To prepare monoclonal antibody to the N protein of porcine reproductive and respiratory syndrome virus(PRRSV),BALB/c mice were immunized with the purified N protein of the PRRSV-2 strain expressed by prokaryotic expression system.Mouse splenocytes were fused with myeloma cells using hybridoma technique,hybridoma cells were identified by indirect ELISA method and indirect immunofluorescence assay(IFA),and positive hybridoma cells were screened for subclones using the limited dilution method.The results showed that a monoclonal antibody cell line 4A7 was successfully obtained,and the results of Western blot and IFA indicated that the monoclonal antibody could accurately recognize the N proteins of type 1 and type 2 PRRSV.Mean-while,the N protein gene was truncated and expressed by prokaryotic expression system,and the amino acid sequence of the B-cell antigenic epitope recognized by 4A7 was screened as 51EKPHF55 using Western blot.Comparison of epitope amino acids in the N protein gene sequences of different strains revealed that the antigenic epitope 51EKPHF55 recognized by the monoclonal antibody 4A7 has no amino acid difference in the sequences of three subtypes among the PRRSV-1 strains and nine lineages among the PRRSV-2 strains,indicating a high degree of conservation.The results of the study provide a foundation the development of PRRSV diagnostic kits and novel vaccines.

To prepare monoclonal antibody to the N protein of porcine reproductive and respiratory syndrome virus(PRRSV),BALB/c mice were immunized with the purified N protein of the PRRSV-2 strain expressed by prokaryotic expression system.Mouse splenocytes were fused with myeloma cells using hybridoma technique,hybridoma cells were identified by indirect ELISA method and indirect immunofluorescence assay(IFA),and positive hybridoma cells were screened for subclones using the limited dilution method.The results showed that a monoclonal antibody cell line 4A7 was successfully obtained,and the results of Western blot and IFA indicated that the monoclonal antibody could accurately recognize the N proteins of type 1 and type 2 PRRSV.Mean-while,the N protein gene was truncated and expressed by prokaryotic expression system,and the amino acid sequence of the B-cell antigenic epitope recognized by 4A7 was screened as 51EKPHF55 using Western blot.Comparison of epitope amino acids in the N protein gene sequences of different strains revealed that the antigenic epitope 51EKPHF55 recognized by the monoclonal antibody 4A7 has no amino acid difference in the sequences of three subtypes among the PRRSV-1 strains and nine lineages among the PRRSV-2 strains,indicating a high degree of conservation.The results of the study provide a foundation the development of PRRSV diagnostic kits and novel vaccines.

Objective::The effectiveness of statins in reducing atherosclerotic calcification remains controversial. The aim of this study was to confirm that simvastatin reduces atherosclerotic calcification and stabilizes plaque by restricting endoplasmic reticulum stress (ERS)-mediated apoptosis.Methods::Twenty-four 8-week-old male apolipoprotein E (ApoE) -/- mice (C57BL/6J genetic background) were selected and randomly divided into model ( n = 12) and simvastatin ( n = 12) groups. Twelve male C57BL/6J mice were selected as control group ( n = 12). The mice were adaptively fed for 2 weeks and were put on a high-fat diet thereafter. After 9 weeks, they were treated with simvastatin (20 mg/kg) or phosphate-buffered saline daily for 8 weeks. Aortic sinus samples were obtained from ApoE -/- and C57BL/6J mice for hematoxylin and eosin, von Kossa, alizarin Red S, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling, and immunohistochemical staining after in vivo treatment with simvastatin. In addition, mouse vascular smooth muscle cells were analyzed after exposure to simvastatin in vitro.Results::Administration of simvastatin in vivo drastically attenuated the atherosclerosis, calcification, and apoptosis, and decreased the serum levels of triglycerides, total cholesterol, low-density lipoprotein cholesterol, and high-density lipoprotein cholesterol. The expression levels of glucose-regulated protein, 78 kDa (GRP78), C/EBP homologous protein (CHOP), and caspase 12 (CASP12) in the aortic sinus decreased in the simvastatin group compared with the model group. In vitro, simvastatin or simvastatin plus ERS inhibitor (taurine) attenuated calcification and apoptosis, and reduced the expression of ERS-related proteins GRP78, CHOP, and CASP12. Conclusion::Treatment with simvastatin suppressed atherosclerotic calcification. This effect may be mediated through the inhibition of ERS-related apoptosis.

Objective::The effectiveness of statins in reducing atherosclerotic calcification remains controversial. The aim of this study was to confirm that simvastatin reduces atherosclerotic calcification and stabilizes plaque by restricting endoplasmic reticulum stress (ERS)-mediated apoptosis.Methods::Twenty-four 8-week-old male apolipoprotein E (ApoE) -/- mice (C57BL/6J genetic background) were selected and randomly divided into model ( n = 12) and simvastatin ( n = 12) groups. Twelve male C57BL/6J mice were selected as control group ( n = 12). The mice were adaptively fed for 2 weeks and were put on a high-fat diet thereafter. After 9 weeks, they were treated with simvastatin (20 mg/kg) or phosphate-buffered saline daily for 8 weeks. Aortic sinus samples were obtained from ApoE -/- and C57BL/6J mice for hematoxylin and eosin, von Kossa, alizarin Red S, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling, and immunohistochemical staining after in vivo treatment with simvastatin. In addition, mouse vascular smooth muscle cells were analyzed after exposure to simvastatin in vitro.Results::Administration of simvastatin in vivo drastically attenuated the atherosclerosis, calcification, and apoptosis, and decreased the serum levels of triglycerides, total cholesterol, low-density lipoprotein cholesterol, and high-density lipoprotein cholesterol. The expression levels of glucose-regulated protein, 78 kDa (GRP78), C/EBP homologous protein (CHOP), and caspase 12 (CASP12) in the aortic sinus decreased in the simvastatin group compared with the model group. In vitro, simvastatin or simvastatin plus ERS inhibitor (taurine) attenuated calcification and apoptosis, and reduced the expression of ERS-related proteins GRP78, CHOP, and CASP12. Conclusion::Treatment with simvastatin suppressed atherosclerotic calcification. This effect may be mediated through the inhibition of ERS-related apoptosis.

Objective: To compare the consistency of the biological widths measured by using cone-beam CT (CBCT) and periodontal probe in patients with two different gingival biotypes. Methods: Totally 27 patients [13 males, 14 females, (37.6±13.7) years old], who planned to receive the crown lengthening surgery, were recruited under the inclusion and exclusion criteria in Department of Periodontology, School of Stomatology, The Fourth Military Medical University during November 2017 to June 2018. A total of 40 teeth (14 front teeth, 26 posterior teeth) were involved in this study. The patients were divided into two groups according to their gingival biotypes: thin gingival biotype [5 males, 8 females, (40.2±15.0) years old, 21 teeth] and thick gingival biotype [8 males, 6 females, (35.1±11.9) years old, 19 teeth]. All the teeth were checked before crown lengthening procedures by using CBCT, and the biological widths and sulcus depths were measured during the surgery by using periodontal probes (Hu-Friedy, U S A). The data were recorded and statistically analyzed. Results: There were no significant differences of the biological widths between the two measuring methods amongst all of the 40 teeth [periodonial probe: (1.64±0.26) mm; CBCT: (1.69±0.20) mm], amongst 21 thin gingival biotype teeth [periodontal probe: (1.49±0.19) mm; CBCT: (1.57±0.12) mm] and amongst 19 thick gingival biotype teeth [periodontal probe: (1.80±0.21) mm; CBCT: (1.87±0.18) mm] (P>0.05). There were no significant differences of the biological widths [anterior teeth: (1.59±0.15) mm, posterior teeth: (1.67±0.29) mm, P=0.42] and of the sulcus depths [anterior teeth: (2.00±0.28) mm, posterior teeth: (2.11±0.43) mm, P=0.44] between anterior teeth and posterior teeth. The difference of biological widths, measured by two methods respectively, between thin and thick gingival biotype groups was statistically significant (P<0.01). There were significant differences of the sulcus depths, measured by the periodontal probes, between the thin [(1.93±0.28) mm] and thick [(2.24±0.41) mm] gingival biotype groups (P<0.01). Conclusions The biological widths measured by CBCT is consistent with those measured by using periodontal probes. The biological widths and the depths of the sulcus of thin and thick gingival biotypes are different.

Objective To study the association between H cy,hs-CRP,IMA and transient ischemic attack (TIA).Methods One hundred and twenty-six TIA patients were divided into low risk group (n=42),moderate risk group (n=43) and high risk group (n=43) according to their AB-CD2 score with 20 healthy subjects undergoing physical examinarion served as control group.Their clinical data were recorded and their serum Hcy,IMA and hs-CRP levels were compared.Results The serum levels of TC,TG,LDL,Hcy,IMA and hs-CRP were significantly higher while those of HDL were significantly lower in low risk group,moderate risk group and high risk group than in control group (P＜0.05),in moderate risk group and high risk group than in low risk group (P＜0.05),and in high risk group than in moderate risk group (P＜0.05).The serumlevels of Hcy,hs-CRP and IMA were positively associated with ABCD2 score in TIA patients (r=0.36,r =0.31,r =0.24,P＜0.05) but not associated with each other (P＞0.05).Multivariate logistic regression analysis showed that hyperlidemia and Hcy were the risk factors for TIA (P＜0.05,P＜0.01).Conclusion Serum Hcy,hs-CRP,IMA levels are positively associated with AB-CD2 score.Hyperlipidemia and Hcy are the risk factor for TIA.Measurement of serum Hcy,hsCRP,IMA levels is beneficial to the assessment of TIA.

Adult ; Female ; Humans ; Male ; Middle Aged ; Treatment Outcome ; Ulna ; surgery ; Ulna Fractures ; therapy ; Young Adult

Objective To evaluate the feasibility and efficacy of intravascular optical coherence tomography (OCT) in the assessment of plaque characteristics and drug eluting stent deployment quality in the elderly patients with unstable angina (UA) and non-ST segment elevation myocardial infarction (NSTEMI). Methods OCT was used in elderly patients undergoing percutaneous coronary interventions.Fifteen patients, 9 males and 6 females with mean age of 72.6±5.3 years (range 67-92 years) were enrolled in the study. Images were obtained before initial balloon dilatation and following stent deployment. The plaque characteristics before dilation, vessel dissection,tissue prolapse, stent apposition and strut distribution after stent implantation were evaluated. Results Fifteen lesions were selected from 32 angiographic lesions as study lesions for OCT imaging after diagnostic coronary angiography. There were 7 lesions in the left anterior descending artery, 5 lesions in the right coronary artery and 3 lesions in the left circumflex coronary artery. Among them,12 (80.0%) were lipid-rich plaques, and 10 (66.7%) were vulnerable plaques with fibrous cap thickness 54.2±7.3 μm. Seven ruptured culprit plaques (46.7%) were found; 4 in UA patients and 3 in NSTEMI patients. Tissue prolapse was observed in 11 lesions (73.3%).Irregular stent strut distribution was detected in 8 lesions (53.3%). Vessel dissections were found in 5 lesions (33.3%). Incomplete stent apposition was observed in 3 stents (20%) with mean spacing between the struts and the vessel wall 172±96 mm (range 117-436 mm).Conclusions 1) It is safe and feasible to perform intravascular OCT to differentiate vulnerable coronary plaque and monitor stent deployment in elderly patients with UA and USTEMI. 2) Coronary plaques in elderly patients with UA and USTEMI could be divided into acute ruptured plaque, vulnerable plaque, lipid-rich plaque, and stable plaque. 3) Minor or critical plaque rupture is one of the mechanisms of UA in elderly patients. 4) Present drug eluting stent implantation is complicated with multiple tissue prolapses which are associated with irregular strut distributions. 5) The action and significance of tissue prolapse on acute vessel flow and in-stent thrombus and restenosis need to be further studied.