Objective: To analyze the characteristics of the healthy state of TCM (Traditional Chinese Medicine) of female, and preliminarily constructs the model of TCM health status identification of female with menstrual cycle. Methods: The text of disease diagnosis and syndrome differentiation of menstrual-cycle-linked disorders from Guidelines for diagnosis and treatment of common disease of gynecology in Traditional Chinese Medicine was analyzed, and the symptoms related with viscera functions, the waxing and waning of qi and blood, and pathogenic properties were extracted. The questionnaires of diseases and syndrome elements differentiation of female by calculating the weight relationship between symptoms and health status were designed to estimate the interior state of waxing and waning of yin-yang by figuring out the different periods of menstrual, and in the last step, Constitution in Chinese medicine Questionnaire was used to identify the constitution. Through the above four identification methods, a comprehensive identification of the female's health status of TCM was formed. Results: Through the disease identification model, we distinguished the state of disease and yet disease. And through the syndrome elements differentiation model, we knew the viscera functions, the waxing and waning of qi-blood and yin-yang, and pathogenic properties. And by identifying the internal qi-blood and yin-yang status, we initially built the model that can identify health status of female integrally with the constitution. Conclusion:The model identification results can reflect the comprehensive health status of female in multiple dimensions. It can make a fine classification of women.s TCM health status. It can not only help to know the previous health status but also help to speculate the future health trend, which contributes to the formulation of personalized health interventions of follow-up.

Objective To investigate the expression of transient receptor potential vanilloid 1(TRPV1)and transient receptor po-tential melastatin member 8(TRPM8)in the intestinal and spinal dorsal root ganglion(DRG)in experimental colitis mice induced by dextran sodium sulfate(DSS),and further explore the connection and related pathways.Methods A total of 20male C57BL/6mice were selected and randomly divided into blank control group and DSS group,with 10mice in each group.Mice in the DSS group were treated with 30g/L DSS for 7days to construct colitis model.The hair,body mass,fecal characteristics(granular,loose stool,bloody stool,etc)and perianal conditions(redness,swelling,bloody stool,etc)of every group were observed and recorded at the same time every day,the colitis related disease activity index(DAI)calculated,and colon histopathological score were calculated according to the pathological sec-tions.The protein expression levels of TRPV1,TRPM8,Gαq in colon tissue were detected by Western blot.The expression levels of in-terleukin-6(IL-6),interleukin-1β(IL-1β)in the colon tissue were detected by real-time quantitative polymerase chain reaction(RT-PCR).The localization and expression of TRPV1,TRPM8,Gαq in colon tissue and DRG were detected by immunofluorescence.Results Compared with the blank control group,the colon pathological damage was obvious in the DSS group,and DAI score of colon tissue was significantly increased(P＜0.05),inflammatory factors including IL-1β,IL-6 and TRPV1,Gαq proteins were up-regula-ted significantly(P＜0.05),TRPM8 expression was down-regulated(P＜0.05).Meanwhile,co-expression of TRPV1/TRPM8,TR-PV 1/Gαq were observed in colonic mucosa and submucosa,and TRPV1/TRPM8 were co-expression in DRG.Compared with the blank control group,TRPV1 expression was increased and TRPM8 was decreased in DSS group.Conclusion The increased TRPV1 expres-sion and decreased TRPM8 expression are found in the colonic tissue of experimental colitis mice,and TRPV1/TRPM8 can be co-expressed in the colonic tissue and DRG.There may be some balance mechanism between them to maintain the stability of intestinal function.

Background: Studies have shown that transient receptor potential (TRP) channels play important roles in gastroesophageal reflux disease (GERD), however, the relationship between TRPV1 and TRPM8 in reflux esophagitis (RE) remains unclear. Aims: To investigate the expressions of TRPV1, TRPM8 and their correlation in guinea pigs with RE. Methods: Thirty male guinea pigs aged 3⁃4 weeks were randomly divided into 3 groups: blank control group, negative control group and model group, with 10 animals in each group. Guinea pigs in model group and negative control group were given esophageal perfusion with 0.1 mol/L HCl containing 0.5% pepsin and normal saline, respectively, once a day for 14 days; guinea pigs in blank control group were free to drink sterile water for 14 days. On day 15, the esophagus was dissected for macroscopic and histopathological examination, and Western blotting and/or real⁃time PCR were used to detect the expression levels of TRPV1, TRPM8, GNAQ (an isoform of G protein), and the tight junction proteins and proinflammatory cytokines in esophageal tissue. The co⁃localization of TRPV1 and TRPM8 was assessed by immunofluorescence. Results: Esophageal mucosal congestion, hyperplasia of esophageal epithelial cells, infiltration of inflammatory cells, as well as up⁃regulation of proinflammatory cytokines and down⁃regulation of tight junction proteins were observed in esophageal tissue of guinea pigs in model group, which indicated the successful RE model construction. As compared with the negative control group, expression levels of TRPV1 and GNAQ mRNA and protein were significantly increased, while expression levels of TRPM8 mRNA and protein were significantly reduced in esophageal tissue of guinea pigs in model group (all P<0.05). TRPV1 and TRPM8 channels were co ⁃ localized in the lamina propria of esophageal mucosa. Conclusions: There is a certain equilibrium mechanism between TRPV1 and TRPM8 channels in RE models. G protein⁃coupled receptor signaling pathway and the downstream TRPV1/TRPM8 might be involved in the occurrence and development of GERD.