To evaluate the effect of preoperative anaemia and blood transfusion on 30-day postoperative morbidity and mortality in patients undergoing gynecological surgery. Data were analyzed from 12,836 women undergoing operation in the American College of Surgeons National Surgical Quality Improvement Program. Outcomes measured were; 30-day postoperative mortality, composite and specific morbidities (cardiac, respiratory, central nervous system, renal, wound, sepsis, venous thrombosis, or major bleeding). Multivariate logistic regression models were performed using adjusted odds ratios (OR_adj) to assess the independent effects of preoperative anaemia (hematocrit <36.0%) on outcomes, effect estimates were performed before and after adjustment for perioperative transfusion requirement. The prevalence of preoperative anaemia was 23.9% (95%CI: 23.2–24.7). Adjusted for confounders by multivariate logistic regression; preoperative anaemia was independently and significantly associated with increased odds of 30-day mortality (OR: 2.40, 95%CI: 1.06–5.44) and composite morbidity (OR: 1.80, 95%CI: 1.45–2.24). This was reflected by significantly higher adjusted odds of almost all specific morbidities including; respiratory, central nervous system, renal, wound, sepsis, and venous thrombosis. Blood Transfusion increased the effect of preoperative anaemia on outcomes (61% of the effect on mortality and 16% of the composite morbidity). Preoperative anaemia is associated with adverse post-operative outcomes in women undergoing gynecological surgery. This risk associated with preoperative anaemia did not appear to be corrected by use of perioperative transfusion.

Raynaud's phenomenon (RP) is characterized by exaggerated cold-induced vasoconstriction. This augmented vasoconstriction occurs by virtue of a reflex response to cooling via the sympathetic nervous system as well as by local activation of α2C adrenoceptors (α2C-AR). In a cold-initiated, mitochondrion-mediated mechanism involving reactive oxygen species and the Rho/ROCK pathway, cytoskeletal rearrangement in vascular smooth muscle cells (VSMCs) orchestrates the translocation of α2C-AR to the cell membrane, where this receptor readily interacts with its ligand. Different parameters are involved in this spatial and functional rescue of α2C-AR. Of notable relevance is the female hormone, 17β-estradiol, or estrogen. This is consistent with the high prevalence of RP in pre-menopausal women compared to age-matched males. In addition to dissecting the role of these various players, the contribution of pollution as well as genetic background to the onset and prevalence of RP are also discussed. Different therapeutic approaches employed as treatment modalities for this disease are also highlighted and analyzed. The lack of an appropriate animal model for RP mandates that more efforts be undertaken in order to better understand and eventually treat this disease. Although several lines of treatment are utilized, it is important to note that precaution is often effective in reducing severity or frequency of RP attacks.

Diabetic nephropathy (DN), a major complication of diabetes, is characterized by hypertrophy, extracellular matrix accumulation, fibrosis and proteinuria leading to loss of renal function. Hypertrophy is a major factor inducing proximal tubular epithelial cells injury. However, the mechanisms leading to tubular injury is not well defined. In our study, we show that exposure of rats proximal tubular epithelial cells to high glucose (HG) resulted in increased extracellular matrix accumulation and hypertrophy. HG treatment increased ROS production and was associated with alteration in CYPs 4A and 2C11 expression concomitant with alteration in 20-HETE and EETs formation. HG-induced tubular injury were blocked by HET0016, an inhibitor of CYPs 4A. In contrast, inhibition of EETs promoted the effects of HG on cultured proximal tubular cells. Our results also show that alteration in CYPs 4A and 2C expression and 20HETE and EETs formation regulates the activation of the mTOR/p70S6Kinase pathway, known to play a major role in the development of DN. In conclusion, we show that hyperglycemia in diabetes has a significant effect on the expression of Arachidonic Acid (AA)-metabolizing CYPs, manifested by increased AA metabolism, and might thus alter kidney function through alteration of type and amount of AA metabolites.