Objective To explore the correlation of complex inflammation indexes,neutrophil-to-lymphocyte ratio(NLR)and platelet-to-lymphocyte ratio(PLR)with the severity of acute ische-mic stroke(AIS).Methods A total of 278 patients with brain MRI-confirmed AIS admitted in our department between March 2018 and September 2023 were enrolled retrospectively,and according to the National Institutes of Health Stroke Scale(NIHSS)score at admission,they were divided into a mild stroke group(NIHSS score≤3,n=157)and a moderate-severe stroke group(NIHSS score＞3,n=121).Clinical data and results of laboratory tests at admission were collec-ted,and NLR and PLR were calculated.Multivariate logistic regression analysis was performed to assess the association of NLR and PLR with AIS severity.Results Compared with the mild stroke group,the moderate-severe stroke group had significantly older age,larger proportions of atrial fibrillation and pre-morbid Modified Rankin Scale(mRS)score＞1,higher NLR and PLR,and higher ratio of culprit large vessel stenosis,and a lower rate of transient ischemic attack(TIA)(P＜0.05,P＜0.01).Multivariate logistic regression analysis showed that TIA(95％CI:0.017-0.455,P=0.004)was a protective factor,and pre-morbid mRS＞1(95％CI:1.451-6.700,P=0.004),NLR(95％CI:1.041-1.346,P=0.010)and culprit large vessel stenosis(95％CI:1.370-4.415,P=0.003)were risk factors for the severity of AIS.Conclusion Inflammation is involved in the pathogenesis of AIS,and the complex inflammatory index,NLR may be an inde-pendent risk factor for the severity of AIS.

Objective To explore the correlation of complex inflammation indexes,neutrophil-to-lymphocyte ratio(NLR)and platelet-to-lymphocyte ratio(PLR)with the severity of acute ische-mic stroke(AIS).Methods A total of 278 patients with brain MRI-confirmed AIS admitted in our department between March 2018 and September 2023 were enrolled retrospectively,and according to the National Institutes of Health Stroke Scale(NIHSS)score at admission,they were divided into a mild stroke group(NIHSS score≤3,n=157)and a moderate-severe stroke group(NIHSS score＞3,n=121).Clinical data and results of laboratory tests at admission were collec-ted,and NLR and PLR were calculated.Multivariate logistic regression analysis was performed to assess the association of NLR and PLR with AIS severity.Results Compared with the mild stroke group,the moderate-severe stroke group had significantly older age,larger proportions of atrial fibrillation and pre-morbid Modified Rankin Scale(mRS)score＞1,higher NLR and PLR,and higher ratio of culprit large vessel stenosis,and a lower rate of transient ischemic attack(TIA)(P＜0.05,P＜0.01).Multivariate logistic regression analysis showed that TIA(95％CI:0.017-0.455,P=0.004)was a protective factor,and pre-morbid mRS＞1(95％CI:1.451-6.700,P=0.004),NLR(95％CI:1.041-1.346,P=0.010)and culprit large vessel stenosis(95％CI:1.370-4.415,P=0.003)were risk factors for the severity of AIS.Conclusion Inflammation is involved in the pathogenesis of AIS,and the complex inflammatory index,NLR may be an inde-pendent risk factor for the severity of AIS.

Two strains of porcine reproductive and respiratory syndrome virus (PRRSV) were isolated in 2006 and 2016 and designated as FZ06A and FZ16A, respectively. Inoculation experiments showed that FZ06A caused 100% morbidity and 60% mortality, while FZ16A caused 100% morbidity without death. By using genomic sequence and phylogenetic analyses, close relationships between a Chinese highly pathogenic PRRSV strain and the FZ06A and FZ16A strains were observed. Based on the achieved results, multiple genomic variations in Nsp2, a unique N-glycosylation site (N³³→K³³), and a K151 amino acid (AA) substitution for virulence in the GP5 of FZ16A were detected; except the 30 AA deletion in the Nsp2-coding region. Inoculation experiments were conducted and weaker virulence of FZ16A than FZ06A was observed. Based on our results, a 30 AA deletion in the Nsp2-coding region is an unreliable genomic indicator of a high virulence PRRSV strain. The Nsp2 and GP5 differences, in addition to the virulence difference between these two highly pathogenic PRRSV strains, have the potential to be used to establish a basis for further study of PRRSV virulence determinants and to provide data useful in the development of vaccines against this economically devastating disease.
Asian Continental Ancestry Group ; China ; Genomics ; Humans ; Mortality ; Phylogeny ; Porcine Reproductive and Respiratory Syndrome ; Porcine respiratory and reproductive syndrome virus ; Vaccines ; Virulence

ObjectiveThe aim of this study is to investigate whether oral administration of collagen Ⅱ peptide (250-270)[C Ⅱ (250-270)]-cholera toxin B subunit (CTB)complex could effectively set up oral immune tolerance to collagen-induced arthritis (CIA) in mice. MethodsDBA/1 mice were divided into Ⅰ, Ⅱ, Ⅲ and Ⅳgroups. Group Ⅰ was normal control group. Collagen type Ⅱ emulsified in Freund's complete adjuvant were injected to mice of groups Ⅱ , Ⅲ and Ⅳ twice from the base of the tail. Mice of group Ⅲ were fed with C Ⅱ (250-270)-CTB covalent complex twice after the arthritis was developed. Mice of group Ⅳ were fed with C Ⅱ(250-270) and CTB mix at the 14th day after primary immunization. Visual scores and histopathologic scores of arthritis were recorded. The frequencies of arthritis between the groups were compared usingFisher's exact test. The clinical and histological severity of arthritis were analyzed by ANOVA.Results The frequencies of arthritis in groups Ⅰ , Ⅱ , Ⅲ and Ⅳ were 0, 100％, 100％ and 25％ respectively. Average accumulative scores of arthritis were 0, 5.0±1.7, 10.8±2.8 and 1.0±2.0 respectively. Average accum-ulative histopathological scores of arthritis were 0, 16±8, 32±13 and 7±6 respectively. Conclusion Oral administration of C Ⅱ (250-270) and CTB mix in arthritis mice after C Ⅱ immunization can suppress the onset and severity of arthritis. Oral administration of C Ⅱ (250-270)-CTB covalent complex in the acute stage of arthritis can accelerate arthritis.

Objective:To study the effects of dexamethasone(DEX)on the cytotoxicity and apoptosis of NK-92MI cells and the mechanisms involved.Methods:NK-92MI cells were treated with different doses of DEX.The proliferative rate and cytotoxicity of the NK-92MI cells were detected by MTT colorimetry.The cell apoptotic rate was observed by flow cytometry with Annexin V and propidium iodide(PI)double staining.The expression of apoptosis-related gene,Bcl-2 and Bax was detected by RT-PCR.Results:After treated with 1?10-8mol/L to 1?10-3mol/L of DEX for 24 h,48 h and 72 h,the proliferation of NK-92MI cells was significant inhibited(P