Effects of garlic on lipid metabolism were studied in three experiments using different aged male rats fed a diet containing 1% cholesterol or 15% lard. Lyophilized garlic was supplemented at 2% and 4% of the diet. Plasma glucose was not changed by dietary treatments. Rats fed cholesterol and lard diets increased plasma cholesterol and triglycerides compared to controls. Garlic decreased plasma cholesterol in cholesterol- and lard-fed rats, but decreased plasma triglycerides only in the lard-fed group. Garlic supplementation decreased very low density lipoprotein cholesterol and increased high density lipoprotein cholesterol. The liver weight, total liver lipid and cholesterol were increased in rats fed the cholesterol diet but a supplementation of garlic decreased those parameters by about 30%. Dietary cholesterol and lard decreased hepatic glucose-6-phosphate dehydrogenase and malic enzyme activities: the garlic supplementation further decreased these enzyme activities. Garlic feeding increased the excretion of the neutral steroids in both 16-week and 10-week-old rats and bile acids in only 16-week-old pair-fed rats. Garlic at the 2% level was similarly effective on lipid metabolism as at 4%. These results demonstrate that garlic increases the excretion of neutral and acidic steroids and exerts hypocholesterolemic effects in cholesterol-fed rats.

Abbreviations & AcronymsObjective: To determine the correlation between metabolic syndrome and the distribution of stone components in patients with urolithiasis. Methods: Between January 2007 and December 2010, renal or ureteral stones were collected from 712 patients (432 males, 280 females) who underwent surgical intervention at three hospitals in South Korea. Metabolic syndrome was defined according to the latest definition of the International Diabetes Federation, using ethnicity-and sexspecific cut-off values for central obesity. Patients were assessed by factors used in metabolic syndrome. All urinary stones were analyzed using infrared spectrophotometry and categorized according to their main component. Results:The patients' mean age was 55.9 years (range 19-93 years). Of the 712 patients, 347 (48.7%; 205 males, 142 females) had a diagnosis of metabolic syndrome. Calcium oxalate (71.5%), uric acid (15.3%), carbonate apatite (8.0%) and struvite (4.1%) calculi were found as the main stone components. Overall, the proportion of uric acid calculi was markedly higher in patients with rather than without metabolic syndrome (19.6 vs 11.2%; P = 0.002). However, the proportion of calcium oxalate, carbonate apatite and struvite calculi did not differ between the two groups. The multivariableadjusted odds ratio for uric acid calculi according to the metabolic syndrome components indicated that the presence of metabolic syndrome was associated with a 93% increased odds ratio of uric acid calculi compared with the absence of metabolic syndrome. Impaired fasting glucose and hypertriglyceridemia were independent risk factors for uric acid calculi. Conclusions: Metabolic syndrome is associated with a significantly increased risk of uric acid calculi development, especially those with impaired fasting glucose and hypertriglyceridemia.

What’s known on the subject? and What does the study add? We found that resistin, a member of adipokine family, is expressed in human prostate cancers and induces prostate cancer cell proliferation through PI3K/Akt signaling pathways. We are studying the effect of resistin on other urogenital tract diseases besides prostate cancer, and the relationship between other adipokines and the urogenital tract diseases. OBJECTIVES • To determine whether resistin, a novel adipokine, induces prostate cancer cell proliferation. • To identify the mechanisms underlying the activation of prostate cancer cells by resistin. MATERIALS AND METHODS • Semi‐quantitative reverse transcriptase‐polymerase chain reaction and immunohistochemical staining were performed to investigate the intensity of prostate epithelial resistin expression. • Human full‐length resistin gene (RETN) was transfected into the PC‐3 cells using the pEGFP‐N1 vector to assess the effect of overexpression of resistin in prostate cancer cell line PC‐3. • Various concentrations of human recombinant protein resistin were added to the hormone‐insensitive prostate cancer cell lines PC‐3 and DU‐145 for 48 h, and cell proliferation was assessed by a water‐soluble tetrazolium salt assay. RESULTS • Human prostate cancer cell lines PC‐3 and DU‐145 were found to express the human resistin mRNA. • Resistin protein was strongly detected in high‐grade prostate cancer tissue, whereas BPH or low‐grade prostate cancer tissue revealed fainter expression of resistin. • Cell proliferation was stimulated by both the full‐length resistin gene overexpression and resistin treatment. • Akt phosphorylation occurred after addition of resistin to PC‐3 and DU‐145 cells. LY294002, a pharmacological inhibitor of phosphatidylinositol 3‐kinase (PI3K), significantly inhibited PC‐3 and DU‐145 cell proliferation after resistin treatment. CONCLUSIONS • Resistin is expressed in human prostate cancers. • Resistin induces prostate cancer cell proliferation through PI3K/Akt signalling pathways. • The proliferative effect of resistin on prostate cancer cells may account in part for prostate cancer progression.

In this cohort of healthy men hemodilution from increased plasma volume may be responsible for the observed decreased tumor marker concentration in men with a higher body mass index. In addition, an increase in body mass index may predict a lower tumor marker concentration in an individual.

PurposeFollowing the introduction of medical therapy for benign prostatic hyperplasia (BPH), we determined the effect of the change in trends in medical therapy on the indication and outcome of surgical intervention for BPH.Materials and MethodsWe compared the basic characteristics of, weight of resected tissue of, transfusions in, and postoperative complications of patients who underwent surgery between 1985 and 1989 (before the advent of medical therapy for BPH), between 1995 and 1999 (when medical therapy was developed and became widely used as alternative treatment), and between 2005 and 2009 (when medical therapy superseded surgical intervention to become first-line treatment and when combination therapy became widely adopted).ResultsAt our institution, the mean age and BMI of patients increased over the past two decades (p<0.001). Hypertension, operation history, and other comorbidities also increased significantly (p<0.001, p=0.005, and p<0.001, respectively). The indications for surgery in 1985 to 1989, 1995 to 1999, and 2005 to 2009 were as follows: acute urinary retention in 34.7%, 20.2%, and 15.1% of patients and symptomatic deterioration in 61.1%, 72.3%, and 73.0% of patients, respectively. Prostate volume and the weight of resected tissue increased from 34.4±14.5 ml to 61.3±32.4 ml and from 7.2±6.4 g to 10.8±7.6 g, respectively, over two decades. Patients who underwent surgery in 2005 to 2009 had their catheters removed earlier (p<0.001). Secondary hemorrhage within four postoperative weeks and repeat transurethral resection of the prostate within 1 year decreased significantly (p=0.03 and p=0.003, respectively). No statistically significant change in impaired detrusor contractility was found (p=0.523).ConclusionsAlthough patients who underwent surgery were older after widespread use of medical therapy for BPH, advancements in surgical techniques have benefitted these patients.

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The apoptotic effect of fluoxetine (FLX), an antidepressant, against human epithelial ovarian cancer cell lines OVCAR-3 and SK-OV-3 was investigated in relation to the mitochondria-mediated cell death process and nuclear factor (NF)-jB activation. FLX-induced mitochondrial membrane permeability change and formation of reactive oxygen species, leading to cell death. FLX-induced increase in mitochondrial Bax levels, decrease in cytosolic Bid and Bcl-2 levels, loss of the mitochondrial transmembrane potential, cytochrome c release, caspase-3 activation and up-regulation of p53. Oxidant scavengers and Bay 11-7085 [an inhibitor of nuclear factor kappaB (NF-jB) activation] prevented the FLX-induced cell death, increase in phosphorylated inhibitory jB-a and NF-jB p65 levels, and binding of NF-jB p65 to DNA. Results from this study suggest that FLX may exhibit apoptotic effect against ovarian cancer cell lines by inducing the mitochondrial membrane permeability change, which leads to cytochrome c release and subsequent caspase-3 activation, through reactive oxygen species-dependent activation of NF-jB.

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