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The etiology of tic disorders (TDs) is not precisely known, although several lines of evidence suggest involvement of the immune system in pathogenesis. Here, we aimed to determine the expression levels of pro-inflammatory and anti-inflammatory cytokines in children with TD and compare them with those of healthy controls. Furthermore, we also evaluated their association with clinical variables in the TD group. Within the study period, 88 children with tic disorders and 111 healthy control children were enrolled. Most children with tic disorders were diagnosed with Tourette’s disorder (n = 47, 53.4%) or persistent motor tic disorder (n = 39, 44.3%), while the remainder (n = 2, 2.3%) were diagnosed with persistent vocal tic disorder. We found that children with tic disorders had significantly elevated levels of IL-1β, TNF-α, IL-6 and IL-4 expression, while we detected lower expression levels of IL-17 in children with tic disorders. Our findings provide a molecular landscape of cytokine expression in children with TD, which may suggest a proinflammatory state not affected by the presence of comorbidity and symptom severity. Delineating the contribution of alterations in the immune system to the pathogenesis of tic disorders may pave the way for better therapeutic interventions.

Necrosis, apoptosis and autophagic cell death are the main cell death pathways in multicellular organisms, all with distinct and overlapping cellular and biochemical features. DNA damage may trigger different types of cell death in cancer cells but the molecular events governing the mode of cell death remain elusive. Here we showed that increased BH3-only protein BIK levels promoted cisplatin- and UV-induced mitochondrial apoptosis and biphasic ROS production in HCT-116 wild-type cells. Nonetheless, early single peak of ROS formation along with lysosomal membrane permeabilization and cathepsin activation regulated cisplatin- and UV-induced necrosis in p53-null HCT-116 cells. Of note, necrotic cell death in p53-null HCT-116 cells did not depend on BIK, mitochondrial outer membrane permeabilization or caspase activation. These data demonstrate how cancer cells with different p53 background respond to DNA-damaging agents by integrating distinct cell signaling pathways dictating the mode of cell death.

Breast cancer is the most common cancer with a high rate of mortality and morbidity among women worldwide. Estrogen receptor status is an important prognostic factor and endocrine therapy is the choice of first-line treatment in ER-positive breast cancer. However, most tumors develop resistance to endocrine therapy. Here we demonstrate that BH3 profiling technology, in particular, dynamic BH3 profiling can predict the response to endocrine therapy agents as well as the development of acquired resistance in breast cancer cells independent of estrogen receptor status. Immunofluorescence analysis and subcellular fractionation experiments revealed distinct ER-α and ER-β subcellular localization patterns in breast cancer cells, including mitochondrial localization of both receptor subtypes. shRNA-mediated depletion of ER-β in breast cancer cells led to resistance to endocrine therapy agents and selective reconstitution of ER-β in mitochondria restored sensitivity. Notably, mitochondria-targeted ER-α did not restore sensitivity, even conferred further resistance to endocrine therapy agents. In addition, expressing mitochondria-targeted ER-β in breast cancer cells resulted in decreased mitochondrial respiration alongside increased total ROS and mitochondrial superoxide production. Furthermore, our data demonstrated that mitochondrial ER-β can be successfully targeted by the selective ER-β agonist Erteberel. Thus, our findings provide novel findings on mitochondrial estrogen signaling in breast cancer cells and suggest the implementation of the dynamic BH3 technique as a tool to predict acquired endocrine therapy resistance.

The diagnosis of autism spectrum disorder (ASD) in a child affects family processes, increases parenting stress and marital conflicts, and may lead to parental psychopathology. It may also affect the prognosis for their children. The aim of this study is to determine depression and burnout levels as well as their predictors among parents of children with ASD compared with those of healthy children. We also sought to evaluate rate of complementary and alternative medicine (CAM) interventions among parents and explore the associations of this phenomenon in an exploratory fashion. 145 children with ASD and 127 control children were enrolled along with their mothers and fathers. Beck Depression Inventory and Maslach Burnout Inventory were used to evaluate parents’ depression symptoms and burnout levels. Symptoms of children with ASDs were evaluated according to the Childhood Autism Rating Scale by the clinicians. Family, child and CAM variables were screened by means of a sociodemographic data form. Descriptive, bivariate and correlation analyses were used in statistical evaluations. Predictors of burnout were evaluated with multiple regression analysis. Burnout and depression levels among parents of children with ASD were significantly elevated compared to controls. Burnout levels of mothers were significantly elevated compared to fathers while depression scores of fathers were significantly elevated compared to mothers. Maternal burnout was significantly predicted by presence of functional speech in child while paternal burnout was significantly predicted by paternal vocation. Maternal depression was associated with paternal depression, lack of speech in child and attendance of child to special education services. Paternal depression was associated with autistic symptom severity and maternal depression. More than half the parents sought CAM interventions. Education level did not affect search for CAM interventions while both maternal and paternal psychopathology and presence of epilepsy among children increased use of CAM methods. Psychological support should be provided to both mothers and fathers of a child receiving a diagnosis of ASD. Addressing parents’ burnout and stress levels and facilitating their negotiation of knowledge on etiology and treatments for ASD may be beneficial for the family unit as a whole.

Ovarian cancer remains one of the most frequent causes of cancer-related death in women. Many patients with ovarian cancer suffer from de novo or acquired resistance to chemotherapy. Here, we report that RAB25 suppresses chemotherapy-induced mitochondrial apoptosis signaling in ovarian cancer cell lines and primary ovarian cancer cells. RAB25 blocks chemotherapy-induced apoptosis upstream of mitochondrial outer membrane permeabilization by either increasing antiapoptotic BCL-2 proteins or decreasing proapoptotic BCL-2 proteins. In particular, BAX expression negatively correlates with RAB25 expression in ovarian cancer cells. BH3 profiling assays corroborated that RAB25 decreases mitochondrial cell death priming. Suppressing RAB25 by means of RNAi or RFP14 inhibitory hydrocarbon-stapled peptide sensitizes ovarian cancer cells to chemotherapy as well as RAB25-mediated proliferation, invasion and migration. Our data suggest that RAB25 is a potential therapeutic target for ovarian cancer.

The original version of the article has unfortunately missed the revised affiliations for the following authors.

Bu çalışmada, Erwinia herbicola ve onun Vitreoscilla hemoglobin geni (vgb) klonlanmış suşu (vgb+) ile vgb içermeyen (vgb-) rekombinant suşları kullanılmıştır. Vitreoscilla hemoglobinin (VHb) E. herbicola'da indol-3-asetik asit, β-karoten, likopen, C vitamini, fenazin, meropenem, ATP ve NAD üretimi üzerindeki etkisi araştırılmıştır. E. herbicola'da bu şekilde endojen rekombinant bir oksijen alım sisteminin bu metabolitlerin üretimi üzerindeki etkisi ilk defa çalışılmıştır.Diğer iki suşla karşılaştırıldığında, vgb+ rekombinant suşunun düşük konsantrasyonda L-triptofan eklenen zengin kültür ortamının ileri kültür fazı ile yüksek glukozlu M9 ortamında önemli derecede yüksek indol-3-asetik asit seviyesine sahip olduğu belirlendi. Yine bu suşun diğer suşlara göre zengin besiyerinde daha yüksek β-karoten ve likopen seviyesine sahip olduğu gözlendi. VHb'nin C vitamini üretimini hem glukozlu M9 ortamı ve hem de zengin besiyerinde pozitif yönde etkilediği saptanırken, fenazin üretiminin fruktoz ortamında ve meropenem üretiminin ise sükroz ortamında VHb varlığından pozitif yönde etkilendiğ belirlendi. Ayrıca, rekombinant suşların konakçıdan önemli derecede yüksek oksijen alımına sahip oldukları belirlendi. Zengin besiyerinde vgb+ suşunun hem ATP hem de NAD düzeyleri konakçı ve vgb- rekombinantından daha yüksek bulundu.

Bu çalışmada Zea mays cv. Martha F1 formu üzerinde Callisto'nun pigmentasyon ve antioksidan sistem üzerine etkileri araştırılmıştır.Zea mays (mısır) bitkisine kontrol grubuna karşı 13, 18, 25, 35, 49, 69, 96, 134, 188, 264 ve 369 ppm dozlarında Callisto uygulandı. Bu örneklerde klorofil a (Kla), klorofil b (Klb), karotenoid, total klorofil, glutatyon seviyeleri ve glutatyon- s-transferaz ile glutatyon redüktaz enzim aktiviteleri tanımlanmıştır.Klb ve total klorofil seviyeleri 1. gün örneklerinde kontrol gruplarından daha düşük çıkmıştır. Bununla beraber, Klorofil a ve Karotenoid seviyeleri aynı gruplarda artış göstermiştir. Kla, Klb ve total klorofil miktarları 5., 10. ve 15. gün örneklerinde genel olarak düşüş göstermiştir. Diğer taraftan karotenoid miktarları aynı gruplarda dikkate değer şekilde artış göstermiştir.Ayrıca bu örneklerde antioksidan sistemi üzerine Calliston'un etkileri de araştırılmıştır. glutatyon, glutatyon-S-transferaz ve glutatyon redüktaz aktivitelerinde farklı etkiler kaydedilmiştir. Özellikle, glutatyon-S-transferaz aktivitesinde günlere bağlı olarak artış dikkat ii çekmektedir. Glutatyon redüktaz aktivitesinde ve glutatyon seviyesinde hem konsantrasyonlara hem de günlere bağlı olarak değişimler gözlenmiştir.

IntroductionPlasma chemerin, which has chemotactic and adipogenic functions, is increased in several inflammatory diseases. However, its relationship with multiple sclerosis (MS) has not been explored yet. In this study, we aimed to determine chemerin levels and their possible role in MS.MethodsChemerin serum concentrations were evaluated by using ELISA kit in 91 clinically definite MS patients and 52 healthy controls. The mean serum chemerin, insulin, and cholesterol levels were compared. Patients were divided into two groups according to the body mass index (BMI), and the relationships between clinical and metabolic parameters were evaluated.ResultsSerum chemerin levels were 10.46 ± 1.65 ng/mL in MS patients and 10.26 ± 2.14 ng/mL in the control group. No significant difference was found between patients and controls (p = 0.55). We found no difference regarding age, gender, and BMI between two groups (p = 0.053, p = 0.54, p = 0.41). However, female patients with MS had higher chemerin levels than male patients. There were no associations between serum chemerin levels and EDSS score, annualized relapse rate, BMI, insulin resistance, and serum cholesterol levels in MS patients.ConclusionIn this study, we aimed to determine serum chemerin levels in patients with MS. However, in our study, there was no significant difference between serum chemerin levels of MS patients and healthy controls’. Additionally, chemerin levels were not associated with other metabolic parameters, as well as cognitive dysfunction. Further studies are needed to evaluate the role of chemerin in MS patients.

Objective: C1q/tumor necrosis factor-related protein-5 (CTRP5) is a novel peptide hormone involved in the metabolism of energy regulation. Polycystic ovary syndrome (PCOS), which is a reproductive and metabolic disorder, is associated with insulin resistance. The aim of the current study was to compare circulating levels of CTRP5 in women with and without PCOS and to investigate possible associations between CTRP5 and metabolic-hormonal parameters. Material and Methods: The present cross-sectional study contained 80 women with PCOS and 80 age and body mass index-matched women without PCOS. Circulating levels of CTRP5 were calculated using an enzyme-linked immunosorbent assay. We also measured hormonal and metabolic parameters. Results: Patients with PCOS had lower levels of circulating CTRP5 compared with women without PCOS (6.90±2.64 vs 11.73±3.66 ng/mL, p<0.001). CTRP5 was negatively correlated with insulin resistance, free-androgen index, and body mass index in both the PCOS and control groups. Moreover, patients with PCOS who had insulin resistance showed lower circulating CTRP5 levels compared with those without insulin resistance. In both the control and PCOS groups, overweight subjects had lower circulating levels of CTRP5 compared with participants of normal weight. Logistic regression analyses indicated that subjects in the lowest tertile for CTRP5 level had higher risk for PCOS compared with those in the highest tertile of CTRP5. Conclusion: Decreased circulating levels of CTRP5 were associated with higher risk of PCOS, as well as having metabolic disturbance among women with PCOS. (J Turk Ger Gynecol Assoc 2019; 20: 89-96)