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INTRODUCTIONGeneral surgeons dealing with laparoscopic herniorrhaphy should be aware of the aberrant obturator artery that crosses the superior pubic ramus and is susceptible to injuries during dissection of the Bogros space and mesh stapling onto Cooper’s ligament. The obturator artery is usually described as a branch of the anterior division of the internal iliac artery, although variations have been reported.MATERIALS AND METHODSThe present study was conducted on 98 pelvic halves of embalmed cadavers, and the origin and course of the obturator artery were traced and noted.RESULTSIn 79% of the specimens, the obturator artery was a branch of the internal iliac artery. It branched off at different levels either from the anterior division or posterior division, individually or with other named branches. In 19% of the cases, the obturator artery branched off from the external iliac artery as a separate branch or with the inferior epigastric artery. However, in the remaining 2% of the specimens, both the internal and the external iliac arteries branched to form an anastomotic structure within the pelvic cavity.CONCLUSIONThe data obtained in this study show that it is more common to find an abnormal obturator artery than was reported previously, and this observation has implications for pelvic surgeons and is of academic interest to anatomists. Surgeons dealing with direct, indirect, femoral, or obturator hernias need to be aware of these variations and their close proximity to the femoral ring.

Tarocystatin from Colocasia esculenta, a group‐2 phytocystatin, is a defense protein against phytopathogenic nematodes and fungi. It is composed of a highly conserved N‐terminal region, which is homological to group‐1 cystatin, and a repetitive peptide at the C‐terminus. The purified recombinant proteins of tarocystatin, such as full‐length (FL), N‐terminus (Nt) and C‐terminus (Ct) peptides, were produced and their inhibitory activities against papain as well as their antifungal effects were investigated. Kinetic analysis revealed that FL peptide exhibited mixed type inhibition (Kia = 0.098 μm and Kib = 0.252 μm) and Nt peptide showed competitive inhibition (Ki = 0.057 μm), whereas Ct peptide possessed weak papain activation properties. A shift in the inhibitory pattern from competitive inhibition of Nt peptide alone to mixed type inhibition of FL peptide implied that the Ct peptide has an regulatory effect on the function of FL peptide. Based on the inhibitory kinetics of FL (group‐2) and Nt (group‐1) peptides on papain activity, an inhibitory mechanism of group‐2 phytocystatins and a regulatory mechanism of extended Ct peptide have each been proposed. By contrast, the antifungal activity of Nt peptide appeared to be greater than that of FL peptide, and the Ct peptide showed no effect on antifungal activity, indicating that the antifungal effect is not related to proteinase inhibitory activity. The results are valid for most phytocystatins with respect to the inhibitory mechanism against cysteine proteinase.

Prebiotics alter bacterial content in the colon, and therefore could be useful for obesity management. We investigated the changes following addition of inulin oligofructose (IO) in the food of rats fed either a corn starch (C) diet or a high-carbohydrate, high-fat (H) diet as a model of diet-induced metabolic syndrome. IO did not affect food intake, but reduced body weight gain by 5·3 and 12·3 % in corn starch + inulin oligofructose (CIO) and high-carbohydrate, high-fat with inulin oligofructose (HIO) rats, respectively. IO reduced plasma concentrations of free fatty acids by 26·2 % and TAG by 75·8 % in HIO rats. IO increased faecal output by 93·2 %, faecal lipid excretion by 37·9 % and weight of caecum by 23·4 % and colon by 41·5 % in HIO rats. IO improved ileal morphology by reducing inflammation and improving the density of crypt cells in HIO rats. IO attenuated H diet-induced increases in abdominal fat pads (C 275 (SEM 19), CIO 264 (SEM 40), H 688 (SEM 55), HIO 419 (SEM 32) mg/mm tibial length), fasting blood glucose concentrations (C 4·5 (SEM 0·1), CIO 4·2 (SEM 0·1), H 5·2 (SEM 0·1), HIO 4·3 (SEM 0·1) mmol/l), systolic blood pressure (C 124 (SEM 2), CIO 118 (SEM 2), H 152 (SEM 2), HIO 123 (SEM 3) mmHg), left ventricular diastolic stiffness (C 22·9 (SEM 0·6), CIO 22·9 (SEM 0·5), H 27·8 (SEM 0·5), HIO 22·6 (SEM 1·2)) and plasma alanine transaminase (C 29·6 (SEM 2·8), CIO 32·1 (SEM 3·0), H 43·9 (SEM 2·6), HIO 33·6 (SEM 2·0) U/l). IO attenuated H-induced increases in inflammatory cell infiltration in the heart and liver, lipid droplets in the liver and plasma lipids as well as impaired glucose and insulin tolerance. These results suggest that increasing soluble fibre intake with IO improves signs of the metabolic syndrome by decreasing gastrointestinal carbohydrate and lipid uptake.

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Population studies have shown that compared to diabetic men, diabetic women are at a higher risk of cardiovascular disease. However, the mechanisms underlying this gender disparity are unclear. Our studies in young murine models of type 2 diabetes mellitus (T2DM) and cardiovascular disease show that diabetic male rats develop increased cardiac fibrosis and suppression of intracardiac anti-fibrotic cytokines, while premenopausal diabetic female rats do not. This protection from cardiac fibrosis in female rats can be an estrogen-related effect. However, diabetic female rats develop early subclinical myocardial deformation, cardiac hypertrophy via elevated expression of pro-hypertrophic miR-208a, myocardial damage, and suppression of cardio-reparative Angiotensin II receptor 2 (Agtr2). Diabetic rats of both sexes exhibit a reduction in cardiac capillary density. However, diabetic female rats have reduced expression of neuropilin 1 that attenuates cardiomyopathy compared to diabetic male rats. A combination of cardiac hypertrophy and reduced capillary density likely contributed to increased myocardial structural damage in diabetic female rats. We propose expansion of existing cardiac assessments in diabetic female patients to detect myocardial deformation, cardiac hypertrophy and capillary density via non-invasive imaging, as well as suggest miR-208a, AT2R and neuropilin 1 as potential therapeutic targets and mechanistic biomarkers for cardiac disease in females.Extensive clinical observations over the past decade have linked diabetes to cardiovascular disease (CVD) and concluded that an estimated 70% of the diabetic population die from CVD 1 . In the non-diabetic population, women typically develop CVD nearly a decade later than men. However, this sex difference in CVD is not seen after menopause, leading to the notion that estrogen 'protects' women from developing CVD. Importantly, results from the 20 year Framingham Study show that diabetic women, independent of age, are at significantly higher risk of developing CVD compared to age-matched men, which suggests a deviation from the theory that women are 'protected' from CVD due to elevated estrogen 2,3 . In fact, subsequent long-term clinical studies show that diabetic women are an increased risk-group for CVD compared to age-matched non-diabetic women and diabetic men [4][5][6][7][8][9][10][11][12][13] . The mechanisms underlying the increased CVD risk in diabetic women and their poorer outcomes, compared to their male counterparts, are unknown and require further characterization.In order to investigate these mechanisms, as well as better characterize the biological sex-based differences in diabetes and CVD development, we compared several key cardiac functional and metabolic parameters between four cohorts comprised of healthy male and female Zucker Lean (ZL) rats and hyperglycemic male and female Zucker diabetic fatty (ZDF) rats. ZL males (ZL-M) and ZDF males (ZDF-M) have been extensively characterized [14][15][16][17] . While ZDF-M have similar body weights a...

Increased seaweed consumption may be linked to the lower incidence of metabolic syndrome in eastern Asia. This study investigated the responses to two tropical green seaweeds, Ulva ohnoi (UO) and Derbesia tenuissima (DT), in a rat model of human metabolic syndrome. Male Wistar rats (330–340 g) were fed either a corn starch-rich diet or a high-carbohydrate, high-fat diet with 25% fructose in drinking water, for 16 weeks. High-carbohydrate, high-fat diet-fed rats showed the signs of metabolic syndrome leading to abdominal obesity, cardiovascular remodelling and non-alcoholic fatty liver disease. Food was supplemented with 5% dried UO or DT for the final 8 weeks only. UO lowered total final body fat mass by 24%, systolic blood pressure by 29 mmHg, and improved glucose utilisation and insulin sensitivity. In contrast, DT did not change total body fat mass but decreased plasma triglycerides by 38% and total cholesterol by 17%. UO contained 18.1% soluble fibre as part of 40.9% total fibre, and increased magnesium, while DT contained 23.4% total fibre, essentially as insoluble fibre. UO was more effective in reducing metabolic syndrome than DT, possibly due to the increased intake of soluble fibre and magnesium.

Persistent inflammation promotes development and progression of heart failure (HF). TWEAK (TNF-Related WEAK Inducer Of Apoptosis), a NF-κB- and/or AP-1-responsive proinflammatory cytokine that signals via TWEAK receptor (TWEAKR), is expressed at high levels in human and preclinical models of HF. Since the adapter molecule TRAF3IP2 (TRAF3 Interacting Protein 2) is an upstream regulator of various proinflammatory pathways, including those activated by NF-κB and AP-1, we hypothesized that targeting TRAF3IP2 inhibits TWEAK-induced proinflammatory and pro-fibrotic responses in vitro and in vivo. Consistent with the hypothesis, forced expression of TRAF3IP2 upregulated TWEAK and its receptor expression in cultured adult mouse cardiac fibroblasts (CF). Further, exogenous TWEAK upregulated TRAF3IP2 expression in a time- and dose-dependent manner, suggesting a positive-feedback regulation of TRAF3IP2 and TWEAK. TWEAK also promoted TRAF3IP2 nuclear translocation. Confirming its critical role in TWEAK signaling, silencing TRAF3IP2 inhibited TWEAK autoregulation, TWEAKR upregulation, p38 MAPK, NF-κB and AP-1 activation, inflammatory cytokine expression, MMP and TIMP1 activation, collagen expression and secretion, and importantly, proliferation and migration. Recapitulating these in vitro results, continuous infusion of TWEAK for 7 days increased systolic blood pressure (SBP), upregulated TRAF3IP2 expression, activated p38 MAPK, NF-κB and AP-1, induced the expression of multiple proinflammatory and pro-fibrotic mediators, and interstitial fibrosis in hearts of wild type mice. These proinflammatory and pro-fibrotic changes occurred in conjunction with myocardial hypertrophy and contractile dysfunction. Importantly, genetic ablation of TRAF3IP2 inhibited these TWEAK-induced adverse cardiac changes independent of increases in SBP, indicating that TRAF3IP2 plays a causal role, and thus a therapeutic target, in chronic inflammatory and fibro-proliferative diseases.