Effects of recombinant fusion protein interleukin-18 on expression of immune-inflammatory factors in mice infected with Staphylococcus aureus / 中国当代儿科杂志

<p><b>OBJECTIVE</b>To observe the effects of recombinant fusion protein interleukin (IL)-18 on the expression of immune-inflammatory factors in the mice infected with Staphylococcus aureus (SA), and to investigate the mechanism of action of IL-18 in defense of SA infection in vivo.</p><p><b>METHODS</b>A total of 40 specific pathogen-free female BLAB/c mice were randomly divided into four groups: control, SA infection, immunized, and intervention. A mouse model of SA infection was established by nasal inoculation with SA liquid. The immunized group and the intervention group were intranasally given IL-18 before SA modeling, and then the SA infection group and the intervention group received the nasal inoculation with SA liquid; the control group was treated with phosphate buffered saline instead. The levels of IL-4, interferon (IFN)-γ, tumor necrosis factor (TNF), granulocyte colony-stimulating factor (G-CSF), IgM in the serum and bronchoalveolar lavage fluid (BALF) of mice were measured by enzyme-linked immunosorbent assay. The expression of macrophage inflammatory protein (MIP)-1α mRNA and MIP-2β mRNA in the lung tissue of mice were determined by real-time fluorescent quantitative PCR.</p><p><b>RESULTS</b>Compared with the control group, the SA infection group and the immunized group had significantly higher levels of IL-4, G-CSF, and IgM in the serum and BALF and expression of MIP-1α mRNA and MIP-2β mRNA in the lung tissue (P<0.05); the SA infection group had a significantly lower level of IFN-γ and a significantly higher level of TNF in the serum and BALF (P<0.05); the immunized group had a significantly higher level of IFN-γ in the serum and BALF (P<0.05). Compared with the SA infection group, the intervention group had significantly higher levels of IL-4, IFN-γ, G-CSF, and IgM in the serum and BALF and expression of MIP-1α mRNA in the lung tissue. In contrast, the intervention group showed a significantly lower level of TNF in the serum and BALF and expression of MIP-2β mRNA in the lung tissue (P<0.05). All the above indicators in the intervention group were significantly higher than those in the control group (P<0.05), except the serum level of IFN-γ.</p><p><b>CONCLUSIONS</b>In the mice infected with SA, the recombinant fusion protein IL-18 by mucosal immunity can affect inflammatory factors in the serum and BALF and the expression of MIP-1α mRNA and MIP-2β mRNA in the lung tissue to promote the anti-infective immune response and enhance the ability to clear pathogens.</p>

Current research and development trend of swallowable biotelemetry systems / 中国医疗器械杂志

Swallowable biotelemetry systems are one kind of implantable biotelemetry systems. The research about swallowable biotelemetry systems is rapidly growing recently because they can be used to measure physiological and pathological parameters of human gastrointestinal tracts in vivo and they significantly improve patient comfort. This paper presents the current research of swallowable biotelemetry systems domestically and abroad. The development trend of these systems is analyzed at the end of the paper.

Mutation analysis of fibroblast growth factor receptor 3 gene in an achondroplasia family / 中华医学遗传学杂志

<p><b>OBJECTIVE</b>To clarify the patients' pathogenic mechanism in an achondroplasia family not according with the genetic law of autosomal dominant inheritance disease at gene level.</p><p><b>METHODS</b>Genomic DNA from peripheral blood of all members in this family was used for amplification of the exon 10 of fibroblast growth factor receptor 3(FGFR3) gene by PCR; mutation was detected by DNA sequencing and identified by restriction endonuclease MaeIII.</p><p><b>RESULTS</b>A new mutation of A to T at nucleotide 1180 was found in patients but not in unaffected members.</p><p><b>CONCLUSION</b>Combined with pedigree analysis, it was summarized that achondroplasia patients in this family might result from this new mutation.</p>