This study examines the hemocompatibility of gellan-gum-based hybrid hydrogels, with varying gellan-gum concentrations and constant sodium alginate and silk fibroin concentrations, respectively, in accordance with ISO 10993-4 standards. While previous studies have focused on cytocompatibility, the hemocompatibility of these hydrogels remains underexplored. Hydrogels were formulated with 0.3%, 0.5%, 0.75%, and 1% gellan gum combined with 3% silk fibroin and 4.2% sodium alginate separately, using physical and ionic cross-linking. Swelling behavior was analyzed in phosphate (pH 7.4) and acetic (pH 1.2) buffers and surface morphology was examined by scanning electron microscopy (SEM). Hemocompatibility tests included complete blood count (CBC), coagulation assays, hemolysis index, erythrocyte morphology, and platelet adhesion analysis. Results showed that gellan gum–sodium alginate hydrogels exhibited faster swelling than gellan gum–silk fibroin formulations. SEM indicated smoother surfaces with sodium alginate, while silk fibroin increased roughness, further amplified by higher gellan-gum concentrations. Hemocompatibility assays confirmed normal profiles in formulations with 0.3%, 0.5%, and 0.75% gellan gum, while 1% gellan gum caused significant hemolytic and thrombogenic activity. These findings highlight the excellent hemocompatibility of gellan-gum-based hydrogels, especially the sodium alginate variants, supporting their potential in bioengineering, tissue engineering, and blood-contacting biomedical applications.

Colorimetric determination of proteins in serum is proposed based on the biuret method and replacing ultraviolet-visible spectrometric (UV-Vis) detection with a simple and affordable smartphone digital image colorimetric (SDIC) method. Optimum SDIC conditions were found as a detection wavelength of 555 nm, a region of interest of 1600 px², and 9.0 cm between the detection camera and sample solution. Under the optimum conditions, the coefficient of determination was 0.9982 within a linear dynamic range of 0.022 to 0.35 g dL⁻¹. The precision of the method based on the percent relative standard deviation was below 5%. The limit of detection and limit of quantitation were found to be 0.007 and 0.022 g dL⁻¹ respectively, which were sufficient for the quantification of the total protein, albumin, and globulin in serum. The method was validated with an independent experiment using a UV-Vis method and both methods showed good statistical agreement, indicating the accuracy of the proposed SDIC method.

Background: Hepatic ischemia-reperfusion causes histologic injury to the intestinal mucosa. We investigated the effects of diosmin, a phelobotrophic drug with antioxidant and antiinflammatory effects, on intestinal injury in the experimental liver ischemia-reperfusion model. Materials and methods: Fourty rats were divided into four groups: sham group (Group 1), control group (Group 2), perop diosmin group (50 mg/kg) treatment group (Group 3) and preop 10-day diosmin (50 mg/kg) treatment group (Group 4). Ischemia-reperfusion model was carried out by clamping the hepatic pedicle for 60 min and then reperfusing the liver for 90 min. At the end of procedures, blood and ileum tissue samples were obtained for biochemical and histopathological assessments. Results: According to the results of liver function tests (AST, ALT and LDH) there was a significant difference between the control and other groups (p<0.001 for all). According to the plasma and ileum oxidative stress parameters (MDA, GSH-Px and XO), there was a significant difference between the control and other groups (p<0.05 for all). Histopathologically; the specimens in Group 2 showed specific morphological abnormalities (the epithelial lining of the apical surface of villi was degenerated and desquamated to the lumen). Group 3 and 4 showed ileal histomorphology similar to the sham group. Pathological scores were significantly different between Group 2 and other groups. Conclusions: Diosmin can be administered for protection from destructive effects of hepatic ischemia-reperfusion injury on intestine in both emergent and elective hepatic surgical operations in which the possible ischemic periods are expected (Tab. 4, Fig. 1, Ref. 39) . Full Text in free PDF www.bmj.sk .

Asporin is secreted by theca cells in the mouse ovaries and is an effective marker at the gonadotropin-independent stage in secondary follicle development. It has an inhibitory effect on transforming growth factor beta and bone morphogenic proteins, which are involved in androgenesis process. Our aim was to compare serum asporin levels of polycystic ovary syndrome and control groups and examine the relationship between asporin and hyperandrogenism. A total of 60 patients, i.e., 30 polycystic ovary syndrome group and 30 controls, were included in the study. The demographic characteristics, hormonal status, and serum asporin levels of patients were evaluated and compared for each group. In addition, polycystic ovary syndrome patients were analyzed according to the presence of hyperandrogenism. Receiver operating characteristic curve analysis was performed for asporin levels in order to distinguish polycystic ovary syndrome patients from controls. Body mass index, serum asporin and androgen levels, free androgen index, and insulin resistance values were statistically significantly higher in polycystic ovary syndrome group. Serum asporin levels were statistically significantly higher in hyperandrogenic polycystic ovary syndrome patients compared to non-hyperandrogenic polycystic ovary syndrome women (p=0.010). Receiver operating characteristic curve analysis was done for serum asporin levels to distinguish between polycystic ovary syndrome patients and healthy controls (area under the curve=0.676, standard error: 0.070, 95%CI: 0.539-0.812, p=0.019, 63.3% sensitivity, and 70% specificity). The elevation of serum asporin levels in patients with polycystic ovary syndrome may be associated with the pathogenesis of this syndrome, or it may be the consequence of the disease. This relationship may be explained through the androgen mechanism.