Immunological rejection is the major barrier to successful transplantation.The immune response to an allograft is an ongoing dialogue between the innate and adaptive immune system that will lead to the rejection of allograft.Activation of elements of the innate immune system,triggered as a consequence of tissue injury sustained during cell isolation or organ retrieval and ischemia reperfusion,will initiate and amplify the adaptive response.Identifying the molecular pathways that trigger tissue injury,signal transduction and rejection facilitates the identification of targets for the development of immunosuppressants.

With the continuous development of the cancer stem cell theory,biomarkers for CSCs (Cancer stem cells) have gradually become the hot issues in tumor research.As the most commonly used CSCs biomarker,CD44 gains lots of attentions.This paper will review recent research about CD44 molecule and its powerful role in regulating tumor progenesis and progression.

Tumor occurrence and development is a complicated process.Previous studies confirm that DNA mutations result in activation of downstream pathways of tumor cells.Recently,studies of post-translational modifications showed that RNA editing play an important role in transcriptional mechanism.Thus,RNA editing further enrich the diversity of RNA and protein,participate in the process of many diseases,including cancer.Recently,many studies have focused on the RNA editing enzymne ADAR1 because of the complexity role in tumorigenesis and progression.This article mainly reviewed the role of ADAR1 in the occurrence and development of tumors.

Objective To analyze the dynamic changes of perinatal defects in Lishui city from 2005 to 2014.Methods According to hospital-based data,87 294 fetuses and infants aged from 28 weeks of gestation to 7 days after birth were monitored for birth defects in Lishui city from 2005 to 2014.Results Among 87 294 perinatal infants,birth defects were found in 1 914 cases with a incidence of birth defects of 219.3/ten thousand,which was on the rise year by year except 2009.The incidence of birth defects was 235.1/ten thousand (737/31 352) in urban areas,which was significantly higher than that in rural areas (210.4/ten thousand,1 177/55 942) (x2 =5.705,P ＜ 0.05).The incidence of birth defects of boys and girls was 221.1/ten thousand (1 005/45 453) and 212.8/ten thousand (890/41 822),respectively (x2 =0.707,P ＞ 0.05).Among 1 914 cases of defects,657 were detected prenatally and 1 257 case were detected within 7 days after birth.Congenital heart disease was the most common birth defect,followed by polydactyly,cleft lip,microtia and syndactyly.Birth defect accounted for 32.74％ (278/849) of all perinatal deaths and the ratio was on the rise since 2010.Conclusion There is an upward trend in incidence of birth defects in Lishui city in the last decade;the incidence of birth defects in urban areas is significantly higher than that in rural areas;the incidence of congenital heart disease is high,and birth defects are the main cause of perinatal death.

Objective To observe the reception of using pig bone marrow stromal cells (BMSCs) that were transfected with human tissue factor pathway inhibitor (TFPI) to resolve the dysregulation of coagulation after liver xenotransplantation.Methods Pig BMSCs were immortalized by transfection with lentivirus containing SV40T and then transfection with human TFPI.At last the cells were tested for their ability to inhibit clotting in a model by co-incubation of human plasma,human monocytes and pig aortic endothelial cells.Results After transfection with SV40T,pig BMSCs were immortalized and similar to primary cells.The immortalized pig BMSCs showed a stable TFPI expression after transfection with human TFPI by lentivirus.Moreover,they showed the potential of regulating coagulation dysregulation in vitro.Conclusion Pig BMSCs transfected with human TFPI could solve the regulation dysregulation caused by TF activation effectively,and have the potential of resolving coagulation dysregulation in liver xenotransplantation.

Acute liver failure is a culmination of liver diseases which develop in a common pathophysiologic procession.The mortality rate is very high due to complicated etiology and diagnostic difficulties.Presently,the main method for acute liver failure treatment is dialysis,adjuvant therapy,and liver transplantation.We reviewed new research findings for the treatment of this disease and particular attention was given to practical matters for clinicians to consider in approaching patients.

BACKGROUND:It is confirmed that the absence of hypoxia-inducible factor-1α (HIF-1α) accelerates the degenerative process in the intervertebral discs, and microRNAs have an important role in degeneration of the intervertebral discs.
OBJECTIVE:To evaluate the changes of microRNAs in the intervertebral discs of HIF-1α-deficient (HIF-1α-/-) mice which may mediate the signaling pathway of HIF-1α in the intervertebral discs.
METHODS: As previously reported, HIF-1α-/- mice were established. HIF-1α-/- mice and HIF-1αflox/flox mice (control mice) aged 4 weeks were used. MRI and histological staining were used to evaluate the degeneration of the intervertebral discs. Total RNAs were extracted from the intervertebral discs tissues by Trizol, and the differential expression profile of microRNAs was harvested by significance analysis of microarrays and Cluster, based on microarray screening. Real-time quantitative reverse transcription-PCR was applied to verify the reliability of microRNA array results.
RESULTS AND CONCLUSION:The number of nucleus pulposus cels in the intervertebral discs of HIF-1α-/- mice was decreased, the cels presented with smal size and the color deepened in the cytoplasm. Finaly, differential expression profile of microRNAs (n=10) was obtained, seven of which were upregulated and three were downregulated. In conclusion, the loss of HIF-1α may cause the imbalance of some important miRNAs, which may result in a large amount of dead nuclear pulposus cels and mediate disc degeneration in HIF-1α-/- mice.

Objective The aim of this study was to investigate how different concentrations of dextran sulfate sodi-um ( DSS) influence the establishment of mouse model of inflammatory bowel disease ( IBD) and the effect of DSS on the expression of colitis-associated immune factors.Methods The DSS solution in different concentrations (3%, 5%, 7%) were given to male C57BL/6J mice to generate mouse inflammatory bowel disease model.The IBD mice were observed by defecation characteristics, body weight, and survival time.The animals were sacrificed at 6 days after the start of DSS drinking.The general appearance of colons was observed and scored.Moreover, the pathological changes of the colon were examined and analyzed by routine histology.The expression of immune factors in the spleen was detected by real-time PCR.Results The mice in the 3%, 5%, 7% DSS groups developed murine colitis.In addition, the incidence of IBD and mouse mortality rate was directly proportional to the increase of DSS concentration.Furthermore, the higher concentra-tion of DSS induced the expression of proinflammatory factors including TNF-α, IFN-γand IL-17A, but cause a decrease of anti-inflammatory factors such as IL-4, IL-10 and Treg-related transcription factor Foxp3.Conclusions Our data suggest that giving 5%DSS solution to C57BL/6J mouse is appropriate to efficiently establish a murine IBD model.This laid an important foundation for further studies of the pathogenesis of IBD, biological characteristics, and intervention factors.

Objective To investigate the inhibitory effect of Glycyrrhizin in MHCC97-H cell line in vitro and explore the relevant mechanism.Methods MHCC97-H cells were cultured in vitro and treated with Glycyrrhizin in different concentrations and then cell viability was assayed at different time points.The concentration and time were selected with 50％ cell viability.MHCC97-H cell plate clone formation assay and invasion-migration experiment were also performed to study the tumor-suppressor efficacy of Glycyrrhizin.Acridine orange staining was used to evaluate the formation of autophagic vacuoles.Meanwhile,3-MA and Atg7-siRNA were both employed to avoid the autophagy activation in MHCC97-H cells and cell viability was reassessed.Western-blot was carried out to study the expression of autophagic proteins of LC3B,p-mTOR and p-ERK1/2.Results It showed Glycyrrhizin significantly inhibited MHCC97-H cell viability and the concentration and time at 50％ cell viability were 2 mmol/L and 48 h respectively.Clone number in Glycyrrhizin group was significantly smaller than that in the control group (176.7 ± 14.5 vs.410.0 ± 32.1).Invasion-migration rate was also lower in Glycyrrhizin group compared with the control group (41.0％ ±3.8％ vs.100％).Autophagic vacuoles was increased in MHCC97-H cells when treated with Glycyrrhizin and expression of LC3B-Ⅱ was enhanced and LC3B-Ⅱ/I Ratio was increased,at the same time degradation of P62 was accelerated.Reduced p-mTOR in concurrence with upregulated p-ERK1/2 could be observed in MHCC97-H cells administered with Glycyrrhi-zin.Cell groups additionally treated with 3-MA or Atg7-siRNA exerted higher cell viability (64.3％ vs.45.9％ and 67.7％ vs.47.1％,respectively).Conclusion Glycyrrhizin can induce excessive autophagy in hepatocellular carcinoma cells to cause autophagic cell death and exhibit great potential in clinical application.