High levels of sTNFR1 and sTNFR2 in euthymic patients showed that it may support that proinflammatory process continues in euthymic period. This is the first study which showed increased sTNFR2 levels in euthymic period, which could be interpreted as a compensatory mechanism and again the first which deals with verbal memory.

BackgroundThe role of inflammation in the pathogenesis and progression of atherosclerosis has been increasingly discussed. Although the seroepidemiological studies have suggested a relationship between Helicobacter pylori (H. pylori) infection and atherosclerosis; the issue is still controversial. It is well known that abnormal lipid profil is related to atherosclerosis and the measurement of carotid-intima media thickness (CIMT) is one of the surrogate marker of atherosclerosis. The serum concentration of high-density lipoprotein (HDL-C) has been known to have an inverse correlation with the development of atherosclerosis. Paraoxonase-1 (PON1) is a major anti-atherosclerotic component of HDL-C. PON1 activity is related to lipid peroxidation and prospective cardiovascular risk. The aim of this study was to investigate CIMT and serum PON1 activities along with lipid parameters in H. pylori positive and negative subjects.MethodsThirty H. pylori positive subjects and thirty-one negative subjects were enrolled. H. pylori infection was diagnosed by the presence of positivity of stool H. pylori antigen test or Carbon 14 labeled urea breath test. Serum PON1 activity was measured spectrophotometrically. Traditional cardiovascular risk factors were investigated and laboratory analysis included measurement of serum triglycerides (TG), total cholesterol (TC), high-density lipoprotein (HDL-C) and low-density lipoprotein cholesterol (LDL-C). We assessed CIMT by high-resolution ultrasound of both common carotid arteries.ResultsWe found that the mean and maximum values of right and overall CIMT in H. pylori positive subjects were significantly thicker than those of H. pylori negative subjects. There was no significant differences in serum HDL-C, LDL-C, TC levels and TC/HDL-C ratios between two groups. Serum TG levels of H. pylori positive subjects were significantly higher than those of H. pylori negative subjects (p = 0.014). We found that PON1 activities were significantly lower in H. pylori positive subjects compared with negative subjects. No significantly correlation was observed between PON1 and CIMT values.ConclusionsThere is an increase in CIMT values in patients with H. pylori positive compared to H. pylori negative subjects. PON1 activity decrease significantly in H. pylori positive subjects. However, an association between PON1 and CIMT was not found. These data indicated that H. pylori may have a role in atherosclerotic processes, however, further studies are needed to evaluate the exact mechanisms.

Background: The kidney is often affected in plasma cell dyscrasias, usually due to the effects of nephrotoxic monoclonal-free light chains. Renal failure due to a monoclonal gammopathy may be detected by the highly sensitive serum-free light-chain (sFLC) ratio yet missed by electrophoretic assays. The aim of this study was to assess sFLC levels in relation to markers of renal function. Methods: Five-hundred thirteen patients were included in this study. sFLC levels were measured by Freelite Õ (The Binding Site Group Ltd, Birmingham, UK) assay using the BNII nephelometer (Siemens Diagnostics, Germany). Kappa/lambda (k/) sFLC ratio was calculated. Serum creatinine levels were analyzed by modified Jaffe method in Cobas 8000 analyser. GFR was estimated by the CKD-EPI (Chronic Kidney Disease Epidemiology Collaboration) equation. Patients were assigned to two groups depending on their eGFR values: 60 mL/min/1.73 m

The purpose of this study is to investigate the potential protective effect of the flavonoid Luteolin on ischemia-reperfusion (IR) injury in mouse intestine, which has not previously been studied. Twenty-four female C57BL/6 mice were randomly assigned to four groups, each consisting of 6 mice: a sham group (laparotomy, but no IR injury), a sham + Luteolin group (no IR, and Luteolin was administered intraperitoneally 30 min after laparotomy), IR group (30 min occlusion of the superior mesenteric artery (SMA) then 2 hr' reperfusion), IR + Luteolin (30 min occlusion of the SMA then 2 hr' reperfusion; Luteolin was administered intraperitoneally before reperfusion). Intestine tissues were harvested from the mice for histopathological and biochemical analysis. Total oxidant status (TOS) and total antioxidant capacity (TAC) of the intestinal tissues were measured using Erel's method. Oxidative stress index (OSI) was calculated using the TOS/TAC ratio. Intestinal histological changes were significantly decreased in the IR + Luteolin group compared with the IR group (p = .037). TOS tissue levels were also significantly decreased in the IR + Luteolin group compared with the IR group (p = .005). TAC levels did not increase significantly in the IR treatment group and were not affected by Luteolin treatment (p > .05). The results of this study show that Luteolin administration provides considerable protection against IR injury in the mouse intestine.

Cystatin C is a good marker of GFR in renal transplant patients, especially in those with no tubular injury; however, BTP is not as good as cystatin C in that regard.

To evaluate the effects of Caspase-3 (CASP3) gene expression and serum levels on preventing severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. A total of 41 individuals (male: 21; female: 20) with SARS-CoV-2 infection were included in the current study. Hemograms were examined from patient blood samples, and CASP3 gene expression levels were detected. Also, human CASP3 levels were determined from the serum samples of patients. The mean age of patients was 56.220 ± 18.937 years. Significant differences were detected among all groups for CASP3 2 C −ΔΔ t (p = 0.014) and CASP3 concentration (p = 0.024). The relationship between CASP3 2 C −ΔΔ t levels and hemoglobin (p = 0.023), between CASP3 2 C −ΔΔ t levels and C-reactive protein (CRP) (p = 0.001), between CASP3 2 C −ΔΔ t levels and ferritin (p = 0.003), between CASP3 2 C −ΔΔ t levels and lactate dehydrogenase (p = 0.001), and between CASP3 2 C −ΔΔ t levels and SpO 2 (p = 0.006) were statistically significant. Also, the relationship between CASP3 concentration levels and SpO 2 was statistically significant (p < 0.046). The CASP3 gene and/or its products have an important function to prevent injury caused by SARS-CoV-2 infection. They play crucial roles in maintaining cellular homeostasis and viability. Perhaps CASP3 levels may provide information about the severity of the disease.

Glioblastoma (GBM) is classified as a stage‐IV glioma. Unfortunately, there are currently no curative treatments for GBM. Poly(rC)‐binding protein 1 (PCBP1) is a cytosolic iron chaperone with diverse functions. PCBP1 is also known to regulate autophagy, but the role of PCBP1 in ferroptosis, iron‐dependent cell death pathway, remains unrevealed in GBM cells. Here, we investigated the effects of borax, a boron compound, on the ferroptosis signaling pathway mediated by PCBP1 and autophagy. The study analyzed cell viability, proliferation, and cell cycle on U87‐MG and HMC3 cells to investigate the effects of borax. After determining the cytotoxic concentrations of borax, morphological analyzes and measurement of PCBP1, Beclin1, malondialdehyde (MDA), glutathione (GSH), glutathione peroxidase 4 (GPx4) and acyl‐CoA synthetase long chain family member 4 (ACSL4) levels were performed. Finally, expression levels of PCBP1, Beclin1, GPx4 and ACSL4, and caspase‐3/7 activity were determined. We found that borax reduced U87‐MG cell viability in a concentration‐ and time‐dependent manner. Additionally, borax altered cell proliferation and remarkably reduced S phase in the U87‐MG cells and exhibited selectivity by having an opposite effect on normal cells (HMC3). According to DAPI staining, borax caused nuclear deficits in U87‐MG cells. The result showed that borax in U87‐MG cells induced reduction of the PCBP1, GSH, and GPx4 and enhancement of Beclin1, MDA, and ACSL4. Furthermore, borax triggered apoptosis by activating caspase 3/7 in U87‐MG cells. Our study indicated that the borax has potential as an anticancer treatment for GBM via regulating PCBP1/Beclin1/GPx4/ACSL4 signaling pathways.

This study demonstrated that cystatin C and β-trace protein do not reflect GFR with sufficient accuracy.