Objective To evaluate the relationship between the intestinal motility alterations and intercellular adhesion molecule-1 ( ICAM-1 ) expression within the rat intestinal muscularis after ischemia reperfusion. Methods Thirty Wistar rats were divided randomly into IIR, monoclanal anti-ICAM-1 and sham group (n = 10), HR models were established by clamping-releasing the superior mesenteric artery. Gut transit was measured in vivo and intestinal circular muscle contractions were measured in an organ bath. The expression of ICAM-1 mRNA was detected by RT-PCR and immunohistochemisty. Leukocyte infiltration and myeloperoxidase (MPO) activity were quantified in sham and ischemia/reperfusion rats with and without monoclonal anti-ICAM-1 antibody treatment. Results The gut transit of monoclonal anti-ICAM-1 group was improved obviously as compared with IIR group. Circular smooth muscle contractility stimulated by ICAM-1 mRNA expression was 1.69 ± 0. 57 and 1.76 ± 0. 32 within the muscularis; Leukocyte infiltration into the muscularis was (5.6 ±2. 2) c/f and ( 18. 2 ±3. 1 ) c/f. MPO activity was (2. 03 ±0. 56) U/g and (6. 41 ± 1.25 ) U/g respectively. The differences were all statistically significant between IIR and treatment groups ( P ＜ 0. 05 ). The expression of ICAM-1 protein in IIR and anti-ICAM-1 groups was not significantly different (P ＞ 0. 05). Conclusions The up-regulated expression of ICAM-1 after ⅡR injury calls forth local infiltration of PMN within the intestinal muscularis, leading to intestinal motility dysfunction.

Brucellosis is a zoonotic disease of global importance for infecting humans .The early diagnosis of brucellosis infection plays a significant role in the treatment and rehabilitation .This paper reviews the different methods used to diagnose brucellosis ,particularly introduces the basic principles and applications of fluorescence polarisation assay as a diagnostic tool for brucellosis ,which could provide the reference for clinical diagnosis and epidemiological investigation on brucellosis .

Objective:To explore the effects of MiR-199a-3p on promoting the development of mycoplasma pneumonia via the silent information regulator 1(SIRT1)/nuclear factor-κB (NF-κB) pathway.Methods:Totally 80 SPF-grade BALB/c mice were randomly divided into a control group, a model group, a miR-199a-3p group, and a inhibitory group, with 20 rats in each group. Excep the control group, the model group was established as a mouse model of mycoplasma pneumoniae through a continuous nasal drip of a high-load mycoplasma pneumoniae bacterial solution for 3 days. After modeling, mice in each group had tail vein injections. The miR-199a-3p group and the inhibitory group mice were injected with agomir solution and antagonir solution, respectively. And the model group and control group mice were injected with the same amount of physiological saline through the tail vein. After the experiment, mice of all groups were killed and their blood was collected from the eyeballs, and interleukin-4 (IL-4), interleukin-6 (IL-6), interleukin-1β (IL-1β), and tumor necrosis factor-α (TNF-α) levels were detected by the enzyme-linked immunosorbent assay method. Subsequently, the lung tissues of the mice were taken for HE staining to observe pathological changes in the lung tissue. Real-time fluorescence quantitative PCR was used to detect miR-199a-3p gene expression levels in lung tissue, and Western Blot was used to detect SIRT1/NF-κB signaling pathway protein expression in lung tissue. Results:Compared with the model group, IL-4, IL-6, IL-1β, and TNF-α levels in the serum of the miR-199a-3p group were decreased, with a significant difference ( P < 0.05). The HE staining results showed that the lung tissue structure of the control group mice was nearly normal and there was no alveolar exudation or inflammatory response. The other three groups all had varying degrees of alveolar interstitial widening, alveolar exudation, and inflammatory cell infiltration. Compared with the model group, miR-199a-3p gene and SIRT1 protein expression levels in the miR-199a-3p group increased, with a significant difference (all P < 0.05). While NF-κB protein expression levels in the miR-199a-3p group decreased, there was a significant difference ( P < 0.05). Conclusions:The expression of miR-199a-3p gene is reduced in the lung tissue of mycoplasma pneumoniae mice. Increasing the level of miR-199a-3p gene has a protective effect on lung tissue damage in mycoplasma pneumoniae mice through anti-inflammatory effects, and its mechanism may be related to its regulatory effect on the SIRT1/NF-κB pathway.