Effects of TLR-2/NF-κB signaling pathway on the occurrence of degenerative knee osteoarthritis: an in vivo and in vitro study.

The study aims to explore the effects of TLR-2/NF-κB signaling pathway on the occurrence of degenerative knee osteoarthritis (OA). Degenerative knee OA and normal cartilage samples were collected from patients with degenerative knee OA receiving total knee arthroplasty and amputation. Expressions of TLR-2, NF-κB and MMP-13 were determined by qRT-PCR and immunochemistry. The chondrocytes were divided into control, IL-1ß, IL-1ß + anti-TLR-2 and IL-1ß + PDTC groups. MTT assay and flow cytometry were performed to determine proliferation and apoptosis of the chondrocytes. Expressions of TLR-2, NF-κB and MMP-13 were measured by Western blotting. ELISA was conducted to detect the expressions of related inflammatory factors. The positive expressions of TLR, NF-κB and MMP13 were associated with body mass index (BMI), family history, exercise, and WOMAC scores of OA patients. Logistic regression analysis showed that OA influencing factors were TLR, NF-κB, MMP13, BMI, family history and exercise. Compared with normal chondrocytes, the expressions of TLR-2, NF-κB, MMP-13 and related inflammatory factors increased in degenerative knee OA. The chondrocytes in the IL-1ß + anti-TLR-2 and IL-1ß + PDTC groups showed lower apoptosis rates than those in the IL-1ß group. Compared with the control group, increased expressions of TLR-2, NF-κB, phosphorylated-NF-κB (p-NF-κB), MMP-13, IL-1, IL-6 and TNF-α were found in the IL-1ß group. In the IL-1ß + anti-TLR-2 and IL-1ß + PDTC groups, decreased expressions of NF-κB, p-NF-κB, MMP-13, IL-1, IL-6 and TNF-α were found compared with those in the IL-1ß group. TLR-2/NF-κB signaling pathway contributes to the occurrence of degenerative knee OA.

The SDF-1/CXCR4 axis promotes recovery after spinal cord injury by mediating bone marrow-derived from mesenchymal stem cells.

This study aims to explore the role of the SDF-1/CXCR4 axis in mediating BMSCs and SCI recovery. BMSCs were collected and SCI rat models were established. Wistar rats were assigned into the blank control, sham, SCI, SCI + BMSCs, SCI + BMSCs + SDF-1, SCI + BMSCs + AMD3100 (an inhibitor of SDF-1/CXCR4 axis) and SCI + BMSCs + SDF-1 + AMD3100 groups. Hind limb motor function was measured 7, 14, 21 and 28 days after operation. qRT-PCR, western blotting and ELISA was performed to determine the expressions of SDF-1, CXCR4, NGF, BDNF, GFAP and GAP-43, TNF-α, IL-1ß, L-6 and IFN-γ. Hind limb motor function scores 7 days after the operation were reduced in the SCI rats of the blank control and sham groups. Hind limb function was found to be better in the SCI + BMSCs and SCI + BMSCs + SDF-1 groups than in the SCI, SCI + BMSCs + AMD3100 and SCI + BMSCs + SDF-1 + AMD3100 groups 14, 21 and 28 days after operation. Furthermore, the SCI group had lower SDF-1, CXCR4, NGF, BDNF and GAP-43 expressions but higher GFAP, TNF-α, IL-1ß, IL-6 and IFN-γ than the blank control and sham groups 28 days after operation. While, the SCI + BMSCs, SCI + BMSCs + SDF-1 and SCI + BMSCs + SDF-1 + AMD3100 groups displayed opposite trends to the SCI and SCI + BMSCs + AMD3100 groups. In conclusion, SDF-1/CXCR4 axis promotes recovery after SCI by mediating BMSCs.

Crystal structure of 4-{[(1H-1,2,4-triazol-1-yl)meth-yl]sulfan-yl}phenol.

In the title compound, C9H9N3OS, the plane of the benzene ring forms a dihedral angle of 33.40 (5)° with that of the triazole group. In the crystal, mol-ecules are linked by O-H⋯N hydrogen bonds involving the phenol -OH group and one of the unsubstituted N atoms of the triazole ring, resulting in chains along [010]. These chains are further extended into a layer parallel to (001) by weak C-H⋯N hydrogen-bond inter-actions. Aromatic π-π stacking [centroid-centroid separation = 3.556 (1) Å] between the triazole rings links the layers into a three-dimensional network.

[Analysis of the test results of HBV serum markers and HBV DNA of the neonates born to HBsAg-positive mothers].

OBJECTIVE: To observe the HBV serum markers and HBV DNA expressions of the neonates born to the HBsAg-positive mothers. METHODS: By detecting serum immunity markers of hepatitis B virus (5 items) and serum HBV DNA of 283 neonates (a pair of twins) born to 282 HBsAg-positive mothers. RESULTS: 12 patterns emerge from the study of the hepatitis B serum markers of 283 neonates. Topping the list is the combination of HBeAg and anti-HBc positive accounting for 48.41% (137/283), followed by the combination of anti-HBe and anti-HBc positive accounting for 22.26% (62/283). The third highest combination is that of HBsAg, HBeAg and anti-HBc positive accounting for 12.37% (35/283). There are five combinations accounting for 16.61% (47/283), each with HBsAg-positive. No case is found of the five items all negative or only HBsAb positive. Five cases are detected of serum HBV DNA > or = 1 x 103 IU/ml accounting for 1.77%. CONCLUSIONS: Neonates born to HBsAg-positive mothers display complex patterns of serum hepatitis B markers, the dominant pattern being the combination of HBeAg and anti-HBc positive. Cases of serum HBV DNA > or = 1 x 10(3) IU/ml are rare.

[Instructional significance of HBV-DNA load in maternal milk on breastfeeding of postpartum women infected with HBV].

OBJECTIVE: To study the instructional significance of HBV-DNA load in maternal milk on breastfeeding of postpartum women infected with HBV. METHODS: HBV-DNA levels in serum and breast milk were detected by FQ-PCR in 152 postpartum women infected with HBV, and HBV-DNA ≥ 1.0 × 10(3) U/ml was defined as HBV positive. Correlation analysis was also conducted to estimate if there were relations in HBV levels in serum and breast milk. RESULTS: HBV-DNA positive rate were 50.66% (77/152) and 36.18% (55/152) in serum and breast milk, respectively. When HBeAg was positive, HBV-DNA positive rate were 95.38% (62/65) and 76.92% (50/65) in serum and breast milk; however when HBeAg was negative, HBV-DNA positive rate were 17.24% (15/87) and 5.75% (5/87) in serum and breast milk. When the concentration of HBV-DNA was 3-4 lg U/ml in serum, HBV-DNA positive rate was 20.00% (5/25) in breast milk; However, when the concentration of HBV-DNA was higher than 5 lg U/ml in serum, HBV-DNA positive rate was 96.15% (50/52) in breast milk. CONCLUSION: The HBV-DNA level in breast milk in postpartum women infected with HBV increased with the HBV-DNA levels in serum. Breastfeeding should be avoided when the concentration of HBV-DNA is higher than 1.0 × 10(3) U/ml in milk.

[Detection of peripheral blood HBV-LHBs transactivation function and its relationship with anti-viral efficacy].

OBJECTIVE: Explore the serum of patients with CHB of HBV large envelope protein (HBV-LHBs) trans-activation function and antiviral therapy effect relationship. METHODS: 60 cases of anti-viral treatment of patients with chronic hepatitis B to take every 3 months HBVDNA, HBV-LHBs, as well as detection of hepatitis B immune markers to observe the changes in indexes. RESULTS: Income group 60 cases of anti-virus group HBVDNA with HBV-LHBs have a higher detection rate of the consistency of the results found no statistical significance (P > 0.05), HBV-LHBs-positive rate and positive rate of HBeAg differences (chi2 = 4.08, P < 0.05). After 24 months of antiviral therapy HBV-LHBs expression always HBVDNA in 29 cases of which occurred 24 months after the negative reaction of the 20 cases, continuous positive were seven cases of non-negative. 60 cases of patients 24 months found no HBsAg seroconversion, four cases of emergence of HBeAg seroconversion. CONCLUSION: (1) detection of serum HBV-LHBs to reflect the hepatitis B virus replication with HBVDNA good correlation. (2) anti-viral treatment of dynamic observation of the process of HBV-LHBs expression can predict the effectiveness of anti-viral therapy.

[The roles of saliva testing for preventing hepatitis B virus spreading].

OBJECTIVE: To discuss the significance of testing hepatitis B virus (HBV) from saliva in HBV patients. METHODS: HBV DNA content in serum and saliva of 200 HBV patients and 20 healthy subjects were detected by fluorescence quantitative polymerase chain reaction. According to the serum level of HBV content, four groups were divided: control group A, group B negative, low virus C (1 x 10(3) - 1 x 10(5) copies/ml) and high-group D ( > 1 x 10(5) copies/ml). The relationship of serum and virus content in saliva was analysed. RESULTS: Of 200 HBV cases, 180 were found HBV DNA in serum with positive rate of 90.0%; while 145 were found HBV DNA in saliva with positive rate of 72.5%, and there was no significant difference (chi2 = 1.35, P > 0.05). The significant difference was observed in testing serum and saliva in Group C (100.0% vs. 38.5%; Z = 14.11, P < 0.01). In group D, there was no significant difference found either (100.0% vs. 83.8%; chi2 = 1.05, P > 0.05). Group D virus serum had a high average level of (6.63 +/- 1.55) log copies/ml virus and in the saliva had an average level of (5.21 +/- 1.85) log copies/ml; saliva had serum viral load lower than an order of magnitude average. No HBV DNA was found in serum or saliva from 20 health subjects. CONCLUSION: When the serum contains a high content of HBV DNA virus, the content of saliva HBV DNA virus should be likely high, which might pose a threat of source of infection. A precise quantitative detection of HBV DNA in saliva might be used as evaluation of the level of virus in the body copy for judgment of infection.

[HBVcccDNA of patients with hepatitis B in the serum, PBMC and liver tissue distribution].

OBJECTIVE: Hepatitis B virus covalently closed circular DNA in the serum of patients with hepatitis B, peripheral mononuclear cells (PBMC) and liver tissue distribution. METHODS: Serum HBV DNA > 10(5) copies/ml 50 cases of hepatitis B patients, serum HBV DNA < 10(5) copies/ml 30 cases of hepatitis B patients, patients with fatty liver (hepatitis B) 20 cases, using real-time quantitative polymerase chain reaction for detection of serum, and liver tissue in PBMC HBVcccDNA the existence. RESULTS: Of 50 serum HBV DNA > 10(5) copies/ml cccDNA the serum specimens were 28 cases, 56% detection rate, 29 cases were PBMC HBVcccDNA, 58% detection rate, liver tissue HBVcccDNA were 44 cases, 88% detection rate, serum, the PBMC were detected in liver tissue were significant differences in P < 0.005, compared serum PBMC were no significant differences in P > 0.005. 30 serum HBV DNA < 10(5) copies/ml the serum specimens, PBMC cccDNA detected two cases were 6.67% detection rate, liver tissue cccDNA were six cases 20% detection rate, serum, PBMC, were among the liver tissue was not significantly different P > 0.005. 20 in the serum of patients with fatty liver, liver tissue in PBMCwere not detected HBVcccDNA. CONCLUSION: HBVcccDNA mainly in the liver of patients with hepatitis B, hepatitis B patients and also cccDNA PBMC in the presence of liver tissue but a few of many.

[Clinical significance of intrahepatic hepatitis B core antigen (+) in patients with chronic hepatitis B].

OBJECTIVE: This study aimed to assess the clinical significance of intrahepatic hepatitis B core antigen (HBcAg) (+) in patients with chronic hepatitis B (CHB). METHODS: 200 CHB patients were prospectively studied using fluorescence quantitative PCR (FQ-PCR), combined PCR with fluorescence probe hybridization technique, to determine serum HBV DNA. Serum HBeAg was measured quantitatively. Liver biopsies were performed and immunohistochemistry stained liver slides were examined in all the cases. Correlation analyses were performed. RESULTS: Based on the HBV DNA levels, the patients were divided into 5 groups: group A (<3 log10 copies/ml) n=20, group B (>or=3 log10 copies/ml-<5 log10 copies/ml) n=13, group C (>or=5 log10 copies/ml-<6 log10 copies/ml) n=24, group D (>or=6 log10 copies/ml-<8 log10 copies/ml) n=116, and group E (>or=8 log10 copies/ml) n=27, and 87.5% of the CHB patients were intrahepatic HBcAg (+). The rate of HBcAg (+) was 55.0% (11/20) in group A, 53.8% (7/13) in group B, 75.0% (19/24) in group C, 96.6% (112/116) in group D, and 100% (27/27) in group E. A strong correlation was found between the rate of HBcAg (+) and the level of serum HBV DNA (r=0.80). This type of association also appeared between serum HBV DNA levels and HBeAg (+) (r=0.47). Of 20 CHB patients who were serum HBV DNA negative, 25% (5) were HBeAg (+), and 55% (11) were HBcAg (+), whereas 15 patients were both HBV DNA (-) and HBeAg (-), and 46.7% (7) were HBcAg (+). CONCLUSIONS: Intrahepatic HBcAg (+) in CHB patients might be more reliable in reflecting HBV replication. Determination of HBcAg (+) may have clinical significance for evaluating the efficacy of antiviral therapy and for predicting the therapeutic responses to different antiviral agents.