ABSTRACT
Objective To investigate the expression and immune function of NOD2 signal in MyD88-/- mice. Methods MyD88-/- mice and wild-type C57 BL/6 mice were characterized by PCR. Mice model of pulmonary infection was constructed by tracheal instillation of BCG vaccine strain(attenuated strain of Mycobacterium). PBS tracheal instillation was used as negative control.Peripheral blood sample and lung tissue were collected aseptically 24 h after Mycobacterium challenge. Real-time PCR and Western blot were used to detect the expression of NOD2 gene and protein. IL-6 level in the peripheral blood was determined by enzymelinked immunosorbent assay. Results The expression of NOD2 protein in BCG infected mice was significantly higher than PBS negative control group. NOD2 protein expression in MyD88-/- mice was higher than in wild-type mice. BCG infection was associated with higher NOD2 protein expression than infection-free PBS control in both groups of animals. The IL-6 level in peripheral blood was significantly higher after BCG infection than PBS group in both MyD88-/- mice and wild type mice. Conclusions BCG can activate the NOD2 signaling pathway when MyD88-dependent pathway is deficient.
ABSTRACT
<p><b>OBJECTIVE</b>To find an inhibitor to reduce the volatilization of formalin.</p><p><b>METHOD</b>The saturated solution of sodium hydrosulphite (SHS) was sprayed on the surface of the anatomy specimens, then the concentration of formaldehyde in the air was tested.</p><p><b>RESULTS</b>The concentration of formaldehyde in the air of SHS sprayed group [(3.10 +/- 1.22) mg/m3] was significantly lower than that of the control group [(8.36 +/- 4.11) mg/m3, P < 0.01].</p><p><b>CONCLUSION</b>SHS may be a volatilization inhibitor for formalin, which could reduce the concentration of formaldehyde in the air.</p>