ObjectiveTo investigate the effects of chitosan/PVA nerve conduits which used for repairing sciatics nerve defect in rats.MethodsTwenty-seven rats were divided into 3 groups randomly,with 9 rats in each group. Firstly, the 15mm defects in the left sciatic nerves were made in the rats and were respectively repaired with chitosan/PVA conduits graft (group A), the silicon conduits graft (group B),and autografts (group C). At 12 weeks after the operations, the left sciatic nerves were taken out, and the comparative evaluation was made on the repairing effects by wet weight of gastrocnemius and soleus muscles, histological examination,computerized imaging analysis and True Blue retrograde tracing. ResultsThe wet weight of gastrocnemius and soleus muscles showed no significant difference between the chitosan/PVA graft and autograft groups (P ＞ 0.05). The wet weight of gastrocnemius and soleus muscles in significant difference between the chitosan/PVA graft and the silicon group at 12 weeks after the operation(P ＜ 0.05). The nerve fiber density showed no statistically significant differences between the chitosan/PVA and autograft groups(P＞ 0.05).The regenerative nerve fiber in group B had normal morphological and structural characters under transmission electron microscope.True Blue-labeled neuron cell bodies were found within both anterior horn of gray matter in the spinal cord and dorsal root ganglions (DRGs) ipsilateral to the operated side of the tested rats on illumination with ultra-violet light 1 week after the injection of True Blue.Conclusion Chitosan/PVA nerve conduit can effectively promote the nerve regeneration and myelinization of rat sciatic nerve, which is expected to substitute for autograft to repair nerve defects succesfully.

Objective To observe the safety of telbivudine (LdT) application throughout pregnancy in women with chronic hepatitis B (CHB),and to provide evidence-based treatment recommendations for women of childbearing age with chronic hepatitis B.Methods Women with hepatitis B virus (HBV) infection who took LdT before pregnancy and in early pregnancy were followed up prospectively for evaluating maternal and newborn adverse events.All newborns received block of HBV mother-to-child transmission (MTCT) after birth and were followed up for neonatal disorders and effects of maternal and child block.Results Among the 145 cases of pregnant women,143 were diagnosed as CHB and 2 decompensated cirrhosis.One hundred and five (72.4％) patients had HBV DNA＜500 copy/mL and 125 (86.0％) had positive hepatitis B e antigen.There were total 154 times pregnancies including 17 spontaneous abortions,4 ectopic gestation and 9 pregnancies after abortion.One hundred and one cases finished pregnancy,with 100 full term deliveries,1 preterm delivery and 2 twin pregnancies.One fetal with cleft lip and palate was aborted by induced labor in 24 weeks gestation.One baby was born with right double ears; one had benign lymph node under the left ear; and another one was diagnosed with congenital heart disease.Seven of the pregnant women had creatine kinase increased.Eight developed drug resistance.However,none had disease progression during pregnancy.None of the 63 infants was hepatitis B surface antigen positive over the 6 months of follow-up.The prevention of HBV MTCT was 100％ successful.Conclusion It is safe and effective for women with chronic HBV infection to receive LdT treatment throughout pregnancy.

OBJECTIVE To identify the pop strain of Staphylococcus aureus hospital acquired infection by random amplification of polymorphic DNA(RAPD),and to study the molecular mechanism of antibiotic(resistance),so as to reduce the occurrence of drug resistance and infection acquired in hospital.METHODS 1.DNA from 21 strains of S.aureus were extracted by the phenol-chloroform method and analyzed by using arbitrary(primer) polymerase chain reaction(AP-PCR).2.Amplifying mecA,GyrA and GrlA by PCR,and testing the(variation) of these genes by using Hinf Ⅰ-digested analysis.RESULTS Twenty one S.aureus strains were divided into 3(genetic) types.Type Ⅰ is the pop strain in our hospital which including 12 strains.Fourteen from 17 clinical stains were resistant to meticillin and quinolones,of which 13 strains had mecA except isolate 13064.And they all had(variation) in(GyrA) and/or GrlA.CONCLUSIONS RAPD provides markers for the typing of clinical strains and is suitable for(molecular) epidemiologic studies with high type ability,powerful discrimination,simplicity and(rapidness). Type Ⅰ is the pop S.aureus strain in hospital-acquired infection of our hospital.The majority of these strains are multi-(resistant) to meticillin,quinolones and other antibiotics.

Epigenetics is the study of heritable changes in gene expression other than the changes in the underlying DNA sequence. Such changes include DNA methylation,genomic imprinting,X chromosome inactivation and non-coding RNA regulation. Recent progresses on epigenetics offer new ideas to tackling these problems in forensic science,including determination of the necessary allele in paternity,identification of fetal paternity testing in embryonic period,discrimination of identical twins,origination analysis of tissue,and individual age estimation. This review focuses on the main concept of epigenetics and its application in the field of forensic science.

OBJECTIVE To study the molecular mechanism of antibiotic resistance in hospital acquired(Staphylococcus) epidermidis infection,so as to reduce the occurrence of drug resistance and infection(acquired) in hospital.METHODS DNA from 18 strains of S.epidermidis were extracted by the phenol-chloroform method,and mecA,gyrA and grlA were amplified by PCR,then the variation of gyrA and grlA was tested by Hinf Ⅰ-(digested)(analysis).RESULTS Fifteen from 18 S.epidermidis strains were resistant to meticillin,and all of them had mecA gene. Eleven from 18 S.epidermidis strains were resistant to meticillin,quinolones and other(antibiotics).And they all had a mutant in gyrA and/or grlA.The mutated spots were gyrA Ser84(TCA→TTA) and GrlA Ser80(TCC→TTC).CONCLUSIONS The majority of hospital acquired S.epidermidis strains are multi-resistant to meticillin,quinolones and other antibiotics,which are caused by acquirement of drug-resistance gene or(mutation) of drug-targeting genes.Medical institutions must strictly standardize the application of antibiotics to(reduce)(development) of drug resistance.

Objective: To explore the correlation between BMI and gut microbiota of college students in Inner Mongolia,and to provide a reference basis for revealing the relationship between intestinal flora and obesity. Methods: Totally 88 college students from Inner Mongolia Medical University were enrolled, Height and weight were measured,and the feces samples were collected. The bacterial metagenome was extracted from dry feces samples for the concentration detection in per gram of dry feces,expressed as μg/μL. Correlation between BMI and metagenomics concentration of gut microbiota was statistically analyzed. Meanwhile,the metagenomics concentration of gut microbiota in different BMI groups was compared with each other. Results: There was a negative correlation between BMI and the metagenomics concentration of gut microbiota(r=-0.27,P<0.05). Significant difference in the concentration of gut microflora was observed between the normal group and the obesity group,the normal group and the overweight/obesity group(F=3.62,P<0.05). Among the female volunteers,there were significant differences between normal group and overweight group,between normal group and obesity group(F=1.87,P<0.05). No significant differences in metagenomics concentration of gut microbiota were found in different BMI groups(F=0.60, P>0.05). Conclusion There is a correlation between BMI and gut microbiota of college students in Inner Mongolia，the concentration of gut microflora metagenome in overweight and obese people decreased significantly.

Traumatic brain injury(TBI)is a multifaceted disease with a complex pathogenesis for which there are currently no effective therapeutic interventions.Research has shown that bone marrow mesenchymal stem cell-derived extracellular vesicles(BMSC-EVs)may play a therapeutic role in TBI.They attenuate neuroinflammatory responses at the site of the lesion and promote neurovascular regeneration.However,the exact mechanisms underlying their actions are not fully understood.This article aims to review the current state of research on the therapeutic mechanisms of BMSC-EVs in TBI.It also aims to discuss possible future research directions and potential clinical applications of BMSC-EVs.

Purpose: The incidence rate of breast cancer (BC) has increased annually. Downstream neighbor of son (DONSON) critically affects cell cycle progression and maintains stable genomic properties; however, its relevant effects on BC growth and progression require indepth investigation. Methods: DONSON upregulation was validated in public databases. DONSON expression in matched BC and adjacent tissues and cell lines (MDA-MB-231, BT-549, and HS-578T) was determined using quantitative reverse transcription polymerase chain reaction. In vitro apoptosis, invasion, migration, and proliferation tests were performed to ascertain the functions of DONSON in BC cell lines. Then, using western blot analysis, the levels of DONSON downstream proteins were determined. Results: Compared to the control, DONSON was expressed at higher levels in BC tissues and cell lines. DONSON knockdown facilitated apoptosis and limited proliferation, migration, invasion, and S/G2 transition of BC cells In vitro. Furthermore, DONSON overexpression promoted BC cell proliferation and inhibited apoptosis In vitro. Moreover, DONSON knockdown reduced cyclin A1 and cyclin-dependent kinase 2 levels. Moreover, DONSON knockdown limited the progression of epithelial-mesenchymal transition. Conclusion DONSON critically affects BC growth and serves as a possible target and marker for the efficacy of subsequent therapies.

Diabetic retinopathy （DR） is one of the most common chronic microvascular complications of diabetes mellitus. It has a high rate of blindness， and the age of onset is gradually getting younger， which seriously affects the physical and mental health and quality of life of patients. The disease is retinal damage induced by diabetes mellitus， which is a kind of fundus disease with the main manifestations of fundus hemorrhage， hard exudation， microhemangioma， cotton-wool spots， neovascularization， etc. In traditional Chinese medicine （TCM）， it is classified into the category of "diabetic cataracts" and other diseases. At present， there is no effective method to prevent the progress of the disease in modern medicine， so it is particularly important to choose a reasonable and effective intervention to prevent and treat DR. Studies have confirmed that TCM has unique advantages in the treatment of DR. It can use its advantages of multiple bioactive components， multiple targets， and multiple pathways to intervene in the development process of DR from various aspects. By searching for the relevant literature on the progress of the intervention of DR with TCM monomers and compounds， this paper mainly reviews the relevant research results of the treatment of DR with multiple signaling pathways such as phosphatidylinositol 3-kinase （PI3K）/protein kinase B （Akt）， nuclear factor kappa-B（NF-κB）， p38 mitogen-activated protein kinase （p38 MAPK）， nuclear factor erythroid 2-related factor （Nrf2）/hemeoxygenase-1 （HO-1）， Hippo， advanced glycation end products （AGEs）/receptor for advanced glycation end products （RAGE）， and Akt/glycogen synthase kinase-3β （GSK-3β）， so as to provide more ideas and directions for the clinical prevention and treatment of DR.

Objective:Percutaneous coronary intervention(PCI)is one of the most important treatments for coronary artery disease(CAD).However,in-stent restenosis(ISR)after PCI is a serious complication without effective measures for prevention and treatment.This study aims to investigate the Ras-related protein 1A(Rap1A)level in ISR patients and in the tumor necrosis factor-α(TNF-α)-induced inflammatory injury model of human umbilical vein endothelial cells(HUVECs),to explore the role of Rap1A in regulating TNF-α-induced inflammation in HUVECs and to provide a new potential target for ISR prevention and treatment. Methods:A total of 60 CAD patients,who underwent PCI between December 2020 and July 2022 from the Department of Cardiovascular Medicine of Xiangya Hospital,Central South University,and re-examined coronary angiography(CAG)1 year after the operation,were included.After admission,27 patients were diagnosed with ISR and 33 patients were diagnosed with non-in-stent restenosis(non-ISR)according to the CAG.Clinical data were collected,and the plasma Rap1A level was determined by enzyme linked immunosorbent assay(ELISA).In cell experiments,an inflammatory injury model was established with TNF-α treatment(10 ng/mL,24 h)in HUVECs.The mRNA and protein expression levels of Rap1A,interlukin-6(IL-6),and vascular cell adhesion molecule-1(VCAM-1)were measured by real-time reverse transcription PCR and Western blotting.Small interfering RNA(siRNA)was used to explore the role of Rap1A in regulating TNF-α-induced inflammation in HUVECs. Results:Compared with the non-ISR patients,a higher proportion of ISR patients had a history of smoking(P=0.005)and diabetes(P=0.028),and higher levels of glycosylated hemoglobin(HbA1c)(P=0.012),low-density lipoprotein cholesterol(LDL-c)(P=0.014),and hypersensitive C-reactive protein(hs-CRP)(P=0.027).The remaining projects did not show significant differences(all P＞0.05).The plasma level of Rap1A in the ISR group was significantly higher than that in the non-ISR group[942.14(873.28 to 1 133.81)μg/mL vs 886.93(812.61 to 930.98)μg/mL;P=0.004].Diabetes,LDL-c,and Rap1A were risk factors for ISR by univariate logistic regression analysis(all P＜0.05).The mRNA and protein expression levels of inflammatory factors IL-6 and VCAM-1 were increased in HUVECs after 10 ng/mL TNF-α treatment for 24 h compared with the control group(all P＜0.05),while the mRNA and protein levels of Rap1A were increased(both P＜0.05).After inhibition of Rap1A in HUVECs,the mRNA and protein expression levels of IL-6 and VCAM-1 were significantly decreased(all P＜0.05). Conclusion:The plasma Rap1A level was significantly elevated in patients with ISR,suggesting that Rap1A may be a potential biomarker for predicting ISR.In the TNF-α-induced HUVECs inflammatory injury model,the expression level of Rap1A was increased.The level of TNF-α-induced endothelial cell inflammation was decreased after inhibition of Rap1A expression,suggesting that Rap1A may be a potential target for the treatment of endothelial cell inflammation in ISR.