734 research outputs found

    Role of Condom Negotiation on Condom use among Women of Reproductive Age in three Districts in Tanzania.

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    ABSTRACT: BACKGROUND: HIV/AIDS remains being a disease of great public health concern worldwide. In regions such as sub-Saharan Africa (SSA) where women are disproportionately infected with HIV, women are reportedly less likely capable of negotiating condom use. However, while knowledge of condom use for HIV prevention is extensive among men and women in many countries including Tanzania, evidence is limited about the role of condom negotiation on condom use among women in rural Tanzania. METHODS: Data originate from a cross-sectional survey of random households conducted in 2011 in Rufiji, Kilombero and Ulanga districts in Tanzania. The survey assessed health-seeking behaviour among women and children using a structured interviewer-administered questionnaire. A total of 2,614 women who were sexually experienced and aged 15--49 years were extracted from the main database for the current analysis. Linkage between condom negotiation and condom use at the last sexual intercourse was assessed using multivariate logistic regression. RESULTS: Prevalence of condom use at the last sexual intercourse was 22.2% overall, ranging from12.2% among married women to 54.9% among unmarried (single) women. Majority of the women (73.4%) reported being confident to negotiate condom use, and these women were significantly more likely than those who were not confident to have used a condom at the last sexual intercourse (OR = 3.13, 95% CI 2.22-4.41). This effect was controlled for marital status, age, education, religion, number of sexual partners, household wealth and knowledge of HIV prevention by condom use. CONCLUSION: Confidence to negotiate condom use is a significant predictor of actual condom use among women in rural Tanzania. Women especially unmarried ones or those in multiple partnerships should be empowered with condom negotiation skills to enhance their sexual and reproductive health outcomes

    Detection of autoantibodies against reactive oxygen species modified glutamic acid decarboxylase-65 in type 1 diabetes associated complications

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    <p>Abstract</p> <p>Background</p> <p>Autoantibodies against glutamate decarboxylase-65 (GAD<sub>65</sub>Abs) are thought to be a major immunological tool involved in pathogenic autoimmunity development in various diseases. GAD<sub>65</sub>Abs are a sensitive and specific marker for type 1 diabetes (T1D). These autoantibodies can also be found in 6-10% of patients classified with type 2 diabetes (T2D), as well as in 1-2% of the healthy population. The latter individuals are at low risk of developing T1D because the prevalence rate of GAD<sub>65</sub>Abs is only about 0.3%. It has, therefore, been suggested that the antibody binding to GAD<sub>65 </sub>in these three different GAD<sub>65</sub>Ab-positive phenotypes differ with respect to epitope specificity. The specificity of reactive oxygen species modified GAD<sub>65 </sub>(ROS-GAD<sub>65</sub>) is already well established in the T1D. However, its association in secondary complications of T1D has not yet been ascertained. Hence this study focuses on identification of autoantibodies against ROS-GAD<sub>65 </sub>(ROS-GAD<sub>65</sub>Abs) and quantitative assays in T1D associated complications.</p> <p>Results</p> <p>From the cohort of samples, serum autoantibodies from T1D retinopathic and nephropathic patients showed high recognition of ROS-GAD<sub>65 </sub>as compared to native GAD<sub>65 </sub>(N-GAD<sub>65</sub>). Uncomplicated T1D subjects also exhibited reactivity towards ROS-GAD<sub>65</sub>. However, this was found to be less as compared to the binding recorded from complicated subjects. These results were further proven by competitive ELISA estimations. The apparent association constants (AAC) indicate greater affinity of IgG from retinopathic T1D patients (1.90 × 10<sup>-6 </sup>M) followed by nephropathic (1.81 × 10<sup>-6 </sup>M) and uncomplicated (3.11 × 10<sup>-7 </sup>M) T1D patients for ROS-GAD<sub>65 </sub>compared to N-GAD<sub>65</sub>.</p> <p>Conclusion</p> <p>Increased oxidative stress and blood glucose levels with extended duration of disease in complicated T1D could be responsible for the gradual formation and/or exposing cryptic epitopes on GAD<sub>65 </sub>that induce increased production of ROS-GAD<sub>65</sub>Abs. Hence regulation of ROS-GAD<sub>65</sub>Abs could offer novel tools for analysing and possibly treating T1D complications.</p

    Skin autofluorescence is increased in patients with carotid artery stenosis and peripheral artery disease

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    Advanced glycation end products (AGEs) have a pivotal role in atherosclerosis. We evaluated skin autofluorescence (SAF), a non-invasive measurement of tissue AGE accumulation, in patients with carotid artery stenosis with and without coexisting peripheral artery occlusive disease (PAOD). SAF was measured using the AGE Reader™ in 56 patients with carotid artery stenosis and in 56 age- and sex-matched healthy controls without diabetes, renal dysfunction or known atherosclerotic disease. SAF was higher in patients with carotid artery stenosis compared to the control group: mean 2.81 versus 2.46 (P = 0.002), but especially in the younger age group of 50–60 years old: mean 2.82 versus 1.94 (P = 0.000). Patients with carotid artery stenosis and PAOD proved to have an even higher SAF than patients with carotid artery stenosis only: mean 3.28 versus 2.66 (P = 0.003). Backward linear regression analysis showed that age, smoking, diabetes mellitus, renal function and the presence of PAOD were the determinants of SAF, but carotid artery stenosis was not. SAF is increased in patients with carotid artery stenosis and PAOD. The univariate and multivariate associations of SAF with age, smoking, diabetes, renal insufficiency and PAOD suggest that increased SAF can be seen as an indicator of widespread atherosclerosis

    Antihyperlipidemic and antiperoxidative effect of Diasulin, a polyherbal formulation in alloxan induced hyperglycemic rats

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    BACKGROUND: This study was undertaken to investigation the effect of Diasulin, a poly herbal drug composed of ethanolic extract of ten medicinal plants on blood glucose, plasma insulin, tissue lipid profile, and lipidperoxidation in alloxan induced diabetes. METHODS: Ethanolic extract of Diasulin a, poly herbal drug was administered orally (200 mg/kg body weight) for 30 days. The different doses of Diasulin on blood glucose and plasma insulin in diabetic rats were studied and the levels of lipid peroxides [TBARS, and Hydroperoxide] and tissue lipids [cholesterol, triglyceride, phospholipides and free fatty acids] were also estimated in alloxan induced diabetic rats. The effects were compared with glibenclamide. RESULT: Treatment with Diasulin and glibenclamide resulted in a significant reduction of blood glucose and increase in plasma insulin. Diasulin also resulted in a significant decrease in tissue lipids and lipid peroxide formation. The effect produced by Diasulin was comparable with that of glibenclamide. CONCLUSION: The decreased lipid peroxides and tissue lipids clearly showed the antihyperlipidemic and antiperoxidative effect of Diasulin apart from its antidiabetic effect

    Cell free hemoglobin in the fetoplacental circulation: a novel cause of fetal growth restriction?

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    Cell free hemoglobin impairs vascular function and blood flow in adult cardiovascular disease. In this study, we investigated the hypothesis that free fetal hemoglobin (fHbF) compromises vascular integrity and function in the fetoplacental circulation, contributing to the increased vascular resistance associated with fetal growth restriction (FGR). Women with normal and FGR pregnancies were recruited and their placentas collected freshly postpartum. FGR fetal capillaries showed evidence of erythrocyte vascular packing and extravasation. Fetal cord blood fHbF levels were higher in FGR than in normal pregnancies (P < 0.05) and the elevation of fHbF in relation to heme oxygenase-1 suggests a failure of expected catabolic compensation, which occurs in adults. During ex vivo placental perfusion, pathophysiological fHbF concentrations significantly increased fetal-side microcirculatory resistance (P < 0.05). fHbF sequestered NO in acute and chronic exposure models (P < 0.001), and fHbF-primed placental endothelial cells developed a proinflammatory phenotype, demonstrated by activation of NF-κB pathway, generation of IL-1α and TNF-α (both P < 0.05), uncontrolled angiogenesis, and disruption of endothelial cell flow alignment. Elevated fHbF contributes to increased fetoplacental vascular resistance and impaired endothelial protection. This unrecognized mechanism for fetal compromise offers a novel insight into FGR as well as a potential explanation for associated poor fetal outcomes such as fetal demise and stillbirth

    Curcumin-induced inhibition of cellular reactive oxygen species generation: novel therapeutic implications

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    There is evidence for increased levels of circulating reactive oxygen species (ROS) in diabetics, as indirectly inferred by the findings of increased lipid peroxidation and decreased antioxidant status. Direct measurements of intracellular generation of ROS using fluorescent dyes also demonstrate an association of oxidative stress with diabetes. Although phenolic compounds attenuate oxidative stress-related tissue damage, there are concerns over toxicity of synthetic phenolic antioxidants and this has considerably stimulated interest in investigating the role of natural phenolics in medicinal applications. Curcumin (the primary active principle in turmeric, Curcuma longa Linn.) has been claimed to represent a potential antioxidant and antiinflammatory agent with phytonutrient and bioprotective properties. However there are lack of molecular studies to demonstrate its cellular action and potential molecular targets. In this study the antioxidant effect of curcumin as a function of changes in cellular ROS generation was tested. Our results clearly demonstrate that curcumin abolished both phorbol-12 myristate-13 acetate (PMA) and thapsigargin-induced ROS generation in cells from control and diabetic subjects. The pattern of these ROS inhibitory effects as a function of dose-dependency suggests that curcumin mechanistically interferes with protein kinase C (PKC) and calcium regulation. Simultaneous measurements of ROS and Ca2+ influx suggest that a rise in cytosolic Ca2+ may be a trigger for increased ROS generation. We suggest that the antioxidant and antiangeogenic actions of curcumin, as a mechanism of inhibition of Ca2+ entry and PKC activity, should be further exploited to develop suitable and novel drugs for the treatment of diabetic retinopathy and other diabetic complications
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