Ydetroelsen8536

Intake of probiotic bacteria may improve or preserve insulin sensitivity. Fetuin-A and sestrin 3 have emerged as promising candidate biomarkers for crucial roles in insulin signaling pathway. Therefore, the effect of oral supplementation with the probiotic bacterium Lactobacillus delbrueckii subsp. lactis PTCC1057 on proteins involved in insulin signaling pathway was investigated in normal and streptozotocin (STZ)-induced diabetic mice. The 6-8-week-old female mice were divided into a non-diabetic control, diabetic control, and diabetic experimental and non-diabetic experimental groups (5 mice each group). Diabetic and non-diabetic experimental groups treated with 3 × 107 CFU mL-1 L. delbrueckii subsp. lactis PTCC1057 by gavage feeding approach daily for 28 days. Serum glucose, fetuin-A, and sestrin 3 levels were measured by standard methods. The result showed that oral administration of L. delbrueckii significantly decreased serum glucose in comparison to diabetic control group (P = 0.01). Serum fetuin-A level was higher in diabetic control group than non-diabetic group and oral administration of L. delbrueckii subsp. lactis PTCC1057 significantly decreased fetuin-A level in diabetic experimental group in comparison with non-diabetic groups (P = 0.001). Sestrin 3 level significantly was lower in diabetic control group than non-diabetic control group (P = 0.03) and it significantly increased in diabetic experimental group in comparison with diabetic control group after intervention of L. delbrueckii subsp. lactis PTCC1057 (P = 0.02). The results show that feeding the STZ-induced diabetic mice with L. delbrueckii subsp. lactis PTCC1057 terminated to decrease in fasting blood glucose and fetuin-A level and increase in serum sestrin 3 level. Therefore, the L. delbrueckii subsp. find more lactis PTCC1057 can be considered as excellent candidate for future studies on diabetes mellitus.Mesenchymal stem cells (MSCs) are multi-potent cells characterized by long term self-renewal and by potential for differentiation into cells of different mesenchymal tissue types such as fibroblasts, osteocytes, chondrocytes, and adipocytes. Their unique properties offer broad therapeutic potentials. Bone marrow has been used as the most common MSCs source, but it is gradually going to be replaced by adipose tissue which showed to contain more MSCs per unit than the bone marrow and clinical application of MSCs procured from the adipose tissue have been demonstrating at least similar results. Post-burn scars result frequently in severe both functional and aesthetic impairments in restitution and rehabilitation periods of the burn disease. Despite extensive research in the last decades, the exact mechanisms of scar formation remains unclear. The development of post-burn scars is influenced by multiple factors such as initial depth of the burn, methods of burn wound therapy, duration of the open wound until finaructed scar and required volume of transferred fat. Isolation of MSCs following procurement was provided by the Central Tissue Bank cell culture laboratory which is one of the parts of the burn department. The average time of scars duration was 79 months, ranging from 6 to 216 months. The postburns scars were assessed clinically according to Vancouver Scar Scale (VSS) prior to surgery, including photo documentation, and re-evaluated after 6 months following MSCs application. As the results have shown, the average VSS score before treatment was 7.88 points ranging from 4 to 11 points. The average VSS 6 months after surgical procedure and MSCs application was 2.34 points ranging from 1 to 4 points. According to the results obtained, the favourable effect of adipose tissue derived autologous MSCs application on scar remodelling following surgical reconstruction of post-burn scars could be promising.Here, we aim at developing a novel biomatrix from decellularized bovine spinal meninges for tissue engineering and regenerative medicine applications. Within this concept, the bovine spinal meninges were decellularized using 1% Triton X-100 for 48 h, and residual nuclear content was determined with double-strand DNA content analysis and agarose gel electrophoresis. The major matrix components such as sulfated GAGs and collagen before and after the decellularization process were analyzed with DMMB, hydroxyproline assay and SDS-PAGE. Subsequently, the native bovine spinal meninges (nBSM) and decellularized BSM (dBSM) were physiochemically characterized via ATR-FTIR spectroscopy, TGA, DMA and tensile strength test. The dsDNA content in the nBSM was 153.39 ± 53.93 ng/mg dry weight, versus in the dBSM was 39.47 ± 4.93 ng/mg (n = 3) dry weight and DNA fragments of more than 200 bp in length were not detected in the dBSM by agarose gel electrophoresis. The sulfated GAGs contents for nBSM and dBSM were observed to be 10.87 ± 1.2 and 11.42 ± 2.01 μg/mg dry weight, respectively. The maximum strength of dBSM in dry and wet conditions was found to be 19.67 ± 0.21 MPa and 13.97 ± 0.17 MPa, while nBSM (dry) was found to be 26.26 ± 0.28 MPa. MTT, SEM, and histology results exhibited that the cells attached to the surface of dBSM, and proliferated on the dBSM. In conclusion, the in vitro preliminary study has demonstrated that the dBSM might be a proper and new bioscaffold for tissue engineering and regenerative medicine applications.Non-Herlitz junctional epidermolysis bullosa (JEB-nH), an autosomal recessive bullous genodermatosis, is characterized by generalized skin blistering from birth onward, dental anomalies, universal alopecia and nail dystrophy. The underlying defect is mutation of the COL17A1 gene encoding the type XVII collagen, resulting in losing structure for attachment of basal epithelial cells to the matrix. In present study, we described one case of congenitally affected female child aged 10 years, with skin blistering. Dermatologic examination revealed sparse, mild blisters on the face and hand, with profound enamel pitting of the teeth. Skin biopsy from proband's bullous skin displayed subepidermal bulla formation without acantholysis. The immunofluorescence of anti-type XVII collagen antibody staining showed loss of type XVII collagen staining at the basement membrane zone. A combination of whole exome sequencing (WES) and Sanger sequencing revealed the novel heterozygous mutations (c.4324C>T;p.Q1442* and c.1834G>C;p.