The impact of apelin-13 on cisplatin-induced endocrine pancreas damage in rats: an in vivo study.

Apelin-13 is a peptide hormone that regulates pancreatic endocrine functions, and its benefits on the endocrine pancreas are of interest. This study aims to investigate the potential protective effects of apelin-13 in cisplatin-induced endocrine pancreatic damage. Twenty-four rats were divided into four groups: control, apelin-13, cisplatin, and cisplatin + apelin-13. Caspase-3, TUNEL, and Ki-67 immunohistochemical staining were used as markers of apoptosis and mitosis. NF-κB/p65 and TNFα were used to show inflammation. ß-cells and α-cells were also evaluated with insulin and glucagon staining in the microscopic examination. Pancreatic tissue was subjected to biochemical analyses of glutathione (GSH) and malondialdehyde (MDA). Apelin-13 ameliorated cisplatin-induced damage in the islets of Langerhans. The immunopositivity of apelin-13 on ß-cells and α-cells was found to be increased compared to the cisplatin group (p = 0.001, p = 0.001). Mitosis and apoptosis were significantly higher in the cisplatin group (p = 0.001). Apelin-13 reduced TNFα, NF-κB/p65 positivity, and apoptosis caused by cisplatin (p = 0.001, p = 0.001, p = 0.001). While cisplatin caused a significant increase in MDA levels (p = 0.001), apelin caused a significant decrease in MDA levels (p = 0.001). The results demonstrated a significant decrease in pancreatic tissue GSH levels following cisplatin treatment (p = 0.001). Nevertheless, apelin-13 significantly enhanced cisplatin-induced GSH reduction (p = 0.001). On the other hand, the serum glucose level, which was measured as 18.7 ± 2.5 mmol/L in the cisplatin group, decreased to 13.8 ± 0.7 mmol/L in the cisplatin + apelin-13 group (p = 0.001). The study shows that apelin-13 ameliorated cisplatin-induced endocrine pancreas damage by reducing oxidative stress and preventing apoptosis.

Effect of fibromyalgia on demographic, biochemical, metabolic and inflammatory profiles: a single-centre retrospective study.

OBJECTIVES: The objective of this study is to ascertain the disparities in demographic features and biochemical profiles between individuals diagnosed with fibromyalgia (FM) and a control group of healthy individuals. METHODS: This retrospective, cross-sectional study compared the demographic, biochemical, metabolic, and inflammatory indexes and rates of 174 FM patients diagnosed using the American College of Rheumatology 2016 diagnostic criteria between January 2023 and January 2024, and 186 healthy control groups. RESULTS: There was no difference between the FM and control groups in terms of alcohol consumption, marital status, or diabetes mellitus. The smoking rate is higher, and the educational level was found to be lower for FM versus the control. There was no significant difference between FM and controls regarding waist-height ratio, triglyceride-glucose index, plasma atherogenic index, vitamin B12, and folate levels. Monocyte HDL ratio, cardiometabolic index, magnesium, HbA1c, and ferritin levels were significantly higher in the control than in FM (p<0.001, p=0.039, p=0.007, p<0.001, p<0.001, respectively). C-reactive protein, erythrocyte sedimentation rate, systemic immune-inflammatory index, neutrophil-lymphocyte rate, platelet lymphocyte rate, and vitamin D levels were found to be higher in FM compared to control (p=0.001, p=0.032, p=0.003, p=0.030, p=0.003, p<0.001, respectively). A weak positive correlation was observed between the fibromyalgia impact questionnaire (FIQ) score and disease duration, as well as between pain degree and ESR, and pain degree and CRP. The study revealed a weak inverse relationship between Widespread Pain Index (WPI) and waist circumference. CONCLUSIONS: This study highlights fthe association f ibromyalgia with elevated inflammatory markers, altered metabolic parameters, and specific demographic characteristics.

The potential antioxidant effect of N-acetylcysteine on X-ray ionizing radiation-induced pancreas islet cell toxicity.

PURPOSE: Previous research has highlighted the impact of X-ray irradiation-induced organ damage, on cancer patients after radiation therapy. The ionizing radiation-induced oxidative stress causes injury to the pancreatic islet cells of Langerhans. We used histopathological, immunohistochemical, and biochemical analyses to examine α- and ß-cells in the islets of Langerhans in rats undergoing whole-body x-ray ionizing radiation, a group of which was treated with NAC. MATERIAL AND METHODS: Twenty-four male rats were randomly divided into 3 groups, one control, and two experimental groups. Group I (Control) was administered only saline solution (0.09% NaCl) by oral gavage for 7 days. Group II (IR) was administrated whole body single dose 6 Gray ionizing radiation (IR) and saline solution (0.09% NaCl) by oral gavage for 7 days. Group III (IR + NAC) was administered 300 mg/kg NAC (N-acetylcysteine) by oral gavage for 7 days, 5 days before, and 2 days after 6 Gray IR application. RESULTS: In the X-ray irradiation group, we observed diffuse necrotic endocrine cells in the islets of Langerhans. In addition, we found that Caspase-3, malondialdehyde (MDA) levels increased, and insulin, glucagon, and glutathione (GSH) levels decreased in the IR group compared to the control group. In contrast, we observed a decrease in Caspase-3, and MDA levels in necrotic endocrine cells, and an increase in insulin, glucagon, and GSH levels in the IR + NAC group compared to the IR group. CONCLUSION: This study provides evidence for the beneficial effects of N-acetyl cysteine on islets of Langerhans cells with X-ray ionizing-radiation-induced damage in a rat model.

The Effects of Dexmedetomidine on Abdominal Aortic Occlusion-Induced Ovarian Injury via Oxidative Stress and Apoptosis.

Ischemia/reperfusion (I/R) induced ovarian damage is caused by various diseases such as ovarian torsion, ovarian transplantation, cardiovascular surgery, sepsis, or intra-abdominal surgery. I/R-related oxidative damage can impair ovarian functions, from oocyte maturation to fertilization. This study investigated the effects of dexmedetomidine (DEX), which has been shown to exhibit antiapoptotic, anti-inflammatory, and antioxidant effects, on ovarian I/R injury. We designed four study groups: group 1 (n = 6): control group; group 2 (n = 6): only DEX group; group 3 (n = 6): I/R group; group 4 (n = 6): I/R + DEX group. Then, ovarian samples were taken and examined histologically and immunohistochemically, and tissue malondialdehyde (MDA) and glutathione (GSH) levels were measured. In the I/R group MDA levels, caspase-3, NF-κB/p65, 8-OHdG positivity, and follicular degeneration, edema, and inflammation were increased compared to the control group (p = 0.000). In addition, GSH levels were significantly decreased in the I/R group compared to the control group (p = 0.000). On the other hand, in the I/R + DEX treatment group MDA levels, caspase-3, NF-κB/p65, 8-OHdG positivity, follicular degeneration, edema, and inflammation findings were decreased than in the I/R group (p = 0.000, p = 0.005, p = 0.005, p = 0.001, p = 0.005, respectively). However, GSH levels increased significantly in the I/R + DEX treatment group compared to the I/R group (p = 0.000). DEX protects against ovarian I/R injury through antioxidation and by suppressing inflammation and apoptosis.

Histopathological evaluation of the effects of dexmedetomidine against pituitary damage induced by X-ray irradiation.

Background: The present study, aimed to investigate the potential negative effects of x-ray radiation and the effects of the α2-adrenergic receptor agonist dexmedetomidine on the pituitary gland.Methods: Twenty-four Sprague-Dawley rats were divided into three groups: Rats in Group 1 (control group). Group 2 (X-ray irradiation) and group 3 (X-ray irradiation + Dexmedetomidine) were given a total of 10 Gy external beam total body irradiation. Group 3 was given a single intraperitoneal dose of 200 µg/kg dexmedetomidine 30 minutes before RT.Results: In sections obtained from the x-ray irradiation group, we observed many necrotic in adenohypophysis and neurohypophysis. In addition, there were extensive oedematous areas and vascular congestions due to the necrotic cells in both the adenohypophysis and neurohypophysis. In contrast, we observed a reduction in necrotic chromophobic and chromophilic cells in adenohypophyseal tissue and a reduction in necrotic pituicytes in neurohypophyseal tissue in the dexmedetomidine treatment group. In addition, we determined lower caspase-3 and TUNEL expression in the dexmedetomidine treatment group compared with the x-ray irradiation group. Dexmedetomidine reduced x-ray radiation-induced pituitary damage by preventing apoptosis.Conclusions: The present study demonstrated the use of dexmedetomidine in situations related to radiation toxicity and offers the potential for a comprehensive study.

The hepatoprotective potential of resveratrol in an experimental model of ruptured abdominal aortic aneurysm via oxidative stress and apoptosis.

The mortality rate in ruptured abdominal aortic aneurysms can today be reduced through cardiovascular surgery. However, ischemia and reperfusion-induced tissue damage develop due to aortic cross-clamping applied during surgery. The present study aimed to reduce oxidative stress-induced hepatic damage resulting from ischemia and reperfusion due to aortic cross-clamping during surgery by means of resveratrol administration. Forty male Sprague-Dawley rats were randomly assigned into four groups: control (healthy), glycerol+ischemia/reperfusion (I/R) (sham), I/R, and I/R + Resveratrol. In all groups scheduled for I/R, 60 min of shock was followed by 60 min of ischemia. In the I/R + Resveratrol group, 10 mg/kg of resveratrol was administered 15 min before ischemia and immediately before reperfusion via the intraperitoneal route. In addition, 120 min of reperfusion was applied under anesthesia after ischemia in all groups. Intralobar and interlobar necrosis, vascular congestion, and edematous fields resulting from aortic occlusion were present. Liver tissue malondialdehyde (MDA) levels and cleaved caspase-3 positivity increased, while glutathione (GSH) levels decreased. However, resveratrol administration reduced intralobular and interlobar necrosis, vascular congestion and edematous fields, cleaved caspase-3 positivity, and MDA levels, and increased GSH levels. Our findings suggest that resveratrol is effective against aortic occlusion-induced liver injury by reducing oxidative stress and apoptosis.

Effects of gadolinium-based MRI contrast agents on liver tissue.

BACKGROUND: MRI with contrast is often used clinically. However, recent studies have reported a high accumulation of gadolinium-based contrast agents (GBCAs) in kidney, liver, and spleen tissues in several mouse models. PURPOSE: To compare the effects on liver tissue of gadolinium-based MRI contrast agents in the light of biochemical and histopathological evaluation. STUDY TYPE: Institutional Review Board (IRB)-approved controlled longitudinal study. ANIMAL MODEL: In all, 32 male Sprague-Dawley rats were divided into a healthy control group subjected to no procedure (Group 1), a sham group (Group 2), a gadodiamide group (Group 3), and a gadoteric acid group (Group 4). FIELD STRENGTH/SEQUENCE: Not applicable. ASSESSMENT: Liver tissues removed at the end of the fifth week and evaluated pathologically (scored Knodell's histological activity index [HAI] method by two histopathologists) immunohistochemical (caspase-3 and biochemical tests (AST, ALT, TAS, TOS, and OSI method by Erel et al) were obtained. STATISTICAL TESTS: Differences between groups were analyzed using the nonparametric Kruskal-Wallis test followed by the Tamhane test, and one-way analysis of variance (ANOVA) followed by Turkey's HSD test. RESULTS: An increase was observed in histological activity scores in sections from rats administered gadodiamide and gadoteric acid, and in caspase-3, AST and ALT values (P < 0.05). In contrast, we determined no change in TOS (P = 0.568 and P = 0.094, respectively), TAS (P = 0.151 and P = 0.055, respectively), or OSI (P = 0.949 and P = 0.494, respectively) values. DATA CONCLUSION: These data suggest that gadodiamide and gadoteric acid trigger hepatocellular necrosis and apoptosis by causing damage in hepatocytes, although no change occurs in total antioxidant and antioxidant capacity. LEVEL OF EVIDENCE: 1 Technical Efficacy: Stage 4 J. Magn. Reson. Imaging 2018;47:1367-1374.

Effects of Infliximab against Methotrexate Toxicity in Splenic Tissue via the Regulation of CD3, CD68, and C200R in Rats.

Methotrexate (MTX), which has been used in clinical practice for approximately 70 years, is still widely employed in the treatment of rheumatoid arthritis (RA), psoriasis, and cancer. Although MTX toxicity causes nephrotoxicity, hepatotoxicity, bone marrow suppression, pulmonary fibrosis, and gastrointestinal damage, previous studies have not addressed splenic toxicity. This is the first study to examine the effectiveness of infliximab (INF) against MTX-induced toxicity in splenic tissues via the regulation of CD3, CD68, and C200R. We investigated the effects of MTX on macrophages and T lymphocytes in the spleen at the molecular level and examined the protective potential of the tumor necrosis factor (TNF)-α antagonist INF against MTX toxicity. Three groups of rats were set up. Group 1 received saline solution only, group 2 a single dose of MTX (20 mg/kg), and group 3 INF (7 mg/kg) before administration of a single dose of MTX (20 mg/kg). All injections were given intraperitoneally. Spleen tissues were removed 5 days after MTX administration and evaluated for CD3, CD68, and CD200R using immunohistochemical staining. Finally, the mean numerical density of CD3+, CD68+, and CD200R+ cells was estimated by a histopathologist using StereoInvestigator 8. MTX increased the numerical densities of CD3+, CD68+, and CD200R+ cells (p < 0.05). We also observed that INF reduced the numerical densities of these cells following MTX administration (p < 0.05). INF may, therefore, be a promising candidate for the prevention of the deleterious effects on spleen tissue of MTX, used in the treatment of RA and cancer.

Protective effects of beta glucan in brain tissues of post-menopausal rats: a histochemical and ultra-structural study.

Decline of estrogen during menopause has been associated with numerous significant changes that have been linked to many pathophysiological complications. In addition, ovarian hormone deficiency increases the production of reactive oxygen radicals which could result in oxidative stress and cell damage. While estrogen therapy is often considered to overcome the behavioral and physiological shortcomings, antioxidants are gaining popularity for their beneficial property. For this purpose, in the present study, utilizing the antioxidant properties of beta glucan has been examined in treatment of menopause induced oxidative stress in cerebral neurons. Four groups of female Wistar rats were used: control, ovariectomy, ovariectomy + estrogen treated and ovariectomy + beta glucan treated. We observed a significant increase in neural degeneration in ovariectomized rats as compared to controls. Moreover, increased oxidative stress in the brains of the ovariectomized rats has been detected by performing immunohistochemical analysis. A large number of immuno-positive cerebral neurons have been observed in ovariectomy group rat brains. Interestingly, providing beta glucan treatment to ovariectomized rats reduced the number of degenerated neurons. Our study is the first to examine light and electron microscopic examination and immunohistochemical and stereological analysis of estrogen depletion in rats and to test protective role of beta glucan in the experimental study.

Protective effects of estrogen and bortezomib in kidney tissue of post-menopausal rats: an ultrastructural study.

PURPOSE: Symptoms and disorders related to menopause and its associated estrogen deficiency have become a considerable health concern worldwide. Ovarian hormone depletion/estrogen deficiency can be usefully studied using animal models after removal of the ovaries [ovariectomy (Ovx)]. This study assessed renal changes after Ovx-induced estrogen deficiency in a rat model. METHODS: Rats were randomly allotted into one control group (group I, healthy) and three study groups (group II, Ovx group; group III, Ovx +17ß-estradiol group; and group IV, Ovx + bortezomib group). RESULTS: In the Ovx group (group II), thickening of glomerular capillary walls, narrowing of Bowman's capsular space, glomerular hypertrophy, atrophic tubules, and loss of the basal membranes of the tubules were observed. Mesangial cell proliferation was observed, particularly in the glomerulus. Immunohistochemical (IHC) staining studies in this group showed dense staining in the mesangial cells, tubular cell Nf-KB/p65, and caspase-3. Groups III and IV (Ovx +17ß-estradiol and Ovx + bortezomib) showed decreased NF-kB/p65 and caspase-3 expression compared with the Ovx group (p < 0.05). CONCLUSION: In renal failure related to estrogen deficiency caused by Ovx, 17ß-estradiol and bortezomib have a protective effect on renal tissue.

The Effect of Anti-Tumor Necrosis Factor Therapy on The Plasma Atherogenic Index in Rheumatic Diseases.

Background: The risk of atherosclerosis is increased in individuals with rheumatological disease. The objective of this study is to examine the heightened susceptibility to atherosclerosis in persons afflicted with rheumatological disorders. This study aimed to assess the impact of anti-tumor necrosis factor (anti-TNF) medication on the plasma atherogenic index (PAI) in persons diagnosed with rheumatological disease. Methods: This study used a retrospective cross-sectional design to investigate a cohort of 136 patients with rheumatological disease who were undergoing anti-TNF therapy (Group 1), as well as a comparison group of 117 patients getting conventional therapy (Group 2). Measurements of PAI were conducted at the initial baseline and again at the sixth month of treatment. Results: Initially, there was no statistically significant disparity observed in PAI values between the two cohorts. After a period of 6 months, a notable reduction in PAI was identified in the group receiving anti-TNF medication (P = 0.01), while no significant alteration was detected in the group receiving conventional treatment. Conclusion: It provides findings showing that anti-TNF therapy can reduce the PAI in individuals with rheumatological disease. This may indicate a potential cardiovascular protective effect of anti-TNF therapy.

Comparative Analysis of Epigallocatechin-3-Gallate and TNF-Alpha Inhibitors in Mitigating Cisplatin-Induced Pancreatic Damage Through Oxidative Stress and Apoptosis Pathways.

Oxidative stress and inflammation caused by cisplatin, which is frequently used in the treatment of many cancers, damage healthy tissues as well as cancer cells. In this study, we aimed to investigate the effect of epigallocatechin-3-gallate (EGCG) and infliximab (INF) administration on pancreatic endocrine cells in rats treated with systemic cisplatin (CDDP). The rats were randomly divided into 6 groups: group 1 (control group), group 2 (EGCG group), group 3 (CDDP group), group 4 (EGCG + CDDP group), group 5 (CDDP + INF group), and group 6 (EGCG + CDDP + INF group). The study's findings demonstrated that EGCG and INF effectively reduced the cellular damage induced by CDDP in histopathologic investigations of the pancreas. EGCG and INF, whether used individually or in combination, demonstrated a significant reduction in malondialdehyde (MDA) levels and an increase in glutathione (GSH) levels in the rat pancreas compared to the CDDP group. Immunohistochemically, the enhanced presence of insulin and glucagon positivity in the EGCG and INF groups, along with the absence of TUNEL immunopositivity, indicate that both treatments reduced CDDP-induced apoptosis. Furthermore, the observed lack of immunopositivity in TNF-α and 8-OHdG in the groups treated with EGCG and INF, compared to those treated with CDDP, indicates that these substances can inhibit inflammation. EGCG and INF, whether provided alone or together, can potentially reduce the damage caused to pancreatic islet cells by cisplatin. This effect is achieved through their anti-inflammatory and antioxidant properties during the early stages of the condition.

Dexmedetomidine on the interplay of IL-6 and STAT3 pathways in adrenal gland damage-induced scalding burns in rats.

Scalding burns are a common form of thermal injury that often leads to systemic complications. Pro-inflammatory cytokines like interleukin-6 (IL-6) and the activation of signal transducer and activator of transcription 3 (STAT3) pathways have been linked to the pathophysiology of organ damage caused by burns. This study aimed to investigate the potential therapeutic effects of dexmedetomidine, an α2-adrenergic receptor agonist with anti-inflammatory properties, on the interplay of IL-6 and STAT3 pathways in adrenal gland damage following scalding burns in rats. Twenty-eight rats were divided randomly into four groups. Rats in group 1 (n=7, control) were given only 0.9% intraperitoneal (i.p.) NaCl. Rats in group 2 (n=7, DEX) were exposed to 25°C water for 17 s on day 1 and received 100 mcg/kg/day dexmedetomidine i.p. for 3 days; for rats in group 3 (n=7, Burn), boiling water of 94°C was applied inside for 17 s. Rats in group 4 (n=7, Burn+DEX) were exposed to 94°C water for 17 s and received 100 mcg/kg/day dexmedetomidine i.p. for 3 days. Adrenal gland tissues were histopathological examined, and STAT3, IL-6, and TUNEL staining were performed using immunohistochemically. Our results revealed that scalding burns increased IL-6 and STAT3 expression in the adrenal glands of rats. Histological analysis demonstrated that dexmedetomidine administration ameliorated adrenal gland damage and reduced inflammatory cell infiltration. Our findings suggest that dexmedetomidine protects the adrenal glands in scalding burns. This protection appears to be mediated, at least in part, by its modulation of IL-6 and STAT3 pathways.

Interleukins: Pathogenesis in Non-Alcoholic Fatty Liver Disease.

Inflammatory cytokines have been implicated as crucial contributors to the onset and progression of non-alcoholic fatty liver disease (NAFLD). The exact mechanisms by which interleukins (ILs) contribute to NAFLD may vary, and ongoing research is aimed at understanding the specific roles of different ILs in the pathogenesis of this condition. In addition, variations in environmental factors and genetics in each individual can influence the onset and/or progression of NAFLD. The lack of clinical studies related to the potential therapeutic properties of IL-1 inhibitors currently does not allow us to conclude their validity as a therapeutic option, although preclinical studies show promising results. Further studies are needed to elucidate their beneficial properties in NAFLD treatment.

Relationship of Vitamin B12 Levels With Different Degrees of Obesity and Diabetes Mellitus.

INTRODUCTION: The potential influence of micronutrient status on obesity should be considered. Nevertheless, previous research examining the relationship between serum vitamin B12 levels and obesity has yielded inconclusive results. The objective of this study was to investigate the associations between serum vitamin B12 levels and obesity and diabetes mellitus (DM) in a population consisting of persons aged 18 years and older. METHODS: A retrospective case-control research was undertaken on a sample of 1024 individuals aged 18 years and older who were admitted to a tertiary healthcare facility (Recep Tayyip Erdogan University Education and Research Hospital, Rize) for either overweight-related issues or routine check-ups. The primary objective of this study was to assess the B12 levels of these individuals. The researcher recorded the body mass index (BMI) and history of DM for all subjects. RESULTS: The study comprised a total of 1024 participants, consisting of 834 females and 190 males. The levels of vitamin B12 in women were found to be 308±113 pg/mL, while in men, the levels were 304±125 pg/mL. The results of the statistical analysis indicate that there is no statistically significant disparity in vitamin B12 levels between males and females (p=0.748). There was a statistically significant positive correlation seen between age and B12 levels; however, the magnitude of this connection was found to be minor (p=0.000, R2=0.017). The study findings revealed that out of the 1,024 individuals evaluated, 179 individuals exhibited B12 levels below 200, while 845 individuals displayed vitamin B12 levels above 200. The study findings indicated that there was no statistically significant distinction observed in the occurrence of obesity and DM in relation to vitamin B12 deficiency (p = 0.938, p = 0.08, respectively). CONCLUSION: The results of this study offer empirical support for the notion that there is no significant difference in vitamin B12 levels between individuals afflicted with obesity and diabetes and those unaffected by these conditions. Interestingly, it was shown that serum B12 levels exhibited a modest increase with advancing age.

Relationship Between Overnight Dexamethasone Suppression Test and Aging.

Background This study aims to investigate the relationship between suppressed cortisol levels measured after the 1-mg dexamethasone suppression test (DST) and age based on the hypothesis that aging can alter the activity of the hypothalamic-pituitary-adrenal (HPA) axis. Methodology Data obtained by the retrospective evaluation of suppressed 1-mg overnight DST results of adults aged ≥18 years with adrenal incidentaloma or suspected endogenous hypercortisolemia between December 2021 and March 2023 were subjected to age-dependent correlation analysis. Individuals aged between 18 and 90 years (n = 1111) were classified into the following four groups: <30 years, 30-49 years, 50-69 years, and >70 years. DST results were compared according to age groups. Results Median post-DST cortisol was 18.49 nmol/L, with a level of 17.9 nmol/L in females and 20.7 nmol/L in males. The overall rate of DST suppression was 62.7%, with a rate of 63.8% in females and 59.7% in males. On pairwise comparisons of all age groups, there was a difference in post-DST cortisol levels (p = 0.000). Our statistical analysis revealed a strong positive correlation between age and cortisol levels after DST. Conclusions The negative feedback mechanism for cortisol may be altered in older patients. Therefore, the 1-mg DST may yield a higher rate of false positives in the elderly.

Relationship Between Serum Endocan Levels and Other Predictors of Endothelial Dysfunction in Obese Women.

Endocan, or endothelial cell-specific molecule-1 (ESM-1), is a potential inflammatory marker implicated in endothelial dysfunction. The purpose of this study was to determine the correlation between serum endocan levels and the presence and severity of endothelial dysfunction, and the relationships with serum intracellular adhesion molecule-1 (ICAM-1), adiponectin (a marker of inflammation), high sensitivity C-reactive protein (hsCRP) levels, and carotid intima-media thickness (cIMT) in obese subjects. Serum endocan, ICAM-1, adiponectin, hsCRP levels, and cIMT were evaluated in 76 obese women (BMI > 30 kg/m2) and 53 controls (BMI < 25 kg/m2). ICAM-1 (P = .01), hs-CRP (p < 0.001), and cIMT (p < .001) were significantly higher, while adiponectin (P = .006) was significantly lower, in obese women compared with the controls. Serum endocan levels were similar between the obese (470.5 ± 171.3 pg/mL) and controls (471.9 ± 146.3 pg/mL) (P = .732). There was no correlation between serum endocan values and the endothelial dysfunction markers, hsCRP (r = -.021), ICAM-1 (r = -.054), adiponectin (r = .113), or cIMT (r = -.060) in obesity. Endocan is not a suitable marker of endothelial dysfunction in the context of obesity. More research is required to evaluate the role of endocan in the regulation of inflammatory processes in obesity.

The Relationship Between Laboratory Findings and Mortality in COVID-19 Patients Requiring Intensive Care.

INTRODUCTION: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) shows a wide clinical manifestation from asymptomatic infection to life-threatening respiratory failure. This study aimed to determine the relationship between the survival and demographic data, comorbidity status, and laboratory parameters of coronavirus disease 2019 (COVID-19) patients requiring intensive care. MATERIAL AND METHODS: We retrospectively analyzed 236 patients requiring intensive care whose diagnosis was confirmed by the SARS-CoV-2 reverse transcription-polymerase chain reaction (RT-PCR) test. The patients were divided into two groups in terms of survival. Demographic data; procalcitonin and C-reactive protein (CRP) levels; leukocyte, lymphocyte, and neutrophil counts in hemogram and neutrophil-to-lymphocyte ratio (NLR) levels; and lower respiratory and blood cultures were examined, and the relationships between these parameters and survival were evaluated with hypothesis testing. RESULTS:  In the study, 156 (66.1%) males and 80 (33.9%) females, a total of 236 patients, were included. Sixty-seven (28.3%) surviving patients were determined as Group 1, and 169 (71.7%) deceased patients were determined as Group 2. A statistically significant difference was found between the groups in terms of mean age (p<0.001) and gender distribution (p=0.011). In laboratory parameters, a significant difference was observed between the groups in lymphocyte count (p=0.001), NLR (p<0.001), and procalcitonin levels (p<0.001). Although leukocyte (p=0.075), neutrophil (p=0.031), and CRP (p=0.112) levels were higher in Group 2, there was no statistical difference. Mortality was found to be higher in patients with comorbidity (p=0.012) or co-infection (p=0.002). CONCLUSION: High levels of neutrophil count, NLR, and procalcitonin; low lymphocyte count; the presence of comorbidity; and secondary bacterial infection were found to be associated with mortality in COVID-19 patients in the intensive care unit.

Neuroprotective effects of Vaccinium myrtillus on damage-related brain injury.

Traumatic brain injury may trigger the secondary brain injury, which has the potential to be reversible and thus preventable. Anthocyanins are phylotherapeutic plants, which are reported to exhibit anti-inflammatory properties. This study aimed to evaluate the therapeutic efficiency of an anthocyanin, namely Vaccinium myrtillus, to alleviate secondary brain injury and identify possible mechanism of actions. It is hypothesized that lipid peroxidation and Na+ -K+ -ATPase activity may be involved in neuronal ischemia. Thus, brain tissue Malondialdehyde content, Na+ -K+ -ATPase content, and cleaved caspase-3 content was investigated following moderate head trauma in a rat model. Twenty-four Sprague-Dawley male rats were allocated into four groups: Control, Trauma, Solvent-Control, and Treatment. Trauma and Solvent-Control groups showed more prominent brain edema, neuronal ischemia, vascular congestion, increase in brain tissue Malondialdehyde and cleaved caspase-3 levels, and decreased Na+-K+-ATPase activity compared to the Control group. Although the Treatment group had comparable histological signs to the Trauma and Solvent-Control groups, Malondialdehyde level and Na+-K+-ATPase activity was similar to Control group, and cleaved caspase-3 levels were lower compared to Trauma and Solvent-Control groups. We conclude that anthocyanin extracts may alleviate secondary brain injury via anti-oxidative and anti-apoptotic mechanisms.