AIM: To study the pathological change in mouse organs immunitied by inactivated SARS-CoV vaccine. METHODS: Inactivated SARS-CoV vaccine was injected into BALB/c and C57BL/6 mice. Anti-SARS antibody was analyzed by ELISA. After 8 weeks, the immunitied mice were killed and those organs were analyzed by pathological methods. RESULTS: Anti-SARS antibody in mice was positive after 8 days. Only minimal injury was observed in a few lungs and livers, but the other organs were not. CONCLUSIONS: Inactivated SARS-CoV vaccine induced mice to create antibody, whereas they did not cause severe injury. This result will be valuable for vaccine into clinical research. [

Objective To provide scientific evidence to identify and confirm severe acute respiratory syndrome (SARS) by laboratory detection.Methods Multiple clinical specimens were collected serially and systematically from the 4 suspected SARS patients, which occurred between Dec.2003 to Jan.2004 in Guangdong Province. The samples were tested by serologic and molecular methods.Results IgM or IgG antibodies against SARS-CoV were detectable after 6—8 days of the onset in four patients. The four-fold or greater rising in antibodies was clearly detected in three of the four patients, while the fourth patient’s seroconversion was from negative to positive. The results analysed by enzyme-linked immunosorbent assay( ELISA), immunoflourescence assay (IFA), and neutralization test were highly correlated. SARS-CoV RNA was just detected in 3 throat swab specimens from case 1 by real-time PCR. M, N and S genes were amplified by reverse transcriptase polymerase chain reaction (RT-PCR) from the positive samples. Sequencing results showed that they were SARS-CoV gene segments, and most closely matched SARS-CoV gene sequences were isolated from civet cats in Guangdong Province. Nevertheless, SARS-CoV was not isolated from any samples of the 4 patients.Conclusion Based on these results, the 4 reported cases were laboratorily confirmed as SARS cases.

Chronic atrophic gastritis （CAG） is a common and intractable disease in the digestive system characterized by the reduction or disappearance of gastric mucosal glands. The intestinal metaplasia or dysplasia in CAG is called precancerous lesion， which greatly increases the risk of cancerization. Dysactivation of nucleotide-binding oligomerization domain-like receptor protein 3 （NLRP3） inflammatory corpuscles can release a large number of inflammatory factors， induce inflammatory cascade reactions， and participate in the process of many diseases. As reported， the dysactivation of NLRP3 inflammatory corpuscles can cause long-term chronic inflammatory infiltration of gastric mucosa and induce the development of CAG. Mitochondrial dysfunction plays an important role in the activation of NLRP3 inflammatory corpuscles. The accumulation of reactive oxygen species （ROS） produced by mitochondrial dysfunction is the key to activating NLRP3 inflammatory corpuscles. Professor LIU Youzhang put forward the theory of "spleen-mitochondrion correlation"， which holds that the spleen mainly transports water and grains， generates qi and blood， transports nutrients to the whole body， and supplies energy and materials needed by the body. Adenosine triphosphate （ATP） generated by mitochondria through the circulation of tricarboxylic acid is the main energy source of the human body. The view that both of them serve as human energy processing plants coincides in terms of physiology. Pathologically， spleen deficiency is associated with mitochondrial oxidative phosphorylation dysfunction. Pathological products such as dampness， turbidity， phlegm， and blood stasis due to failure in transportation because of spleen deficiency are consistent with metabolites generated by mitochondrial dysfunction. Based on the theory of "spleen-mitochondrion correlation"， this study discussed the pathogenesis of CAG in traditional Chinese medicine （TCM）， analyzed the relationship between NLRP3 inflammatory corpuscles and the pathogenesis of CAG， and proposed that the activation of NLRP3 inflammatory corpuscles by mitochondrial dysfunction was the modern biological basis of the pathogenesis of spleen deficiency in CAG. The spleen-strengthening method may be related to improving the mitochondrial function and inflammatory response of patients with CAG and alleviating the damage of gastric mucosa， providing a new idea for TCM in the prevention and treatment of CAG.

Ulcerative colitis （UC） is a chronic non-specific inflammatory disease characterized by the damage of the epithelial barrier of the colon and the destruction of immune homeostasis. It has a long course， no recovery and high recurrence rate， and is recognized as a difficult digestive disease. MicroRNA （miRNA） has been confirmed to be specifically or differentially expressed in both UC patients and UC animal models， so miRNA can be used as markers for UC diagnosis or reference for treatment evaluation. TCM therapy has a definite therapeutic effect， a wide range of effects， and minimal side effects in the treatment of UC， so this article takes miRNA as the starting point and systematically elaborates on the mechanism of TCM regulating UC related signaling pathways by regulating the expression of miRNA. The results show that chlorogenic acid， Anchang decoction， and Fuyang huoxue jiedu formula can regulate the expressions of miR-155， miR-146a and miR-31-5p， etc.， thereby inhibiting signal transducer and activator of transcription （STAT） signal pathway transduction to improve UC. Limonin， ginsenoside Rh2， artesunate， etc. can inhibit nuclear factor-κB （NF-κB） signaling pathway conduction to improve UC by regulating the expressions of miR-214， miR- 155 and miR-19a， etc. Nitidine chloride， berberine， resveratrol， etc. can regulate the expressions of miR-31， miR-146a， miR- 146b， etc.， thereby inhibiting the Toll-like receptor 4 （TLR4） signaling pathway to improve UC. Mango polyphenolics， Compound qinbai granules， and Astragalus membranaceus polysaccharides can regulate the expressions of miR-126 and miR-193a-3p， thereby inhibiting the phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin （PI3K/AKT/mTOR） signaling pathway to improve UC.