Bone marrow stromal antigen 2 (BST-2) is a kind of host restriction factor. Since it was discovered to be responsible for the defect in virion release of HIV-1 mutants lacking the accessory gene vpu in 2008, it was thought to mainly restrict the viruses by directly tethering viral particles at the plasma membrane. Recent reports suggest that BST-2 also can inhibit the the release of HBV particles, which are budding in the intracellular vesicles, expanding the antiviral spectrum of BST-2. Futhermore, the machanism that BST-2 used to restrict HBV release in multivesicular bodies (MVBs) is similar to that used to restrict HIV at the plasma membrane. However, HBV have evolved strategies to antagonize the antiviral action of BST-2. There are two different opinions about the antagonist. One is HBV inactivated BST-2 by HBx requiring a hepatocyte-specific environment. Another thought envelope protein HBs counteract the antiviral action of BST-2. In this review, we focus on the current advances in the anti-HBV activity of BST-2.
Animals ; Antigens, CD ; genetics ; immunology ; GPI-Linked Proteins ; genetics ; immunology ; Hepatitis B ; genetics ; immunology ; virology ; Hepatitis B virus ; genetics ; physiology ; Host-Pathogen Interactions ; Humans ; Virus Release

Objective:To observe the diagnosis effect about the MRI and CT examination for the patients with lacunar cerebral infarction(LAC).Methods: 82 cases early LAC patients during April 2014- June 2016 were diagnosed by two methods, MRI and CT, respectively. And the application effect of the two methods were compared based on image result.Results: In 82 cases of LAC 742 lesions confirmed by MRI and only 145 lesions confirmed by CT, and there was statistical significant between the two methods; especially in front lobe and thalamic, lesions detection rate using MRI was higher than CT, and there was statistical significant between the two methods(x2=6.59,x2=5.64,x2=6.42;P<0.05); the difference of detection rate in capsula internal also was statistical significant(x2=7.43,P<0.05); the number of lesion diameter less than 5mm was 256 using MRI and it was 3 using CT, the difference also was statistical significant(x2=6.39,P<0.05).However, in parietal lobe, basal ganglia and brainstem, all of the difference were not statistical significant (x2=0.18,x2=1.25,x2=0.81;P>0.05);Conclusion: Both of CT and MRI can be used in early diagnosis of LAC, and MRI examination is more accurate for early or micro lesions and lesions happened in the frontal lobe, thalamus, capsula internal than CT. Therefore, MRI can be used as first choice eximination method in early diagnosis of LAC.

Objective Two single nucleotide polymorphisms(SNPs)in TBX1 gene,G2857C(rs737868)and G2963A(rs28649236),were chosen to investigate their distribution in contruncal defects(CTD)patients and normal controls in order to determine the relationship between TBX1 gene and CTD.Methods By PCR-RFLP,genotypes of these two SNPs were analyzed in 100 patients with CTD and 100 normal controls during Mar.2004 to May.2006. 2 test was applied to analyze the genotype frequency and allele frequency between CTD groups and control groups.Results Remarkable significance were observed at G2963A between CTD groups and normal controls,the G allele frequency in CTD groups were much higher than that in normal controls(?2=5.30,P

Objective To study the treatment of sepsis caused by G - bacteria, anti-lipid A antibodies of bacterial endotoxin were screened from phage antibody library. Methods The mRNA was extracted from human B-lymphocytes against lipid A of bacterial endotoxin, reversely transcripted and amplified by polymerase chain reaction using general primers scanning Fd and light chain of IgG. The amplified fragments were inserted into pCOMB3 vector and electrotransfected competent E.coli XL 1-blue cells. Furthermore, the recombinant phage was lysed by coculture with helper VCSM13. Results Fab displayed on the surface as fusion protein with the N terminal of coat protein Ⅲ, and 4.8?10 6 clone library was established. Antibodies against lipid A of bacterial endotoxin were screened. Specific antibodies against lipid A of bacterial endotoxin were enriched by 100 times after three rounds of panning with lipid A.Conclusions Three clones exhibited specific binding to lipid A is identified by direct and competitive ELISA methods. The succcess of isolating anti-lipid A proves the usefulness of phage display system in human McAb preparation. The result shows that we have got the recombinant phage antibody.

Objective To investigate the value of cystatin CysC on early renal damage in patients with essential hypertensive.Methods Hundred-four patients who were diagnosed as essential hypertensive with microalbuminuria (Urinary microalbumin:20-200 mg/L) with essential hypertensive (58 males and 46 females) were enrolled and 54 healthy subjects (30 males and 24 females) were selected as controls.Serum CysC (CysC)、Crea(Cr) 、BUN、uric acid (UA) were measured and ROC curve was established based on the examination.Results There were significant difference on the level of Serum CysC[1.22(0.91,1.51 ) mg/L vs 0.73 (0.61,0.79 ) mg/L,Z=3.30,P＜0.01],BUN [6.40 ( 4.43,9.06 ) mmol/L vs 5.10 ( 4.34,5.93 ) mmol/L,Z=5.94,P＜0.01],Cr [96.3 (72.6,122.0 ) μmol/L vs 70.5 (56.2,76.0 ) μmol/L,Z=8.30,P＜0.01],UA [375.7 ( 312.3,431.8 ) μmol/L vs 328.7 ( 271,379.3 ) mmol/L,Z=3.28,P＜0.01] between essential hypertensive group and control group.According to ROC curve,the area of CysC under the ROC curve (AUC) in 104 patients was 0.87,significantly different with CR(0.78),BUN(0.66),UA(0.66) (P＜0.05 or P＜0.01 ) The Youden index of CysC was 0.69,and the corresponding sensitivity and specificity of CysC were 76％ and 93％ respectively.Conclusion The diagnostic value of serum CysC on early renal damage in patients with essential hypertensive is superior to Cr,BUN and UA,and changes of renal function can be found earlier according to the level of serum CysC,It plays a key role in the diagnosis,treatment and prognosis of the early renal damage in patients with essential hypertension.

Small RNAs(sRNAs) play a significant role in the regulation of bacterial growth.When sensing certain environmental cues such as fluctuation of nutrient concentration, temperature, pH, and osmolarity, sRNAs can influence the expression of target genes.The formation of biofilms is initiated by bacteria transitioning from the planktonic to the surface-associated mode of growth, which is a self-produced extracellular matrix composed of proteins, polysaccharides, and DNA.Recent evidences have shown that small RNA plays an important role in the regulation of bacterial biofilm formation.sRNAs have key roles in biofilm formation process by base pairing with target mRNAs or interaction with modulating proteins.This review discussed the regulation mechanism and pathway of sRNAs in bacterial biofilms formation, and summarized three classical regulatory models of sRNAs in bacterial biofilms formation, this review also gives the research status and development direction of sRNAs in bacterial biofilms formation.

We identified and characterized the full-length genome of a GI.8 norovirus strain CHN/Huzhou/N10 isolated in an outbreak in Huzhou,China.The full-length genome of CHN/Huzhou/N10 was amplified using five pairs of primers which were designed according to the full-length GI norovirus genome sequences published in GenBank database.Multiple alignments were performed using DNAStar,the phylogenetic relationship of CHN/Huzhou/N10 and the representative NoV (Norovirus) strains from each genogroup were assessed using the software MEGA version 6.0.The viral genome of CHN/Huzhou/N10 was 7 740 nucleotides in length,which was consist of three ORFs spanning 5-5 404 nt (ORF1),5 388-7 019 nt(ORF2),and 7 019-7 660 nt (ORF3),respectively.Phylogenetic analysis based on polymerase and capsid sequences VP1 and VP2 region indicated that CHN/Huzhou/N10 belonged to GI.8 genotype.The amino acid sequence analysis of the VP1 region showed that CHN/Huzhou/N10 had 16 mutations compared with the representative strain Boxer/2001/US,12 of these variations were located in the P2 subregion.Moreover,a single amino acid change (T347S) occurred at histo-blood group antigen (HBGA) binding site Ⅱ and another single amino acid change (T397E) occurred at HBGA binding site Ⅲ.In this study,the first full genome of norovirus GI.8 isolated in Huzhou,China was extensively characterized.The data would be helpful not only for the epidemiology study,but also for the diagnostic tool development and effective vaccine design in the future.

BACKGROUND:Long-term use of corticosteroids (hereinafter referred to as hormone) after renal transplantation could obviously lead to adverse reactions. Immunosuppressive regimen with less and no hormone has been a hot focus in the study of renal transplantation al over the world. However, reduction or withdrawal of hormones has a certain risk. At present, there is no unified scheme. Because urine protein can be immediately detected after tubular injury, to monitor urine protein can find the renal dysfunction after transplantation in recipients undergoing renal transplantation, which can gain time for clinical therapy. OBJECTIVE:To discuss the influence of hormone (prednisone) removal on the occurrence of urine protein in recipients undergoing renal transplantation. METHODS:A total of 35 recipients undergoing renal transplantation after removal of prednisone received immunosuppressive regimen of cyclosporine A or tacrolimus+mycophenolate mofetil bivalent. Initial dose of prednisone was 30 mg/d, and then gradual y reduced by 5 mg per week, and withdrawn at 1 month after renal transplantation. There were 16 cases in cyclosporine A group and 19 cases in tacrolimus group. Urine protein was measured and quantified at 3, 6, 12 and 24 months after renal transplantation and 3, 6 and 12 months after addition of prednisone in both groups. Simultaneously, serum creatinine, fasting glucose, body mass increases, the rate of acute rejection, infection, patient/graft survival at 2 years after renal transplantation and urine protein at 24 hours before and after adding hormone were recorded. RESULTS AND CONCLUSION:For the two groups, urineα1-microglobulin started to rise after 6 months of removal of prednisone. Urinary microalbumin, urinaryα1-microglobulin, and urinary transferrin ascended obviously at 12 months. Urinary protein was positive in five cases of cyclosporine A group and in three cases of tacrolimus group. At 24 months, urinary microalbumin, urinaryα1-microglobulin, urinary transferrin and urinary IgG ascended obviously. Urinary protein was positive in cyclosporine A group with 11 cases and in tacrolimus group with 10 cases. 24-hour urinary protein quantity was more than 1 g in every case. On this base, we made the patients to take more prednisone for 6 months, so urineα1-microglobulin and urinary microalbumin began to descend. Each group had one case of positive urinary protein turning to negative. Twelve months after the adjustment of the prednisone, urinary microalbumin, urinaryα1-microglobulin, and urinary transferrin descended respectively. Positive urinary protein turned into negative:in cyclosporine A group with two cases and in tacrolimus group with three cases. 24-hour urinary protein quantity was around 0.7 g. Two years after renal transplantation, serum creatinine and acute rejection rates were higher in the cyclosporine A group than in the tacrolimus group (P<0.05). No significant difference in fasting glucose, body mass increase, infections, and patient/graft survival was detectable between both groups. Results suggested that removal of prednisone greatly affected urine protein in recipients undergoing renal transplantation. In particular, at 2 years after renal transplantation, urinary microalbumin, urinaryα1-microglobulin, urinary transferrin and urinary IgG ascended obviously, and the security needs further research.

Objective To investigate the clinical application of fecal calprotectin in inflammatory bowel disease (IBD).Methods Colonoscopy took 79 patients with IBD that were diagnosed with pathology,including 47 cases of ulcerative colitis (UC) patients,32 cases of Crohn's disease (CD).Moreover,42 cases of IBD patients without abdominal pain,diarrhea and other intestinal inflammation were used as disease control group,and 34 cases of healthy people were used as healthy control group.The level of fecal calprotectin in each group was detected by enzyme-linked immunosorbent assay (ELISA).Results The positive rate of fecal Calprotectin in IBD group,disease control group and the healthy control group was 57.0％,19.0％,and 0,respectively; each positive rate in IBD group was significantly higher than the other two groups (P ＜ 0.05).The serum concentration of fecal calprotectin in IBD group [(493.86 ±204.18) μg/g] was significantly higher than the disease control group [(71.46 ± 60.51) μg/g] and the healthy control group [(36.19 ± 13.46) μg/g] (P ＜ 0.05) ; IBD active calprotection [(1015.23 ± 324.96) μg/g] was significantly higher than resting [(52.69 ±34.71) μg/g] (P ＜0.01).Conclusions Fecal calprotectin test benefits early diagnosis of IBD,and may be taken as the diagnostic index of IBD activity.It has extensively clinical value.

Objective To obtain the Cyclin D1 through cloning and prokaryotic expression of Cyclin D 1 gene.Methods The total RNA was extracted from liver cancer tissue .The Cyclin D1 cDNA was obtained by reverse transcriptase polymerase chain reaction (RT-PCR).The Cyclin D1 cDNA was sequenced, and sub-cloned to the PET32a+.The prokaryotic expressed was used to obtain the Cyclin D1.Results The 483 bp Cyclin D1 cDNA was obtained.The sequence of Cyclin D1 was corrected.The 36 KD CyclinD1 was obtained by prokaryotic expression .Conclusions The Cyclin D1 cDNA was obtained.Cyclin D1 was expressed in BL21.