Shah N. IAP growth monitoring guidelines for chilidren from birth to 18 years. Indian Pediatr. 2007;44:187-197. van Zeben D, Bieger R, van Wermeskerken R, Castel A, Hermans J. Evaluation of microcytosis using serum ferritin and red blood cell distribution width. European Journal of Haematology. 1990;44:105-108. Martín Núñez G, Ramos Fernández de Soria R, Fernández Galán M, Sánchez Gil F, Cuesta P, Martín Borregón J, et al. Detection campaign for hemoglobinopathies and thalassemias among school children in northern Extremadura. Sangre(Barc.). 1995 Dec;40(6):459-464. Basu S, Chakraborty A, Bhatacharya D, Roy Chowdhury N, Chowdhury A. Population screening and control of thalassemia in Eastern Indian Population - a preliminary report (May 1999 - March 2002): Diagnostic and Research Laboratory, Thalassemia Foundation, Kolkata. Pune:; February 2002. Modell C, Berdoukas V. The clinical approach to thalassaemia New York: Grune and Stratton; 1984. Kattamis C, Kattamis A. Management of thalassemias: growth and development, hormone substitution, vitamin supplementation, and vaccination. Semin Hematol. 1995;32:269–279. Fucharoen S, Ketvichit P, Pootrakul P, al e. Clinical manifestations of Beta thalassemia/ Hemoglobin E disease. J Pediatr Hematol Oncol. 2000;22(6):552-557. Weatherall D. The Thalassemias. In Beutle E, Lichtman M, Coller B, Kipps T, Selingsohn U, editors. Williams Hematology. 6th ed.: McGraw Hill Medical Publishing division. 547-574.

Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-52411010EnglishN2018May30HealthcarePhylloides Tumor - A Study of Spectrum of its Histomorphological Parameters along with Ki-67 Expression English3538Manish GuptaEnglish Mustafa AliEnglish Objective: Aim of the study was to evaluate different parameters that are used to categorise phylloides tumor into benign, borderline and malignant type and also to know frequency of Ki-67 expression in different category. Method: It was a prospective study of two year duration carried out in the department of pathology, King George's medical university and included total 30 cases. Results: Most of patients in the entire category were more than 35 years of age and also severity of all the parameters increased as tumor spectrum shift from benign to malignant side. Conclusion: Patient age and tumor size increases as the lesions progress from benign to malignant phyllodes tumor so is the ki-67 expression. Also Ki-67 antigen is a useful adjunct in the diagnosis and prognosis of phylloides tumor. EnglishPhylloides, Histomorphology, Ki-67 antigenINTRODUCTION Phyllodes tumor which derives from the greek word “phullon” or leaf  are group of biphasic fibroepithelial tumors of  breast of varying malignant potential ranging from benign tumor to fully malignant sarcomas. They were first fully characterized by Johannes Muller in 18381 and constitute 0.3% to 1% of all breast neoplasm. The term cystosarcoma phyllodes was initially described by Muller based on the tumor's “leaflike” projections in to the cystic spaces, sarcomatous stroma and “fleshy” gross appearance. This term has since been discouraged because greater than 70% of these lesion follow a benign course and only rarely exhibit cystic degeneration; phyllodes tumor, coined by the world health organization (WHO) in 1981, is now the preferred term.2 In 2003, WHO divided breast phyllodes tumor in three groups as benign, borderline and malignant, based up on the following criteria3 1. Stromal overgrowth 2. Stromal cellularity 3. Nuclear pleomorphism 4. Mitotic activity 5. Microscopic tumor border (circumscribed or infiltrating). Depending upon the above criteria benign tumors were classified when there was moderate stromal cellularity, mitotic figures were few if any per 10 high power field, well circumscribed border and absence of or mild nuclear pleomorphism. On the other hand malignant phyllodes tumor were diagnosed when they showed extensive stromal overgrowth, marked stromal cellularity, more than 10 mitotic figures per 10 high power field, infiltrating border and marked nuclear pleomorphism. Borderline phyllodes tumors were more atypical than benign but did not fulfil all the criteria of malignancy. All grades of phyllodes tumor have the potential of local recurrence, but the metastasis is mostly identified in borderline and malignant grades. Although a grading system has been set up, the criteria of this system are not rigidly defined and vary widely among the pathologist and it is often difficult to predict the clinical behaviour from the histology alone. In addition to the routine histomorphology, the study of Ki-67 antigen expression may be useful to differentiate benign, borderline and malignant phyllodes tumor and are also helpful in predicting the clinical behaviour. MATERIAL AND METHODS It is a prospective study of two year duration that included all the cases diagnosed as phylloides in Department of pathology and then were assessed and compared by histomorphological parameters used in the diagnosis. Finally Immunohistochemistry using Ki-67 was performed and its expression was recorded. Positive tissue control (Lymphoma for Ki-67) and negative control (Omission of primary antibody) were taken. Hematoxylin and Eosin staining procedure: (Standard protocols were used) Immunohistochemistry:  (Standard protocols were used) Primary Antibody Dako, Monoclonal Mouse Antibody Anti-Human Ki-67 Antigen, product code: IS626; Ready-to-use and Anti-Human CD10, Product code: IS648; Ready-to-use) Interpretation of the Ki-67 immunostaining: Presence of brown colored end product at the site of target antigen was indicative of positive reactivity. KI-67 antigen is expressed in the nucleus and Ki-67 labelling index is defined as the percentage of cells that showed a positive nuclear stain. At least 1000 stromal cells were counted for this analysis, and all Ki-67 indices were determined by one observer. Statistical Analysis The results are presented in Mean±SD (standard deviation), Median and Percentages.  The dichotomous / categorical variables are compared by using Chi-square test. The one way analysis of variance (ANOVA) test is used to compare the continuous variables among the final diagnosis. The Tukey's multiple comparison test is used for pair wise multiple comparison between two groups, if found significant in ANOVA test analysis. The p-value Englishhttp://ijcrr.com/abstract.php?article_id=2489http://ijcrr.com/article_html.php?did=24891. Muller J, Ueber den feinen bau unddie furmen der krankhafte Geschwulste. Berlin: G Reimer; 1838; 1: 54-57. 2. Tavassoli FA, Devilee P, et al. Pathology and Genetics of Tumors of the Breast and Female Genital Organs. Lyon, France: International agency for research on cancer; 2003. 3. Fattaneh A, Tavassoli FA, Devilee P. WHO classification of tumors: Tumors of the breast and female genital organs. IARC, Lyon, pp 100-103, 2003. 4. Tse GM, Tsang AK, Putti TC, Scolyer RA, Lui PC, Law BK, Karim RZ, Lee CS. Stromal CD10 expression in mammary fibroadenomas and phyllodes tumors. J Clin Pathol. 2005; 58(2):185-189. 5. K.S. Kim. Correlation of CD10 and EGFR Expression in Phyllodes Tumors of the Breast.  Ann Oncol (2012)23 (suppl 2): ii17-ii24. 6. Ivan Ili?, Pavle Ran?elovi?, Ratko Ili?, Vuka Kati?, Maja Milentijevi?, Ljubinka Veli?kovi?, Miljan Krsti?. An approach to malignant mammary phyllodes tumors detection. Vojnosanit Pregl .2009; 66(4): 277–282. 7. Ki Beom Ku, Mi Ji Bang, Jong Woo Choi, Yoon Sik Lee, Jin Hyun Park, Hyun Ok Kim,  Min Hee Jeong, Hoon Gyu Oh, and Jin Gu Bong. Clinical, Pathologic and Immunohistochemical feature of Phyllodes Tumors of the Breast. J Breast Cancer. 2004; 7(3):185-192. 8. Timothy W. Jacobs, Yunn-Yi Chen, Donald G. Guinee, Joseph A. Holden, Imok Cha, Donald E et al. Fibroepithelial Lesions with Cellular Stroma on Breast Core Needle Biopsy. Are There Predictors of Outcome on Surgical Excision? Am J Clin Pathol 2005;124:342-354. 9. Yu-Jan Chan, Be-Fong Chen, Chin-Long Chang, Tsen-Long Yang, Chi-Chen Fan. Expression of p53 protein and Ki-67 Antigen in Phyllodes Tumor of The Breast. J Chin Med Assoc.2004; 67:3-8. 10. Nicole Nicosia Esposito, Deepak Mohan, Adam Brufsky, Yan Lin, Malathy Kapali, David J. Dabbs. Phyllodes Tumor: A Clinicopathologic and Immunohistochemical study of 30 cases. Arch Pathol Lab Med. 2006; 130:1516–1521. 11. Y Singh, T Hatano, Y Uemura, N Shikata, H Senzaki, K Hioki, A Tsubura. Immunohistochemical profile of phyllodes tumors of the breast. Oncology Reports.1996; 3(4):677-681. 12. Umekita Y, Yoshida H. Immunohistochemical study of MIB1 expression in phyllodes tumor and fibroadenoma. Pathology international.1999; 4 9(9):807-10.

Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-52411010EnglishN2018May30HealthcareSeroepidemiology of Equine Brucellosis and Role of Horse Carcass Processors in Spread of Brucella Infection in Enugu State, Nigeria English3945Emmanuel Okechukwu NjogaEnglish Joseph Ikechukwu OnunkwoEnglish Samuel Okezie EkereEnglish Ugochinyere Juliet NjogaEnglish Okoro Winifred N.English Aim: The study was undertaken to obtain baseline data on seroepidemiology of equine brucellosis and role of horse carcass processors in spread of Brucella infection in Enugu State. Materials and Methods: Rose Bengal plate test was used to screen for presence of Brucella antibody in 402 horses slaughtered for human consumption in the State. Structured and pretested questionnaire was used to obtain information on socioeconomic characteristics and involvement of 94 randomly selected horse carcass processors in slaughterhouse practices that facilitate spread of Brucella infection during slaughterhouse operations. Results: An overall seroprevalence of 3% (12/402) was recorded. Seroprevalence of 8.8 %, 2.1% and 1.9% were obtained from young (1-5 years), adult (6-12 years) and old (>12 years) horses respectively. Similarly, seroprevalence of 6.8% and 1.4% were recorded for females and males respectively while 4% and 2.2% seroprevalence were documented during the rainy and dry seasons respectively. Significant association (p EnglishBrucellosis, Brucella antibodies, Horses, Risk factors, NigeriaINTRODUCTION The domestic horse (Equus caballus is an odd-toed (perissodactyla) ungulate mammal belonging to the Equidae family, made up of horses, asses and zebras. In Nigeria, horses are treasured animals used for diverse purposes such as draft, transport, sports, exhibitions, research, recreation, security, crowd control, food (meat and milk), ceremonial and religious festivals, as well as source of variety of products and medicines [1]. In addition, horses are used in rural parts of northern Nigeria, for shepherding ruminants by nomadic herdsmen [2]. The multipurpose use of horse makes them very important in the epidemiology of transmission of Brucella infection at both the animal-animal and animal-human interfaces. Brucellosis caused by bacteria of the genus Brucella is an important zoonosis ravaging most parts of the world especially the tropics. Although many Brucella species have been described, B. abortus, B. melitensis and B. suis are the principal agents responsible for more than 90% of brucellosis burden globally [3]; preferentially infecting cattle, goats and pigs respectively [4]. Despite their distinct host preferences, these agents can under favorable conditions cause brucellosis of varying degree in most terrestrial animals and humans [4]. Equine brucellosis is caused mainly by B. abortus and to a lesser extent by B. suis biovar 3 and B. melitensis [5].  Horses usually acquire Brucella infection orally by licking vaginal or prepucial discharges from infected animals [6], generally via coitus or use of infected semen for artificial insemination [7], via inhalation of aerosolized Brucella agents in overstocked stables [8], through lactation by an infected dam [9] and by direct or indirect wound contamination with infected tissues and fluids [7, 10]. Brucellosis in horses is characterized by a clinical manifestation called “poll-evil” or “fistulous withers”[1]. This lesion results from the inflammation of supraspinous or supra-atlantal bursa and the associated connective tissue; leading to pus formation and fistulation of the affected parts of the body[1, 10]. Other signs and symptoms of the disease include middle or late term “abortion storm” due to Brucella invasion of the developing fetus and gravid uterus structures[9]; birth of weak/unthrifty foals, retained placenta, neonatal losses and un-thriftiness, repeat breeder syndrome, increased foaling interval, lameness due to polyarthritis, carpal bursitis, orchitis and epididymitis in stallions [7, 9, 10]. Brucellosis is associated with tremendous economic loses and enormous public health problems. The economic importance of equine brucellosis is based on infertility problems and decrease productivity or performance associated with the disease in most stables and recreational centers [5]; costs of treatment and biosecurity or control programs against the disease, financial losses due to emergency slaughter of infected animals and trade restrictions in animals or their products [11]. Studies on the impact of brucellosis on econometrics of livestock production in Nigeria are few and dated but the most recent report in 1996 estimated an annual loss of US$3.2 million in only two States in the country [12]. The public health importance of brucellosis lies in very low infective dose of B. melitensis and B. abortus, estimated at 10 - 100 colony-forming units [13] and ease of transmission of Brucella agents from animals to humans via multiple routes, especially consumption of raw or undercooked animal products (meat and milk) from infected animals [14]. Control of human infection with zoonotic food borne pathogens such as Brucella is a daunting task because food habits are very difficult to change. Horses are slaughtered for human consumption and the meat sometime preferred over other meat types in parts of Enugu State. Slaughterhouse workers and others in the livestock industry are occupationally at risk of Brucella infection but strict adherence to workplace safety measures, such as use of protective wears (PWs) during routine duties, may greatly reduce the odds of the infection. In most developed countries, brucellosis has been effectively controlled but the disease continues to devastate most parts of tropical Africa and Asia; where livestock production is incidentally a major means of livelihood [3, 6]. Establishment of appropriate control measures against brucellosis in a population depends on estimation of the disease burden in the population [15]. Serological test such as Rose Bengal Plate Test (RBPT) has been recommended for epidemiological screening for brucellosis because the test is sensitive, economical and easy to perform [16]; especially in resource limited parts of the world, where other methods of brucellosis diagnosis are rarely undertaken, due to cost, skills and laboratory infrastructural issues [3]. There is no published data on equine brucellosis in Enugu State despite the endemicity of the disease in Nigeria [4]; and large scale multipurpose use of horses in the study area. Additionally, there is dearth of information on the role of horse carcass processors on practices that facilitate dissemination of Brucella infections during routine slaughterhouse operations. The importance of horses in the epidemiology of transmission of Brucella infection, due to its close association with ruminants (considered reservoir of Brucella infection to horses) and human, may be significant and therefore needs to be investigated. Consequently, the study was conducted to determining the seroepidemiology of equine brucellosis and role of horse carcass processors in spread of Brucella infection in Enugu State, Nigeria. MATERIALS AND METHODS Sample collection Research visits to various horse slaughter points in Enugu State for blood sample collection, were made once weekly for six months; covering three months of dry season (December to February) and another three months of rainy season (June to August). Simple random sampling method was used to select horses to be sampled. The sex of each selected animal was determined by visual examination. The age was estimated as described by Richardson et al. [17] and then categorized as young (1- 5 years), adult (6-12 years) and old (> 12 years). Foals (Englishhttp://ijcrr.com/abstract.php?article_id=2490http://ijcrr.com/article_html.php?did=2490 Ihedioha IJ, Agina O. Haematological profile of Nigerian horses in Obollo-afor, Enugu State. Journal of Veterinary and Applied Sciences 2014; 4:1-8. Ehizibolo DO, Gusi AM, Ehizibolo PO, Mbuk EU, Ocholi RA. Serologic prevalence of brucellosis in horse stables in two northern states of Nigeria. Journal of Equine Science 2011; 22:17-19 Ducrotoy M, Bertu WJ, Matope G, Cadmus S, Conde-Álvarez R, Gusi AM et al.  Brucellosis in Sub-Saharan Africa: Current challenges for management, diagnosis and control. Acta Tropica 2017; 165: 179-193. Onunkwo JI, Njoga EO, Nwanta JA, Shoyinka SVO, Onyenwe IW, Eze JI. Serological survey of porcine Brucella infection in Southeast, Nigeria. Nigerian Veterinary Journal 2011; 32: 60-62. Colavita G, Amadoro C, Rossi F, Fantuz F, Salimei E. Hygienic characteristics and microbiological hazard identification in horse and donkey raw milk. Veterinaria Italiana 2016; 52; 21-29. Ducrotoy MJ, Bertu WJ, Ocholi RA, Gusi AM, Bryssinckx W, Welburn S et al. Brucellosis as an emerging threat in developing economies: Lessons from Nigeria. PLoS Neglected Tropical Diseases 2014; 8: e3008. Ocholi RA, Bertu WJ, Kwaga JK, Ajogi I, Bale OOJ, Okpara J. Carpal bursitis associated with Brucella abortus in a horse in Nigeria. Veterinary Record 2004; 155: 566-567. Nicoletti PL. Brucellosis. In: Sellon DC, Long MT (editors). Equine infectious disease. Missouri: Saunders Elsevier: 2007. p. 281-295. Ardo MB, Abubakar DM. Seroprevalence of horse (Equus caballus) brucellosis on the Mambilla plateau of Taraba State, Nigeria. Journal of Equine Science 2016; 27: 1-6. Tijjani AO, Junaidu AU, Salihu MD,  Farouq AA, Faleke OO, Adamu SG, Musa HI, Hambali IU. Serological survey for Brucella antibodies in donkeys of north-eastern Nigeria. Tropical Animal Health and Production 2017; 49:1211-1216. McDermott J, Grace D, Zinsstag J. Economics of brucellosis impact and control in low-income countries, Revue scientifique et technique (International Office of Epizootics) 2013; 32: 249-261. Brisibe F, Nawathe DR. Bot CJ. Sheep and goat brucellosis in Borno and Yobe States of arid Northeastearn Nigeria. Small Ruminant Research 1996; 20: 83-88. Pappas G, Panagopoulou P, Christou L, Akritidis N. Brucella as a biological weapon. Cellular and Molecular Life Science 2006; 63: 2229 -2236. Dean AS, Crump L, Greter H, Schelling E, Zinsstag J. Global burden of human brucellosis: a systematic review of disease frequency. PLoS Neglected Tropical Diseases 2012; 6:e1865. Kaltungo BY, Saidu SNA, Sackey AKB, Kazeem HM. A review on diagnostic techniques for brucellosis. African Journal of Biotechnology 2014; 13: 1-10. Diaz R, Casanova A, Ariza J, Moriyon I. The Rose Bengal test in human brucellosis: a neglected test for the diagnosis of a neglected disease. PLoS Neglected Tropical Diseases 2011; 5:e950. Richardson JD, Cripps PJ, Hillyer MH, O'Brien JK, Pinsent PJ, Lane JG. An evaluation of the accuracy of ageing horses by their dentition: a matter of experience? Veterinary Record 1995; 137: 88-90. Alton GG, Jones IM, Angus RD, Verger JM. Techniques for brucellosis laboratory. Institut National de la Recherche Agronomique (National Institute of Agricultural Research), 1998; Paris France. Petersen E, Rajashekara G, Sanakkayala N, Eskra L, Harms J, Splitter G. Erythritol triggers expression of virulence traits in Brucella melitensis. Microbes and Infection 2013; 15: 440-449 Anonymous, Equine reproductive maturity in mares and stallions. Available at http://equimed.com/health-centers/reproductive-care.  Accessed online on March 10, 2018. Sabrina R, Taha MH, Bakir M, Asma M, Khaoula B. Detection of Brucella spp. in milk from seronegative cows by real-time polymerase chain reaction in the region of Batna, Algeria, Vet. World, 2018; 11: 363-367.

Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-52411010EnglishN2018May30Life SciencesEffect of Terminalia chebula and Gallic Acid on Increased Adiposity of High-Fat Diet Induced Hyperlipidemic Mice English4652Sarada S.English Padmini E.English Objective: To elucidate the role of Terminalia chebula and Gallic Acid on increased adiposity and as a regulator of Lipogenesis and its associated factors in high-fat diet induced hyperlipidemic mice. Methods:  The study was performed on C57BL/6J Male mice aged 6-8 weeks. Control was fed with normal diet and the other 3 groups were fed with commercial hyperlipidemic diet. Adipose tissue markers Peroxisome proliferator-activated receptorgamma, CCAAT/enhancer-binding proteins-beta, 4-Hydroxy-2-nonenal, Thioredoxin, Tumour necrosis factor-?, adiponectin and leptin were estimated using adipose tissue by ELISA. Results:  The diet-induced hyperlipidemic C57BL/6J Male mice showed a marked reduction in the levels of transcription factors, oxidative stress markers and pro-inflammatory markers when treated with Terminalia chebula (Peroxisome proliferator-activated receptor-gamma (PEnglishTerminalia chebula, Hyperlipidemia, Adiposity, Gallic AcidINTRODUCTION Hyperlipidemia is a metabolic syndrome which includes lipid abnormalities (1,2). Regular intake of high-fat diet can result in hyperlipidemia (3). Hyperlipidemia is associated with an increase in the number of adipocytes due to enhanced adipogenesis. Adipose tissue is an important organ involved in dynamic regulation of metabolism in living body (4), our present study monitored the biochemical changes in adipose tissue by examining the expression of 4-Hydroxy-2-nonenal, Thioredoxin, adipogenic transcriptional factors, and adipokines. The important transcriptional factors Peroxisome proliferator-activated receptor-gamma and CCAAT/enhancer-binding proteins-beta required for adipogenesis and lipid metabolism are up-regulated in individuals whose diet composed of fatty foods (5,6) demanding the need for their screening during Hyperlipidemia. 4-Hydroxy-2-nonenal (HNE) an, α β-unsaturated aldehyde generated due to the lipid peroxidation (7) may alter the expression of antioxidants. One of the antioxidant playing a vital role in regulating redox status is Thioredoxin (8). Adipokines are peptides produced by adipose tissue involved in the regulation of glucose and lipid metabolism (9). Since adipokines were bound to fluctuate in the hyperlipidemic condition associated with adiposity (10,11), the expression of pro-inflammatory adipokine such as  leptin, tumor necrosis factor-alpha, and anti-inflammatory adipokine- adiponectin was observed in adipose tissue In the present study, Gallic acid and Terminalia chebula were used for assessing their effect during hyperlipidemia. Gallic acid is 3, 4, 5, - trihydroxybenzoic acid, used for the treatment of a vast number of diseases such as cancer, cardiovascular diseases, ulcers, arthritis, gout etc. It is found to be antihyperglycemic, antihyperlipidemic, antioxidant, and cardioprotective (12). Terminalia chebula is a common herbaceous plant used in ayurvedic preparations as it possesses diverse medicinal properties which include antimicrobial, antioxidant, antiviral, anticarcinogenic, antihyperlipidemic, etc. Ellagic acid, gallic acid, chebulinic acid, chebugalic acid and corilagin present in this fruit have a beneficial effect in the treatment of hyperlipidemia (13,14). MATERIALS AND METHODS Preparation of T. chebula aqueous powder : Terminalia chebula [Haritaki] dried fruits were collected from the Deciduous forest area in Kombankaddu area [Kodaikanal to Palani route]. It was authenticated at CAPTAIN SRINIVASA MURTI RESEARCH INSTITUTE OF AYURVEDA AND SIDDHA DRUG DEVELOPMENT, Arignar Anna Government Hospital Campus, Arunbakkam, Chennai, Tamil Nadu. Seeds from the individual fruit were removed, washed thoroughly and then air-dried on a drier table at room temperature. Then the dried pulp crushed in an electrical mixer-grinder into a coarse powder. The powder was stored in a closed vessel for future use. Animals: Mice -C57BL/6J Male aged 6-8 weeks obtained from CPCSEA approved Breeder were taken for this experiment and kept at Centre for Toxicology and Developmental Research (CEFT) Sri Ramachandra University (SRU). All animal experiments were conducted as per the instructions of Institutional Animal Ethics Committee (IAEC/XLVIII/SRU/495/2016). Experimental Design: Grouping: Animals were randomised and grouped based on the stratified body weight. Induction of hyperlipidemia Hyperlipidemia was induced to all the animals (GII – GIV) by giving commercially procured High fat diet (HFD) for a period of 15 weeks except Group I. Group I animals received standard rodent pellet diet for 15 weeks. Solubility / Suspendability, Stability, and Homogeneity of Formulation Solubility / Suspendability of the test and reference item (Gallic acid and Terminalia chebula) were ensured one day before dosing. 0.5% CMC Vehicle was selected based on the nature of test and reference drug. 0.5% CMC as a vehicle used for the preparation of test and reference drug. The homogeneity of test item in 0.5 % CMC was ensured using glass rod while dosing. Histopathology Liver, adipose were collected from all animals of the all dose groups and preserved in 10% neutral buffered formalin. The fixed tissues were processed, embedded in paraffin wax, sectioned approximately at 3-5 microns thick and stained with Haematoxylin and eosin for histopathological examination. ELISA Studies 200 mg of adipose tissue was homogenized in standard homogenization buffer with anti-proteases (20 mM Tris-HCl, 1 mM EDTA, 255 mM sucrose, pH 7.4, anti-protease). The homogenates were centrifuged at 1,000 g for 10 min and the subnatant (whole tissue extract) below the lipid cake was aspirated and denatured by adding SDS to a final concentration of 0.06% and boiling for 10 min at 100ºC. Total protein concentrations of the tissue extracts were measured using the method of Bradford (1976). Based on the requirement, the sample was diluted to acquire 100 µg of protein by using PBS buffer and used for the ELISA. PPAR-γ was quantified using  ELISA kit (MBS005886, MyBioSource, USA)   C/EBP-β was quantified using ELISA kit (MBS006925, MyBioSource, USA) Leptin  was quantified using Leptin ELISA kit (11-LEPHU-E01, ALPCO, India) Adiponectin was quantified using Total Adiponectin ELISA kit (47-ADPHUT-E01, ALPCO, India) Tumour necrosis factor-α  was quantified using ELISA kit (K0331131, Koma Biotech, Korea) 4-Hydroxy-2-nonenal was quantified using 4 hydroxy nonenol ELISA kit (MBS161454 96T, My Biosource, USA) Thioredoxin was quantified using Trx ELISA kit (MBS009625, MyBioSource, USA). Statistical Analysis The results were expressed as mean value standard deviation. Statistical analysis of the data was carried out using SPSS software. Statistical significance was arrived by comparing results of One Way ANOVA of Group I and II with III and IV. Results Histopathological Findings             Histopathology of adipose tissue of Group I (Control) showed the normal size of adipose cells. However, the adipose of Group II (HFD) showed marked hypertrophy of adipose cells with a minimal degree of severity of inflammatory cell infiltration in crown shaped structure between adipose cells. In Group III (HFD + Gallic acid treatment group) Histopathology of adipose tissue revealed decrease in the size of adipose cells and no infiltration in crown shaped structure when compared to high-fat diet (G2) group animals and Group IV (HFD + Terminalia chebula treatment group) revealed normalization of adipose cells when compared with normal control group animals. The remarkable decrease in severity and incidence of lesions in adipose tissues of animals was observed in Group 4 animals as compared to the high-fat diet (G2) and gallic acid (G3) treated animals. Transcription Factors in Adipose From the ELISA studies conducted on the adipocytes of all the 4 groups the levels of Peroxisome proliferator-activated receptor-gamma and CCAAT/enhancer-binding proteins-beta were found to be significantly increased in Group compared to Group I. The levels of Peroxisome proliferator-activated receptor-gamma and CCAAT/enhancer-binding proteins-beta were found to decrease significantly compared to HFD in Group IV (HFD +Terminalia chebula ) than the Group III (HFD + Gallic Acid ) ( Table I). Adipokine Levels From the Elisa studies conducted on the adipocytes of all groups, the levels of Adiponectin and Leptin were found to be normal in Group I which was remarkably reduced in Group II (HFD). On receiving treatment the levels of Adiponectin and Leptin were found to increase considerably compared to HFD in Group IV (HFD +Terminalia chebula) than the Group III (HFD + Gallic Acid). However the levels of Tumour necrosis Factor -α which was found to be less in Group I (Normal) and increased in Group II (HFD) decreased remarkably in Group IV (HFD +Terminalia chebula ) than the Group III (HFD + Gallic Acid ) as compared to HFD. (Table II) Oxidative stress in Adipose Tissue The ELISA studies conducted on the adipocytes of 4 groups revealed normal levels of 4-Hydroxy-2-nonenal and Thioredoxin in Group I (Normal) which was notably increased in Group II (HFD). On treatment, the levels of 4-Hydroxy-2-nonenal and Thioredoxin were found to decrease appreciably in Group IV (HFD +Terminalia chebula ) than the Group III (HFD + Gallic Acid )( Table III). Discussion Adipose tissue is an important organ where excess fat in our body is stored. It is a dynamic organ that plays an important role in energy balance and homeostasis of our body. It acts as a sensor for lipid levels in our body and controls hunger, satiety and sleep patterns. Adipocytes are considered a major endocrine organ as they secrete lipid and protein factors which produce an impact on the metabolism of other tissues, regulation of appetite, immunological responses and vascular disease etc (15). The development of hyperlipidemia as a result of High fat diets (HFD) lead to an expansion of adipose tissue along with increase in size and number. The Adipose tissue inflammation is an important marker for hyperlipidemia. Our study observed changes in the structure of adipocyte in group II (HFD) mice which shows marked hypertrophy of adipose cells with minimal degree of inflammatory cell infiltration in crown shaped structure in the histopathological report of the adipose tissue. Herbal treatment by Terminalia chebula has resulted in decrease in hypertrophy of adipose tissue as assimilation of fat is decreased in the body. The results are more predominant than Group III –Treatment with pure compound Gallic as Terminalia chebula is rich in fibre which reduces lipid absorption in the small intestine. Adipose tissue is composed of more of fatty acids and phospholipids and less of triglyceride in the form of neural fat. The presence of redox systems in microsomes in the adipose tissue results in high activity of lipid peroxidation (16). Oxidative stress and inflammation go hand-in-hand in the many tissues that are affected because oxidative stress induces the production of inflammatory cytokines, and the cytokines in turn induce free radical production. Lipid peroxidation (LP), an autocatalytic process is initiated by free radical attack on the unsaturated bonds of membrane fatty acids which leads to 4-Hydroxy-2-nonenal . In our study the levels of 4-Hydroxy-2-nonenal were found to increase significantly in Group II (HFD) as compared to Group I (Normal diet) as a result of high incidence of lipid peroxidation due to hyperlipidemia. The increase in HNE levels indicates damage to adipose tissue which is confirmed by the histopathological report (17). The levels of 4-Hydroxy-2-nonenal were found to be reduced in group IV (HFD+ Terminalia chebula) as inflammation and oxidative stress is found reduced by the herbal drug. ( Table III) The results are far more appreciable than treatment with Gallic acid as Terminalia chebula is a better drug in controlling fat assimilation in the adipose ( evident from histopathological reports and Fig 6). Thioredoxin (TRX) is a redox protein that is involved in many biological functions which controls a number of transcription factors (18). Increased lipid peroxidation associated with increase in the levels of LDL results in the formation of oxLDL. This oxLDL further aggravates the problem by increasing its uptake by macrophages in adipocytes. This increases Thioredoxin expression and so the levels of Thioredoxin were found to be increased by the consumption of high fat diet as compared to mice that was given normal diet (Table III). The treatment by the herbal drug reduced the levels of LDL and lipid peroxidation causing decrease in the levels of Thioredoxin and this effect was more pronounced than treatment with Gallic Acid, pure compound suggesting that Terminalia chebula is a better drug in treating oxidative stress and its associated complications caused by hyperlipidemia (19) (Table III and Fig 7). Further increase in the levels of lipids leads to increased Adipogenesis. Fat cell formation or adipogenesis is a process characterised by changes in factors that determine the structure of adipocyte (20). It is a process in which preadipocytes develop into mature adipocytes. This is a multistep process controlled by various transcriptional factors (15). The two factors that have a pronounced effect on this synthesis are Peroxisome proliferator-activated receptor-gamma and CCAAT/enhancer-binding proteins-beta (21). CCAAT/enhancer-binding proteins-beta genes are rapidly induced to express which then activate Peroxisome proliferator-activated receptor-gamma (22). Peroxisome proliferator-activated receptor-gamma can initiate adipogenesis program, giving rise to fat cells by activating the adipogenic genes responsible for adipogenesis (23). In our study increased levels of both Peroxisome proliferator-activated receptor-gamma and CCAAT/enhancer-binding proteins-beta were observed in group II( HFD) compared to group I (Normal diet) which has lead to increased adipogenesis evident from the histopathological studies which indicate increase in fat depots of adipose tissue (Table I and Fig 1 and 2) . The adipokines which keep the adipogenesis at check by reducing lipogenesis and favouring lipolysis are leptin and adiponectin which are drastically reduced in hyperlipidemia (24) (Table II). The deficiency of leptin or leptin receptor is seen in animals fed with high fat diet which leads to extreme obesity (25) (Fig 3). Adiponectin is a peptic hormone which decreases serum FFA, glucose, and triacylglycerol concentrations in the adipose tissue (26). However adiponectin concentrations fall with increasing obesity which was observed in group II (HFD) mice (Table II, Fig 4) which indicated both decreased adiponectin and leptin levels. The herbal drug Terminalia chebula is more efficient than Gallic Acid in increasing the levels of both adiponectin and leptin which is evident from their levels in group III (HFD+GA) and group IV (HFD+TC) and thereby decreasing adipogenesity. ( Fig 3 and 4) However, the Tumor necrosis factor-alpha (TNF alpha) a multifunctional cytokine which exerts a series of biological actions on adipose and regulates or interfere with adipocyte metabolism by regulating fatty acid metabolism (27) is downregulated more effectively by Terminalia chebula than pure compound Gallic Acid. (Table II and Fig 5). Our study indicates that herbal treatment with Terminalia chebula brings about a reduction in fat content of adipose as it reduces adipogenesis by down-regulating the transcription factors, Tumour necrosis factor α, and oxidative stress markers and brings about lipid breakdown or lipolysis by increased production of adiponectin and leptin more effective than pure compound Gallic Acid. Conclusion These results suggest that Terminalia chebula could decrease adipose tissue mass by down-regulation of transcriptional factors- Peroxisome proliferator-activated receptor-gamma, CCAAT/enhancer-binding proteins-beta, Pro-inflammatory cytokine-TNF α, Oxidative stress markers - 4-Hydroxy-2-nonenal, Thioredoxin and upregulation of adipokines that favor lipolysis - adiponectin and leptin. This effect has been far more pronounced than group III mice treated with Pure compound Gallic Acid (50 mg-Kg body wt)). Further, to confirm the anti-adipogenic activity of Terminalia chebula more effective than Gallic Acid by histopathological examination of adipose tissue. The following results prove Terminalia chebula a more potent antihyperlipidemic factor than pure compound Gallic Acid.       Acknowledgement          The authors acknowledge the immense help received from the scholars whose article cited and included in references of this manuscript. The authors are also grateful to authors/editors/publishers of all those articles, journals and books from where the literature for this article has been reviewed and discussed. Authors acknowledge the immense help received from the scholars whose articles are cited and included in references of this manuscript. The authors are also grateful to authors / editors / publishers of all those articles, journals and books from where the literature for this article has been reviewed and discussed. Conflict of interest : nil Financial Support : nil Ethical Clearance : (IAEC/XLVIII/SRU/495/2016) Englishhttp://ijcrr.com/abstract.php?article_id=2491http://ijcrr.com/article_html.php?did=2491 Asmare Amuamuta Bahir Dar, 2014, A Review on Risk Factors/Indicators and Effects of Hyperlipidemia. Middle-East Journal of Scientific Research 22 (6): 886-893. Bragg DA, Walling A , 2015, Metabolic Syndrome: Hyperlipidemia. FP Essent.;435:17-23. 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Curr Cardiol Rev, 6(4): 309-324. Benson T. Akingbemi , 2013, G Protein-Coupled Receptors in Energy Homeostasis and Obesity Pathogenesis. Progress in Molecular Biology and Translational Science Volume 114, Pages 317-342 William P. Cawthorn and Jaswinder K. Sethi, 2008, TNF-α and adipocyte biology. FEBS Lett.  582(1): 117-131. Sanet van Zyla et al, 2017, The relationship between obesity, leptin, adiponectin and the components of metabolic syndrome in urban African women, Free State, South Africa. South African Journal of Clinical Nutrition 30(3):68–73. Snehal S. Patel and Ramesh K. Goyal , 2011, Cardioprotective effects of gallic acid in diabetes-induced myocardial dysfunction in rats. Pharmacognosy Res 3(4): 239–245. Rubaiat Nazneen Akhand et al , 2013 , Sub-chronic oral administration of the ethanolic extracts of dried Terminalia chebula  mature fruits in streptozotocin (STZ)-induced type 2 diabetes mellitus (T2DM) model of  Long-Evans (L-E) rats improve glycemic, lipidemic and anti-oxidative status. Journal of Applied Pharmaceutical Science Vol. 3 (05), pp. 027-032. Priya F, Velpandian V, Ayyasamy S, Pitchiahkumar M , 2013 , Hypolipidemic activity of Kadukkai Chooranam (Terminalia chebula) in Triton WR - 1339 induced hyperlipidemic rats. Journal of Pharmacy and Biological Sciences (IOSR-JPBS) Volume 5, Issue 5 PP 77-84. Aus TariqAli , 2013 ,Adipocyte and adipogenesis, Volume 92, Issues 6–7,  Pages 229-236. Hai-LuZhao et al, 2008, Fat redistribution and adipocyte transformation in uninephrectomized rats. Kidney International Volume 74, Issue 4, 2 August 2008, Pages 467-477. Mark P. 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Radiance Research AcademyInternational Journal of Current Research and Review2231-21960975-52411010EnglishN2018May30Life SciencesUnusual Changes in Stratospheric Ozone and Water Vapor Over Antarctica and its Relation to Mesosphere Dynamics during a Minor Sudden Stratosphere Warming English5358G. Venkata ChalapathiEnglish S. EswaraiahEnglish P. Vishnu PrasanthEnglish Jaewook LeeEnglish K. Niranjan KumarEnglish Yong Ha KimEnglish Objective: Usually, the stratospheric ozone will show its significance in the variability of mesospheric tides in normal days over the low-latitude region. But during sudden stratosphere warmings, the water vapor and ozone over the polar region will change and shows some different effects on mesosphere tides. In the present study, we have provided the unusual changes in both water vapor and ozone over Antarctica and their role in altering the mesospheric tides. Method: Using MLS data in the stratosphere and Rothera (68oS, 68oW) MF radar observations in the mesosphere, the variability of Antarctica ozone and H2O during sudden stratospheric warming (SSW) winter 2010, and their influence on mesosphere dynamics has presented. The unusual increment of ozone reduction is noticed and consequent enhancement in H2O and HNO3 is also observed during the warming period. Mesospheric tidal components (diurnal, semi-diurnal and terr-diurnal) have been estimated using the hourly wind data from the MF radar. Result: The unusual changes in H2O and Ozone were observed during the warming period the similar behavior was observed in semi-diurnal tidal components during 2010 winter and their relation to ozone enhancement is discussed. Conclusion: The observations indicate that the enhancement of H2O and HNO3 leads to produce the ozone during warming period and hence the increment in ozone reduction is achieved over the polar region. Further, the enhancement of Brewer- Dobson mean circulation was clearly noticed through ozone transport during the warming period. The tidal enhancement after the SSW could be due to the non-linear interaction between planetary waves and tides. EnglishSudden Stratospheric Warming, Ozone and H2O variability, Mesospheric Tides, MF RadarIntroduction             It is well known that in the winter polar stratosphere, stratospheric sudden warming (SSW) occurs as a result of the interactions between vertically propagating planetary waves and the zonal winds (15). Ozone destruction occurs over both the polar regions in local winter-spring. In the Antarctic, essentially complete removal of lower-stratospheric ozone currently results in an ozone hole every year (14). In the winter polar lower stratosphere, low temperatures induce condensation of water vapor (H2O) and nitric acid (HNO3) into polar stratospheric clouds (PSCs). Further, it is understood that PSCs along with cold aerosols provide surfaces for heterogeneous conversion of chlorine from longer-lived reservoir species, such as chlorine nitrate (ClONO2) and hydrogen chloride (HCl), into reactive (ozone-destroying) forms, with chlorine monoxide (ClO) predominant in daylight (20). In the Antarctic, enhanced ClO is usually present for 4-5 months (through to the end of September) (19), leading to the destruction of most of the ozone in the polar vortex between 14 and 20 km altitude. Understanding the variabilities of H2O and ozone in particular during the SSW events is important to understand the variabilities of mesospheric tides, as the forcing of the semi-diurnal tide, in particular, is mainly due to the absorption of ultraviolet radiation by ozone in the stratosphere and mesosphere. Few studies have been established on the tidal variabilities at high-latitudes in relation to the major SSW events over NH hemisphere (2,12). Such studies over SH hemisphere are sparse. It is well established that ozone reduction takes place in the polar region especially in Antarctica region and hence ozone hole during winter. The chemistry of ozone formulation and its reduction during normal year winters and during 2010 minor SSW period is well explained by de Latt et al. (5). In their study, they identified that ozone reduction has been enhanced during the 2010 winter period. In the present study, we are going to explain how this ozone enhancement during 2010 winter will affect the tides in the MLT (Mesosphere lower thermosphere) region. Such study was not done so far, for the first time we are providing in detail study on the variability of MLT tides during the minor event occurred in 2010. Data In the present study, we make use of stratospheric zonal winds and temperatures obtained from ERA-Interim reanalysis datasets provided by the European Center for Medium-range Weather Forecasts (ECMWF) (1) for the evaluation of 2010 minor SSW event. The water vapor and ozone profiles are retrieved from Microwave Limb Sounder (MLS) and mesosphere tides from Rother MF (Medium Frequency) radar. Methodology The ERA-Interim reanalysis provides the data between the pressure levels 1000 and 1 hPa (~0-48 km) with a latitudinal and longitudinal grid of 1.5o × 1.5o. We have utilized zonal mean temperature and zonal winds at 10 hPa. Earth Observing System (EOS) Microwave Limb Sounder, hereafter called MLS, is one of the four instruments aboard NASA’s Aura satellite, and it has a radiometer that retrieves temperature from the bands near the O2 spectral line at 118 and 239 GHz. It measures the temperature from 316 to 0.001 hPa pressure levels with a track resolution of 230 km, which includes the global coverage from 82oS to 82oN with ~ 15 orbits per day, providing ~30 samples daily for given latitude. Details of the MLS and temperature validation are given in Schwartz et al. (17). In the present study, we have used the H2O, HNO3, temperature, and ozone (O3) profiles derived at 80oS. To study the mesosphere dynamics during the 2010 minor SSW period, we used a Rothera MF Radar (68oS, 68oW) wind measurements, which is a coherent, spaced-antenna system and has been operated since 1997. The radar has a transmitting power of 25 kW at a frequency of 1.98 MHz and provides winds in the mesosphere at 4 km altitude resolution every hour (11). The hourly wind profiles during 2010 have been used in the present analysis. Results and Discussion Evolution of 2010 SSW in SH Fig. 1 depicts daily zonal mean temperature at 80oS (Fig.1a) and zonal wind at 60oS (Fig.1b) obtained from ERA-Interim reanalysis dataset for the year 2010 observed at 10 hPa. The daily mean amplitude of PW of zonal wavenumber (k) 1 and 2 at 10 hPa over 60oS is displayed in Fig.1c. The PW amplitudes of k=1 and k=2 were computed from the distribution of geopotential heights along the constant latitude. It is clear from the figure that during 2010 three episodic minor warming events occurred in early August (day 212), mid-September (day 259) and in the end of October (day 300), marked with dotted vertical lines. Though three episodic warmings occurred in 2010, September (day 259) event was the record one and influenced the mesosphere largely (6,7). During 2010 the temperature indicates that the warming lasted for more than eight days with temperature increases of ~10-15K from the normal days and the second event (day 259) was the most noticeable. The zonal wind was weakened by ~20-25 m/s in each episodic warming. During 2010 minor SSW, the amplitude of PW (k=2) over 60oS was comparable to that of PW (k=1) during the first episodic warming (Fig.1c) and later PW (k=1) is stronger than PW (k=2). Further, the PW (k=1) amplitude during 2010 winter was weaker than the 2002 major SSW, and hence the PW interaction with the mean flow may lead to only deceleration, not a reversal, of zonal wind over 60oS at 10 hPa (Fig. 1b).  Reduction in ozone destruction: 2010 SSW Figure 2 presents the daily mean variability of HNO3, H2O and O3 for the 2010 minor SSW year and also other years at different heights (~22, 32 and 68 hPa) derived from MLS measurements at 80oS. H2O is given in parts per billion (ppbv) and ozone is given in parts per million (ppmv). Further, the five-day running mean was functional in order to reduce noise if any of the data and to obtain better clarity in comparison with different years. In the figure top panel shows the HNO3, H2O variability at mid stratosphere ~22 hPa (25 km) and corresponding ozone (Figs.(2)a)-2(c)), lower two panels show the similar behavior at lower stratosphere ~32 hPa (23.5 km) and ~68 hPa (19 km)). From the figure, it is clear that the reduced photochemical ozone destruction is evident in 2010 at 25 km, during mid-August and in early September when the HNO3 and H2O are moderately increased and it could be due to an increase of stratopause temperatures during SSW. However, at lower stratosphere heights the process is continuing and following as usual winter trend and not affected by SSW and hence photochemical ozone destruction is unaffected. Usually, during winter, a strong polar vortex forms over Antarctica and it inhibits the mixing of warm mid-latitude air and enhances radiative cooling in absence of solar radiation. The average minimum winter temperatures over Antarctica will be~193K. If the temperature drops below~195 K, polar stratospheric clouds (PSCs) are formed in the Antarctica ozone layer. The most common type of PSCs forms from nitric acid (HNO3) and water (H2O). The PSC formation will occur on an average of 1-2 months in Arctic and 5-6 months in Antarctic regions. Once formed, PSC particles will undergo vertical transport to lower altitudes due to gravity, they trigger the chemical reactions (denitrification and dehydration) in the stratosphere and cause the highly reactive chlorine gas (ClO) to be formed, which catalytically destroys ozone. As long as temperatures remain sufficiently low, PSC formation will continue and hence the ozone destruction. However, once the sunlight increase due to season transition vortex warms, the PSC will disappear slowly and halogen spices are deactivated and hence the ozone reproduction starts. Both H2O and HNO3 in the stratosphere will affect directly or indirectly on ClO production in PSC reaction and reduce the amount of ClO production and hence reduce the ozone destruction. The clear mechanism for the reduction of photochemical ozone destruction at 22 hPa is shown in Fig. 3. The figure depicts five-day running mean MLS measurements of HNO3, O3, H2O and temperature as a function of time for the 2010 minor SSW year and other non-SSW years 2012,2013 at 22 hPa (~25 km), where the ozone reproduction is greater due to SSW effect compared to other lower altitudes. Once temperatures drop below the PSC formation temperature around the day 150 (~1 June), denitrification starts as evidenced by the decrease in HNO3. However, full denitrification will be reached within about 20 days. At the same time, the chlorine reservoir HCl is empty (18) due to chemical reactions of HCl on PSC’s. Usually, dehydration starts about 20 days later than denitrification as the pure ice formation temperatures are delayed by 20 days after PSC formation temperature. Due to decrease of solar isolation in August (~day225) ozone is being destroyed slowly by halogens as ClO start to increase around day 225. When ClO is abundant around day’s 250-270 (mid-September), ozone destruction is maximum. During late winter /transition period starts (~day 270), temperatures increases to above the PSC formation threshold level, PSCs starts to evaporate and the active halogens are rapidly deactivated back into reservoir species like HCl. The slow increase in HNO3 and H2O starting around DOY 270 also shows that mixing is taking place. However, after day300 (~late October – early November) ozone slowly increases again, mainly by mixing of mid-latitude air. This behavior is very similar for all years but different in SSW years (2010). In contrast, during 2010 SSW, the warming occurred during late August (day 212) and mid-September (259) and lasted for about a week and significantly affected the mesosphere and thermosphere (6). However, in 2010 the chemical species and ozone are greatly affected by the warmings that occurred in the occurred in the stratosphere. For instance, during 2010 winter the first warming was noticed on the day 212 and the temperature was increased, even crossed the PSC threshold level and hence HNO3 and H2O suddenly raised and ClO decreases which result in an increase of HCl on the day212. The net photochemical chemical reactions result in increasing ozone around the day 250, instead of reduction; showing that catalytic ozone depletion at 22 hPa in 2010 is not unusual. In the following subsections, we will discuss, how these ozone increase around the days 250-270 affects the MLT dynamics. Sudden Stratospheric Warming-Ozone effects on the mesospheric tides  Fig.4 depicts the daily variability of zonal diurnal, semi-diurnal and terr-diurnal tides measured by Rothera MF radar during SH winter at 80 km. Fig. 4(a) shows the variability of tides in 2010 SSW year. Fig. 4(b) shows the variability of stratospheric ozone during 2010 SSW year and non-SSW years 2012, 2013, respectively. It is clear from the figure that the semi-diurnal tidal amplitude is increasing (~ 40 m/s) during last 15 days of the October (day 285-300). Usually, the tidal amplitudes are falling below 20 m/s in SH winter. The role of stratospheric ozone in coupling the low-latitude stratosphere and MLT region has been studied by Goncharenko, et al. (10). They suggested that the increase in the ozone density at 2 hPa (~ 43.5 km) lasts ~35 days following the SSW long after the downfall of PWs, causing enhancement in SDT amplitude. However, at the polar latitudes, the mechanism is different. The meridional circulation forced by PWs in the polar region during SSW leads to transport of ozone from pole to equator (9,16), and thus increases the peak ozone heating rate at ~ 43 km at low-latitudes, resulting in the amplification of SDT in the MLT region (10,13). As shown in Fig.4b, the ozone density at 22 hPa (the ozone is usually generated at this altitude) is gradually increasing in the winter from the day 200 onwards and attains maximum value during warming day (259) and after that it extremely deviates from the normal seasonal trend, except a small hike around the day 300. The variation in ozone trend in 2010 winter could be due to the strong B-D circulation forced by enriched PWs at polar region. The circulation transported the ozone from SH to NH high latitudes as a consequence of pole-pole circulation (Figure 1 of Butchart, 2014) or it could be transported to low latitudes. Alternatively, the ozone could be downward transported to lower altitudes in SH itself. The small upturn in the O3 density around the day 300 could be due to the minor warming that occurred on the day 300 (6). Since MLS satellite is located in a Sun-synchronous orbit, the zonal mean values of O3 might have been aliased with the migrating tides. Figure 5 indicates that even when ozone density is lower than the usual value, the SDTs are enhanced during the days 270-310. This may suggest that ozone alone may not play a dominant role in the amplification of tides over the Antarctic MLT region. Further, we also verified the O3 anomaly during 2010 SSW winter and 2012 non-SSW winter periods and presented in Figure 5.  It is clear from the figure (Fig.5a) that the ozone density is high at tropical region at starting of winter at 43 km (2 hPa), where the tides will generate and as soon as reaching peak warming day, the ozone is transported towards NH high-latitude region and more ozone is ascertained at 60oN, it could be due to B-D circulation at the stratosphere (Butchart, 2014, Figure 1). The B-D circulation at the stratosphere (~43 km) shown with a curved arrow in Fig.5(a) and the ozone density is comparatively low at ~ 60oS. In a normal year (Non-SSW) (Fig.5(b)) the circulation was not observed, and the usual trend was apparent at 43 km. It states that the strong mean circulation forced by enriched PWs at polar region, transported the ozone from SH to NH high latitudes as a consequence of pole-pole circulation (Butchart,2014) or it could be downward transported to lower altitudes at SH itself. So, we may conclude that the enhancement of SDT amplitudes at high-latitudes are due to different effect than those observed at low latitudes (4,8,21). It tells that, the effect of ozone and water vapor is less significant on the Antarctic mesospheric tides. Thus, the above discussion suggests that the enhancement in SDT amplitudes could be due to the PWs-tidal interaction. Conclusions             In the present communication, we described the variability of Antarctica ozone and H2O during the winter period of 2010 SSW year, and their influence on mesospheric tides. The tidal components (diurnal, semi-diurnal and terr-diurnal) in the MLT region have been estimated using the hourly wind data from both Rothera (68oS, 68oW) MF radar. The main findings are summarized as follows; In 2010, we noticed record minor stratosphere warming (SSW) in mid-September (day 259) using ERA-interim data analysis. It is noticed that the stratosphere chemistry below 50hPa is not affected by SSW. The chemical species ClO, H2O, HNO3 plays a key role in destruction (ClO) and reconstruction (H2O, HNO3) of ozone in the middle and upper stratosphere.  Though the SSW occurs during the days 250-270, the Ozone will not rise due to ozone destruction element ClO element is abundant even when H2O, HNO3 slowly increasing (Fig.3). During the days 270-300 the ClO is falling rapidly and H2O and HNO3 increase shows the vertical mixing and produces more ozone. The unusual behavior was observed in semi-diurnal tidal components during SSW year 2010. The Semi-diurnal tidal enhancement is noticed during the days 270-310, irrespective of the day of peak warming occurred in 2010. The reason why tidal amplitudes are enhancing during the days 270-300, may be explained like this: Since the ozone destruction between 20-25 km is reduced to 60% during SSW years compared to other years and the recovery of ozone is fast between the days 270-300 due to downward transport of chemical species, rather than horizontal mixing, and transport of humid rich air (H2O) and hence change in vertical propagating tides. However, the effect could be low since the ozone density is less during the days 270-300.                  The above discussion suggests that though the ozone destruction is reduced during SSW period, ozone alone cannot affect the tidal enhancement, it may be due to planetary wave (PW)-tidal interaction. To quantify this, issue the non-linear interaction between tides-and PWs should be discussed. Acknowledgements: We deeply appreciate the ERA-Interim and MLS team for providing the data used in the present study. SE acknowledges for financial support by the Korea Polar Research Institute (PE17020), Korea and Chungnam National University, Daejeon, Korea. Our sincere thanks to Prof. Dennis Riggin for providing the Rothera MF radar data.  Authors acknowledge the immense help received from the scholars whose articles are cited and included in references of this manuscript. The authors are also grateful to authors / editors / publishers of all those articles, journals and books from where the literature for this article has been reviewed and discussed. Figure 1. (a) Daily variation of zonal mean Polar Stratospheric Temperature (PST) at 10 hPa over 80oS. (b) Daily variation of zonal mean zonal wind at 10 hPa over 60oS during 2010 minor SSW. (c) Planetary wave amplitude of zonal wavenumbers 1 and 2 at 10 hPa over 60oS. The dashed horizontal line in (b) indicates zero wind line and the dashed vertical line indicates the warming periods in 2010. Figure 2. Daily mean variability of HNO3, H2O and Ozone (O3) in the stratosphere using MLS measurements during normal years (2012, 2013) and comparison with minor warming event year (2010) at 22 hPa (a-b), at 32 hPa (d-f), and at 68 hPa (g-h). All profiles are at ~ 80oS. Figure 3. The five-day running mean MLS measurements of H2O, HNO3, O3 and temperature at ~ 22hPa for the years 2010,2012 and 2013 during DOY 100-350. All profiles are at ~ 80oS. Figure 4. (a)Variability of diurnal, semi-diurnal and terr-diurnal zonal components measured by Rothera MF radar (68oS,68oW) during 2010 SH winter at 80 km, (b) daily mean variability of Ozone (O3) in stratosphere using MLS measurements during Non-SSW years (2012,2013) and comparison with minor warming event years (2010) at 22 hPa. All profiles are at ~ 80oS. Vertical lines indicate the day of peak warming. Figure 5.  Zonal mean ozone mass mixing ratio anomaly (ppmv) profiles calculated from the south pole to north pole at 2 hPa (~43 km) altitude for the SSW year 2010 (Top Panel) and the non-SSW year 2012 (bottom panel). The vertical line indicates the day of peak warming. The horizontal line indicates 60o latitude. Curved arrow in top panel shows the transport of ozone due to mean circulation. Englishhttp://ijcrr.com/abstract.php?article_id=2492http://ijcrr.com/article_html.php?did=2492 Berrisford, P., Dee, D., Fielding, K., Fuentes, M., Kallberg, P., Kobayashi, S. , Uppala, S., 2009. The ERA-interim archive. European Centre for Medium Range Weather Forecasts. Shinfield Park, Reading, Berkshire RG2 9AX, United Kingdom, pp. 1–16. Bhattacharya, Y., Shepherd, G. G., & Brown, S.,2004. Variability of atmospheric winds and waves in the Arctic polar mesosphere during a stratospheric sudden warming. Geophysical Research Letters, 31(23), L23101. Butchart, N., 2014. The Brewer-Dobson circulation. 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An unusual reduction in the mesospheric semi-diurnal tidal amplitude over Tirunelveli (8.7°N, 77.8°E) prior to the 2011 minor warming and its relationship with stratospheric ozone. Journal of Atmospheric and Solar-Terrestrial Physics, 89(Supplement C), 27–32. https://doi.org/10.1016/j.jastp.2012.07.012 Figure captions: Figure 1. (a) Daily variation of zonal mean Polar Stratospheric Temperature (PST) at 10 hPa over 80oS. (b) Daily variation of zonal mean zonal wind at 10 hPa over 60oS during 2010 minor SSW. (c) Planetary wave amplitude of zonal wavenumbers 1 and 2 at 10 hPa over 60oS. The dashed horizontal line in (b) indicates zero wind line and the dashed vertical line indicates the warming periods in 2010. Figure 2. Daily mean variability of HNO3, H2O and Ozone (O3) in the stratosphere using MLS measurements during normal years (2012, 2013) and comparison with minor warming event year (2010) at 22 hPa (a-b), at 32 hPa (d-f), and at 68 hPa (g-h). All profiles are at ~ 80oS. Figure 3. The five-day running mean MLS measurements of H2O, HNO3, O3 and temperature at ~ 22hPa for the years 2010,2012 and 2013 during DOY 100-350. All profiles are at ~ 80oS. Figure 4. (a) Variability of diurnal, semi-diurnal and terr-diurnal zonal components measured by Rothera MF radar (68oS,68oW) during 2010 SH winter at 80 km, (b) daily mean variability of Ozone (O3) in stratosphere using MLS measurements during Non-SSW years (2012,2013) and comparison with minor warming event years (2010) at 22 hPa. All profiles are at ~ 80oS. Vertical lines indicate the day of peak warming. Figure 5.  Zonal mean ozone mass mixing ratio anomaly (ppmv) profiles calculated from the south pole to north pole at 2 hPa (~43 km) altitude for the SSW year 2010 (Top Panel) and the non-SSW year 2012 (bottom panel). The vertical line indicates the day of peak warming. The horizontal line indicates 60o latitude. Curved arrow in top panel shows the transport of ozone due to mean circulation.