Altered Cortical Thicknesses of Left Pars Opercularis and Left Lateral Occipital Gyrus Can Be Associated with Psychotic Symptoms in Patients with Alzheimer's Disease

OBJECTIVE: The aims of this study was to present an association between the presence of psychotic symptoms and cortical thicknesses/subcortical volumes in patients with Alzheimer's disease (AD). METHODS: Fourteen AD patients with psychotic symptoms and 41 without psychotic symptoms underwent 3T MRI scanning. After adjusting the effects of confounding variables, the cortical thicknesses were compared between the AD patients with and without psychotic symptoms in multiple regions, across the continuous cortical surface. In addition, the subcortical volumes were compared with a structure-by-structure manner. RESULTS: AD patients with psychotic symptoms were characterized by significant smaller cortical thickness of left pars opercularis (F=4.67, p=0.02) and left lateral occipital gyrus (F=6.05, p=0.04) rather than those without psychotic symptoms, after adjusting the effects of age and scores on the Stroop test, non-psychotic items of Neuropsychiatry Inventory and Clinical Dementia Rating, triglyceride level and total intracranial volume. However, there were no significant differences in the subcortical volume between the two groups. CONCLUSION: These results suggest that AD psychosis may reflect more severe deterioration of neuropathologic change in specific brain region.

The Expressions of iNOS and the Effects of iNOS Inhibitor in the Rats of Cisplatin Induced Nephrotoxicity / 대한비뇨기과학회지

PURPOSE: This study was designed to investigate the role of NO in cisplatin induced nephrotoxicity of rats, especially in association with expressions of inducible nitric oxide synthase(iNOS) and the effects of iNOS inhibitor. MATERIALS AND METHODS: Male, Sprague-Dawley rats weighing 170-190gm were used. Nephrotoxicity was induced by single intraperitoneal administration of cisplatin(10mg/kg). Aminoguanidine sulfate (300mg/kg), a relatively specific iNOS inhibitor, was administrated 30 minutes prior to cisplatin administration. Individual kidneys were obtained from control, cisplatin single treated and cisplatin combined with aminoguanidine treated rats at 6, 12, 24, 48, 72hours and 7days after cisplatin administration. Serum BUN/creatinine(mg/dl), the unit weight of rat kidney (kidney wet weight/body weight) were estimated. HE stain was performed for histologic evaluation of nephrotoxicity. The expressions of iNOS were assessed by Western blotting and RT-PCR. RESULTS: Serum BUN/creatinine levels in aminoguanidine treated groups were suppressed its increment significantly at 12, 24 and 48 hours compared with cisplatin single treated groups (p<0.05). The unit weight of kidneys in aminoguanidine treated groups were decreased significantly at 24 and 48hours compared with cisplatin single treated groups (p<0.05). Western blotting represents intense iNOS protein bands (117KDa) at 24,48 and 72hours in cisplatin single treated groups. RT-PCR assay for iNOS mRNA (429bp) were weakly expressed in control groups and intense expressions were identified cisplatin single treated and cisplatin combined with aminoguanidine treated groups at 6, 12, 24 and 72hours. CONCLUSIONS: From these results, it is suggested that cisplatin induced nephrotoxicity may be partly mediated by NO. Aminoguanidine may delay or suppress the cisplatin induced nephrotoxicity of rat kidney.