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Biomedical subjects

P Sodhi

Publications and source records attributed to P Sodhi.

7 recordsLinked to original sources

Fetus-in-fetu.

Fetus-in-fetu (FIF) is a rare congenital condition first described in early nineteenth century. In this anomaly, a malformed parasitic twin is found within the body of its partner. Less than 100 cases have been described in the English-language literature.

Female↗

Unusually severe ABO hemolytic disease of newborn.

ABO-hemolytic disease of newborn (ABO-HDN) is a common cause of neonatal hyperbilirubinemia. Most of the cases are however mild. We describe a neonate with ABO-HDN with unusually severe course.

Erythroblastosis, Fetal↗

Anaesthetic management of a patient with pemphigus vulgaris for emergency laparotomy.

A 45-year-old man with a long-standing history of duodenal ulcer presented with symptoms and signs of perforation peritonitis. He also had lesions of pemphigus vulgaris throughout the body, involving both skin and mucous membranes. Care was taken to avoid pressure and friction during placement of monitoring devices, intravenous and arterial lines. Since the patient had to undergo exploratory laparotomy, intubation was performed in an atraumatic manner after rapid sequence induction. However, there was minor bleeding from the mucous lesions of the oral cavity, which was controlled by a saline adrenaline throat pack. The patient was extubated at the end of the surgery and steroids were continued in the peri-operative period.

Anesthesia, General↗

Systemic or local administration of azide produces striatal lesions by an energy impairment-induced excitotoxic mechanism.

Sodium azide is an inhibitor of cytochrome oxidase which produces selective striatal lesions in both rodents and primates. In the present study we investigated the neurochemical and histologic effects of both intrastriatal and systemic administration of sodium azide, as well as the age dependence and mechanism of the lesions. Intrastriatal administration of sodium azide produced dose-dependent lesions. Neurochemical and histologic evaluation showed that markers of both spiny projection neurons (GABA, substance P) and aspiny interneurons (somatostatin, neuropeptide Y, NADPH-diaphorase) were equally affected. Subacute systemic administration of sodium azide resulted in lesions with a similar neurochemical profile; however, in contrast to intrastriatal injections there was sparing of dopaminergic striatal afferents. Prior decortication significantly attenuated lesions produced by intrastriatal administration of sodium azide, consistent with an excitotoxic process. Chronic administration of sodium azide for 1 month lead to striatal neuropathological changes. Lesions produced by intrastriatal administration of sodium azide in 1-, 4-, and 12-month-old animals showed age dependence. Both freeze-clamp measurements and chemical-shift magnetic resonance spectroscopy confirmed that sodium azide impairs oxidative phosphorylation in the striatum following either intrastriatal or systemic administration. These results show that the striatum is particularly vulnerable to oxidative stress produced by sodium azide, and that it produces striatal lesions by a secondary excitotoxic mechanism.

3,4-Dihydroxyphenylacetic Acid↗

Reduced apolipoprotein epsilon 4 allele frequency in the oldest old Alzheimer's patients and cognitively normal individuals.

Recent genetic studies show that the apolipoprotein E epsilon 4 allele (ApoE-epsilon 4) is a risk factor for Alzheimer's disease (AD). If ApoE-epsilon 4 individuals develop AD as they get older, we would expect a decrease in ApoE-epsilon 4 allele frequency with increasing age. We found a marked decline in ApoE-epsilon 4 allele frequency with advancing age in both AD and cognitively normal controls (p < 0.003), although in all age groups the ApoE-epsilon 4 allele was overrepresented (p < 0.0001). Nonetheless, a few cognitively normal nonagenarians were ApoE-epsilon 4 positive. Thus, our data support two new conclusions: (1) the ApoE-epsilon 4 associated risk for AD is age-dependent, probably due to censoring by the earlier development of AD in ApoE-epsilon 4 individuals, and (2) despite the ApoE-epsilon 4 associated risk for AD, it is possible to reach extreme old age with normal cognition.

Aged↗