Preservation of frontal white matter tracts in ventricular surgery: favoring an anterior interhemispheric transcallosal approach vs a transcortical transfrontal transventricular approach

Neurosurgical Review - Secondary to the creation of a surgical corridor and retraction, white matter tracts degenerate, causing long-term scarring with potential neurological consequences. Third...     

Protein-Restricted diet alters concentration of plasma membrane glycoproteins in rat liver

Malnutrition is known to have adverse effects on the physiology and morphology of the liver. The aim of this investigation was to examine the effect of protein restriction on the content of plasma membrane proteins residing in the sinusoidal and bile canalicular domains of rat liver. Post-weanling rats maintained on low protein isocaloric diets showed marked growth retardation concomitant with reduced liver protein concentration compared to control animals. The content of leucine aminopeptidase, a bile canalicular enzyme, and asialoglycoprotein receptor, a sinusoidal receptor, in livers of protein-restricted rats was 66% and 50%, respectively, of control livers. In contrast, the relative concentrations of dipeptidyl peptidase IV and a cell adhesion molecule (GP 110), both canalicular proteins, were 160% and 121%, respectively, in rat livers upon protein restriction. After a 4-week rehabilitation period, the concentrations of all canalicular membrane proteins were similar to those in control livers, while the sinusoidal receptor was only 68% of control values. Protein restriction was found to adversely affect the concentrations of protein constituents, but not their localization in the hepatocyte plasma membrane. In general, altered concentrations of hepatocyte membrane proteins were reversed on the administration of a normal protein diet.     

Synthesis and in vitro antibacterial evaluation of novel imidazo[2',1':5,1]-1,2,4-triazolo[4,3-c]-quinazoline derivatives of 5-thioxo-1, 2, 4-triazole, 4-oxothiazolidine, and their open-chain counterparts

Two novel series of imidazo[2', 1':5, 1]-1, 2, 4-triazolo[4, 3-c]quinazolines bearing 5-thioxo-1, 2, 4-triazoles, 6a-f, and 4-oxothiazolidines, 7a-f, were synthesized from corresponding thiosemicarbazide derivatives, 5a-f. The stepwise methodology applied to the preparation of compounds 5a-f was initiated with reaction of the parent 3-amino-1, 2, 4-triazolo[4, 3-c]quinazolines, 2, with ethyl 2-chloroacetoacetate resulting in annelation of the imidazole ring to give esters, 3a-c. However, hydrazinolysis of these ester derivatives gave the corresponding acid hydrazides, 4a-c, which on reaction with the appropriate alkyl isothiocyanate yielded compounds 5a-f. In turn, compounds 5, were cyclized with potassium hydroxide or with ethyl bromoacetate to give the corresponding thioxotriazoles 6 and oxothiazolidines 7, respectively. All synthesized compounds were screened for their in vitro antibacterial activity against various Gram-positive and Gram-negative bacteria. Some test compounds were found to possess potent antibacterial activities. Compound, 7f, exhibited much higher potency than the reference standard ciprofloxacin, against both types of bacteria, particularly, Gram-positive organisms.     

Pathological characterization of occult hepatitis B virus infection in hepatitis C virus-associated or non-alcoholic steatohepatitis-related hepatocellular carcinoma

Occult hepatitis B virus (HBV) infection, by definition, is a state in which infection with this virus does not manifest with the conventional diagnostic laboratory criteria reserved for the obvious form of HBV infection. As a result, occult HBV infection is commonly a surprise finding discovered accidently during the evaluation of other apparent liver diseases, such as hepatitis C virus (HCV) infection or non-alcoholic fatty liver disease and, more importantly, their evolution into life-threatening hepatocellular carcinoma. As infection with HCV and occult HBV is rarely considered when assessing these more obvious conditions, and in an attempt to offer a better understanding of this phenomenon, this study attempted to shed some light onto the uniqueness of occult HBV infection by addressing the natural history of HBV and HCV infections, as well as non-alcoholic fatty liver disease. This was carried out by taking into account the exclusive integration process undertaken by the HBV genome into infected host hepatocytes, with consideration given to conditions which afford reactivation of the occult infection and stress on the molecular mechanisms that underlie occult HBV infection. Finally, the clinical outcome of occult HBV infection and its relation to hepatocellular carcinoma is analyzed.