Objective To evaluate the feasibility,safety and operation timing of laparoscopic cholecys-tectomy in treatment of gallbladder calculi incarceration. Methods The data of 280 cases of gallbladder stone incarceration performed by LC were retrospectively analyzed. Results Eight out of 280 cases were converted to open cholecystectomy. The successful rate of LC was 97. 1%. There were no complications such as bile and intestinal injury. Conclusion LC for gallbladder calculi incarceration is safe and feasible as long as operators have skilled technique and make right decisions on operation timing.

Angiotensin II (ANGII) plays an important role in the pathogenesis of atherosclerosis by inducing proliferation of vascular smooth muscle cells (VSMCs). In our study, we observed the effects of valsartan on proliferation of cultured VSMCs treated with or without ANGII by cell counting and methyl thiazolyl tetrazolium (MTT) assay, and detected the expression of mitofusin 2 (Mfn2), a newly discovered cell proliferation inhibitor and a related cell proliferation signaling pathway protein by Western blotting. ANGII at a concentration of 10(-6) mol/L significantly stimulated VSMCs proliferation, down-regulated the expression of Mfn2 and up-regulated the expression of Raf and ERK1/2. Valsartan inhibited such effects of ANGII at concentrations of 10(-5) and 10(-6) mol/L, but not at 10(-7) mol/L. Valsartan had no significant effect on the proliferation of untreated VSMCs. These results suggest that valsartan inhibits ANGII-induced proliferation of VSMCs in vitro via Mfn2-Ras-Raf-ERK/MAPK signaling pathway.

BACKGROUND:Hydroxyapatite/gel nano-composite has the same mechanical strength to the natural bone, but its ability to repair bone defects and osteogenic effect need to be confirmed by further studies.
OBJECTIVE:To explore the repair effect of hydroxyapatite/gel bionic composite in skul defects of rabbits.
METHODS: The hole-like calvarium defect models were established in rabbits, and treated with hydroxyapatite/ gel composites (hydroxyapatite/gel group), autologous skul as positive control (autologous bone group) and
nothing as negative control (blank group). The repairing condition in the skul defect areas were observed and analyzed by X-ray and CT at 4, 8, 12 weeks after implantation.
RESULTS AND CONCLUSION: After 8 weeks, X-ray assessment showed that normal-like bone tissue appeared in the defect region of the autologous bone group; in the hydroxyapatite/gel group, dense bone with similar
morphology to normal bone tissue was found in the central site of defect region, and the boundary was slightly blurred. After 12 weeks, the hydroxyapatite/gel showed blurred edge compared with autologous bone, and the center of the composite was disconnected; in the blank group, a clear and regular transmitted shadow was
observed. After 12 weeks, CT examination showed that the hydroxyapatite/gel was connected tightly with the surrounding normal bone tissue. As a new bionic composite, the hydroxyapatite/gel can achieve good effect in repairing skul defects of rabbits.

We investigated the distribution characteristics of Yersinia enterocolitica in Ningxia ,China .In accordance with the requirements of the National Yersinia enterocolitica Disease Monitoring Scheme ,Y .enterocolitica were isolated from differ‐ent kinds of specimens collected in Ningxia in 2008 to 2013 .Then they were serotyped and detected for virulence gene and ana‐lyzed the pulsed‐field gel electrophoresis (PFGE) in Chinese CDC .It was found that 173 strains were isolated from various types of 9 643 specimens ,and the detection rate was 1 .79% .There were statistical differences among detection rates in differ‐ent years and in different specimens (P<0 .01) .Pathogenic serotypes O∶3 and O∶9 carried ail gene and ystA gene were de‐tected from specimens of pigs and diarrhea patient .Non‐pathogenic serotypes O∶5 and O∶8 and non‐typeable strains didn't carry ail gene and ystA gene ,and also can't be detected from swine ,cattle ,sheep ,chickens and dogs .In conclusion ,Y .en‐terocolitica was widely distributed in Ningxia and pigs were the dominant animal host .In all pathogenic serotypes ,the highest proportion was O∶3 following by O∶9 .It was no time and regional difference in the distribution of that in Ningxia ,China .

Objective To explore the clinical effect of gluteal pressure sore repaired by superior and inferior perforating artery island flap with rotation and joint propulsion.Methods From January 2014 to April 2018,37 patients (27 males,10 females,aged 35～79 years) with hip decubitus were admitted to the First People's Hospital of Yulin City for treatment of hip decubitus.According to the situation of the wound surface,the perforating site of superior and inferior perforator arteries and the local soft tissue,the corresponding perforator arteries were selected as the pedicle to form island skin flap,and the wound surface was transferred by rotation and propulsion.Results All the flaps sur vived well.33 cases healed in the first stage,but 4 cases dehisced and infected in the incision.After dressing change,the wounds healed in the second stage and the wounds were locally smooth.Conclusions The rotational combined push type gluteal superior and inferior perforator island flap is a good method to repair gluteal pressure sore.

Angiotensin Ⅱ (ANG Ⅱ) plays an important role in the pathogenesis of atherosclerosis by inducing proliferation of vascular smooth muscle cells (VSMCs).In our study,we observed the effects of valsartan on proliferation of cultured VSMCs treated with or without ANG Ⅱ by cell count ing and methyl thiazolyl tetrazolium (MTT) assay,and detected the expression of mitofusin 2 (Mfn2),a newly discovered cell proliferation inhibitor and a related cell proliferation signaling pathway protein by Western blotting.ANGⅡ at a concentration of 10-6 mol/L significantly stimulated VSMCs proliferation,down-regulated the expression of Mfn2 and up-regulated the expression of Raf and ERK1/2.Valsartan inhibited such effects of ANG Ⅱ at concentrations of 10-5 and 10-6 mol/L,but not at 10-7 mol/L.Valsartan had no significant effect on the proliferation of untreated VSMCs.These results suggest that valsartan inhibits ANGⅡ-induced proliferation of VSMCs in vitro via Mfn2-Ras-Raf-ERK/MAPK signaling pathway.

Decellularized matrix transplantation has emerged as a promising therapeutic approach for repairing tissue defects, with numerous studies assessing its safety and efficacy in both animal models and clinical settings. The host immune response elicited by decellularized matrix grafts of natural biological origin plays a crucial role in determining the success of tissue repair, influenced by matrix heterogeneity and the inflammatory microenvironment of the wound. However, the specific immunologic mechanisms underlying the interaction between decellularized matrix grafts and the host immune system remain elusive. This article reviews the sources of decellularized matrices, available decellularization techniques, and residual immunogenic components. It focuses on the host immune response following decellularized matrix transplantation, with emphasis on the key mechanisms of Toll-like receptor, T-cell receptor, and TGF-β/SMAD signaling in the stages of post-transplantation immunorecognition, immunomodulation, and tissue repair, respectively. Furthermore, it highlights the innovative roles of TLR10 and miR-29a-3p in improving transplantation outcomes. An in-depth understanding of the molecular mechanisms underlying the host immune response after decellularized matrix transplantation provides new directions for the repair of tissue defects.

Decellularized matrix transplantation has emerged as a promising therapeutic approach for repairing tissue defects, with numerous studies assessing its safety and efficacy in both animal models and clinical settings. The host immune response elicited by decellularized matrix grafts of natural biological origin plays a crucial role in determining the success of tissue repair, influenced by matrix heterogeneity and the inflammatory microenvironment of the wound. However, the specific immunologic mechanisms underlying the interaction between decellularized matrix grafts and the host immune system remain elusive. This article reviews the sources of decellularized matrices, available decellularization techniques, and residual immunogenic components. It focuses on the host immune response following decellularized matrix transplantation, with emphasis on the key mechanisms of Toll-like receptor, T-cell receptor, and TGF-β/SMAD signaling in the stages of post-transplantation immunorecognition, immunomodulation, and tissue repair, respectively. Furthermore, it highlights the innovative roles of TLR10 and miR-29a-3p in improving transplantation outcomes. An in-depth understanding of the molecular mechanisms underlying the host immune response after decellularized matrix transplantation provides new directions for the repair of tissue defects.

Decellularized matrix transplantation has emerged as a promising therapeutic approach for repairing tissue defects, with numerous studies assessing its safety and efficacy in both animal models and clinical settings. The host immune response elicited by decellularized matrix grafts of natural biological origin plays a crucial role in determining the success of tissue repair, influenced by matrix heterogeneity and the inflammatory microenvironment of the wound. However, the specific immunologic mechanisms underlying the interaction between decellularized matrix grafts and the host immune system remain elusive. This article reviews the sources of decellularized matrices, available decellularization techniques, and residual immunogenic components. It focuses on the host immune response following decellularized matrix transplantation, with emphasis on the key mechanisms of Toll-like receptor, T-cell receptor, and TGF-β/SMAD signaling in the stages of post-transplantation immunorecognition, immunomodulation, and tissue repair, respectively. Furthermore, it highlights the innovative roles of TLR10 and miR-29a-3p in improving transplantation outcomes. An in-depth understanding of the molecular mechanisms underlying the host immune response after decellularized matrix transplantation provides new directions for the repair of tissue defects.

Decellularized matrix transplantation has emerged as a promising therapeutic approach for repairing tissue defects, with numerous studies assessing its safety and efficacy in both animal models and clinical settings. The host immune response elicited by decellularized matrix grafts of natural biological origin plays a crucial role in determining the success of tissue repair, influenced by matrix heterogeneity and the inflammatory microenvironment of the wound. However, the specific immunologic mechanisms underlying the interaction between decellularized matrix grafts and the host immune system remain elusive. This article reviews the sources of decellularized matrices, available decellularization techniques, and residual immunogenic components. It focuses on the host immune response following decellularized matrix transplantation, with emphasis on the key mechanisms of Toll-like receptor, T-cell receptor, and TGF-β/SMAD signaling in the stages of post-transplantation immunorecognition, immunomodulation, and tissue repair, respectively. Furthermore, it highlights the innovative roles of TLR10 and miR-29a-3p in improving transplantation outcomes. An in-depth understanding of the molecular mechanisms underlying the host immune response after decellularized matrix transplantation provides new directions for the repair of tissue defects.