Diagnostic Utility of Epithelial Membrane Antigen (EMA) and Calretinin (CAL) in Effusion Cytology.

INTRODUCTION: Fluid cytology and subsequent utilization of immunocytology on cell block is being used commonly for increasing the diagnostic accuracy in effusion cytology. AIM: To do cytological analysis of fluids and evaluate the role of Epithelial Membrane Antigen (EMA) and Calretinin (CAL) to differentiate between reactive and malignant cell in pleural and peritoneal fluids. MATERIALS AND METHODS: This was a prospective study carried out in Department of Pathology, Shri Guru Ram Rai Institue of Medical and Health Science, for a period of 18 months from January 2014 to June 2015. A total of 253 samples of pleural and peritoneal fluid were studied by May-Gruenwald-Giemsa (MGG) stain and Papanicolaou (Pap) staining. In 73 cases which were suspicious for malignancy, cell blocks were prepared and IHC was done using two immunomarkers- EMA and CAL. RESULTS: A total of 253 cases of effusion cytology were studied out of which 73 were found positive for malignant cells. Maximum cases of malignant cells or atypical cells were seen in peritoneal fluid. A total of 34 cases were histologically positive for malignancy. All these cases showed strong membranous and cytoplasmic positivity for EMA. Most of cases also showed 2%-5% positivity for CAL. There were 38 cases categorized as atypical or reactive mesothelial cell hyperplasia. These cases showed nuclear and cytoplasmic staining for calretinin and none of these were positive for EMA, although 5 cases showed score 2-3, which was considered as negative. CONCLUSION: The distinction between reactive and malignant mesothelial cells in cytological specimens can be problematic. A combination of CAL and EMA may help in accurate diagnosis.

Hyperglycemia / hypoglycemia-induced mitochondrial dysfunction and cerebral ischemic damage in diabetics.

Enhancement of ischemic brain damage is one of the most serious complications of diabetes. Studies from various in vivo and in vitro models of cerebral ischemia have led to an understanding of the role of mitochondria and complex interrelated mitochondrial biochemical pathways leading to the aggravation of ischemic neuronal damage. Advancements in the elucidation of the mechanisms of ischemic brain damage in diabetic subjects have revealed a number of key mitochondrial targets that have been hypothesized to participate in enhancement of brain damage. The present review initially discusses the neurobiology of ischemic neuronal injury, with special emphasis on the central role of mitochondria in mediating its pathogenesis and therapeutic targets. Later it further details the potential role of various biochemical mediators and second messengers causing widespread ischemic brain damage among diabetics via mitochondrial pathways. The present review discusses preclinical data which validates the significance of mitochondrial mechanisms in mediating the aggravation of ischemic cerebral injury in diabetes. Exploitation of these targets may provide effective therapeutic agents for the management of diabetes-related aggravation of ischemic neuronal damage.