Vitamin D deficiency in patients with chronic hepatitis D viral infection.

AIM OF THE STUDY: Vitamin D deficiency is known to be associated with disease severity, unresponsiveness to treatment, and morbidity among patients with chronic viral hepatitis B and C, autoimmune hepatitis, and alcoholic hepatitis. This study aims to research vitamin D levels in patients suffering from cirrhotic and non-cirrhotic phases of hepatitis D. MATERIAL AND METHODS: 170 individuals in total were included in the study in the form of two groups: the first group of 100 patients with chronic hepatitis D (CHD), 30 of whom had cirrhosis, and the second control group of 70 individuals with similar characteristics to those of the first group in terms of age, type, and seasonal sampling. Levels of 25-hydroxy vitamin D [25(OH)D] were measured in the serum collected from patients and the control group. RESULTS: The lowest 25(OH)D levels were identified in patients with cirrhotic CHD. When these levels were compared with those of the control group, they were found to be significant (15.30 ±6.92 and 18.90 ±8.30 ng/ml, respectively, p = 0.04). 25(OH)D deficiency (< 10 ng/ml) was detected at significantly higher rates in patients with both cirrhotic and non-cirrhotic CHD compared to the healthy controls (30%, 25%, and 8.5%, respectively, p = 0.01). A significant correlation was established between 25(OH)D levels and bilirubin in patients with CHD (r = 0.252, p = 0.012). Multivariate analysis showed that chronic hepatitis D (odds ratio [OR] = 3.608, 95% confidence interval [CI]: 1.31-9.89, p = 0.013) and age (OR = 1.04, 95% CI: 1.00-1.08, p = 0.033) were associated with vitamin D deficiency. CONCLUSIONS: Frequency of 25(OH)D vitamin deficiency is higher in patients with CHD. The identification of vitamin D levels and the replacement of any deficiency may create a positive effect on disease progression, morbidity, and mortality levels.

The relationship of serum SCUBE-1, -2 and -3 levels with clinical findings and ultrasonographic skin thickness in systemic sclerosis patients.

AIM: This study aimed to investigate the relationship between the level of serum signal peptide-CUB-EGF domain-containing protein (SCUBE)-1, SCUBE-2 and SCUBE-3 and clinical findings and ultrasonographic skin thickness in systemic sclerosis (SSc). MATERIAL AND METHODS: Thirty patients who met the American College of Rheumatology/European League against Rheumatism 2013 SSc classification criteria and 44 healthy volunteers who were compatible with the patient group in terms of age and gender were included in the study. Serum SCUBE levels were measured by enzyme-linked immunosorbent assay. Ultrasonographic skin thickness measurements were simultaneously performed. RESULTS: No significant difference was found between the serum SCUBE levels of SSc patients and serum SCUBE levels of the control group. A negative correlation was detected between serum SCUBE-1 level and forced expiratory volume in 1 second (FEV1 ). While a positive correlation was detected between serum SCUBE-2 level and the Duruöz Hand Index and serum C4 level, a negative correlation was determined with the forced vital capacity (FVC) value. A negative correlation was determined between serum SCUBE-3 level and echocardiographic pulmonary artery pressure (PAP). A correlation could not be determined between serum SCUBE levels and ultrasonographic skin thickness. However, a positive correlation was observed between ultrasonographic skin thickness and the modified Rodnan skin score. CONCLUSION: In this study, a correlation was observed between serum SCUBE levels and some clinical and laboratory parameters (FEV1 , FVC, PAP, C4, and Duruöz Hand Index) in SSc patients. New clinical studies are needed to better understand the contribution of these molecules in the progression and pathogenesis of SSc.

Expression of endothelin-1 and Ki-67 in normotensive and severe preeclamptic placentas / Expresión de endotelina-1 y Ki-67 en placentas normotensas y preeclampsia severa

SUMMARY: Severe preeclampsia (HELLP syndrome) is a life-threatening pregnancy complication, usually a severe form of preeclampsia. In this study, we aimed to examine histopathologic changes and Endothelin-1 and KI-67 expression levels by immunohistochemical methods in severe preeclamptic placentas. Severe preeclampsia and obstetric characteristics and biochemical and hematological characteristics of healthy subjects were compared. Placenta sections were stained with hematoxylin-eosin for histopathological examination. In the histopathological examination of severe preeclamptic placenta, degeneration in synaptic and cytotrophoblastic cells, increase in insidious knots, fibrinoid necrosis, degeneration in endothelial cells, calcification and hyaline villous stains were observed. In the severe preeclampsia group, Ki-67 expression increased in decidua cells and inflammatory cells, while endothelial cells in the vessel wall and inflammatory cells in the villus and intervillous spaces increased. It is thought that angiogenetic and cellular proliferation is induced in a co-ordinated manner and significantly influences fetal development.

RESUMEN: La preeclampsia severa (síndrome de HELLP) es una complicación del embarazo potencialmente mortal, generalmente una forma grave de preeclampsia. En este estudio, nuestro objetivo fue examinar los cambios histopatológicos y los niveles de expresión de Endotelina-1 y Ki-67 mediante métodos inmunohistoquímicos en placentas preeclámpsicas graves. Se compararon la preeclampsia grave y las características obstétricas, además de las características bioquímicas y hematológicas de pacientes sanas. Las secciones de placenta se tiñeron con hematoxilina-eosina para examen histopatológico. En el examen histopatológico de placenta preeclampsia severa, se observó la degeneración en células sinápticas y citotrofoblásticas, un aumento de nudos insidiosos, necrosis fibrinoide, degeneración en las células endoteliales,calcificación y manchas vellosas hialinas. En el grupo de preeclampsia grave, la expresión de Ki-67 aumentó en células deciduas y células inflamatorias, mientras que las células endoteliales en la pared del vaso, y las células inflamatorias en las vellosidades y los espacios intervellosos aumentaron. Se cree que la proliferación angiogenética y celular se induce de forma coordinada y que influye significativamente en el desarrollo fetal.

Neuroprotective effects of Ganoderma lucidum on spinal cord injury / Efectos neuroprotectores de Ganoderma lucidum en la lesión de la médula espinal 1

SUMMARY: Traumatic injury to the spinal cord results in the delayed dysfunction and neuronal death. Impaired mitochondrial function, generation of reactive oxygen species (ROS), and lipid peroxidation occur soon after traumatic spinal cord injury (SCI), while the activation of compensatory molecules that neutralize ROS occurs at later time points. The aim of the current study was to investigate the putative neuroprotective effect of Ganoderma lucidum in a rat model of SCI. In order to induce SCI, a standard weight-drop method that induced a moderately severe injury (100 g/cm force) at T10, was used. Injured animals were given either 20 mL/kg Ganoderma lucidum or saline 30 min post injury per day by gastric gavage. At seven days postinjury, rats were decapitated. Spinal cord samples were taken for histological examination or determination of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity. SCI caused a significant decrease in spinal cord GSH content, which was accompanied with significant increases in MDA levels, MPO activity. On the other hand, Ganoderma lucidum treatment reversed all these biochemical parameters as well as SCI-induced histopathological alterations. Furthermore, impairment of the neurological functions due to SCI was improved by meloxicam treatment. The present study suggests that Ganoderma Lucidum, reduces SCI-induced oxidative stress and exerts neuroprotection by inhibiting lipid peroxidation, GSH depletion.

RESUMEN: La lesión traumática de la médula espinal provoca disfunción retrasada y muerte neuronal. La función mitocondrial deteriorada, la generación de especies reactivas de oxígeno (ERO) y la peroxidación lipídica ocurren poco después de una lesión traumática de la médula espinal (LTE), mientras que la activación de moléculas compensatorias que neutralizan ERO ocurre posteriormente. El objetivo del presente estudio fue investigar el efecto neuroprotector de Ganoderma lucidum en un modelo de LTE en ratas. Con el fin de inducir LTE, se utilizó un método estándar de pérdida de peso que indujo una lesión moderadamente grave (100 g / cm de fuerza) a T10. A los animales lesionados se les administró 20 ml / kg de Ganoderma lucidum o solución salina, por sonda gástrica, 30 minutos después de la lesión. A los siete días después de la lesión, las ratas fueron eutanasiadas por decapitación. Se tomaron muestras de médula espinal para el examen histológico y para la determinación de los niveles de malondialdehído (MDA) y glutatión (GSH), y la actividad de mieloperoxidasa (MPO). LTE causó una disminución significativa en el contenido de GSH de la médula espinal, además de aumentos significativos en los niveles de MDA y la actividad de MPO. Por otro lado, el tratamiento con Ganoderma lucidum invirtió todos estos parámetros bioquímicos así como las alteraciones histopatológicas inducidas por LTE. El deterioro de las funciones neurológicas debidas a LTE mejoró con el tratamiento con meloxicam. El presente estudio sugiere que Ganoderma lucidum, reduce el estrés oxidativo inducido por LTE y ejerce la neuroprotección mediante la inhibición de la peroxidación de los lípidos y agotamiento del GSH.

Effects of Ecballium elaterium on brain in a rat model of sepsis-associated encephalopathy.

Despite recent advances in antibiotic therapy, sepsis remains a major clinical challenge in intensive care units. Here we examined the anti-inflammatory and antioxidant effects of Ecballium elaterium (EE) on brain, and explored its therapeutic potential in an animal model of sepsis-associated encephalopathy (SAE) [induced by cecal ligation and puncture (CLP)]. Thirty rats were divided into three groups of 10 each: control, sepsis, and treatment. Rats were subjected to CLP except for the control group, which underwent laparatomy only. The treatment group received 2.5 mg/kg EE while the sepsis group was administered by saline. Twenty-four hours after laparotomy, animals were sacrificied and the brains were removed. Brain homogenates were prepared to assess interleukin 1beta (IL-1ß), interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-α), total antioxidant capacity (TAC), and total oxidant status (TOS). Brain tissue sections were stained by hematoxylin and eosin (H&E) to semi-quantitatively examine the histopathologic changes such as neuron degeneration, pericellular/perivascular edema and inflammatory cell infiltration in the cerebral cortex. We found a statistically significant reduction in brain tissue homogenate levels of TNF-α 59.5 ± 8.4/50.2 ± 6.2 (p = 0.007) and TOS 99.3 ± 16.9/82.3 ± 7.8 (p = 0.01) in rats treated with EE; although interleukin 6 levels were increased in the treatment group compared to the sepsis group, this was not statistically significant. Neuronal damage (p = 0.00), pericellular/perivascular edema and inflammatory cell infiltration (p = 0.001) were also significantly lower in the treatment group compared to those in the sepsis group. These data suggest that Ecballium elaterium contains some components that exert protective effects against SAE in part by attenuating accumulation of proinflammatory cytokines, which may be important contributors to its anti-inflammatory effects during sepsis.

Hyperbaric Oxygen Preconditioning Provides Preliminary Protection Against Doxorubicin Cardiotoxicity.

BACKGROUND: Doxorubicin (DOX) is generally recognized to have important cardiotoxic side effects. Studies are contradictory about the interaction between hyperbaric oxygen (HBO2) therapy and doxorubicin-induced cardiomyotoxicity. Recent data suggests that HBO2 therapy can lead to preconditioning of myocardium while generating oxidative stress. Herein we have investigated the effect of HBO2 therapy in a DOX-induced cardiomyocyte injury animal model. METHODS: Twenty-one rats were divided into three equal groups as follows: 1) Group 1 is a control group (without any intervention), used for evaluating the basal cardiac structures and determining the normal value of cardiacs and serum oxidative markers; 2) Group 2 is the doxorubicin group (single dose i.p. 20 mg/kg doxorubicin) for detecting the cardiotoxic and systemic effects of doxorubicin; 3) Group 3 is the doxorubicin and HBO2 group (100% oxygen at 2.5 atmospheric for 90 minutes, daily), for evaluating the effect of HBO2 in doxorubicin induced cardiotoxicity. At the end of the protocols, the hearts were harvested and blood samples (2 ml) were obtained. RESULTS: The doxorubicin treated animals (Group 2) had increased oxidative stress markers (both cardiac and serum) and severe cardiac injury as compared to the basal findings in the control group. Nevertheless, the highest cardiac oxidative stress index was detected in Group 3 (control vs. Group 3, p = 0.01). However, histological examination revealed that cardiac structures were well preserved in Group 3 when compared with Group 2. CONCLUSIONS: Our results suggest that HBO2 preconditioning appears to be protective in the doxorubicin-induced cardiotoxicity model. Future studies are required to better elucidate the basis of this preconditioning effect of HBO2.

Effects of local vibration and pulsed electromagnetic field on bone fracture: A comparative study.

The effectiveness of various therapeutic methods on bone fracture has been demonstrated in several studies. In the present study, we tried to evaluate the effect of local low-magnitude, high-frequency vibration (LMHFV) on rat tibia fracture in comparison with pulsed electromagnetic fields (PEMF) during the healing process. Mid-diaphysis tibiae fractures were induced in 30 Sprague-Dawley rats. The rats were assigned into groups such as control (CONT), LMHFV (15 min/day, 7 days/week), and PEMF (3.5 h/day, 7 days/week) for a three-week treatment. Nothing was applied to control group. Radiographs, serum osteocalcin levels, and stereological bone analyses of the three groups were compared. The X-rays of tibiae were taken 21 days after the end of the healing process. PEMF and LMHFV groups had more callus formation when compared to CONT group; however, the difference was not statistically significant (P = 0.375). Serum osteocalcin levels were elevated in the experimental groups compared to CONT (P ≤ 0.001). Stereological tests also showed higher osteogenic results in experimental groups, especially in LMHFV group. The results of the present study suggest that application of direct local LMHFV on fracture has promoted bone formation, showing great potential in improving fracture outcome. Bioelectromagnetics. 38:339-348, 2017. © 2017 Wiley Periodicals, Inc.

Protective effects of l-glutamine against toxicity of deltamethrin in the cerebral tissue.

BACKGROUND: Deltamethrin (DLM) is a broad-spectrum synthetic dibromo-pyrethroid pesticide that is widely used for agricultural and veterinary purposes. However, human exposure to the pesticide leads to neurotoxicity. Glutamine is one of the principal, free intracellular amino acids and may also be an antioxidant. This study was undertaken in order to examine the neuroprotective and antioxidant potential of l-glutamine against DLM toxicity in female Wistar albino rats. MATERIALS AND METHODS: The rats were divided into the following groups (n=10): Group I: control (distilled water; 10 mL/kg, po one dose), Group II: l-glutamine (1.5 g/kg, po one dose), Group III: DLM (35 mg/kg, po one dose), and Group IV: DLM (35 mg/kg, po one dose) and l-glutamine (1.5 g/kg, po one dose after 4 hours). Total oxidant status (TOS), total antioxidant status (TAS), tumor necrosis factor-α, interleukin (IL)-1ß, and IL-6 levels and apoptosis were evaluated in brain tissue. RESULTS: DLM-treated animals had a significant increase in brain biochemical parameters, as well as TOS and TAS. Furthermore, the histopathological examination showed neuronal cell degeneration in the cerebral tissue. l-Glutamine treatment decreased the elevated brain levels of TOS and neuronal cell degeneration. There was no difference in tumor necrosis factor-α, IL-1ß, and IL-6 levels between the groups. CONCLUSION: l-Glutamine may reduce the toxic effects of DLM in the cerebral tissue through antioxidant properties.

Evaluation of New Biomarkers in the Prediction of Malignant Mesothelioma in Subjects with Environmental Asbestos Exposure.

INTRODUCTION: The purpose of this study was to investigate the potential value of certain biomarkers in predicting the presence of malignant pleural mesothelioma (MPM) in individuals environmentally exposed to asbestos. METHODS: This prospective study investigated three groups; a control group composed of 41 healthy subjects, an asbestos exposure group consisting of 48 individuals, and a MPM group consisting of 42 patients. Serum levels of soluble mesothelin-related peptide (SMRP), thioredoxin-1 (TRX), epidermal growth factor receptor (EGFR), fibulin-3, syndecan-1 (SDC-1), and mesothelin were determined. RESULTS: Benign pleural plaques were present in 27 (58.3 %) of the individuals in the asbestos exposure group. The asbestos exposure group had significantly higher mean TRX, SMRP, and mesothelin levels compared to the control group (p = 0.023, p = 0.011, and p < 0.001, respectively). Compared to the asbestos exposure group, the MPM group had significantly higher mean EGFR, TRX, SMRP, and fibulin-3 levels (p = 0.041, p = 0.023, p = 0.002, and p = 0.001, respectively), and significantly lower mean SDC-1 levels (p = 0.002). Unlike the other biomarkers, SMRP and TRX levels increased in a graded fashion among the control, asbestos exposure, and MPM groups, respectively. Area under the curve values for SMRP and TRX were 0.86 and 0.72, respectively (95 % CI 0.79-0.92 and p < 0.001 for SMRP, and 95 % CI 0.62-0.81 and p < 0.001 for TRX). The cut-off value for SMRP was 0.62 nmol/l (sensitivity: 97.6 %, specificity: 68.9 %, positive predictive value (PPV): 56.2 %, and negative predictive value (NPV): 98.3 %) and for TRX was 156.67 ng/ml (sensitivity: 92.9 %, specificity: 77.6 %, PPV: 41.4 %, and NPV: 92.1 %). The combination of the biomarkers reached a sensitivity of 100 %, but had lower specificity (as high as 27.7 %). CONCLUSIONS: Serum biomarkers may be helpful for early diagnosis of MPM in asbestos-exposed cases. SMRP and TRX increased in a graded fashion from the controls to asbestos exposure and MPM groups. These two seem to be the most valuable biomarkers for the diagnosis of MPM, both individually and in combination.

Protective effects of honokiol on ischemia/reperfusion injury of rat ovary: an experimental study.

AIM: The purpose of this study was to investigate the protective effect of honokiol on experimental ischemia/reperfusion injury of rat ovary. MATERIALS AND METHODS: A total of 40 female Wistar albino rats were used in this study. The rats were divided into five groups as follows: sham (Group I), torsion (Group II), torsion + detorsion (Group III), torsion + detorsion + saline (Group IV), and torsion + detorsion + honokiol (Group V). Bilateral adnexa in all the rats except for those in the sham group were exposed to torsion for 3 hours. The rats in Group IV were administered saline, whereas the rats in Group V were administered honokiol by intraperitoneal route 30 minutes before detorsion. Tissue and plasma concentrations of malondialdehyde and nitric oxide were determined. Ovarian tissue was histologically evaluated. Data analyses were performed by means of Kruskal-Wallis test and Mann-Whitney U-test (Bonferroni correction) in SPSS 15.0 (Statistical Package for Social Sciences; SPSS Inc., Chicago, IL, USA). RESULTS: The torsion and detorsion groups had higher scores in vascular congestion, hemorrhage, and inflammatory cell infiltration compared with the sham group (P<0.005). In addition, total histopathological scores were significantly higher in the torsion and detorsion groups compared with the sham group (P<0.005). A significant reduction was observed in hemorrhage, inflammatory cell infiltration, and cellular degeneration scores, of all histopathological scores, in the honokiol group (P<0.005). Ovarian tissue concentrations of malondialdehyde were significantly higher in the torsion and detorsion groups compared with the sham and honokiol groups (P<0.005). Ovarian tissue concentrations of nitric oxide, on the other hand, were significantly higher in the torsion group compared with the sham, saline, and honokiol groups (P<0.005). CONCLUSION: Honokiol has a beneficial effect on ovarian torsion-related ischemia/reperfusion injury.

Serum levels of neopterin, inflammatory markers and oxidative stress indicators in hyperemesis gravidarum.

AIM: To investigate whether serum levels of neopterin and inflammatory markers including C-reactive protein (CRP), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and oxidative status indicators were altered in patients with hyperemesis gravidarum (HG) compared to asymptomatic pregnant women. METHODS: This cross-sectional study was performed including 30 pregnant women with HG (mean age: 30.67 ± 6.68) and 30 asymptomatic pregnant women (mean age: 28.00 ± 5.30). Demographic features, obstetric history, and the Pregnancy Unique Quantification of Emesis/Nausea (PUQE) index were noted. Complete blood count, serum biochemical assay and measurement of CRP, TNF-α, IL-6, total antioxidant status and total oxidative status (TOS) levels were taken and compared between groups. RESULTS: White blood cell count (P = 0.013), platelet count (P = 0.015), TOS (P < 0.001), and PUQE score (P < 0.001) were remarkably higher in HG pregnancies. On the other hand, serum levels of lactate dehydrogenase, (P < 0.001), sodium (P < 0.001), potassium (P < 0.001), chloride (P < 0.001) and TAS (P < 0.001) were higher in the control group. There was no difference in the levels of neopterin, CRP, TNF-α and IL-6. In patients with HG, a positive correlation was detected between TOS and serum levels of lactate dehydrogenase, while TNF-α, IL-6 and neopterin were positively correlated with hemoglobin levels. CONCLUSION: Our results demonstrated no association between inflammation and HG. Elucidation of the pathophysiology and complex interaction between various inflammatory processes in HG necessitates further trials on larger series.

Histopathological and Biochemical Effects of Ecballium elaterium on Sepsis-Induced Lung Injury.

PURPOSE: The aim of this study was to investigate the role of Ecballium elaterium (EE) on sepsis-induced lung injury. MATERIALS AND METHODS: A total of 30 male rats were divided into three groups as follows: control, sepsis, and treatment groups (sepsis + EE) with each group containing 10 rats. A rat model of sepsis induced by cecal ligation and puncture (CLP) was used. In the treatment group, rats were injected intraperitoneally with 2.5 mg/kg EE after CLP. Interleukin-6 (IL-6), tumor necrosis factor (TNF)-α, total antioxidant status (TAS), total oxidant status (TOS), and oxidative stress index (OSI) values after a 24-hr period were measured via cardiac puncture. Animals were harvested after the procedure and biochemical analysis was done and histopathological changes of the tissue sections of lungs were examined thereafter. RESULTS: A statistically significant decrease was observed in the IL-6 (p < .05), TNF-α (p < .05), and TOS (p < .01) levels in the sera of the treatment group compared to those of the sepsis group. Following the treatment, the TOS (p = .01) and OSI (p < .05) levels in the lung tissue of rats indicated a statistically significant decrease compared to those of the sepsis group. The histopathological follow-up undertaken after the administration of the EE treatment to septic rats showed significantly lower values of alveolar wall thickness (p < .001), interstitial edema (p = .018), and neutrophil infiltration (p = .047). CONCLUSION: EE treatment may have beneficial effects on sepsis-induced lung injury, and therefore has potential for clinical use.

The antioxidant effects of pomegranate extract on local and remote organs in a mesenteric ischemia and reperfusion model.

OBJECTIVES: We investigated whether pomegranate extract plays a protective antioxidant role against mesenteric ischemia-reperfusion injury (IR), which can lead to a systemic response and damage distant organs, such as the lung, liver, and kidney. METHODS: Forty female Wistar-Albino rats were separated into four groups: laparotomy, laparotomy + PG, mesenteric IR, and mesenteric IR and pomegranate (IR + PG). In the laparotomy + PG and IR + PG groups, pomegranate (225 mg/kg) was given by oral gavage at the beginning of the study. Ischemia was induced for 30 minutes, and reperfusion was subsequently allowed for 60 minutes in the IR and IR + PG groups. The malondialdehyde (MDA) and total antioxidant activity (AOA) levels were evaluated in blood samples. Additionally, all tissues were removed for the measurement of AOA and total oxidant status as well as for subsequent histopathological evaluation. The oxidative stress index was calculated. RESULTS: Histopathological changes in all organs were significantly higher in the IR group and significantly lower in the IR + PG group vs. the other groups. Serum MDA levels were significantly lower in the IR + PG group than in the IR group. No significant difference was found in AOA levels of the groups. DISCUSSION: These data may explain the positive protective effects of pomegranate based on the histopathologic findings in ischemic conditions in an intestinal IR injury model.

Novel markers of endothelial dysfunction and inflammation in Behçet's disease patients with ocular involvement: epicardial fat thickness, carotid intima media thickness, serum ADMA level, and neutrophil-to-lymphocyte ratio.

The etiology of Behçet's disease (BD) has not been fully elucidated. However, immunological and environmental factors, endothelial dysfunction (ED), and genetic susceptibility have been proposed to play a role. In this study, we aimed to evaluate epicardial fat thickness (EFT) together with serum asymmetric dimethylarginine (ADMA), carotid intima media thickness (CIMT), and neutrophil-to-lymphocyte ratio (NLR) in BD patients with ocular involvement. Thirty-six ocular BD patients (17 active and 19 inactive ocular involvement), and 35 age and sex-matched healthy controls were enrolled to this cross-sectional study. All patients underwent examinations with transthoracic echocardiography and carotid Doppler ultrasound. Serum ADMA levels, CIMT, EFT, and NLR were compared between groups, and their association with disease activity was evaluated. Behçet's disease patients had higher WBC counts, neutrophil counts, NLR, CIMT, EFT values, and serum ADMA levels than do healthy controls. The other biochemical, hematological, and echocardiographic parameters were comparable between the two groups. Behçet's disease duration was positively correlated with EFT and CIMT. Multivariate logistic regression analysis revealed that increased serum ADMA concentration and CIMT are independently associated with BD. Neutrophil counts, NLR, and serum ADMA level were higher, and lymphocyte count was lower in patients with active ocular BD compared to those of inactive ocular BD group. Carotid intima media thickness, serum ADMA level, EFT, and NLR were increased in ocular BD patients compared to healthy subjects. In addition, both serum ADMA level and NLR were associated with disease activity of ocular involvement. Increase in disease duration was associated with increase in CIMT and EFT which suggests that anatomical changes occur in time during the disease course. Increased CIMT, serum ADMA level, EFT, and NLR may provide new clues about the role of ED and inflammation in the etiopathogenesis of BD.

Nebivolol Ameliorates Hepatic Ischemia/Reperfusion Injury on Liver But Not on Distant Organs.

INTRODUCTION: Hepatic ischemia/reperfusion injury may occur after large tumor resection and liver transplantation procedures. Nitric oxide was shown to have protective effects on ischemia/reperfusion injury. Nebivolol is a compound that has been reported to improve nitric oxide release. We evaluated the effects of nebivolol in a rat liver ischemia/reperfusion model. METHODS: A total of 40 rats were randomly divided into four groups (n = 10 each). Group I underwent only laparotomy, Group II was administered nebivolol and then underwent laparotomy, Group III underwent laparotomy and hepatic ischemia/reperfusion, and Group IV was administered nebivolol and then underwent laparotomy and hepatic ischemia/reperfusion. Serum AST, ALT, urea, and creatinine levels, and TAS and TOS levels of liver, lung, and kidney tissues were determined. Histopathological determination was also performed. RESULTS: Nebivolol significantly reduced liver function tests in group IV, but it did not improve renal functions. Oxidative stress and abnormal histopathological findings were found to be reduced in liver tissue in group IV. Although the oxidative stress was increased after hepatic ischemia/reperfusion, nebivolol could not reduce the oxidative stress in kidney tissue. There were no significant differences between group III and group IV in terms of the histopathological changes in kidney tissue. There were no significant differences in lung tissue between the groups. CONCLUSIONS: The results of this study suggest that nebivolol has protective effects on liver but not on distant organs in a hepatic ischemia/reperfusion injury model. These experimental findings indicate that nebivolol may be useful in the treatment of hepatic ischemia/reperfusion injury.

Severe pre-eclampsia complicated by HELLP syndrome alterations in the structure of the umbilical cord (morphometric and immunohistochemical study).

The aim of this study was to evaluate the morphometric and immunohistochemistry in umbilical cords from patients with severe pre-eclampsia with and without haemolysis, elevated liver enzymes and low platelets (HELLP) syndrome. The patient and control groups were similar according to baseline obstetric characteristics. White blood cell count in patients with HELLP syndrome and the control group was significantly increased among patients with HELLP syndrome (p < 0.001). Morphometric examination and endothelial core length were significantly different between the groups. In the umbilical cord cross-section of the HELLP group, endothelial cell degeneration in the vessel wall and basement membrane thickening were observed. In the muscle layer of blood vessels, the following disorders were found: increased collagen fibres in the muscle cell, hyperplasia and separation of muscle fibres as well as edema in the intermediate connective tissue. Immunohistochemical analysis showed that endothelial cells, basal membrane and fibroblast cells in the HELLP group expressed high levels of CD44. Vessel wall and amniotic epithelial basement membrane thickening were observed in the HELLP group. Matrix metalloproteinase 9 (MMP9) was expressed. Fibroblast and smooth muscle cells were fusiform and showed a positive reaction to immunohistochemical staining of α-actin smooth muscle.

Paraoxonase and arylesterase activities in dipper and non-dipper prehypertensive subjects.

Paraoxonase-1, a high-density lipoprotein linked enzyme complex, was shown to be decreased in several cardiovascular diseases. We aimed to explore whether serum paraoxonase and arylesterase activities differ in dipper and non-dipper prehypertensive subjects compared to healthy controls.Sixty prehypertensive subjects and 30 controls were enrolled. All subjects underwent echocardiographic assessment and 24-hour ambulatory blood pressure monitoring (ABPM). According to the blood pressure (BP) course on ABPM, prehypertensive subjects were categorized into two: non-dipper prehypertensive (NDPH) and dipper prehypertensive (DPH) groups. Serum paraoxonase and arylesterase activities were detected spectrophotometrically.Paraoxonase and arylesterase activities were significantly lower in patients with NDPH compared to both DPH and control groups. Both paraoxonase and arylesterase activities showed significant negative correlations with BP and left ventricular mass index.We have demonstrated that NDPH subjects have lower paraoxonase and arylesterase activities compared to DPH subjects and normotensives. Further prospective studies are needed to clarify the role of paraoxonase and arylesterase activities in the development of overt hypertension in prehypertensive subjects.

Glutamine provides effective protection against deltamethrin-induced acute hepatotoxicity in rats but not against nephrotoxicity.

BACKGROUND: The aim of this study was to investigate the protective effects of L-glutamine (GLN) against liver and kidney injury caused by acute toxicity of deltamethrin (DLM). MATERIAL AND METHODS: Thirty-two rats were indiscriminately separated into 4 groups with 8 rats each: control group (distilled water; 10 ml/kg, perorally [p.o.]), DLM group (35 mg/kg p.o. one dose.), GLN group (1.5 gr/kg, p.o. single dose.) and DLM (35 mg/kg p.o. one dose.) + GLN group (1.5 gr/kg, p.o. one dose after 4 hours.). Testing for total antioxidant status (TAS), total oxidant status (TOS), interleukin-1 beta (IL-1ß), tumor necrosis factor-alpha (TNF-α), and interleukin-6 (IL-6) analyses were performed on tissue samples, and alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), urea, and creatinine were analyzed on serum samples. Liver and kidney samples were histopathologically analyzed. RESULTS: The TOS level in liver was significantly higher in the DLM group than in the control group, and the level in DLM+GLN group was considerably lower than in the DLM group. The TAS level in the DLM+GLN group was considerably higher than in the control and DLM groups. The TAS level in kidney tissues was considerably lower in the DLM group than in controls, but was similar to other groups. Histopathological analyses of liver tissues established a significant difference between DLM and DLM+GLN groups in terms of grade 2 hepatic injury. However, no significant difference was found between DLM and DLM+GLN groups in terms of kidney injury. CONCLUSIONS: Glutamine leads to significant improvement in deltamethrin-induced acute hepatotoxicity in terms of histopathologic results, tissue oxidative stress parameters, and serum liver function marker enzymes.

The protective role of glutamine against acute induced toxicity in rats.

CONTEXT: Deltamethrin (DLM) is an insecticide commonly used to protect agricultural crops against pests. QT prolongation with malignant ventricular arrhythmias are amongst the most common cardiovascular complications. DLM intoxication cause decreased level of antioxidant enzymes. Glutamine is the precursor of glutathione which is an antioxidant and has been demonstrated to improve outcome after several critical illnesses. OBJECTIVE: We hypothesized that glutamine, by means of antioxidant characteristics, may antagonize the cardiotoxic effects of DLM. MATERIALS AND METHODS: All experiments were performed on 8-week-old male Wistar albino rats. The rats were divided into following groups (n = 10); Group I: control, Group II: l-glutamine, Group III: DLM, Group IV: DLM and after 4 h l-glutamine. Total antioxidant status (TAS), total oxidant status (TOS) and parameter analyses were performed in cardiac tissue. RESULTS: We found that TAS was higher and TOS lower in DLM group. We also found that interstitial edema and inflammatory cell infiltration was significantly more frequent in DLM group and QT and QTc of DLM group were higher than others. DISCUSSION: Recent studies have shown that several special amino acids, such as glutamine, glycine, arginine and taurine, exhibit cytoprotective effect on the cardiocyte, and have established the cardioprotective properties of glutamine. CONCLUSION: In this study, we showed the protective role of glutamine against cardiotoxic effects of DLM in rats. This protective effect was confirmed by showing both tissue level improvement in oxidative stress markers and improvement in prolonged QT interval.

Effects of Potentilla fulgens as a Prophylactic Agent for Ischemia/Reperfusion Injury in the Rat Ovary.

OBJECTIVE: To investigate the effects of Potentilla fulgens as a prophylactic agent on ischemia/reperfusion (I/R) injury in the rat ovary. STUDY DESIGN: A total of 32 Wistar rats were divided into 4 equal groups: (I) sham, (II) ischemia, (III) ischemia + reperfusion, and (IV) IR + Potentilla fulgens. In groups I and II, ovary torsion was not performed and no drug was administered. In group III, 1 hour of ischemia and 2 hours of reperfusion were performed and no drug was given. Group IV received 400 mg/kg/day Potentilla fulgens intraperitoneally 5 days before I/R injury. RESULTS: The detorsion group showed preantral ovarian follicles and corpus luteum around the blood vessels and positive expression of vascular endothelial growth factor (VEGF). In the Potentilla fulgens group (IV) the stromal vascular endothelium with weak expression of VEGF was detected in small areas, and the ovarian follicles and the corpus luteum showed negative expression of VEGF. In the detorsion group the theca cells and apoptotic cells in preantral follicles showed positive expression of E-cadherin in the ovarian surface epithelium. Moreover, the E-cadherin expression was found to be positive in terms of follicular development, theca cells, granulosa cells, and corpus luteum. Potentilla fulgens, given after ischemic injury and apoptosis, was seen to decrease the effect of Bcl-2 expression. CONCLUSION: These results provide compelling evidence that the expression of E-cadherin in the ovary is an important component of ovarian function.