28 research outputs found

    Reactive oxygen species and male reproductive hormones

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    Reports of the increasing incidence of male infertility paired with decreasing semen quality have triggered studies on the effects of lifestyle and environmental factors on the male reproductive potential. There are numerous exogenous and endogenous factors that are able to induce excessive production of reactive oxygen species (ROS) beyond that of cellular antioxidant capacity, thus causing oxidative stress. In turn, oxidative stress negatively affects male reproductive functions and may induce infertility either directly or indirectly by affecting the hypothalamus-pituitary-gonadal (HPG) axis and/or disrupting its crosstalk with other hormonal axes. This review discusses the important exogenous and endogenous factors leading to the generation of ROS in different parts of the male reproductive tract. It also highlights the negative impact of oxidative stress on the regulation and cross-talk between the reproductive hormones. It further describes the mechanism of ROS-induced derangement of male reproductive hormonal profiles that could ultimately lead to male infertility. An understanding of the disruptive effects of ROS on male reproductive hormones would encourage further investigations directed towards the prevention of ROS-mediated hormonal imbalances, which in turn could help in the management of male infertility

    Foregut caustic injuries: results of the world society of emergency surgery consensus conference

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    Structure and dynamical properties of Au-N, N=12-14 clusters: Molecular dynamics simulation

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    ATIS, Murat/0000-0003-4429-6897WOS: 000229549400007Using molecular dynamics and thermal quenching methods on the basis of Voter-Chen version of the embedded-atom method, we have studied the melting behavior of Au-N (N = 12, 13, 14) clusters. This behavior is described in terms of overall and atom resolved root-mean-square bond-length fluctuations, specific-heat, short- and long-time average coordination numbers of each atom and short-time average temperatures of the clusters. The isomer sampling probabilities are obtained from the thermal quenching of the molten clusters, and their energy-spectrum widths are investigated. Phase change of a cluster takes place with the collective and simultaneous motion of all the atoms

    Transplantation in pediatric aHUS within the era of eculizumab therapy

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    aHUS is caused by the over-activation and dysregulation of the alternative complement pathway. Data regarding outcomes of pediatric aHUS patients after kidney transplantation are still very scarce. Accordingly, the aim of this study was to describe the clinical findings and outcomes of pediatric aHUS patients after renal transplantation. This is a retrospective, multicenter study including 12 patients from the national registry system. Among the 12 patients, eight had received prophylactic eculizumab and none of those patients (except one) had experienced aHUS recurrence during a median follow-up period of 58.5 (min-max, 4-94) months. Although eculizumab had been started on the day before transplantation in one of them, aHUS recurrence occurred during the transplantation procedure. Eculizumab had been stopped in only one patient who had no complement gene mutation after 35 months of therapy, and recurrence had not been observed during the 19 months of follow-up. In three patients, maintenance doses had been spaced out without any recurrence. One additional patient with anti-CFH antibody received only two doses of eculizumab for transplantation and had been followed for 46 months without aHUS recurrence. The remaining three patients had not received anti-C5 therapy and none of those patients experienced aHUS recurrence during a median follow-up period of 21 (min-max, 9-42) months. Prophylactic eculizumab is a safe and effective treatment for the prevention of aHUS recurrence. Eculizumab interval prolongation, discontinuation, and transplantation without eculizumab prophylaxis can be tried in selected patients with close follow-up.C1 [Ozcakar, Zeynep Birsin] Ankara Univ, Div Pediat Nephrol, Dept Pediat, Sch Med, Ankara, Turkey.[Ozaltin, Fatih; Gulhan, Bora; Topaloglu, Rezan] Hacettepe Univ, Div Pediat Nephrol, Dept Pediat, Fac Med, Ankara, Turkey.[Ozaltin, Fatih] Hacettepe Univ, Nephrogenet Lab, Fac Med, Ankara, Turkey.[Comak, Elif] Akdeniz Univ, Div Pediat Nephrol, Dept Pediat, Fac Med, Antalya, Turkey.[Parmaksiz, Gonul] Baskent Univ, Adana Teaching & Res Hosp, Pediat Nephrol, Adana, Turkey.[Baskin, Esra] Baskent Univ, Div Pediat Nephrol, Dept Pediat, Sch Med, Ankara, Turkey.[Kasap Demir, Belde] Izmir Katip Celebi Univ, Div Nephrol & Rheumatol, Dept Pediat, Fac Med, Izmir, Turkey.[Canpolat, Nur] Istanbul Univ, Div Pediat Nephrol, Dept Pediat, Cerrahpasa Fac Med, Istanbul, Turkey.[Yuruk Yildirim, Zeynep] Istanbul Univ, Div Pediat Nephrol, Dept Pediat, Istanbul Fac Med, Istanbul, Turkey.[Demircioglu Kilic, Beltinge] Gaziantep Univ, Div Pediat Nephrol, Dept Pediat, Fac Med, Gaziantep, Turkey.[Yuksel, Selcuk] Pamukkale Univ, Div Pediat Nephrol, Dept Pediat, Sch Med, Denizli, Turkey.[Soylemezoglu, Oguz] Gazi Univ, Div Pediat Nephrol, Dept Pediat, Sch Med, Ankara, Turkey
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