BACKGROUND:The amniotic membrane is the rejected material after birth. Amniotic mesenchymal stem cel s are characterized as easy harvesting, strong proliferation ability, no ethical controversy, and low immunogenicity. OBJECTIVE:To electrotransfer human telomerase reverse transcriptase (hTERT) gene into amniotic mesenchymal stem cel s transplanted into diabetic rats and to explore its effect on diabetic rats. METHODS:Human amniotic mesenchymal stem cel s were isolated, cultured and electrotransferred by hTERT gene. Ten of 50 Sprague-Dawley rats were randomized selected as controls, and the remaining rats were used to establish diabetic models through injection of 45 mg/kg streptozotocin. Thirty-six model rats were randomized into model group, cel transplantation group and hTERT-transfected cel transplantation group, with 12 rats in each group. In the latter two groups, human amniotic mesenchymal stem cel s and hTERT-transfected amniotic mesenchymal stem cel s were injected via sublingual veins, respectively. After transplantation, blood glucose levels were monitored dynamical y, and plasma insulin concentration was detected every week. Pancreas tissues were taken and cut into sections for histological observation using hematoxylin-eosin staining. RESULTS AND CONCLUSION:At 4 weeks after transplantation, the blood glucose levels were significantly lower in the two cel transplantation groups than the model group (P<0.05), and especial y in the hTERT-transfected cel transplantation group, the blood glucose level was close to the normal value (P>0.05). However, the model group stil had a higher blood glucose level. At 6 weeks after transplantation, compared with the model group, the plasma insulin concentration was significantly increased in the two cel transplantation group (P<0.05), and the severity of pancreatic injury was also eased in these two groups (P<0.05), especial y in the hTERT-transfected cel transplantation group (P<0.05). These findings indicate that hTERT-transfected amniotic mesenchymal stem cel transplantation can dramatical y decrease blood glucose level and relieve pancreatic injury in diabetic rats, which is an effective method for treatment of mel itus diabetes in rats.

Objective To investigate the antitumor effect of special promoter-controlled Gibbon ape leukemia virus membrane fusion glycoprotein (GALV.fus) mediated by type Ⅰ herpes simplex virus (HSV-Ⅰ) on lung adenocarcinoma. Methods Recombinant HSV-Ⅰ plasmids encoding GALV.fus was introduced into green monkey kidney cells(Vero)by liposome to amplify the virus, and then the virus was transfected into lung adenocarcinoma (A549), human fetal fibroblasts (HFL-Ⅰ GNHu 5) and human lung adenocarcinoma xenografts which were established in nude mice subcutaneously to observe antitumor and cytotoxic effect in vitro and in vivo; Recombined cytomegalovirus (CMV) containing GALV.fus or enhanced green fluorescence protein were served as control. Results Recombinant HSV-Ⅰ virus were packed successfully. Heterotransplantative tumourigenicity of the tumour was 100% in nude mice after A549 cells were inoculated. Recombinant HSV-Ⅰvirus exerted obvious antitumor effects in vitro, with relative survival rate of 23%, while for CMV virus containing GALV. fus, the rate was 20%, and for CMV virus encoding EGFP, the rate was 68%. Recombinant HSV-Ⅰvirus also showed striking antitumor effect on the implanted tumor. Conclusion GALV.fus has powerful effect against lung cancer in vitro and in vivo and maybe a promising candidate for gene therapy.

Endogenously eliminating the hematoma is a favorable strategy in addressing intracerebral hemorrhage (ICH). This study sought to determine the role of retinoid X receptor-α (RXR-α) in the context of hematoma absorption after ICH. Our results showed that pharmacologically activating RXR-α with bexarotene significantly accelerated hematoma clearance and alleviated neurological dysfunction after ICH. RXR-α was expressed in microglia/macrophages, neurons, and astrocytes. Mechanistically, bexarotene promoted the nuclear translocation of RXR-α and PPAR-γ, as well as reducing neuroinflammation by modulating microglia/macrophage reprograming from the M1 into the M2 phenotype. Furthermore, all the beneficial effects of RXR-α in ICH were reversed by the PPAR-γ inhibitor GW9662. In conclusion, the pharmacological activation of RXR-α confers robust neuroprotection against ICH by accelerating hematoma clearance and repolarizing microglia/macrophages towards the M2 phenotype through PPAR-γ-related mechanisms. Our data support the notion that RXR-α might be a promising therapeutic target for ICH.

Endogenously eliminating the hematoma is a favorable strategy in addressing intracerebral hemorrhage (ICH). This study sought to determine the role of retinoid X receptor-α (RXR-α) in the context of hematoma absorption after ICH. Our results showed that pharmacologically activating RXR-α with bexarotene significantly accelerated hematoma clearance and alleviated neurological dysfunction after ICH. RXR-α was expressed in microglia/macrophages, neurons, and astrocytes. Mechanistically, bexarotene promoted the nuclear translocation of RXR-α and PPAR-γ, as well as reducing neuroinflammation by modulating microglia/macrophage reprograming from the M1 into the M2 phenotype. Furthermore, all the beneficial effects of RXR-α in ICH were reversed by the PPAR-γ inhibitor GW9662. In conclusion, the pharmacological activation of RXR-α confers robust neuroprotection against ICH by accelerating hematoma clearance and repolarizing microglia/macrophages towards the M2 phenotype through PPAR-γ-related mechanisms. Our data support the notion that RXR-α might be a promising therapeutic target for ICH.
Anilides/pharmacology* ; Cerebral Hemorrhage/drug therapy* ; Hematoma/drug therapy* ; Humans ; Macrophages ; Microglia ; Neuroprotection ; PPAR gamma ; Retinoid X Receptor alpha

The adjacent anatomy of the pelvis is complicated, with digestive, urinary, reproductive and other organs as well as important blood vessels and nerves. Therefore, accurate resection of pelvic tumors and precise reconstruction of defects after resection are extremely difficult. The development of medical 3D printing technology provides new ideas for precise resection and personalized reconstruction of pelvic tumors. The “triune” application of 3D printing personalized lesion model, osteotomy guide plate and reconstruction prosthesis in pelvic tumor limb salvage reconstruction treatment has achieved good clinical results. However, the current lack of normative guidance standards such as preparation and application of 3D printing personalized lesion model, osteotomy guide plate and reconstruction prosthesis restricts its promotion and application. The formulation of this consensus provides normative guidance for 3D printing personalized pelvic tumor limb salvage reconstruction treatment.