Objective To observe the effect of interferon combined with kenacort in the treatment of scars. Methods According to random number table,287 patients with scars were randomly divided into treatment group and control group.The treatment group(145 cases) was treated with injection of the mixture of interferon and kenacort. The control group(142 cases) was applied with contratubex.The effect and adverse reaction of the two groups were compared.Results The total effective rate of the treatment group was 95.86%,which was higher than 64.08% of the control group,the difference was statistically significant(χ2 =45.52,P<0.01).The incidence rate of adverse reaction of the two groups had no statistically significant difference(χ2 =1.25,P>0.05).Conclusion These find-ings may shed some light on the clinical application of combined injection therapy on scar treatment,given that the closed dynamic method of injecting interferon combined with kenacort significantly improved scar healing.

Objective To study the effect of intratumor angiogenesis and vascular growth factor(VEGF), basic fibroblase growth factor(bFGF), Platelet-derived growth factor (PDGF), and their receptors(flt-1 bFGFR.PDGFR) on the invasion, metaslasis of pancreatic carcimoma(PC) and the relationship between the expressions of three kinds of angiogenic factors, their receptors and microvessel count(MVC). Methods Tis- sue sections of 51 PC and 32 acute or chronic pancreatitis were examined by in situ hybridization for the expression of VEGF bFGF.PDGF, and by immunohistochemistry for the expression of the three kinds of angiogenic factor receptors and MVC. The correlation of the expressions and pathological characteristics of PC were also studied. Results The positive rate of VEGF mRNA,bFGF mRNA, PDGF mRNA and their receptors in PC were significantly higher than that in acute or chronic pancreatistis( P

Background Environmental noise pollution is serious, and there are few studies on the effects of long-term noise exposure during sleep on cognitive function and possible biological clock mechanism. Objective To explore the cognitive impairment induced by noise exposure during sleep in mice and possible biological clock mechanism, and to provide a theoretical basis for the protection against noise exposure. Methods Twenty male C57BL/6J mice were randomly divided into a control group and a noise-exposed group, 10 mice in each group. The noise-exposed group was exposed to sleep-period noise using a noise generator for 12 h (08:00–20:00) per day for a total of 30 d. The calibrated noise intensity was set at 90 dB. No intervention was imposed on the control group. At the end of the noise exposure, cognitive function of mice was examined using the new object recognition experiment and the open field test, and the hippocampal tissue damage of mice were evaluated by Nissl staining, ionized calcium binding adaptor molecule 1 (Iba1) immunofluorescence staining, and real-time fluorescence quantitative PCR for inflammatory factors and biological clock genes. Oxidative stress indicators in the hippocampus of mice were also detected by assay kit. Results After noise exposure during sleep period, the results of new object recognition experiment showed that the discrimination index of mice in the noise-exposed group was 0.06±0.04, which was significantly lower than that of the control group (0.65±0.13) (P<0.05). The results of open field test showed that the central activity distance of the noise-exposed group was (242.20±176.10) mm, which was significantly lower than that of the control group, (1548.00±790.30) mm (P < 0.05), and the central activity time of the noise-exposed group was (0.87±0.64) s, which was significantly lower than that of the control group, (6.00±2.86) s (P < 0.05). The Nissl staining results showed that compared with the control group, neurons in the hippocampus of the noise-exposed mice were shrunken, deeply stained, disorganized, and loosely connected. The immunofluorescence results showed that microglia in the hippocampus of the noise-exposed mice were activated and the expression of Iba1 was significantly increased compared with those of the control group (P<0.05). The real-time PCR results of showed that the mRNA levels of the biological clock genes Clock, Per2, and Rev-erbα were significantly increased compared with those of the control group (P<0.05), and the mRNA level of Per1 was significantly decreased compared with that of the control group (P<0.05); and the mRNA levels of IL-18, IL-6, iNOS, and NLRP3 in the hippocampal tissues of mice were significantly increased compared with those of the control group (P<0.05). The results of oxidative stress evaluation showed that compared with the control group, reduced glutathione content was significantly reduced in the noise-exposed group (P<0.001). Conclusion Noise exposure during sleep period can lead to the destabilization of biological clock genes in hippocampal tissues and trigger hippocampal neuroinflammation, which can lead to the activation of microglia and cause cognitive impairment in mice.