Objective To understand the antibody levels after the inoculation of measles ,poliomyelitis ,epidemic encephalitis B and hepatitis B vaccines among healthy children aged 7 - < 13 years old in Guangshui City of Hubei province to provide the scientif ‐ic basis for formulating the immune prevention and control strategy and risk assessment in whole city .Methods 4 616 healthy chil‐dren aged 7 - < 13 years old were sampled from the whole city .The enzyme‐linked immunosorbent assays (ELISA) was used to de‐tect the 4‐antibody levels .Results The antibody positive rates of measles ,poliomyelitis ,epidemic encephalitis B and hepatitis B a‐mong healthy children aged 7 - < 13 years old in Guangshui City were 94 .41% ,93 .07% ,93 .78% and 68 .72% respectively .The protection levels of first three kinds of antibody reached more than 85% ;the positive rates had statistical difference among 4 kinds of antibody(χ2 = 1 987 .08 ,P = 0 .000) .The antibody positive rates of epidemic encephalitis B had no statistical difference among different age periods (χ2 = 10 .141 ,P= 0 .071) ;the antibody positive rates of measles ,poliomyelitis and hepatitis B had statistical difference among different age periods(χ2 = 40 .471 ,P = 0 .000 ;χ2 = 25 .174 ,P = 0 .000 ;χ2 = 283 .641 ,P = 0 .000) .The positive rates of 4 kinds of antibody had no statistical difference between different genders (χ2 = 0 .019 ,P= 0 .889 ;χ2 = 1 .017 ,P= 0 .313 ;χ2 = 0 .018 ,P= 0 .892 ;P= 0 .639 ,P= 0 .424) ;the antibody positive rates of measles ,poliomyelitis and epidemic encephalitis B had no statistical differences among 17 villages and towns in the whole city (χ2 = 0 .099 ,P= 1 .000 ;χ2 = 0 .117 ,P= 1 .000 ;χ2 = 0 .134 , P= 1 .000) ,while the antibody positive rate of hepatitis B had statistical difference among these villages and towns (χ2 = 186 .179 , P= 0 .001) .Conclusion The antibody levels of measles ,poliomyelitis and epidemic encephalitis B reach the protection rate ,but the antibody level of hepatitis B needs to be increased .The monitoring work should be continuously strengthened and the seeking missed inoculation and re‐inoculation work should be reinforced .

Objective To explore the risk factors for lung cancer-related cerebral infarction . Methods The hospitalized active lung cancer patients on anti-cancer therapy with no traditional stroke risk factors, who experienced an acute cerebral infarct in the First Affiliated Hospital of Guangxi Medical University from January 2005 to December 2015, were consecutively collected as the LCRS ( lung cancer-related stroke) group.The active lung cancer patients without cerebral infarction hospitalized at the same peroid matched with the LCRS group for age and gender were collected as the LC ( lung cancer ) group. Clinical data from the two groups were analyzed .Results A total of 139 LCRS patients and 139 LC patients were enrolled in the study , with 110 male and 29 female in each group , and there were no significant difference for the mean age between the LCRS group (52.1 ±10.4 years old ) and the LC group (52.1 ± 10.1 years old).Two or more acute ischemic lesions of the brain were showed by MRI in most patients in the LCRS group (117 cases, 84.2%).Compared with the LC group, more patients in the LCRS group were found with adenocarcinoma , metastasis, elevated plasma D-dimer, CA125 and CA199 levels [ 88 cases (63.3%) vs 47 cases (33.8%);98 cases (70.5%) vs 56 cases (40.3%);(468.38 ±291.37) μg/L vs (277.59 ±191.22) μg/L;(221.42 ±146.34) U/ml vs (106.84 ±69.97) U/ml;(254.68 ±185.84) U/ml vs (97.15 ±63.64) U/ml;with all P<0.001].By logistic regression analysis of multiple factors , the elevated plasma D-dimer, CA125 and CA199 levels were showed to be independent risk factors for the cerebral infarction (OR=1.003, 95%CI 1.001 -1.004; OR=1.006, 95%CI 1.003 -1.010; OR=1.011, 95%CI 1.007-1.015).Conclusions The elevated plasma D-dimer, CA125 and CA199 levels are the risk factors for the lung cancer related cerebral infarction , which may lead to hypercoagulation and induce cerebral infarction eventually .

OBJECTIVETo clarify if Epstein-Barr virus encoded LMP1 induces matrix metalloproteinase 9 expression via NF-kappa B or AP-1 signaling pathway, which gives evidence to the elucidation of the mechanism of LMP1- mediated carcinogenesis.

METHODSTo determine whether LMP1 or its mutants contribute to MMP9 production via NF-kappa B or AP-1 transcription factor, MMP9-chloramphenicol acetyl transferase (CAT), NF-kappa B mut 9-CAT, AP-1 mut MMP9-CAT were transfected into human nasopharyngeal carcinoma cells stably expressing LMP1 (HNE2-LMP1) or its mutants, [HNE2-LMP1 (1-185), HNE2-LMP1 (1-231), HNE2-LMP1 delta 187-351] by electroporation technic. The difference of MMP9 reporter activity among those cell lines was detected by CAT assay and expression of MMP9 was determined in nasopharyngeal carcinoma cells stably expressing LMP1 or its mutants by zymographic analysis. In the meantime, efforts were made to demonstrate if LMP1 regulates NF-kappa B or AP-1 activation using reporter gene analysis.

RESULTSIn contrast with vector-transfected cells, MMP9 CAT activity in HNE2-LMP1, HNE2-LMP1 (1-185), HNE2-LMP1(1-231), HNE2-LMP1 delta 187-351 increased 7.2, 1.3, 3.3, 4.0 times respectively. Zymographic analysis demonstrated that the 92 kDa MMP9 expression was induced in HNE2-LMP1, HNE2-LMP1(1-231) and HNE2-LMP1 delta 187-351 cells, whereas it was negative in HNE2-pSG5 and HNE2-LMP1 (1-185) cells. As compared to the HNE2 cells, NF-kappa B or AP-1 reporter activity in HNE2-LMP1 cells were increased 13.8, 8.4 fold respectively. Moreover, In contrast with MMP9 CAT-transfected cells, MMP9 CAT activity in NF-kappa B mut MMP9-CAT or AP-1 mut MMP9-CAT transfected HNE2-LMP1, HNE2-LMP1 (1-185), HNE2-LMP1(1-231) and HNE2-LMP1 delta 187-351 cells were significantly decreased by 18.1% or 16.3%, 35.0% or 33.3%, 29.1% or 26.1% from the original level. However, there was no difference in NF-kappa B mut MMP9-CAT or AP-1 mut MMP9-CAT transfected HNE2-pSG5, HNE2-LMP1 (1-185) cells.

CONCLUSIONIn nasophargyngeal carcinoma, Epstein-Barr virus-encoded LMP1 induces MMP9 transcription and enzymatic activity via an NF-kappa B or AP-1 signaling pathway, which may contribute to invasiveness and metastasis.

Gene Expression ; drug effects ; Herpesvirus 4, Human ; chemistry ; Humans ; Matrix Metalloproteinase 9 ; biosynthesis ; NF-kappa B ; metabolism ; Nasopharyngeal Neoplasms ; pathology ; Signal Transduction ; Transcription Factor AP-1 ; metabolism ; Tumor Cells, Cultured ; Viral Matrix Proteins ; pharmacology

OBJECTIVE: To explore the genetic pathogenesis of X-linked agammaglobulinemia in two patients for clinical diagnosis and family counseling. METHODS: Data was collected from the patients' family including clinical information, blood immunoglobulin level, as well as classification and subgrouping of B lymphocytes. Gene mutations were screened by whole exome sequencing (WES) through next-generation sequencing (NGS), the result was verified with Sanger sequencing. RESULTS: A BTK c.1627T>C (p.Ser543Pro) variant was found in the pedigree. The phenotype and variant have co-segregated in the pedigree. The variant was not found in population database. The variant has affected in the kinase domain which contained no benign variants and is harmful as predicted through bioinformatic analysis. CONCLUSION BTK c.1627T>C (p.Ser543Pro) is a pathogenic variant contributing to X-linked agammaglobulinemia in this pedigree. Above finding has provided reproduction guidance for this family.
Agammaglobulinaemia Tyrosine Kinase/genetics* ; Agammaglobulinemia/genetics* ; DNA Mutational Analysis ; Genetic Diseases, X-Linked ; Humans ; Mutation ; Pedigree

OBJECTIVESTo identify whether Epstein-Barr virus (EBV) encoded latent membrane protein 1 (LMP1) can induce tumor necrosis factor receptor-associated factor 1 (TRAF1) expression and promote its anti-apoptosis activity via the NF-kappaB signaling pathway, and assess that LMP1 suppresses apoptosis in nasopharyngeal carcinoma (NPC).

METHODSA stable transfected cell line HNE2-LMP1 was established by introducing LMP1 cDNA into HNE2 cells. Transactivation of TRAF1 was determined by luciferase reporter assay, while expression of TRAF1 mRNA was detected by RT-PCR and expression of TRAF1 protein and caspase 3 by Western blot analysis. Apoptosis activity was observed through fluorescence staining.

RESULTSLMP1 induced TRAF1 expression in NPC cells and caused a decrease in apoptosis. This induction could be blocked by antisense LMP1. Moreover, LMP1-mediated induction of a TRAF1 promoter-driven reporter gene was significantly impaired when the kappaB site kappaB1 or kappaB5 was disrupted, whereas mutation of kappaB3 had only a minor effect on LMP1 dependent up-regulation of the reporter gene.

CONCLUSIONLMP1 induces TRAF1 expression and promotes its anti-apoptosis activity via the NF-kappaB signaling pathway, which may be one of the mechanisms that LMP1 uses to suppress apoptosis in NPC cells.

Apoptosis ; physiology ; Humans ; NF-kappa B ; physiology ; Nasopharyngeal Neoplasms ; physiopathology ; Protein Biosynthesis ; Signal Transduction ; physiology ; TNF Receptor-Associated Factor 1 ; Tumor Cells, Cultured ; Viral Matrix Proteins ; physiology

Objective To investigate the serum levels of semaphorin 3E(Sema3E)in patients with intracranial aneurysms,revealing the correlation between Sema3E and 1-month poor prognosis after interventional embolization.Methods This study was a prospective single-center cohort study,recruiting 102 consecutive patients with intracranial aneurysms who underwent interventional surgery from June 2020 to January 2022 in our hospital.Among them,11 patients were excluded.Clinical and radiological profiles were collected.Peripheral blood was collected after admission,and serum Sema3E levels were determined by enzyme-linked immunosorbent assay.All the aneurysms were treated with endovascular coil embolization or stent-assisted coil embolization.The primary outcome was evaluated with the Glasgow Outcome Scale(GOS)1 month after interventional therapy.The favorable outcome was defined as a GOS score of 4-5,and a poor outcome was defined as a GOS score of 1-3(severe disability,vegetative state,or death).Univariate and multivariate logistic regression analyses were used to identify potential prognostic factors after interventional therapy.Results The average age of 91 patients with intracranial aneurysm was 59.9±11.0 years old,including 70 cases(76.9%)with favorable prognosis and 21 cases(23.1%)with poor prognosis.The mean preoperative Glasgow Coma Scale(GCS)score of the poor prognosis group(9.4±4.5)was significantly lower than that of the favorable prognosis group(13.3±2.5;P<0.001).In the poor prognosis group,the Hunt-Hess grade(3.6±0.6 vs.2.0±1.3,P<0.001)and the serum Sema3E levels[(6.21±1.58)μg/L vs.(4.38±1.77)μg/L,P<0.001]were significantly higher than those in the favorable prognosis group.Logistic regression analysis showed the Hunt-Hess grade(OR =7.150,P =0.003),stent-assisted coil embolization(OR =15.777,P =0.010),and the serum Sema3E level(OR =1.756,P =0.027)were independent prognostic factors for intracranial aneurysms after interventional therapy.Conclusions The serum Sema3E level is closely correlated with the severity of intracranial aneurysms.The serum Sema3E level is a prognostic factor for interventional treatment,which can be used as a biomarker for predicting poor outcomes.