The application of conventional approaches to diabetic wound regeneration has some limitations. Thus, skin substitutes could be a new therapeutic possibility. In this regard, fibrin scaffolds are promising materials due to their desirable characteristics. Since defective fibroblasts caused by diabetes can disrupt regeneration, it seems that the use of living cells can improve the healing process. Thus, based on this fact, a cellular fibrin membrane was used to evaluate the diabetic wound healing in rats. The fibrin membrane was fabricated using fresh frozen plasma on which isolated fibroblasts were cultured. The wound model was created on 36 diabetic rats that were randomly divided into three groups: control, membrane, and cellular fibrin membrane (CM). Wound photogramography and immuno-histopathological staining were performed during consecutive days after treatment. Macroscopic evaluation of the wounds indicated a noteworthy enhancement of wound closure in the CM group. In the CM group, the re-epithelialization rate on day 7, 10 (p < 0.001), and 14 (p < 0.05), the fibroblast percentage on day 3 (p < 0.01) and 7 (p < 0.05) and the collagenization in all days were significantly higher than those of other groups (p < 0.001). The fibroblast number in the CM group on day 10 was significantly (p < 0.01) lower than that in the other groups. Contrary to the neutrophil and angiogenesis percentages that had no significant difference among the groups at different points of time (p > 0.05), the macrophage percentage on day 7 (P < 0.01), 10, and 14 (p < 0.05) was significantly lower in the CM group as compared to that in other groups. Overall, it seems that the use of a fibroblast-loaded fibrin membrane is an attractive strategy to promote diabetic wound healing.

Myeloproliferative neoplasms (MPN) are heterogeneous diseases that classified by the presence of Philadelphia chromosome into Philadelphia chromosome negative (Ph-neg) and positive (Ph-pos) myeloproliferative neoplasms. In ph-neg group A somatic point mutation (c.1849G>T) in the JAK2 gene, part of the JAK2-STAT signal-transduction pathway, causes substitution of phenylalanine for valine (V617F) in the JAK2 protein and has been identified. This mutation was seen in PV by 65% to 97% and ET (30–57%) and primary myelofibrosis (35–95%). Highly sensitive methods have been used to determine the presence of the JAK2V617F mutation instead of direct sequencing. We aimed to assess JAK2 exon14 mutations by high-resolution melting (HRM) analysis, which allows variation screening in compare to other method for detecting mutation. The mutation analysis included 45 individuals who were subjected for diagnosis of ph-neg MPN. Genomic DNA was isolated and different methods are performed. PCR RFLP, ARMS PCR and HRM method has a detection sensitivity comparable with conventional methods (Qiagen) to identify the mutations and sequencing. For HRM analysis is cost-effective and beside that it is enzyme independence method also this method able to show amount of the mutant allele carried in samples and it’s helpful for treatments follow-up and determining MRD for them.

Background. Neuroprotective effects of stem cells have been shown in some neurologic diseases. In this study, the effect of oral mucosal mesenchymal stem cells (OMSCs) on traumatic brain injury (TBI) was evaluated in long term. Materials and Methods. TBI was induced by Marmarou’s method. The number of 2 × 10⁶ OMSCs was intravenously injected 1 and 24 h after the injury. Brain edema and pathological outcome were assessed at 24 h and 21 days after the injury. Besides, long‐term neurological, motor, and cognitive outcomes were evaluated at days 3, 7, 14, and 21 after the injury. Results. OMSCs administration could significantly inhibit microglia proliferation, and reduce brain edema and neuronal damage, at 24 h and 21 days after the injury. Neurological function improvement was observed in the times evaluated in OMSCs group. Cognitive and motor function dysfunction and anxiety‐like behavior were prevented especially at 14 and 21 days after the injury in the treatment group. Conclusion. According to the results of this study, OMSCs administration after TBI reduced brain edema and neuronal damage, improved neurologic outcome, and prevented memory and motor impairments and anxiety‐like behavior in long term.