Evaluation of the adipokine levels of pregnant women with preeclampsia.

AIM: The aim of this study was to compare maternal blood and umbilical-cord leptin, spexin and visfatin levels during delivery in severe preeclampsia (PE) with controls, and to evaluate whether any clinical or demographic variables had independent associations with them. METHODS: This is a case-controlled observational study consisting of 45 pregnant women with severe PE and a control group consisting of gestational age-matched 45 healthy pregnant women. We examined the leptin, spexin, and visfatin levels in serum samples taken from maternal blood and umbilical cords during cesarean section in both groups. Leptin, spexin, and visfatin levels were measured by enzyme-linked immunosorbent assay. RESULTS: The maternal leptin and visfatin levels were significantly higher and the maternal spexin levels were significantly lower in the PE group than in the control group (p < 0.001). Similar to the maternal adipokine levels, the umbilical-cord leptin and visfatin levels were significantly higher and the spexin levels were significantly lower in the PE group (p < 0.001). We found a significant positive correlation between maternal body mass index and maternal blood and umbilical-cord serum leptin and visfatin levels in both groups (p < 0.001). CONCLUSION: The leptin, spexin and visfatin levels were significantly altered in the nondiabetic preeclamptic women in our study. We believe that the main reason for these changes may be the hypoxic placenta to protect the fetus and maintain its nutrition.

Decreased serum human leukocyte antigen-G levels are associated with gestational diabetes mellitus.

AIM: This study was designed to determine serum human leukocyte antigen-G (HLA-G) levels and establish whether serum HLA-G level is related with gestational diabetes mellitus (GDM). METHODS: Twenty-five GDM patients aged between 24 and 34 years and 24 healthy pregnant women aged between 22 and 33 years were included in this study. Health status of subjects was determined by medical history, physical, and obstetric examinations. Absence of family history for Type 2 diabetes mellitus, absence of diagnosis or clinical evidence of any major disease, and absence of medication use altering glucose metabolism constituted the inclusion criteria. GDM cases who are at their 24-28 weeks of pregnancy and who have not been using any oral hypoglycemic agents were included in GDM group. Control group consisted of healthy pregnant women at their 24-28 weeks of pregnancy. RESULTS: Women with GDM had significantly lower levels of serum HLA-G than controls. HLA-G levels were negatively correlated with all parameters of glucose metabolism including insulin (r = - 0.14; p = 0.338), fasting blood glucose (r = - 0.220; p = 0.129), 1-h oral glucose tolerance test (OGTT) blood glucose (r = - 0.18; p = 0.271), 2-h OGTT blood glucose (r = - 0.314; p = 0.172), homeostasis model assessment (r = - 0.226; p = 0.119), HbA1C (r = -0.342; p = 0.108), and WBC (r = -0.149; p = 0.307). There was a negative correlation between HLA-G and BMI (r = -0.341; p = 0.016). CONCLUSION: Decreased circulating HLA-G level is found to be associated with insulin resistance and GDM, in this study.

Changes in serum levels of calcitonin gene-related peptide, adiponectin, and ghrelin in pregnant women with gestational diabetes mellitus.

AIM: This study was designed to determine serum calcitonin gene-related peptide (CGRP) levels and define whether serum CGRP concentration is associated with adiponectin and ghrelin in pregnant women with gestational diabetes mellitus (GDM). STUDY DESIGN: Thirty-six pregnant women with GDM and 43 normal pregnant women without glucose intolerance were evaluated in this study. The serum concentration of CGRP, adiponectin, and ghrelin were measured in two groups at the last trimester of gestation. MAIN FINDINGS: The serum CGRP level in the GDM group was significantly higher than the control group. Serum levels of adiponectin and ghrelin in the GDM group were significantly lower than in the control group. In pregnant women with GDM, there was a significant negative correlation between serum CGRP level and adiponectin level. However, the correlation between maternal serum CGRP levels and ghrelin levels was not significant. CONCLUSION: Our investigation shows that serum CGRP level was significantly higher in pregnant women with GDM in comparison with the control group. These results suggest that CGRP may play a very important role in GDM pathogenesis.

Peripheral blood mononuclear cell microRNAs in coronary artery disease.

The accuracy of risk prediction for coronary artery disease can be improved with the use of novel molecular or genetic biomarkers. In this study, we investigated the difference of five selected microRNAs (miR or miRNA) in patients with coronary artery disease (CAD) and controls, assessed by coronary angiography. The study population consisted of 85 subjects, aged between 18 and 75 years and underwent invasive coronary angiography. Subjects with more than 30% stenosis in at least one coronary artery, patients with a history of prior percutaneous coronary intervention or coronary by-pass surgery were allocated to the patient group; whereas the subjects without at least 30% stenosis consisted the control group. Groups were similar in age, presence of hypertension, and smoking status. However, the proportion of males and subjects taking angiotensin-converting enzyme inhibitors or angiotensin receptor blockers, beta blockers, nitrates, and statins were higher in the patient group. miR-221 and miR-155 were downregulated (P = .02 and .001, respectively), while miR-21 levels were significantly increased (P = .003) in the patient group compared to controls. Changes in miR-145 and miR-126 did not reach statistical significance (P > .05). miRNA- 21, miR-155, and miR-221 were differentially expressed between the patients and controls. miRNAs are promising biomarkers for CAD diagnosis, however, this requires further research with larger groups.

The effects of bosentan on hyperoxia-induced lung injury in neonatal rats.

BACKGROUND: Bronchopulmonary dysplasia (BPD) remains an important cause of morbidity and mortality in premature infants. There is currently no proven effective treatment modality for BPD, and inflammation and oxidative injury play an important role in the pathogenesis of this disease. This study investigated the histopathological and biochemical effects of bosentan, which is a non-specific endothelin receptor antagonist with known antioxidant and anti-inflammatory properties, on hyperoxia-induced lung injury (HILI) in neonatal rats. METHODS: The experiment was performed on newborn rats from the 3rd to the 13th postnatal day. The rats were randomly divided into six groups: Group 1 (air-exposed + saline, n = 6); Group 2 (HILI, n = 8); Group 3 (air-exposed + bosentan, n = 7); Group 4 (HILI + saline, n = 7); Group 5 (HILI + early bosentan-treated group, n = 6), and Group 6 (HILI + late bosentan-treated group, n = 7). Bosentan was administered (30 mg/kg/day) intraperitoneally. The histopathological effects of bosentan on lung tissue were assessed by their alveolar surface area, fibrosis, and smooth muscle actin (SMA) scores, and the biochemical effects on lung tissue were assessed by interleukin-1 beta (IL-1ß), IL-6, IL-10, and tumor necrosis factor-alpha (TNF-α). RESULTS: The alveolar surface area and fibrosis scores were found to be significantly higher in HILI groups compared with Group 1 (P < 0.01). The SMA scores in HILI groups were also significantly higher than Group 1 (P < 0.01). Bosentan treatment, especially late therapy, reduced all of these histopathological scores and the levels of IL-6 and TNF-α in the hyperoxia groups (P < 0.01). CONCLUSION: This experimental study showed that bosentan had a protective effect on hyperoxic lung injury through its anti-inflammatory properties.

Ischemia-modified albumin in preterm infants born to mothers with pre-eclampsia.

BACKGROUND: Pre-eclampsia (PE) carries an increased risk for maternal and/or fetal mortality or serious morbidity. PE is associated with ischemia and increased oxidative stress in the placenta, which may lead to modification of plasma albumin to ischemia-modified albumin (IMA). The aim of this study was to investigate IMA and hematological parameters in mothers and in premature infants in normal and in pre-eclamptic pregnancies. METHODS: Twenty-five pregnant women with PE and their premature newborns were categorized as the PE group, and 25 normotensive pregnant women and their premature newborns as the control group. Preterm infants are classified as small for gestational age (SGA) or non-SGA according to the Fenton preterm growth chart. Serum IMA, complete blood count (CBC), liver function tests (LFT), renal function tests (RFT), albumin, and C-reactive protein were measured in the mothers immediately before birth, and in the cord blood and serum of the newborns at 6 and 24 h after birth. Clinical and demographic data were recorded for both groups. RESULTS: While IMA, LFT and RFT were significantly increased in the PE group compared with the control group, albumin and CBC were significantly lower in the PE group. A total of 40% of PE newborns were SGA, 30% of whom had severe SGA (birthweight <3rd percentile). Cord IMA was significantly increased in all preterm neonates in the PE group compared with the control group. No mothers or neonates died. CONCLUSION: Serum IMA in addition to the prevalence of SGA were significantly increased in the PE group. Cord blood IMA, therefore, might be a predictive biomarker for SGA in PE pregnancies.

Pentraxin-3 Levels in Beta Thalassemia Major and Minor Patients and Its Relationship With Antioxidant Capacity and Total Oxidant Stress.

Thalassemia major (TM) results in hemolytic anemia, an increase in intestinal iron absorption, and occurrence of iron loading due to erythrocyte transfusion; the disease is characterized by oxidative damage in major organs. Oxidative stress leads to vascular endothelial damage and forms the basis for serious cardiovascular diseases. Pentraxin-3 (PTX-3) is one of the markers of vascular endothelial damage that increases in response to the oxidative stress, which can be used as an early diagnostic marker for inflammation. This study's purpose is to define the relation between PTX-3 and the vascular endothelial damage that increases with oxidative stress in thalassemia patients. Our study included 35 TM patients, 30 ß-thalassemia minor patients, and 30 healthy children. As a result of our study, in TM patients, a positive relation was detected between the PTX-3 levels and the total oxidative stress, triglyceride, and very low-density lipoprotein values, whereas a negative relation was detected with the total antioxidant capacity and high-density lipoprotein values. This result shows that as oxidant stress increases, PTX-3 levels also increase; very low-density lipoprotein and triglyceride contribute to the endothelial damage occurring with oxidative stress. As a result, it was concluded that vascular endothelial damage in thalassemia patients can be evaluated through the serum PTX-3 level.

Serum HLA-G levels in women with polycystic ovary syndrome.

This study was designed to determine serum human leukocyte antigen-G (HLA-G) levels and establish whether serum HLA-G level is related with insulin resistance, oxidative stress, dyslipidemia and ovarian hyperandrogenism in women with polycystic ovary syndrome (PCOS). Twenty-five patients with PCOS and 23 healthy control women were evaluated in this study. Serum HLA-G, lipid fractions, glucose, insulin, malondialdehyde (MDA), glutathione (GSH), white blood cell (WBC), sex hormone-binding globulin (SHBG) and other hormone (gonadotropins and androgens) levels were measured. The estimate of insulin resistance was calculated by homeostasis model assessment (HOMA-IR). Serum luteinizing hormone (LH), total testosterone, fasting insulin, WBC levels and LH/follicle-stimulating hormone (FSH) ratio, free androgen index (FAI) and HOMA-IR values were significantly higher in patients with PCOS compared with healthy women. However, the women with PCOS had considerably lower serum FSH, SHBG, MDA, GSH and HLA-G levels than healthy subjects. HLA-G was inversely related with HOMA-IR, FAI, LH/FSH ratio and WBC, but positively with high-density lipoprotein cholesterol. Decreased serum HLA-G level may be related with insulin resistance, ovarian hyperandrogenism and oxidative stress in women with PCOS. Nevertheless, the exact role of HLA-G in the pathogenesis of the disease remains to be elucidated.

Adipocytokine concentrations in children with different types of beta-thalassemia.

BACKGROUND: Beta-thalassemia is an inherited blood disorder. It results from the impaired production of ß-globin chains, leading to a relative excess of alpha-globin chains. Clinical severity separates this disease into three main subtypes: ß- thalassemia major, ß-thalassemia intermedia and ß-thalassemia minor, the former two being clinically more significant. Inflammatory processes may play an important role in some of the complications of thalassemia. Adipose tissue is one of the most important endocrine and secretory organs that release adipocytokines like adiponectin, resistin and visfatin. AIM: The aim of our study was to analyze adipocytokine concentrations (adiponectin, resistin and visfatin) in different types of ß-thalassemia patients and determine any possible correlations with disease severity. METHODS: We recruited 29 patients who were transfusion-dependent ß-thalassemia-major patients, 17 patients with ß-thalassemia intermedia, 30 ß-thalassemia minor patients. The control group consisted of 30 healthy children. Anthropometric measurements, complete blood count, biochemical parameters, serum concentrations of adiponectin, resistin, visfatin were performed for all subjects. RESULTS: Resistin and visfatin concentrations were significantly higher in ß-thalassemia minor patients than in controls. Adiponetin, resistin and visfatin concentrations were significantly higher in both ß-thalassemia intermedia and major patients than in controls. The concentrations of adiponectin, resistin and visfatin were significantly higher in both ß-thalassemia intermedia and major patients than in ß-thalassemia minor patients. There was no significant difference between ß-thalassemia intermedia and ß-thalassemia major patients for adipocytokines concentrations. CONCLUSION: We speculate that these adipocytokines may play a role in the development of complications in ß-thalassaemia.

Serum Fetuin-A levels, insulin resistance and oxidative stress in women with polycystic ovary syndrome.

This study was designed to determine serum Fetuin-A levels and establish whether serum Fetuin-A level is related with insulin resistance, oxidative stress, ovarian hyperandrogenism and dyslipidemia in women with polycystic ovary syndrome (PCOS). Twenty-two patients with PCOS and twenty-one healthy control women were evaluated in this controlled clinical study. Serum Fetuin-A, lipid fractions, glucose, insulin, malondialdehyde (MDA), myeloperoxidase (MPO), glutathione (GSH), superoxide dismutase (SOD) and other hormone (gonadotropins, androgens) levels were measured. The estimate of insulin resistance was calculated by homeostasis model assessment (HOMA-R). The women with PCOS had significantly higher serum fasting glucose, insulin, luteinizing hormone (LH), MDA, Fetuin-A levels, and LH/follicle-stimulating hormone (FSH) ratio, free androgen index (FAI), HOMA-IR than healthy women. However, sex hormone-binding globulin (SHBG) and GSH levels were significantly lower in patients with PCOS compared with controls. Fetuin-A was positively correlated with insulin, HOMA-IR and FAI. Multiple regression analysis revealed that FAI was strong predictor of serum Fetuin-A level. Serum Fetuin-A level was related with insulin resistance and ovarian hyperandrogenism in women with PCOS. These results suggest that Fetuin-A may have a role in triggering the processes leading to insulin resistance and androgen excess in PCOS.

Aluminium sulphate exposure increases oxidative stress and suppresses brain development in Ross broiler chicks.

BACKGROUND: Aluminium (Al) is known to have neurotoxic effects that can result in oxidative damage to a range of cellular biomolecules. These effects appear to be of significance in the developmental stages of the brain. We therefore investigated the oxidative and histopathological damage induced by Al during growth and development of the chick brain. MATERIAL/METHODS: We used a chick embryonic development model, with Al treatment of 500 µg Al sulphate in 0.1 ml saline injected into the egg air chambers at the beginning of their incubation period. The effects on chick-brain growth and development were then assessed at term (day 21). Determination of malondialdehyde and glutathione levels were used as relevant biological measures for increased oxidative stress in terms of lipid peroxidation and biochemical oxidative damage, respectively. Furthermore, we also monitored neuronal degeneration as estimated stereologically using the Cavalieri brain volume estimation tool. RESULTS: This Al treatment showed significantly increased MDA levels and decreased GSH levels, as indicators of increased biochemical oxidative damage. This was accompanied by significantly decreased brain volume, as a measure of neuronal degeneration during brain development in this chick embryonic development model. CONCLUSIONS: Exposure to Al during chick embryonic development results in increased oxidative stress in the brain that is accompanied by neuronal degeneration.

Cord Blood Levels of Spexin, Leptin, and Visfatin in Term Infants Born Small, Appropriate, and Large for Gestational Age and Their Association with Newborn Anthropometric Measurements

Objective: Children born small for gestational age (SGA) are at risk of future obesity and associated comorbidities. Therefore the identification of risk factors and novel biomarkers which are associated with this risk are needed for early detection and to improve preventive strategies. Spexin (SPX), a novel neuropeptide that is involved in the regulation of obesity and fat metabolism, is a candidate biomarker for predicting obesity and related comorbidities at an early age. The aim of this study was to investigate serum levels of SPX in term infants born small, appropriate, and large for gestational age (LGA) and its association with newborn anthropometric measurements. Methods: One hundred and twenty term newborn babies classified as SGA, appropriate for gestational age (AGA), or LGA and their mothers were included. SPX, leptin and visfatin were measured in cord blood and maternal serum by enzyme-linked immunosorbent assay. Results: Fifty-six (46.7%) neonates were girls and 64 (53.3%) were boys. The mean birth weight was 3170.70±663 g, birth length was 48.9±2.79 cm, and head circumference was 34.5±1.67 cm. Birth weights, lengths, and head circumferences of the neonates in the SGA, AGA, and LGA groups were significantly different. Cord blood SPX and leptin levels in the SGA groups were significantly lower than those of both the LGA and AGA groups. Cord blood visfatin levels were significantly lower in the AGA group than the LGA and SGA groups. Maternal SPX levels of SGA babies were significantly lower than those of the mothers in both the LGA and AGA groups, but no significant difference was observed between the SGA and LGA groups. Maternal visfatin levels of the AGA babies were significantly higher than the maternal levels of SGA and LGA groups. There was no difference in terms of maternal leptin levels. Cord blood SPX and leptin levels were positively correlated with birth weight, length and head circumference. Birth weight increased significantly in line with maternal pregestational body mass index. Conclusion: The lowest SPX levels were found in the SGA babies and cord SPX level was significantly correlated with newborn length, weight, and head circumference.

The effect of phlebotomy and mannitol on acute renal injury induced by ischemia/reperfusion of lower limbs in rats.

BACKGROUND: Abdominal aortic surgery can cause ischemic/reperfusion (I/R) injury not only in the lower limbs but also in remote organs such as kidneys. Venous blood volume exclusion from the inferior vena cava (phlebotomy) or/and mannitol are used as a treatment for I/R injury of kidney in humans, despite the fact that the effectiveness of these treatments is still debated. The aim of this study was to evaluate the effects of phlebotomy or/and mannitol on rat kidneys in a model of lower limbs I/R-induced acute renal injury (ARI). MATERIAL AND METHODS: Thirty male Wistar albino rats were used and divided into five groups: (I) sham-operated group, laparotomy without I/R injury (group [S], n = 6); (II) I/R group, infrarenal aortic cross-clamp was used for lower limbs I/R, 3 hours of ischemia followed by 2 hours of reperfusion (group [I/R], n = 6); (III) I/R + phlebotomy group, identical to group [I/R] except for 1 mL of blood aspiration from the inferior caval vein just after ischemia (group [P], n = 6); (IV) I/R + mannitol-treated group, these rats were subjected to I/R and received a bolus injection of mannitol (group [M], n = 6); and (V) I/R + phlebotomy + mannitol-treated group (group [P + M], n = 6), the same procedures were performed as those described for previous groups. At the end of 2-hour reperfusion, all rats were sacrificed. Both kidneys were harvested for biochemical assay (myeloperoxidase [MPO] and superoxide dismutase [SOD] activities, and malondialdehyde [MDA] and reduced glutathione levels) and for histopathological examination (tubular necrosis and acute inflammation on kidney [ARI score]). RESULTS: Aortic I/R significantly increased the level of MDA (reflecting lipid peroxidation), SOD (enzymatic endogenous antioxidant), and MPO (reflecting neutrophil infiltration) activity (p < 0.05). Phlebotomy or/and mannitol treatments significantly decreased the level of MDA, SOD, and MPO activity and increased glutathione level (nonenzymatic antioxidant in the kidney tissues) (p < 0.05). Histological evaluation of ARI score showed that aortic I/R significantly increased (p value for group [S] versus group [I/R] was 0.012), whereas phlebotomy or/and mannitol treatments significantly decreased tubular necrosis and inflammatory infiltration (p values for group [I/R] versus group [P], [M], and [P + M] were 0.043, 0.043, and 0.003, respectively). CONCLUSION: This experiment clearly indicated that the lower limbs I/R-induced ARI attenuated significantly by phlebotomy or/and mannitol treatments. Phlebotomy plus mannitol is more effective treatment than phlebotomy or mannitol alone in preventing lower limbs I/R-induced ARI in rats. Further clinical studies are required to clarify whether phlebotomy or/and mannitol treatments are beneficial in alleviating of ARI during abdominal aortic surgery.

Mannitol attenuates acute lung injury induced by infrarenal aortic occlusion-reperfusion in rats.

PURPOSE: Mannitol is used as a treatment for ischemia/reperfusion (IR) injury of various organs in humans, despite the fact that its effectiveness in vivo is still disputed. The purpose of this study was to determine the effects of mannitol on acute lung injury (ALI) induced by infrarenal aortic occlusion. METHODS: Male Wistar-albino rats were allocated into five groups: (i) sham-operated group, which received a laparotomy without IR injury (n = 12); (ii) IR group, which received 3 h of ischemia followed by 2 h of reperfusion (n = 12); (iii) IR + inferior caval phlebotomy (ICP) group, which was identical to group 2 except for 1 ml of blood aspiration from the inferior caval vein (n = 12); (iv) IR + mannitol-treated group, for which rats were subjected to IR and received a bolus injection of mannitol (n = 12); and (v) IR + ICP + mannitol-treated group, which underwent the same procedures as described for the previous groups. Arterial blood gas parameters were studied and bronchoalveolar lavage (BAL) was performed. Evans blue dye was injected into half of the rats. We biochemically assessed the degree of pulmonary tissue injury by investigating oxidative stress markers and enzymatic and nonenzymatic antioxidant markers, and evaluated ALI by establishing pulmonary leukosequestration and ALI scoring, histopathologically. Pulmonary edema was estimated by using Evans blue dye extravasation and wet/dry weight ratios. RESULTS: Hypertonic mannitol treatment significantly reduced oxidative stress markers, and significantly increased enzymatic and nonenzymatic antioxidant markers in the lung tissues (P < 0.05). Arterial blood gas parameters were significantly ameliorated (P < 0.05), the BAL cytology was significantly better (P < 0.05), pulmonary leukosequestration and ALI scores were significantly decreased (P < 0.05), and pulmonary edema was significantly alleviated (P < 0.05) by mannitol administration. CONCLUSION: This study clearly showed that mannitol treatment significantly attenuated the aortic IR-induced ALI. Further clinical studies are required to clarify whether mannitol has a useful role in ALI during surgeries in which IR-induced organ injury occurs.

Dose-dependent effects of adalimumab in neonatal rats with hypoxia/reoxygenation-induced intestinal damage.

Tumor necrosis factor-alpha (TNF-α) has an important role in hypoxia/reoxygenation (H/R)-induced intestinal damage. It was shown that blocking TNF-α with infliximab has beneficial effects on experimental necrotizing enterocolitis and hypoxic intestinal injury. However, there is no data about the effect of adalimumab on H/R-induced intestinal damage. Therefore, we aimed to determine potential dose-dependent benefits of adalimumab in such damage in neonatal rats. Wistar albino rat pups were assigned to one of the four groups: control group, hypoxia group, low-dose adalimumab (5 mg/kg/day) treated group (LDAT), and high-dose adalimumab (50 mg/kg/day) treated group (HDAT). On the fourth day of the experiment, all rats except for the control group were exposed to H/R followed by euthanasia. Malondialdehyde (MDA), myeloperoxidase (MPO), TNF-α, total antioxidant capacity (TAC), and total oxidant capacity (TOC) were measured in intestinal tissue. TAC and TOC values were used to calculate the oxidative stress index (OSI). Histopathological injury scores (HIS) were also evaluated in the tissue samples. MDA levels were significantly lower in the LDAT and HDAT groups (p < 0.001). TNF-α levels were significantly lower in the LDAT group (p < 0.001). OSI was significantly higher in the H/R group than in the control and LDAT groups (p < 0.001). Mean HIS values in the LDAT group were significantly lower than those in the H/R and HDAT groups (p < 0.001). This experimental study showed that low-dose adalimumab appears to have a beneficial effect on intestinal injury induced with H/R in neonatal rats.

Serum Caspase-1 levels in women with polycystic ovary syndrome.

OBJECTIVE: Caspase-1 is implicated in several important inflammatory diseases and controls adipocyte differentiation and insulin sensitivity. Interleukin-10 (IL-10) is an anti-inflammatory cytokine and plays an important role in chronic inflammatory conditions. This study was planned to determine if there is any relationship between Caspase-1 and IL-10 levels in women with PCOS. MATERIALS AND METHODS: Forty-two women with PCOS and thirty-seven healthy controls were evaluated in this controlled clinical study. Caspase-1 and IL-10 levels, serum lipid sub-fractions, fasting glucose, fasting insulin and other hormones (gonadotropins, androgens), malondialdehyde (MDA) and glutathione (GSH) levels were measured. Homeostasis model assessment (HOMA-IR) was used to estimate insulin resistance. RESULTS: Free androgen index (FAI), HOMA-IR, MDA and Caspase-1 levels were significantly higher in subjects with PCOS. However, the women with PCOS had considerably lower GSH concentration levels than healthy subjects. Serum IL-10 levels were higher in study subjects than in controls, though it was statistically insignificant. Caspase-1 was positively associated with IL-10. CONCLUSION: These outcomes propose that Caspase-1 may have a role in triggering the processes leading to chronic low-grade inflammation in women with PCOS, independent of insulin resistance, androgen excess and oxidative stress. Nevertheless, the precise role of Caspase-1 in the pathogenesis of the disease remains to be elucidated.

The nitroxide tempol has similar antioxidant effects as physiological levels of 17beta-oestradiol in reversing ovariectomy-induced oxidative stress in mice liver and kidney.

OBJECTIVE: Oestrogen defciency increases oxidative stress postmenopause, while tempol is an intracellular radical scavenger that interferes with the formation or effects of many radicals. We aimed to investigate the effects of oestrogen and tempol on oxidative stress parameters in the kidney and liver of ovariectomized mice. MATERIAL AND METHODS: Forty 8-week-old female Bald/c mice were divided into five groups: sham-operated, ovariectomized mice without treatment, ovariectomized mice treated with tempol, ovariectomized mice treated with 17beta-oestradiol and ovariectomized mice treated with 17beta-oestradiol and tempol. Oxidative stress in liver and kidney tissues was investigated by measuring 2-thiobarbituric acid reactive substances (TBA-RS), reduced glutathione, myeloperoxidase, superoxide dismutase and catalase levels. RESULTS: TBA-RS levels were increased and reduced glutathione, myeloperoxidase, superoxide dismutase levels were decreased in the tissues of ovariectomized mice. This effect of ovariectomy on oxidative stress parameters was opposed significantly by the administration of tempol and 17beta-oestradiol either alone or in combination. Ovariectomy reduced the kidney catalase levels, but the effect was not statistically significant (p>0.05). On the other hand, catalase levels were elevated significantly in all treatment groups compared to those of the ovariectomized group (p<0.05). CONCLUSION: These study findings demonstrate that tempol significantly opposes the oxidative stress generated by ovariectomy. This effect, which is evident in remote tissues such as liver and kidney, is comparable to that of physiological levels of oestradiol.

Urinary excretion of pentraxin-3 correlates with the presence of renal scar following acute pyelonephritis in children.

PURPOSE: Acute pyelonephritis is associated with considerable morbidity and potential for renal scarring. Pentraxin3 (PTX3) is a recently discovered mediator of inflammation. The objective of this study was to investigate the changes in serum and urine PTX3 levels in children who had a history of pyelonephritis and were diagnosed with renal parenchymal scar (RPS) and/or vesicoureteral reflux (VUR). METHODS: The study included 88 children (31 males, 57 females) aged between 3 months and 18 years. The children included in the study were divided into four groups: VUR with RPS (Group 1), RPS without VUR (Group 2), VUR without RPS (Group 3), and healthy children without a history of hydronephrosis or UTI history (Group 4). After the initial evaluation, the participants were further divided into two more groups and re-evaluated: Children with RPS (Group 1 + 2), children without RPS (Group 3 + 4), children with VUR (Group 1 + 3), and children without VUR (Group 2 + 4). RESULTS: We found that urine pentraxin 3 (uPTX3) and uPTX3/Creatinine levels were significantly higher in the groups with renal scar with or without VUR than the ones without RPS [mean uPTX3, 3.5 pg/ml (min-max 0.0022-12.3668) vs. 2.2 pg/ml (min-max 0.0022-18.5868) and uPTX3/creatinine, 10.5 pg/mg (min-max 0.0035-51.1) vs. 5.8 pg/mg (min-max 0.0004-78.7), p < 0.01]. uPTX3 levels were not different among the groups with and without VUR. In addition, serum PTX3 levels were not different among the groups. CONCLUSIONS: We showed that urinary PTX3 increased only in patients with scarred kidneys. These results might be helpful to predict RPS due to past pyelonephritis.

Relationship of Apathy with Depressive Symptom Severity and Cognitive Functions in Geriatric Depression.

INTRODUCTION: Apathy which is known as loss of primary motivation is observed more frequently in elderly depression in comparison with younger adults. It is put forth that apathy is related with depressive symptom severity and cognitive functions, that the existence of apathy may be a predictor of neurocognitive impairment. The objective of this study was to examine the apathy levels in elderly patients with major depression as well as the relationship between depressive symptom severity and cognitive functions. METHODS: The study was carried out with 40 major depressive disorder patients (MDD) aged 60 and above, 40 healthy controls aged 60 and above. Sociodemographic data form, structured psychiatric interview (SCID-I), Hamilton Depression Rating Scale (HAM-D), Hamilton Anxiety Rating Scale (HAM-A), Montgomery-Asberg Depression Rating Scale (MADRS), Standardized Mini Mental State Examination (SMMSE), Montreal Cognitive Assessment Scale (MoCA), Apathy Evaluation Scale (AES) and Sheehan Disability Scale (SDS) were applied to the participants. RESULTS: In our study, HAM-D, HAM-A and MADRS scale scores of MDD group was determined to be higher in comparison with those of the healthy control group. A positive correlation was determined in the MDD groups between the AES scores and depressive symptom severity, whereas a negative correlation was determined between the AES scores and cognitive functions. The SMMSE and MoCA scores of the geriatric MDD group were determined to be lower in comparison with healthy control group. Low performance was observed in the geriatric MDD group especially in the fields of orientation, visual/spatial functions, memory and language. Functionality was found to be lower in MDB group than in the control group, and functionality decreased as the level of apathy increased. CONCLUSION: Our results indicate that the apathy levels in geriatric depression are higher in comparison with the control group. Cognitive functions are affected adversely in geriatric patients in major depressive disorder, depressive symptom severity, impairment in cognitive functions and functionality are observed to be related with apathy level.

Oxidative stress parameters in patients with slow coronary flow.

INTRODUCTION: We investigated the probable role of free-radical damage in the pathogenesis of slow coronary flow (SCF) by using oxidative stress parameters. METHODS: Sixty-four patients with angiographically proven SCF and 63 patients with normal coronary flow (NCF) pattern with similar risk profiles were enrolled in this study. We measured erythrocyte superoxide dismutase (SOD), reduced glutathione (GSH), serum malondialdehyde (MDA), catalase and myeloperoxidase (MPO) levels in all subjects. RESULTS: There were statistically significant differences in the levels of erythrocyte SOD, GSH and serum MDA between the 2 groups. Serum MDA (P = 0.003) and erythrocyte SOD levels (P = 0.0001) were increased in the SCF group. The level of erythrocyte GSH (P = 0.010) was lower in patients with SCF. There were no differences between the groups' serum catalase (P = 0.682) and MPO levels (P = 0.070). CONCLUSION: Our data showed that in patients with SCF, serum MDA and erythrocyte SOD levels were increased while erythrocyte GSH levels were decreased significantly, compared with NCF patients. These results indicate that free-radical damage may play a role in the pathogenesis of SCF.