The epidemiological and clinical features of NCPF have more similarity to IPH than has previously been documented. The development of spontaneous shunts tends to protect these patients from variceal bleeding.

Adamantinoma is a primary low-grade, malignant bone tumor that is predominantly located in the mid-portion of the tibia. The etiology of the tumor is still a matter of debate. The initial symptoms of adamantinoma are often indolent and nonspecific and depend on location and extent of the disease. Histologically, classic adamantinoma is a biphasic tumor characterized by epithelial and osteofibrous components that may be intermingled with each other in various proportions and differentiating patterns. To assure the histological diagnosis, pathologists should employ immunohistochemistry for demonstrating the sometimes sparse epithelial cell nests when the radiological features are suggestive of adamantinoma. There is paucity of compiled data over adamantinoma in the literature, hence authors tried to make a comprehensive review which must be of use to beginners and trained pathologists. Our objective is to further define the clinicoradiologic features and pathologic spectra of adamantinoma.

J. Neurochem. (2010) 112, 77–91. Abstract Several studies have indicated the involvement of oxidative stress in the development of diabetic neuropathy. In the present study, we have targeted oxidative stress mediated nerve damage in diabetic neuropathy using N‐acetyl‐l‐cysteine (NAC), a potent antioxidant. After 8 weeks, streptozotocin‐induced diabetic rats developed neuropathy which was evident from decreased tail‐flick latency (thermal hyperalgesia). This was accompanied by decreased motor coordination as assessed by performance on rota‐rod treadmill. Na+ K+ ATPase, a biochemical marker of development of diabetic neuropathy, was significantly inhibited in sciatic nerve of diabetic animals. NAC treatment at a daily dose between 1.4 and 1.5 g/kg body weight to diabetic animals for 7 weeks in drinking water ameliorated hyperalgesia, improved motor coordination and reversed reduction in Na+ K+ ATPase activity. There was an increase in lipid peroxidation in sciatic nerve of diabetic animals along with decrease in phospholipid levels, while NAC treatment attenuated lipid peroxidation and restored phospholipids to control levels. This was associated with decrease in glutathione and protein thiols. The activities of antioxidant enzymes; superoxide dismutase, catalase, glutathione reductase, glutathione peroxidase and glutathione‐S‐transferase were reduced in sciatic nerve of diabetic animals. Cytochrome c release and active caspase 3 were markedly increased in nerve from diabetic animals suggesting activation of apoptotic pathway. NAC treatment significantly ameliorated decrease in antioxidant defense and prevented cytochrome c release and caspase 3 activation. Electron microscopy revealed demyelination, Wallerian degeneration and onion‐bulb formation in sciatic nerve of diabetic rats. NAC on the other hand was able to reverse structural deficits observed in sciatic nerve of diabetic rats. Our results clearly demonstrate protective effect of NAC is mediated through attenuation of oxidative stress and apoptosis, and suggest therapeutic potential of NAC in attenuation of diabetic neuropathy.

Fine needle aspiration cytology (FNAC) of salivary gland lesions is a safe, effective diagnostic technique. Several amply illustrated reviews are available in the English literature. The reported diagnostic accuracy varies between 86% to 98%. The sensitivity ranges from 62% to 97.6% and specificity is higher from 94.3% to 100%. In this present study, we have analyzed 172 cases of salivary gland aspirates and the histopathological diagnosis was available in 45 cases. There was discordance in cytological and histopathological diagnosis in nine cases. Five cases had discrepancies in benign versus malignant diagnosis with four cases being false negative. The errors in these FNA diagnoses were due to sampling error, observational error and interpretational error. Therefore, this study illustrates high diagnostic accuracy of FNAC in salivary gland lesions and shows that FNAC offers valuable information that allows the planning of subsequent patient management.

Portal hypertension is characterized by an increase in portal pressure (> 10 mmHg) and could be a result of cirrhosis of the liver or of noncirrhotic diseases. When portal hypertension occurs in the absence of liver cirrhosis, noncirrhotic portal hypertension (NCPH) must be considered. The prognosis of this disease is much better than that of cirrhosis. Noncirrhotic diseases are the common cause of portal hypertension in developing countries, especially in Asia. NCPH is a heterogeneous group of diseases that is due to intrahepatic or extrahepatic etiologies. In general, the lesions in NCPH are vascular in nature and can be classified based on the site of resistance to blood flow. In most cases, these disorders can be explained

Necrotizing fasciitis is most often associated with bacterial infections. Zygomycosis is an uncommon infection causing necrotizing fasciitis. We report 18 such cases of zygomycotic necrotizing fasciitis, of these, 15 were immunocompetent. Of the eight cases cultured, five were positive for Apophysomyces elegans. A retrospective case review conducted at a tertiary referral center, from 1998 to 2004, 18 cases of fungal necrotizing fasciitis were diagnosed based on histomorphology of fungal organisms; and in few of the cases diagnosis was supported by mycologic culture reports. Of the total of 18 cases, culture report was available in eight cases, and out of which five of them grew A. elegans. Fifteen patients were immunocompetent. Clinical presentation, mycologic findings and histopathologic results were evaluated. A review of the literature pertaining to A. elegans infection was also done. Histopathologic examination showed broad, predominantly aseptate and occasional pauciseptate, thin-walled fungal hyphae with occasional angioinvasion. To the best of our knowledge, this is the first largest series of zygomycotic necrotizing fasciitis from India. Herein, we present data on 18 cases of necrotizing fasciitis assosiated with zygomycosis. Most of the cases in our series were immunocompetent. Nonsuppurative necrosis with presence of typical fungal profiles was important histologic feature. Zygomycosis must be considered in the differential diagnosis not only in immunocompromised patients but also in the absence of any underlying disorders.

Pulmonary embolism, though treatable, is a devastating disease and an important cause of morbidity and mortality among hospitalized patients. In all, 1000 autopsies were reviewed in adult medical patients. The overall incidence of pulmonary embolism in adult medical autopsies was 15.9% (159/1000). The incidence of pulmonary embolism contributing significantly to the death of the patients (groups 1 and 2) is 126/1000 (12.6%). Thus, pulmonary embolism very significantly contributed to death in 126/159 (79.24%) of group 1 and 2 patients. Pulmonary embolism affected a younger population as 79.87% of the overall patients, 66.67% of the fatal cases (group 1) and 73% of combined group 1 and 2 cases were below the age of 50 years. Sepsis was the primary diagnosis in 32% of total and in 42% of fatal cases. Hence, pulmonary embolism is considered as an important cause of death in patients admitted to the medical wards. It affects a younger population in India and needs to be tackled appropriately.

Animal models of copper toxicosis rarely exhibit neurological impairments and increased brain copper accumulation impeding the development of novel therapeutic approaches to treat neurodegenerative diseases having high brain Cu content. The aim of this study was to investigate the effects of intraperitoneally injected copper lactate (0.15 mg Cu/100 g body weight) daily for 90 days on copper and zinc levels in the liver and hippocampus, on biochemical parameters, and on neurobehavioral functions (by Morris water maze) of male Wistar rats. Copper-administered animals exhibited significantly decreased serum acetylcholinesterase (AChE) activity and impaired neuromuscular coordination and spatial memory compared to control rats. Copper-intoxicated rats showed significant increase in liver and hippocampus copper content (99.1 and 73 % increase, respectively), 40.7 % reduction in hepatic zinc content, and interestingly, 77.1 % increase in hippocampus zinc content with concomitant increase in copper and zinc levels in serum and urine compared to control rats. Massive grade 4 copper depositions and grade 1 copper-associated protein in hepatocytes of copper-intoxicated rats were substantiated by rhodanine and orcein stains, respectively. Copper-intoxicated rats demonstrated swelling and increase in the number of astrocytes and copper deposition in the choroid plexus, with degenerated neurons showing pyknotic nuclei and dense eosinophilic cytoplasm. In conclusion, the present study shows the first evidence in vivo that chronic copper toxicity causes impaired spatial memory and neuromuscular coordination, swelling of astrocytes, decreased serum AChE activity, copper deposition in the choroid plexus, neuronal degeneration, and augmented levels of copper and zinc in the hippocampus of male Wistar rats.