Curcumin could be a potentially therapeutic anti-cancer agent, as it significantly inhibits prostate cancer growth, as exemplified by LNCaP in vivo, and has the potential to prevent the progression of this cancer to its hormone refractory state.

BACKGROUND. Earlier work from our laboratory highlighted the therapeutic potential of curcumin (turmeric), used as a dietary ingredient and as a natural anti-in¯ammatory agent in India and other Southeast Asian countries. This agent was shown to decrease the proliferative potential and induce the apoptosis potential of both androgen-dependent and androgenindependent prostate cancer cells in vitro, largely by modulating the apoptosis suppressor proteins and by interfering with the growth factor receptor signaling pathways as exempli®ed by the EGF-receptor. To extend these observations made in vitro and to study the ef®cacy of this potential anti-cancer agent in vivo, the growth of LNCaP cells as heterotopically implanted tumors in nude mice was followed. METHODS. The androgen-dependent LNCaP prostate cancer cells were grown, mixed with Matrigel and injected subcutaneously into nude mice. Experimental group received a synthetic diet containing 2% curcumin for up to 6 weeks. At the end point, sections taken from the excised tumors were evaluated for pathology, cell proliferation, apoptosis, and vascularity. RESULTS. Curcumin causes a marked decrease in the extent of cell proliferation as measured by the BrdU incorporation assay and a signi®cant increase in the extent of apoptosis as measured by an in situ cell death assay. Moreover, a signi®cant decrease in the microvessel density as measured by the CD31 antigen staining was also seen. CONCLUSIONS. Curcumin could be a potentially therapeutic anti-cancer agent, as it signi®cantly inhibits prostate cancer growth, as exempli®ed by LNCaP in vivo, and has the potential to prevent the progression of this cancer to its hormone refractory state. Prostate 47:293±303,

Many tumors readily convert l-glutamine to α-ketoglutarate. This conversion is almost invariably described as involving deamidation of l-glutamine to l-glutamate followed by a transaminase (or dehydrogenase) reaction. However, mammalian tissues possess another pathway for conversion of l-glutamine to α-ketoglutarate, namely the glutaminase II pathway: l-Glutamine is transaminated to α-ketoglutaramate, which is then deamidated to α-ketoglutarate by ω-amidase.Here we show that glutamine transaminase and ω-amidase specific activities are high in normal rat prostate. Immunohistochemical analyses revealed that glutamine transaminase K (GTK) and ω-amidase are present in normal and cancerous human prostate and that expression of these enzymes increases in parallel with aggressiveness of the cancer cells. Our findings suggest that the glutaminase II pathway is important in providing anaplerotic carbon to the tricarboxylic acid (TCA) cycle, closing the methionine salvage pathway, and in the provision of citrate carbon in normal and cancerous prostate. Finally, our data also suggest that selective inhibitors of GTK and/or ω-amidase may be clinically important for treatment of prostate cancer. In conclusion, the demonstration of a prominent glutaminase II pathway in prostate cancer cells and increased expression of the pathway with increasing aggressiveness of tumor cells provides a new perspective on 'glutamine addiction' in cancers.

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Background: Decompensated liver disease (DCLD) is associated with various cognitive changes. The present study aimed to estimate the prevalence, phenomenology, and course of delirium in decompensated liver disease patients. Methods: This prospective observational study was done on 111 patients admitted to the gastroenterology department with the diagnosis of DCLD. Richmond Agitation Sedation Scale (RASS) and confusion assessment method (CAM) were used to detect delirium for the first five consecutive days. Patients detected to be having delirium were administered a delirium rating scale (DRS) for the next seven days to evaluate the features of delirium. Descriptive analysis was carried out by mean and standard deviation for quantitative variables, frequency, and proportion for categorical variables. For normally distributed quantitative parameters, the mean values were compared using an independent sample t-test. Categorical outcomes were compared between study groups using the chi-square test. coGuide version V.1.0 was used for statistical analysis. Results: The prevalence of delirium among patients with DCLD was 34 (30.63%). All delirious patients continued to have delirium symptoms for the initial three days. Six patients remitted as early as the fourth day of DRS assessment, while nine patients continued to have delirium symptoms even by the seventh day of evaluation. Conclusion: Nearly one-third of patients with DCLD presented with delirium. They presented with insomnia, cognitive deficits, motor retardation, and minimal psychotic symptoms. Many patients completely recovered from delirium within a week, but a few had delirium up to the seventh day.