Objective To investigate the expression and clinical significance of augmenter of liver regeneration (ALR) in patients with HBV related acute on chronic liver failure (ACLF) .Methods The serum and clinical data of patients with ACLF (ACLF group ,n=214) ,patients with mild chronic hepatitis B (mild chronic hepatitis B group ,n=196) were collected from outpatient and inpatient in the hospital ,and control group(n=200) people were the blood transfusion healthy blood donors .The level of ALR was measured by ELISA method .The correlation between ALR and MELD score of patients with ACLF were analyzed by linear regres-sion analysis .Unconditioned binary response logistic regression model was used to determine the correlation between ALR and mor-tality at 24 weeks of patients with ACLF .Results Serum ALR level was higher in ACLF group than in mild chronic hepatitis B group and control group(P<0 .05) .There were negative correlations between the serum ALR level and MELD score of patients with ACLF(r2 = -0 .249 ,F=13 .955 ,P<0 .01) .Serum ALR level of patients with ACLF was more significant in survival group than in dead group(P=0 .004) .Logistic regression analysis identified that high serum ALR level was related to the good prognosis (P=0 .012 ,OR=0 .807) .Conclusion The serum ALR level was significantly increased in patients with HBV related ACLF which played an important role in liver regeneration and improve the prognosis of patients .

PurposeTo observe the effects of rhIGF-1 on kidney in diabetic rats. MethodsUsing biochemistry, radioimmunoassay, molecular biology (RT-PCR). Results(1) 24 h UAER,24 h uriary volume in rhIGF-1 group is lower than that of diabetic control group; (2) The level of sertan IGF-1 ,kidney IGF-1 and IGF-1 mRNA in diabetic control group is lower than that of normal control group;The level of serum IGF-1 in rhIGF-1 group is higher than that of diabetic control group;no differences were found in the levels of kidney IGF-1 and kidney IGF-1 mRNA between diabetic control group and rhIGF-1 group; (3) The level of serum GH in diabetic control group is higher than that of normal control group; The level of serum GH in rhIGF-1 group is lower than that of diabetic control group; (4) rhIGF-1 might have some protective effects on diabetic nephropathy via electron microscope. ConclusionsrhIGF-1 doesn't increase the damage of diabetic kidney tissue.

Objective To investigate the changes of myosin heavy chain ( MyHC) isoforms in rat masseter muscle fibers caused by chronic sleep deprivation ( CSD) and a possible link with the pathogenesis of temporomandibular joint disorders ( TMD ) .Methods Total 180 male rats were randomly divided into three groups( n=60 per group): chronic sleep deprivation group ( CSD),cage control group ( CC),and large-platform control group ( TC ) .Each group was further divided into three subgroups ( n=20 in each group)according to the observation time point(7,14,and 21 days).The expression of MyHC isoforms in mas-seter muscle fibers was investigated by real-time quantitative PCR,Western blotting and immunohistochemi-cal staining.Results The expression of MyHC-Ⅰ,MyHC-ⅡA and MyHC-ⅡB deep and shallow masseter muscle in CSD7d group had differention with the control group(MyHC-Ⅰ:(0.314±0.005,0.134±0.005, P<0.05;MyHC-ⅡA (7.960±0.465,7.090±0.564, P<0.05;MyHC-ⅡB:(2.840±0.054,2.580±0.054, P<0.05) .The expression of MyHC-Ⅰdeep and shallow masseter muscle in CSD 14 d group had differention with the control group(0.284±0.005,0.106±0.015, P<0.05),the same appearance as MyHC-ⅡA deep and shallow masseter muscle(7.030±1.045,6.050±0.976, P<0.05) and MyHC-ⅡB deep and shallow masseter muscle((3.680±0.548,3.850±0.457, P<0.05).CSD groups exhibited increased MyHC-Ⅰexpression in both the deep and shallow muscle fiber layers at 7 days compared with CC and TC groups(P<0.05) ,whereas CSD significantly decreased MyHC-ⅡA and MyHC-ⅡB expression(P<0.05) .The expression of MyHC-Ⅱwas sig-nificantly decreased in CSD 7 d group,while the expression of MyHC-Ⅰwas increased.As the CSD time ex-tended,the MyHC-Ⅱexpression was increased and MyHC-Ⅰexpression was descreased.CSD 21d group ex-hibited significant different from MyHC-Ⅱand MyHC-Ⅰexpression in the deep muscle fiber layer compared with those in CC and TC groups (P<0.05) ,while there was no difference of MyHC-Ⅰor MyHC-Ⅱexpression in the shallow muscle fiber layer between CSD group and CC group (P>0.05) ,and there were no differences between the CC and TC groups at any time point.Conclusion These findings suggest that CSD alters the ex-pression of MyHC isoforms,which may contribute to TMD pathogenesis.

The nervous system is one of the most complicated organ systems in invertebrates and vertebrates. Down syndrome cell adhesion molecule (DSCAM) of the immunoglobulin (Ig) superfamily is expressed widely in the nervous system during embryonic development. Previous studies in Drosophila suggest that Dscam plays important roles in neural development including axon branching, dendritic tiling and cell spacing. However, the function of the mammalian DSCAM gene in the formation of the nervous system remains unclear. Here, we show that Dscam ( del17 ) mutant mice exhibit severe hydrocephalus, decreased motor function and impaired motor learning ability. Our data indicate that the mammalian DSCAM gene is critical for the formation of the central nervous system.
Animals ; Cell Adhesion Molecules ; genetics ; metabolism ; Corpus Callosum ; metabolism ; pathology ; Genotype ; Hydrocephalus ; genetics ; metabolism ; pathology ; Mice ; Mice, Knockout ; Motor Activity ; genetics ; physiology ; Mutation

Objective: To investigate whether N6-methyladenine DNA(6-mA DNA) modification is related to the occurrence of infantile hemangiomas (IH) at the epigenetic level. Methods: The genomic 6-mA DNA data were obtained by MeDIP and high-throughput sequencing. The 6-mA DNA methylation levels in 3 proliferative hemangioma specimens and adjacent skin tissues were compared by u-test. The functional differences of 6-mA modified genes were analyzed by GO analysis. Results: The level of 6-mA DNA modification in IH tissue was higher. The coverage of 6-mA Peaks in the genome was 0.037% in the tumor tissue, and the coverage of 6-mA Peaks in the surrounding skin tissue was 0.013% in the genome. The difference between the two groups was statistically significant (u=5999.87, P=0.00). The gene functions of differentially 6-mA modified genes in tumors were enriched in mesoderm development, stem cell differentiation, mesenchymal development, and cell cycle. These gene functions were closely related to the pathogenesis of IH. Conclusion Abnormal 6-mA DNA modification may be one of the pathogenesis of infantile hemangioma.

Objective To explore the value of combined detection of lipoprotein-associated phospholipase A2(Lp-PLA2),neuron specific enolase(NSE)and S-100 calcium binding protein β(S-100β)in the diagnosis and prognosis evaluation of acute cerebral infarction(ACI)in patients with carbon monoxide poisoning(CMP).Methods A total of 102 patients with CMP complicated with ACI admitted to the hospital from Jan-uary 2020 to November 2021 were selected as the study group,meanwhile,102 patients with simple CMP were enrolled as the control group.Patients in the study group were followed up for 6 months after discharge,ac-cording to the follow-up results,they were grouped into good prognosis group(60 cases)and poor prognosis group(42 cases).The serum levels of Lp-PLA2,NSE and S-100β were detected by enzyme-linked immunosor-bent assay(ELISA).The receiver operating characteristic(ROC)curve was applied to analyze the value of the combination of serum Lp-PLA2,NSE and S-100β in the early diagnosis and prognosis evaluation of patients with CMP and ACI.Results Compared with the control group,the levels of Lp-PLA2,NSE and S-100β in the study group were obviously higher(P<0.05).The ROC curve analysis results showed that the area under the curve(AUC)of the combined detection of serum Lp-PLA2、NSE、S-100β for the diagnosis of CMP complicat-ed with ACI was greater than the AUC of single detection of each indicator(P<0.001).Compared with the good prognosis group,the levels of Lp-PLA2,NSE and S-100β in the poor prognosis group were obviously higher(P<0.05).The results of ROC curve analysis showed that the AUC of the combined detection of ser-um Lp-PLA2、NSE、S-100β for the prognosis of patients with CMP complicated with ACI was greater than the AUC of single detection of each indicator(P<0.05).Conclusion The expression of Lp-PLA2,NSE and S-100β in serum of patients with CMP complicated with ACI is high,and the combined detection of the three has certain value in the diagnosis and prognosis evaluation for patients with CMP complicated with ACI.

Type I interferons play an important role in the pathogenesis of autoimmune diseases such as systemic lupus erythematosus(SLE).Monoclonal antibody shows therapeutic potential by blocking the signaling pathway.This study used recombinant human subunit 1 of the type I interferon receptor(IFNAR1)protein to immunize New Zealand white rabbits,and applied B cell cloning technology to screen and obtain rabbit parental antibodies.After humanization modification,QX006N was obtained.In vitro biological studies showed that QX006N could specifically bind to human IFNAR1 with an affinity of 108 pmol/L,and neutralize the type I interferon signaling pathway and this pathway mediated biological effects.This study provides a solid foundation for the development of antibody drugs targeting the type I interferon signaling pathway for the treatment of SLE.