Homocysteine, hopelessness, rumination, affective temperaments, and clinical course in patients with bipolar disorder-1.

PURPOSE: This study aimed to explore the associations between homocysteine, rumination, affective temperaments, clinical features, and hopelessness in bipolar disorder-1 (BD-1). MATERIALS AND METHODS: In total, 57 euthymic patients with BD-1 and 57 healthy controls were included. The Beck Hopelessness Scale (BHS), Temperament Evaluation of Memphis, Pisa, Paris, and San Diego-Autoquestionnaire (TEMPS-A), and Ruminative Responses Scale Short Form (RRS-SF) were administered. Homocysteine, folate, and vitamin B12 levels were measured. RESULTS: The BHS total (p = 0.047), TEMPS-A irritable (p = 0.007), and TEMPS-A cyclothymic (p= 0.001) scores were significantly higher than the control group in the BD-1 group. Hyperhomocysteinemia (HHcy) was found in 33.3% of the patients (n = 19). In the HHcy group, age of onset of disease (p = 0.020) was significantly lower than the non-HHcy group in patients. Previous suicide attempt number was significantly correlated with scores of reflective pondering, brooding, and global rumination in BD-1 (p Ë‚ 0.05). Except for hyperthymic temperament, all types of affective temperaments were correlated with the scores of RRS-SF brooding (p Ë‚ 0.05) in the BD-1 group. The RRS-SF brooding scores significantly correlated with the BHS total scores (r = 0.263, p < 0.05); the TEMPS-A hyperthymic (ß = -0.351, p = 0.001) and TEMPS-A irritable (ß = 0.536, p < 0.001) scores significantly predicted the BHS total scores in the BD-1 group. CONCLUSIONS: The findings may lead clinical efforts and future clinical trials to explore and intervene in related sources and presentations of BD-1's adverse consequences.

Evaluation of Serum Paraoxonase, Myeloperoxidase, and HDL-Cholesterol Levels in Acute Myeloid Leukemia.

Inflammation and oxidative stress play a significant role in the pathogenesis of acute myeloid leukemia. While myeloperoxidase carries pro-oxidant effects, HDL-cholesterol and paraoxonase have antioxidant properties. Therefore, we evaluated serum paraoxonase, myeloperoxidase, and HDL-cholesterol levels in cases with acute myeloid leukemia. Myeloperoxidase, paraoxonase, and HDL-cholesterol levels in 40 acute myeloid leukemia patients and 18 healthy individuals were determined. The relationship between these parameters and other prognostic factors, as well as their association with response to chemotherapy, was investigated. Myeloperoxidase levels were higher, while paraoxonase and HDL-cholesterol levels were lower in acute myeloid leukemia cases compared to the control group (p < 0.001, p < 0.001, p = 0.006, respectively). The myeloperoxidase level was significantly negatively correlated with paraoxonase and HDL-c levels (r = - 0.64, p < 0.001; r = - 0.27, p = 0.02, respectively). Paraoxonase level was positively correlated with HDL level (r = 0.34, p = 0.04). Lactate dehydrogenase level was negatively correlated with HDL-c and paraoxonase levels and positively correlated with myeloperoxidase level (r = - 0.37, p = 0.019; r = - 0.35, p = 0.04; r = 0.45, p = 0.03, respectively). Following complete remission induction treatment, cases with complete remission had lower myeloperoxidase levels and higher HDL-cholesterol and paraoxonase levels compared to other cases (p = 0.03, p = 0.01, p = 0.04, respectively). Myeloperoxidase levels are higher, while paraoxonase and HDL-cholesterol levels are lower in acute myeloid leukemia cases. The obtained findings emphasize the potential importance of inflammation and oxidative stress in the pathogenesis of acute myeloid leukemia. These parameters can be used as biomarkers for prognosis prediction and prediction of response to chemotherapy.

Release of mercury from amalgam filling and its relationship with metallothionein and superoxide dismutase.

Purpose: This study aims at determining the amount of mercury released over time from amalgam after treatment in healthy subjects and to examine the relation of mercury with serum MT-1 and SOD-1 levels. Materials and methods: Amalgam filling was applied to the 15 subjects aged 19-22 years and blood samples were collected before treatment and 1 day, 7 days, 21 days and 35 days after treatment. Mercury analysis of serum samples was performed using Inductively Coupled Plasma Mass Spectrometry (ICP-MS). In addition, MT-1 and SOD-1 levels in serum samples were measured using commercial enzyme-linked immunosorbent assay (ELISA). Friedman test and Spearman's correlation analysis was performed to analyse the data. p value was interpreted in significance level of 0.05. Results: As a result of the analysis for MT-1, it was found that the values decreased over time and this decrease was statistically significant after 21 days (p<0.05). In addition, it was found that SOD-1 decreased over time, but this decrease was not statistically significant . In terms of released mercury, there was no statistically significant difference among the values of mercury released over time . According to the results of correlation analysis, no statistically significant relationship was found among the variables. Conclusion: The results of the present study indicated that the amount of mercury released from the tested amalgam were found to be tolerable and no significant relationship was found between MT-1 and SOD-1.

Assessment of hypolipidemic and anti-inflammatory properties of walnut (Juglans regia) seed coat extract and modulates some metabolic enzymes activity in triton WR-1339-induced hyperlipidemia in rat kidney, liver, and heart.

Atherosclerosis and cognitive impairment are both influenced by hyperlipidemia. Due to their high margin of safety and low cost, natural chemicals have recently attracted particular attention in the context of the treatment of disease. Hence, the purpose of this study was to investigate the possible amendatory impact of ethanol extract walnut (Juglans regia) seed coat (E-WSC) on some metabolic enzymes (glutathione reductase (GR), paraoxonase-1 (PON1), aldose reductase (AR), sorbitol dehydrogenase (SDH), acetylcholinesterase (AChE), glutathione S-transferase (GST), and butyrylcholinesterase (BChE)) activity in the liver, kidney, and heart of rats with Triton WR-1339-induced hyperlipidemia. Rats were divided into five groups: control group, HL-Control group (Triton WR-1339 400 mg/kg, i.p administered group), E- WSC + 150 (150 mg/kg,o.d given group), E- WSC + 300 (E- WSC 300 mg/kg, o.d given group) and HL+ E-WSC + 300 (Group receiving E- WSC 300 mg/kg, o.d 30 min prior to administration of Triton WR-1339 400 mg/kg, i.p). In HL-Control, AR, SDH, and BChE enzyme activity was significantly increased in all tissues compared to the control, while the activity of other studied enzymes was significantly decreased. The effects of hyperlipidemia on balance were improved and alterations in the activity of the investigated metabolic enzymes were prevented by E-WSC. As a result, promising natural compounds that can be used as adjuvant therapy in the treatment of cognitive disorders and hyperlipidemia may be found in E-WSC powder.

Role of TGF-ß1 and PDGF-B in Crimean-Congo hemorrhagic fever in Eastern Anatolia Region in Turkey.

BACKGROUND & OBJECTIVES: In this study, we aimed to investigate the relationship between serum TGF-ß1 and PDGF-B levels with the pathogenesis, clinical course and prognosis of adult Crimean-Congo hemorrhagic fever (CCHF) patients. METHODS: 50 adult patients and 30 healthy individuals as a control group were included in the study, who were followed up and treated with the diagnosis of CCHF at the Atatürk University Faculty of Medicine Infectious Diseases and Clinical Microbiology Clinic, between March 2017 and September 2019 in Eastern Anatolia Region in Turkey. Blood samples were taken from patients on the first day of their hospitalization and on the sixth day of their complaints. TGF-ß1 and serum PDGF-B levels were studied by ELISA method using commercial kits, from serum samples taken from CCHF patient group and individuals in healthy control group and stored at -80°C. RESULTS: While the serum TGF- ß1 levels of patients with CCHF were found to be significantly higher on the sixth day of their complaints compared to the first day of hospitalization (42.33 ± 15.42, 28.40 ± 7.06, p = 0.001, respectively), the serum PGDF-B levels were found to be significantly lower on the sixth day of their complaints compared to those measured on the day of hospitalization (62.14 ± 19.75, 93.96 ± 20.02, respectively, p = 0.001). INTERPRETATION & CONCLUSION: Serum TGF-ß1 levels are higher and PDGF-B levels are lower in CCHF patients with severe disease, indicating that serum TGF-ß1 and PDGF-B play an important role in the pathogenesis of CCHF.

The protective efficacy of Quercetin and Naringenin against radiation-related submandibular gland injury in female rats: A histopathological, immunohistochemical, and biochemical study.

OBJECTIVE: In this study, we aimed to reveal the effectiveness of Quercetin and Naringenin in preventing radiotherapy-associated submandibular gland injury. DESIGN: The study was conducted using 48 adult female Sprague Dawley rats. The rats were randomly assigned into six groups of eight animals each. Group 1 represented the control group. The rats received only Naringenin was regarded as Group 2, received only Quercetine was regarded as Group 3. The rats exposed to radiotheraphy at a dose of 15 Gy was regarded as Group 4. Rats in group 5 were received Naringenin at a dose of 50 mg/kg daily for one week prior to radiotheraphy exposition while rats in group 6 was received Quercetine at a dose of 50 mg/kg daily for one week prior to radiotheraphy. Rats were sacrificed after radiotheraphy and submandibular glands were dissected for biochemical and immunohistochemical evaluations. RESULTS: Quercetin and Naringenin were found to have protective effect against radiation-induced damage. Naringenin and Quercetin increased the levels of Superoxide dismutase, Catalase, Glutathione Peroxidase, Glutathione and Total antioxidant status while decreasing the levels of Myeloperoxidase and Total oxidant status. Also, these agents inhibited the expression of Tumor Necrosis Factor-α and 8-hydroxy 2-deoxyguanosine immunohistochemically. CONCLUSIONS: With their powerful antioxidant and anti-inflammatory effects, Naringenin and Quercetin exhibit histopathological, immunochemical, and biochemical protection against radiation-related submandibular gland injury. In addition, Quercetin was found to be superior to Naringenin in terms of this efficacy.

The hepato-renal protective potential of walnut seed skin extract against acute renal ischemia/reperfusion damage.

Acute kidney damage is defined as a sudden change in kidney functions that prevents the removal of nitrogenous wastes from the body, thus disrupting the body's fluid and electrolyte balance. When acute kidney injury occurs, the kidneys and liver are most affected in the body. Agents used in the treatment of acute kidney injury often have nonsteroidal anti-inflammatory properties that can produce toxic effects on the gastrointestinal tract and kidneys. Natural antioxidants can be recommended as an alternative to existing treatment or in combination to protect tissues against these toxic effects. Therefore, we conducted our current study on whether walnut seed skin (WSS) extract might have hepato-renal protective effects in kidney-damaged Sprague-Dawley rats. This study is the first to use walnut seed skin extract in liver and kidney tissues in renal ischemia/reperfusion (IR) injury. Female Sprague-Dawley rats were randomly divided into three groups: Healty control (HC), renal IR (50 min ischemia - 3 h reperfusion), and renal IR + 450 mg/kg/p.o. WSS extract (the rats were treated with WSS extract orally once 1 h before the IR procedure). For this purpose, blood, liver and kidney tissues of rats were used. In serum samples, aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), urea and creatinine values were determined separately for the administration groups. We also performed histopathological studies on liver and kidney tissues. Finally, gene markers (endothelial nitric oxide synthase (eNOS), interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α), Caspase-4 and Caspase-9) determined to evaluate the anti-oxidant, anti-inflammatory and apoptotic effect of walnut seed skin were measured by q-RT PCR method. As a result of the study it was determined that pre-application of WSS extract improved the deteriorated serum parameters in rats with renal ischemia. In the histopathological analysis results, it was observed that WSS had a protective effect on kidney and liver tissue. In studies on gene expression, although there were different and contradictory results for liver and kidney tissue, we determined that WSS was more protective on liver tissue. In conclusion, the healing potential of WSS in renal and hepatic tissues seems to act by inhibiting the inflammatory response, oxidative stress and apoptosis. Therefore, the potential of this extract is remarkable and may serve as a potential therapeutic that may protect against acute organ damages due to renal IR.

Evaluation of the relationship between macrophage migration inhibitory factor level and clinical course in patients with COVID-19 pneumonia.

The COVID-19 pandemic, which has ravaged our world for more than a year, still shapes our agenda with a scale of intensity that fluctuates over time. In our study, we aimed to determine the correlation between serum migration inhibitory factor (MIF) level and disease severity in COVID-19 with different prognoses. Between 15 October 2020 and 20 January 2021, 110 patients over the age of 18 who were diagnosed with COVID-19 and 40 volunteer healthcare personnel were included in our study. MIF levels were measured by enzyme-linked immunosorbent assay. In the comparison of serum MIF values in the patient and control group, it was observed that the MIF level was significantly higher in patients with both moderate and severe COVID-19 levels compared to the control group (p = 0.001, 0.001). In the comparison of serum MIF values of moderate to severe COVID-19 patients, it was observed that MIF level was higher in severe patients (p = 0.001). In the receiver operating characteristic curve analysis performed to differentiate between severe and moderate COVID-19 patients with MIF levels, the area under the curve was observed as 0.78. When the cutoff value of the MIF level was taken as 4.455 ng/ml, the sensitivity was 83% and the specificity was 62%. Failure to adequately balance the pro-inflammatory cytokines synthesized in COVID-19 with anti-inflammatory effect is the most important reason for the aggravation of the disease course. Playing a role in pro-inflammatory cytokine synthesis, MIF can provide important information about the disease prognosis in the early period.

Could VEGF-D level have a role in clinical risk scoring, estimation of thrombus burden, and treatment in acute pulmonary thromboembolism?

OBJECTIVE: Pulmonary embolism (PE) is usually a complication of deep vein thrombosis and is an important cause of mortality and morbidity. Vascular endothelial growth factor D (VEGF-D) is a secretory protein that plays a role in the remodelling of blood vessels and the lymphatic system. This study aimed to determine the relationship between VEGF-D level and clinical risk scoring in patients with PE. METHODS: The study included 117 patients admitted for PE that were divided into four groups: high-risk patients (n = 35), high-intermediate-risk patients (n = 30), low-intermediate-risk patients (n = 24), and low-risk patients (n = 28). Plasma VEGF-D was measured from peripheral venous blood samples (5 mL) using a commercial enzyme-linked immunosorbent assay (ELISA) kit. Pulmonary Artery Obstruction Index (PAOI) was calculated from CT angiography imaging. RESULTS: There was no significant difference in troponin-I and NT-proBNP levels between the high-intermediate-risk and high-risk PE patients (P = .134, .146). VEGF-D and PAOI levels were found to be statistically significantly higher in high-risk patients compared with high-intermediate-risk patients (P = .016, .001). VEGF-D level was moderately correlated with mean pulmonary artery pressure and PAOI (r = .481, P = .01; r = .404, P = .01). In ROC curve analysis, a cut-off of 370.1 pg/mL for VEGF-D had 91.4% sensitivity and 67% specificity in the differentiation of high-intermediate-risk and high-risk PE patients. CONCLUSION: This study showed that plasma VEGF-D level was more reliable than troponin-I and NT-proBNP in clinical risk scoring and demonstrating thrombus burden. VEGF-D can be used as a biomarker in clinical risk scoring and estimation of thrombus burden in patients with acute PE.

Determination of Pentraxin-3, Interleukin-8 and Vascular Endothelial Growth Factor Levels in Patients with Gastric Adenocarcinoma.

INTRODUCTION AND AIM: The purpose of this study was to determine the value, in terms of diagnosis, resectability and prognosis of pentraxin-3 (PTX3), interleukin-8 (IL-8) and vascular endothelial growth factor (VEGF) in cases of gastric adenocarcinoma, an important condition both worldwide and in Turkey, and to determine their levels in order to contribute to elucidating the pathogenesis of the disease. MATERIALS AND METHODS: Serum was separated from blood specimens collected from 45 patients diagnosed with gastric adenocarcinoma and from a 30-member healthy control group. Serum PTX3, IL-8 and VEGF levels were studied by ELISA method. RESULTS: Serum PTX3 values differed significantly between the patient group and the control group (p <0.05). Serum IL-8 values also differed significantly between the patient group and the control group (p <0.05). A significant difference was also observed between serum VEGF values in the patient group and the control group (p <0.05). Significant correlation was determined between serum PTX3 and VEGF (p <0.01; r=0.833), between serum PTX3 and IL-8 (p <0.01; r=0.818), and between serum VEGF and IL-8 (p <0.01; r=0.803), measurements when the entire study population was evaluated irrespectively of groups. CONCLUSION: Serum PTX3, IL-8 and VEGF levels decreased in cases of gastric adenocarcinoma compared to the control group, and their levels affected one another.
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Evaluation of the relationship between KIM-1 and suPAR levels and clinical severity in COVID-19 patients: A different perspective on suPAR.

Coronavirus disease 2019 (COVID-19) is one of the most pressing health problems of this century, but our knowledge of the disease is still limited. In this study, we aimed to examine serum-soluble urokinase plasminogen activator receptor (suPAR) and kidney injury molecule 1 (KIM-1) levels based on the clinical course of COVID-19. Our study included 102 patients over the age of 18 who were diagnosed as having COVID-19 between September 2020 and December 2020 and a control group of 50 health workers over the age of 18 whose severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) PCR results were negative. KIM-1 was measured by ELISA and suPAR by suPARnostic™ assay. Analysis of previously identified variables of prognostic significance in COVID-19 revealed high neutrophil to lymphocyte ratio, lactose dehydrogenase, prothrombin time, C-reactive protein, PaO2 /FiO2 , D-dimer, ferritin, and fibrinogen levels in patients with severe disease (p < 0.05 for all). KIM-1 and suPAR levels were significantly higher in COVID-19 patients compared to the control group (p = 0.001 for all). KIM-1 level was higher in severe patients compared to moderate patients (p = 0.001), while suPAR level was lower (p = 0.001). KIM-1, which is believed to play an important role in the endocytosis of SARS-CoV-2, was elevated in patients with severe COVID-19 and may be a therapeutic target in the future. SuPAR may have a role in defense mechanism and fibrinolysis, and low levels in severe patients may be associated with poor prognosis in the early period.

Evaluation of alpha defensin, IL-1 receptor antagonist, and IL-18 levels in COVID-19 patients with macrophage activation syndrome and acute respiratory distress syndrome.

BACKGROUND: Many laboratory parameters have been associated with morbidity and mortality in SARS-CoV-2 (COVID-19), which emerged in an animal market in Wuhan, China in December 2019 and has infected over 20 million people. This study investigated the relationship between serum interleukin (IL)-18, IL-1 receptor antagonist (IL-1Ra), and alpha defensin levels and the clinical course and prognosis of COVID-19. MATERIALS AND METHODS: This study included 100 patients who were admitted to the chest diseases department and intensive care unit of our hospital and diagnosed with COVID-19 by real-time polymerase chain reaction (PCR) of nasopharyngeal swab samples between March 24 and May 31, 2020. The control group consisted of 50 nonsymptomatic health workers with negative real-time PCR results in routine COVID-19 screening in our hospital. RESULTS: Serum alpha defensin, IL-1Ra, and IL-18 levels were significantly higher in patients who developed macrophage activation syndrome (MAS) and acute respiratory distress syndrome (ARDS) compared to patients who did not (p < .001 for all). Alpha defensin, IL-1Ra, and IL-18 levels were significantly higher in COVID-19 patients with and without MAS or ARDS when compared to the control group (p < .001 for all). When the 9 patients who died were compared with the 91 surviving patients, IL-1Ra and IL-18 levels were found to be significantly higher in the nonsurvivors (p < .001). CONCLUSION: Our findings of correlations between alpha defensin and levels of IL-1Ra and IL-18, which were previously shown to be useful in COVID-19 treatment and follow-up, indicates that it may also be promising in treatment.

Low serum Α-SYNUCLEIN and oligomer Α-SYNUCLEIN levels in multiple sclerosis patients.

INTRODUCTION: Multiple sclerosis (MS) is an autoimmune, inflammatory, demyelinating neurodegenerative disease progressing with attacks. Alpha-synuclein (α-Syn), a neuronal protein, has been previously associated with the inflammation and development of neurodegenerative diseases. Although the cause of neurodegeneration in multiple sclerosis is mainly associated with inflammation, α-Syn may play a role in the pathogenesis of MS, as in other classical neurodegenerative diseases such as synucleinopathies. In multiple sclerosis, α-Syn has been directly studied in central nervous system lesions and cerebrospinal fluid (CSF). However, there are few studies approaching variations in peripheral α-Syn in MS. The aim of our study was to investigate the correlation between disease progression and other clinical parameters by measuring serum α-Syn and oligomer α-Syn levels in MS patients. MATERIAL AND METHOD: The study included 60 MS patients aged 18 years or older who were admitted to the Department of Neurology between 01.02.2020-01.04.2020 and diagnosed with MS according to the 2010 MC Donald criteria, and 60 age- and sex-matched healthy controls. Those who were in the MS attack period and received cortisone treatment in the past three months were excluded from the study. The serum α-Syn and oligomer α-Syn levels of the individuals in both groups were measured. The correlation between the serum α-Syn, oligomer α-Syn, oligomer α-Syn/α-Syn ratio levels of the MS patients and their age, disease duration, number of attacks, annualized relapse rate (ARR), disease type, EDSS scores and immunomodulatory drug type used was investigated. Statistical analysis was performed using the SPSS 22.0 software. RESULTS: In our study, 73.3% of the MS patients were female and the mean age of the patients was 36.18 ± 9.5 years. The most common MS disease type was RRMS with 83.3%. Serum α-Syn (79.52 ± 34.81) and oligomer α-Syn (18.79 ± 10.48) levels were significantly lower in the MS patients compared to the control group (p < 0.001). Serum oligomer α-Syn/α-Syn ratio was higher in the MS patients compared to the control group and in SPMS compared to RRMS, but was not statistically significant. There was no significant correlation between the serum α-Syn, oligomer α-Syn and oligomer α-Syn/α-Syn ratio ratio of the MS patients and their age, disease duration, disease type, EDDS, ARR and immunomodulatory treatments. There was a significant positive correlation between α-Syn and oligomer α-Syn in MS patients (r: 0.29, p: 0.02). CONCLUSION: In our study, serum α-Syn and oligomer α-Syn levels were lower in the MS patients compared to the control group. Low levels of α-Syn in MS may play a role in the development of neuroinflammation and may be a result of the diffuse neuronal and synaptic loss. There is a need for further studies on this subject.

Protective Effect of Lycopene against Reperfusion Injury in Rats with Ovarian Torsion: A Biochemical and Histopathological Evaluation.

Objective The aim of our study was to evaluate the effect of two different doses of lycopene, an antioxidant, on experimentally induced ovarian ischemia/reperfusion (IR) injury in rat model. Materials and Methods Twenty-four female rats were randomly divided into four groups: sham operation (group 1), 3-hour ischemia, 3-hour reperfusion (IR) (group 2), and IR + 100 mg/kg lycopene (PO) (group 3), IR + 200 mg/kg of lycopene (group 4). The rats' superoxide dismutase (SOD), myeloperoxidase (MPO) activities, malondialdehyde (MDA), and glutathione (GSH) levels were calculated. Ovarian tissue damage was assessed using a histopathological scoring system. Results Serum parameter levels and histological scores showed that treatment with lycopene may be conservative approach to prevent IR injury after the ovarian detorsion procedure.The improvement with lycopene was higher at 200 mg than at 100 mg. The MPO and MDA values were significantly lower in groups 3 and 4 as compared with group 2 ( p < 0.05), whereas the MPO and MDA values were lower in group 4 as compared with group 3.The SOD and GSH values were significantly higher in groups 3 and 4 as compared with group 2 ( p < 0.05), whereas the SOD and GSH values were higher in group 4 as compared with group 3.Tissue damage scores were elevated in the IR group compared with the sham group, but the treatment with different lycopene doses after reperfusion improved the histopathological tissue damage scores. Conclusion The results showed that lycopene treatment reduced ovarian IR damage. Antioxidant activity was found to increase in a dose-dependent manner. Lycopene treatment may be conservative approach for ovarian torsion patients after the detorsion procedure to prevent IR damage.

Could HIF-1α be a novel biomarker for the clinical course and treatment of pulmonary embolism?

Background/aim: Pulmonary embolism (PE) is associated with high morbidity and mortality rates if not diagnosed and treated rapidly. The aim of our study was to investigate the relationship between levels of hypoxia-induced factor-1 alpha (HIF-1α) and clinical course and prognosis in patients with intermediate low-risk, intermediate high-risk, and high-risk PE. Materials and methods: The study included 240 subjects in 4 groups: a healthy control group (n = 60, mean age = 60 ± 15.2, female/male = 30/30 ), intermediate low-risk PE group (n = 60, mean age = 60 ± 12,5, female/male = 27/33), intermediate high-risk PE group (n = 60, mean age = 61,4 ± 14,8, female/male = 36/24), and high-risk PE group (n = 60, mean age = 62,3 ± 15, female/male = 33/27). Plasma HIF-1α levels were measured using commercial enzyme-linked immunosorbent assay (ELISA) kit. Results: Comparison of HIF-1α levels revealed a statistically significant difference between the groups in proportion to clinical scoring (P = 0.001 for all). Comparison of initial HIF-1α and troponin levels in intermediate high-risk PE patients given thrombolytic therapy and those treated with enoxaparin sodium showed that HIF-1α levels were significantly higher in the group that received thrombolytic therapy (P = 0.001), while there was no difference in troponin levels (P = 0.146). Conclusion: HIF-1α can be used in the PE clinical risk stratification and monitoring of PE and may also serve as a valuable early indicator in intermediate high-risk PE, for which early reperfusion therapy is important.

Is Vimentin the Cause or Effect of Obstructive Sleep Apnea Development?

PURPOSE: In obstructive sleep apnea (OSA), hypoxia secondary to apnea and hypopnea and the resulting systemic inflammatory response are the main causes of comorbidities. The aim of this study was to investigate the relationship between OSA and vimentin, which plays an important role in the activation of cells that synthesize inflammatory cytokines. MATERIALS AND METHODS: The study included 150 OSA patients (50 mild, 50 moderate, and 50 severe OSA) and 50 patients without OSA as a control group. Plasma vimentin levels were measured from peripheral blood samples using a commercial enzyme-linked immunosorbent assay (ELISA) kit. RESULTS: The OSA patients in our study had significantly higher body mass index, apnea-hypopnea index (AHI), triglyceride level, mean oxygen desaturation, and plasma vimentin levels compared to the healthy control group (p = 0.007, 0.001, 0004, 0.001, and 0.001, respectively). Plasma vimentin level was significantly higher in the moderate and severe OSA groups compared to the control and mild OSA groups (p = 0.001 for all). There was no difference between severe and moderate OSA. There were significant correlations between plasma vimentin levels and OSA patients' AHI and mean oxygen desaturation (r = 0.46, p = 0.001; r = 0.214, p = 0.005). CONCLUSION: In this study, we observed significant positive correlations between plasma vimentin level and OSA severity, weight, AHI, and mean oxygen desaturation. Vimentin may have utility as a biomarker in the follow-up and treatment of OSA.

Is Metrnl an Adipokine Involved in the Anti-inflammatory Response to Acute Exacerbations of COPD?

PURPOSE: Chronic obstructive pulmonary disease (COPD) is a common lung disease characterized by airflow limitation and systemic inflammation. Recently, there has been growing interest in adipose tissue-mediated inflammation in the pathogenesis of COPD. The aim of our study was to determine the relationships between a new adipocytokine, meteorin-like protein (Metrnl), and acute exacerbations of COPD, smoking, and comorbidities. MATERIALS AND METHODS: The study included 313 patients aged 40-65 years in four groups: Group 1: ex-smokers (≥ 20 pack-years) with COPD hospitalized for COPD exacerbation (n = 133), Group 2: current-smokers (≥ 20 pack-years) without COPD (n = 60), Group 3: ex-smokers (≥ 20 pack-years) without COPD (n = 60), and Group 4: never-smokers without COPD (n = 60). Peripheral venous blood samples (5 cc) were collected from all participants. Plasma Metrnl levels were measured using commercial enzyme-linked immunosorbent assay (ELISA) kit. RESULTS: Mean Metrnl levels were 28.45 ± 11.27 ng/ml in Group 1, 24.34 ± 4.38 ng/ml in Group 2, 18.84 ± 3.8 ng/ml in Group 3, and 19.44 ± 3.92 ng/ml in Group 4. Group 1 had significantly higher mean Metrnl level compared to the other groups (p = 0.006, p = 0.001, p = 0.001). Metrnl level was also significantly higher in Group 2 when compared with Groups 3 and 4 (p = 0.001, p = 0.005). Group 1 patients with diabetes mellitus and coronary artery disease showed significantly lower Metrnl levels compared to other patients in the group (p = 0.001, p = 0.001). CONCLUSION: The high Metrnl level in COPD exacerbations and active smoking may be important in balancing the inflammatory response. However, plasma Metrnl levels were found to be lower in COPD patients with comorbidities.

Protective effect of gallic acid against cisplatin-induced ototoxicity in rats / Efeito protetor do ácido gálico contra a ototoxicidade induzida por cisplatina em ratos

Abstract Introduction: Cisplatin is an antineoplastic agent widely used in the treatment of a variety of cancers. Ototoxicity is one of the main side-effects restricting the use of cisplatin. Objective: The purpose of this study was to investigate the protective efficacy of gallic acid, in biochemical, functional and histopathological terms, against ototoxicity induced by cisplatin. Methods: Twenty-eight female Sprague Dawley rats were included. Rats were randomly assigned into four groups of seven animals each. Cisplatin group received a single intraperitoneal dose of 15 mg/kg cisplatin. Gallic acid group received intraperitoneal gallic acid at 100 mg/kg for five consecutive days. Cisplatin + gallic acid group received intraperitoneal gallic acid at 100 mg/kg for five consecutive days and a single intraperitoneal dose of 15 mg/kg cisplatin at 3rd day. A control group received 1 mL intraperitoneal saline solution for five consecutive days. Prior to drug administration, all rats were exposed to the distortion product otoacoustic emissions test. The test was repeated on the 6th day of the study. All rats were then sacrificed; the cochleas were removed and set aside for biochemical and histopathological analyses. Results: In cisplatin group, Day 6 signal noise ratio values were significantly lower than those of the other groups. Also, malondialdehyde levels in cochlear tissues were significantly higher, superoxide dismutase and glutathione peroxidase activities were significantly lower compared to the control group. Histopathologic evaluation revealed erosion in the stria vascularis, degeneration and edema in the connective tissue layer in endothelial cells, impairment of outer hair cells and a decrease in the number of these calls. In the cisplatin + gallic acid group, this biochemical, histopathological and functional changes were reversed. Conclusion: In the light of our findings, we think that gallic acid may have played a protective role against cisplatin-induced ototoxicity in rats, as indicated by the distortion product otoacoustic emissions test results, biochemical findings and immunohistochemical analyses.

Resumo Introdução: A cisplatina é um agente antineoplásico amplamente usado no tratamento de vários tipos de câncer. A ototoxicidade é um dos principais efeitos colaterais que restringem o uso da cisplatina. Objetivo: O objetivo deste estudo foi investigar a eficácia protetora do ácido gálico, em termos bioquímicos, funcionais e histopatológicos, contra a ototoxicidade induzida por cisplatina. Método: Vinte e oito ratas Sprague-Dawley foram incluídas. As ratas foram distribuídas aleatoriamente em quatro grupos de sete animais cada. O grupo cisplatina recebeu uma única dose intraperitoneal de 15 mg/kg de cisplatina. O grupo ácido gálico recebeu ácido gálico via intraperitoneal a uma dose de 100 mg/kg durante cinco dias consecutivos. O grupo cisplatina + ácido gálico recebeu ácido gálico via intraperitoneal a uma dose de 100 mg/kg durante cinco dias consecutivos e uma única dose intraperitoneal de 15 mg/kg de cisplatina no terceiro dia. O grupo controle recebeu 1 mL de solução salina via intraperitoneal por cinco dias consecutivos. Antes da administração do fármaco, todos os ratos foram expostos ao teste de emissões otoacústicas - produto de distorção. O teste foi repetido no sexto dia do estudo. Todos os ratos foram então sacrificados; as cócleas foram removidas e reservadas para análises bioquímicas e histopatológicas. Resultados: No grupo cisplatina, os valores da relação sinal-ruído do dia 6 foram significativamente mais baixos aos dos outros grupos. Além disso, os níveis de malondialdeído nos tecidos cocleares foram significativamente mais altos, e as atividades de superóxido dismutase e glutatione peroxidase foram significativamente mais baixas em comparação com o grupo controle. A avaliação histopatológica revelou erosão na estria vascular, degeneração e edema na camada de tecido conjuntivo em células endoteliais, comprometimento das células ciliadas externas e diminuição do número dessas células. No grupo cisplatina + ácido gálico, estas alterações bioquímicas, histopatológicas e funcionais foram revertidas. Conclusão: Tendo em vista os nossos achados, consideramos que o ácido gálico pode ter desempenhado um papel protetor contra a ototoxicidade induzida por cisplatina em ratas, conforme indicado pelos resultados do teste emissões otoacústicas - produto de distorção, achados bioquímicos e análises imuno-histoquímicas.

Levosimendan ameliorates cisplatin-induced ototoxicity: Rat model.

OBJECTIVES: Cisplatin is employed for chemotherapeutic purposes in several types of adult and pediatric cancer. However, side-effects including nephrotoxicity, ototoxicity, gastrointestinal effects and neuropathy restrict the use of the drug due to their adverse impacts on quality of life. This study aimed to determine whether levosimendan exhibits a protective effect against cisplatin-related ototoxicity in a rat model by means of functional, biochemical and histochemical analysis. METHODS: The study was employed with 24 female Sprague Dawley rats. After distortion product otoacoustic emissions (DPOAE) tests applied to all rats, rats were randomly assigned into four groups of six animals each. A single intraperitoneal 15 mg/kg dose of cisplatin was administered to Cisplatin group. Levosimendan group received intraperitoneal levosimendan at a dose of 100 mg/kg for five consecutive days. Cisplatin + Levosimendan group received intraperitoneal levosimendan at a dose of 100 mg/kg for five consecutive days and a single intraperitoneal dose of 15 mg/kg cisplatin at 3rd day of the study. Control group received 8 mL/kg/day intraperitoneal saline solution for five consecutive days. The DPOAE test was repeated on the 6th day of the study. All rats were then sacrificed, the cochleas were removed and set aside for biochemical and histopathological analyses. RESULTS: A significant increase in levels of Malondialdehyde (MDA) and significantly lower activities of superoxide dismutase (SOD) and Glutathione peroxidase (GPx) were observed at rats of cisplatin group. Administration of levosimendan showed significantly lower cochlear MDA levels, while SOD and GPx activities both increased significantly. The DPOAE test performed at 6th day of the study showed a significant impairment in the signal-noise ratio (SNR) levels of rats in Cisplatin group. The SNR levels of rats treated with levosimendan were significantly higher than those of cisplatin group and were similar to those of the control group. Cisplatin impaired the cochlear structure and a severe Caspase 3 and 8-hydroxy-2' -deoxyguanosine (8-OHdG) immunopositivity was observed at cochlea of the rats of cisplatin group. Administration of levosimendan protected the structure of cochlea and there was a mild Caspase 3 and 8OHdG immunopositivity. CONCLUSION: Our data demonstrate that levosimendan protects hearing against cisplatin-induced ototoxicity and obviates cellular degeneration. It also significantly reduces oxidative stress and apoptosis, probable mechanisms involved in ototoxicity.

Protective effect of gallic acid against cisplatin-induced ototoxicity in rats.

INTRODUCTION: Cisplatin is an antineoplastic agent widely used in the treatment of a variety of cancers. Ototoxicity is one of the main side-effects restricting the use of cisplatin. OBJECTIVE: The purpose of this study was to investigate the protective efficacy of gallic acid, in biochemical, functional and histopathological terms, against ototoxicity induced by cisplatin. METHODS: Twenty-eight female Sprague Dawley rats were included. Rats were randomly assigned into four groups of seven animals each. Cisplatin group received a single intraperitoneal dose of 15mg/kg cisplatin. Gallic acid group received intraperitoneal gallic acid at 100mg/kg for five consecutive days. Cisplatin+gallic acid group received intraperitoneal gallic acid at 100mg/kg for five consecutive days and a single intraperitoneal dose of 15mg/kg cisplatin at 3rd day. A control group received 1mL intraperitoneal saline solution for five consecutive days. Prior to drug administration, all rats were exposed to the distortion product otoacoustic emissions test. The test was repeated on the 6th day of the study. All rats were then sacrificed; the cochleas were removed and set aside for biochemical and histopathological analyses. RESULTS: In cisplatin group, Day 6 signal noise ratio values were significantly lower than those of the other groups. Also, malondialdehyde levels in cochlear tissues were significantly higher, superoxide dismutase and glutathione peroxidase activities were significantly lower compared to the control group. Histopathologic evaluation revealed erosion in the stria vascularis, degeneration and edema in the connective tissue layer in endothelial cells, impairment of outer hair cells and a decrease in the number of these calls. In the cisplatin+gallic acid group, this biochemical, histopathological and functional changes were reversed. CONCLUSION: In the light of our findings, we think that gallic acid may have played a protective role against cisplatin-induced ototoxicity in rats, as indicated by the distortion product otoacoustic emissions test results, biochemical findings and immunohistochemical analyses.