Progressive decline in β-cell function and β-cell mass is associated with prolonged exposure to insulin resistance environment in patients of T2DM, more prominently in obese diabetics at the level of skeletal muscle, adipose tissue and liver. Here, a review of the available evidences of therapeutic regimes to preserve and maintain the lifespan of β-cells of pancreas has been made. BACKGROUND DM is now considered one of the most common noncommunicable diseases in the world causing 5% of all deaths per year. Regardless of its aetiology, the end point of DM is β-cell death. Therefore, new therapies should aim at preventing β-cell death and promote β-cell regeneration in patients in order to improve blood glucose without treatment-derived side effects. Deterioration in β-cell function and mass in type 2 diabetics is progressive. Only about 50% of normal islet function remains at the time of diagnosis and a reduction in β-cell mass of about 60% was shown at necropsy. Accelerated apoptosis is considered as the cause of the reduction of β-cell mass. The major factors for progressive loss of β-cell function and mass are glucotoxicity, lipotoxicity, overstimulation, proinflammatory cytokines, leptin and islet cell amyloid deposition. Impaired β-cell function and possibly reduced β-cell mass appear to be reversible, particularly at early stages of the disease. Insulin resistance and β-cell dysfunction both play important roles in the development and progression of T2DM. KEYWORDS(1) It is evident that while insulin resistance lays the foundation for glucose intolerance, the progression to T2DM does occur in parallel to a degree of β-cell dysfunction, allowing Blood Glucose (BG) levels to rise. (2) Analysis of the results of the UKPDS and those of other studies suggests that pertaining to the diagnosis of T2DM, decreasing β-cell function is almost entirely responsible for progression of the disease. (3) At time of entry into the UKPDS, those who were newly diagnosed with diabetes had a reduction in insulin sensitivity of approximately 40% and a reduction in β-cell function of approximately 50%. Over the course of the study, however, β-cell function continued to decline as calculated by Homeostasis Model Assessment (HOMA), while insulin sensitivity remained relatively constant. Pharmacological interventions utilised in the UKPDS were largely unsuccessful

BACKGROUND AND OBJECTIVEManipur is a state located in North Eastern part of India with a huge burden of people living with HIV/AIDS. Studies of cause of death in this group of people is of utmost importance to determine the preventive strategies and to derive prognosis and to compare with trends in other parts of India and World. This study was conducted among the patients who were admitted to JNIMS Hospital.

BACKGROUND AND OBJECTIVES Stroke is a common cause of chronic debilitating disease as a result of the vascular related effect of certain part of the brain. Also the mortality due to the nature of stroke either Intracerebral Haemorrhage (ICH) or Cerebral Infarction (Ischaemic stroke) vary, the earlier causing more fatality. The risk factors of the ICH or the Ischaemic stroke vary to certain degree. Glycaemic state of stroke patients affects the outcome of them. It is of importance to establish clinical correlation of the glycaemic status of the stroke patients with the type and extent of the lesion documented by Computerised Tomography (CT) scan of brain for development of preventive measures and clinical management of such patients for better outcome. Hence, this study was conducted among stroke patients who were admitted in Medicine wards, Jawaharlal Nehru Institute of Medical Sciences (JNIMS), Porompat, Manipur. DATA AND METHODS A study of stroke cases was undertaken in patients who were admitted to Medicine wards, Jawaharlal Nehru Institute of Medical Sciences (JNIMS), Porompat, Manipur from January 2011 till December 2014. All the patients were investigated with CT scan brain, Blood sugar along with Glycosylated Haemoglobin (HbA1C) besides other routine tests and recorded. RESULT Out of the 200 stroke patients registered in 48 months, 120 patients were having hyperglycaemia. All the patients with stress hyperglycaemia were haemorrhagic. 85.71% of the cases among known diabetes were also haemorrhagic. CONCLUSION Glycaemic state of patients presented in stroke gives a picture of clinical difference. The size of the lesion measured by CT scan of brain also varies among different types of hyperglycaemia and the prognosis of the patients and showed that those patients with higher glucose level had haemorrhagic lesions with bigger size and had higher mortality rate. The deteriorating glucose tolerance with age also contributes to the increased incidence of stroke with age. The newly diagnosed diabetics also had higher mortality rate and it indicates the importance of early detection of diabetes and stress hyperglycaemia and suggested the needful timely management of the glycaemic state of the patient to prevent or reduce the incidence of hyperglycaemia and related stroke.

BACKGROUNDAn appreciably large fraction of the population of Manipur has been diagnosed as HIV/AIDS positive and an increase in the number of patients with HCV co-infection was observed, that led to dilemma of ART initiation at the background of liver problem. This study was taken up to solve such dilemma.

Sarcoidosis is a granulomatous lesion affecting multi organs, mainly the lungs, kidney, skin, lymph nodes etc. occurring mainly in African American blacks and Nordics. A 45 year old female presented with progressively increasing generalised skin eruption, fatigue and joint pains. Further work up of the patient reveals Hypothyroidism, Rheumatoid factor positive and Lipid profile showed isolated hypertriglyceridemia. CXR-PAV showed bilateral hilar lymphadenopathy. Calcium profile was normal. Bone marrow examination for anemia showed non-caseating well formed epithelioid granuloma strongly suggestive of Sarcoidosis. High ACE level of 114 clinched the diagnosis for Sarcoidosis. The patient responded to steroid and is on remission.