Based on the close structural and functional associations of the Shaoyang （少阳） channel and related zang-fu （脏腑） organs with the brain and the pharynx， this paper proposes that the pathogenesis of post-stroke dysphagia involves constraint and stagnation of the pivot mechanism， binding of phlegm and stasis， frenetic stirring of ministerial fire， and incoordination of the spirit mechanism， ultimately leading to loss of pharyngeal function. An acupuncture therapy centered on regulating the pivot and unblocking the orifice is established. Acupoints of the Shaoyang channel， including Fengchi （GB 20）， Wangu （GB 12）， Yifeng （SJ 17）， and Waiguan （SJ 5）， are selected to regulate the pivot and treat the root； acupoints of the Du （督） and Ren （任） channels， including Fengfu （GV 16）， Lianquan （CV 23）， and Tiantu （CV 22）， are used to unblock the orifice and treat the branch. In addition， staged treatment can be applied according to syndrome differentiation. In the acute stage with predominant phlegm turbidity， Fenglong （ST 40）， Yinlingquan （SP 9）， Jinjin （EX-HN 12）， and Yuye （EX-HN 13） are added to resolve phlegm and facilitate orifice function. During the recovery stage with excess ministerial fire scorching the pharynx， Zulinqi （GB 41） and Zhaohai （KI 6） are added to drain fire and nourish yin； when ministerial fire disturbs the spirit， Tongli （HT 5） and Neiguan （PC 6） are added to calm the spirit and the heart. During the chronic stage with blood deficiency and collateral stasis， Zusanli （ST 36） and Sanyinjiao （SP 6） are added to nourish blood and unblock collaterals. In clinical practice， the angle and depth of needling are adjusted based on the stage of dysphagia， with the combination of elongated needles and medicinal moxibustion are used to enhance the therapeutic effect.

The intestinal barrier is the primary defense that separates the host from the external environment, possessing several crucial physiological functions, including nutrient digestion, absorption, and protection against potentially harmful dietary antigens and pathogenic microorganisms. Nevertheless, various factors, such as diet, medications, circadian rhythm disturbances, gut microbiota, microbial metabolites, and genetic predisposition, can disrupt the intestinal barrier. Such disruption may lead to bacterial translocation, subsequently triggering enterohepatic and systemic inflammation. Impaired intestinal barrier has been implicated in the pathogenesis of numerous diseases, particularly chronic gut and liver diseases. In this review, we will summarize the fundamental functions of intestinal barrier and discuss clinical correlations between intestinal barrier dysfunction and diseases such as colitis, colorectal cancer, and chronic liver diseases including metabolic dysfunction-associated steatohepatitis, alcohol-associated liver disease, and primary sclerosing cholangitis. Additionally, we will also highlight some potential therapeutic strategies aimed at restoring barrier integrity to improve disease management.

Objective : To investigate the effect and mechanism of ARRB1 on Armillariella tabescens polysaccharides reversal of 5-fluorouracil ( 5-FU ) -induced chemotherapeutic intestinal mucosal injury． Methods : Twelve ARRB1 knockout ( ARRB1 －/ － ) and wild-type ( WT) C57BL /6 mice were randomly divided into Control，Model and ATPS groups (200 mg / kg) ，respectively．5-FU (50 mg / kg) was injected intraperitoneally for 7 days to establish a model of chemotherapeutic intestinal mucosal injury．The histopathological damage of jejunum was evaluated by HE staining ; the activity of serum superoxide dismutase (SOD) and diamine oxidase (DAO) was measured by kits ; the expression of tight junction protein (TJ) markers ZO-1，Occludin，Claudin-1 and proliferation-associated protein Ki-67 was detected by immunohistochemistry．Crypt isolation and organoid culture were used to detect the growth status of small intestinal organoids. Results : 5-FU chemotherapy reduced body weight，aggravated histopathological damage in small intestine，decreased SOD level，TJ protein and Ki-67 protein expression，increased serum DAO level，decreased spherical structure formation rate and organoid formation rate ; compared with the model group，after ATPS treatment，WT mice recovered body weight，decreased pathological damage，increased serum SOD level，TJ protein and Ki-67 protein expression，DAO levels decreased，and the rates of spherical structure for- mation and organoid formation were significantly higher．However，ARRB1 －/ － mice failed to reverse the effect of 5- FU after ATPS treatment． Conclusion ATPS reverses 5-FU-induced intestinal mucositis through the protective effects of ARRB1 on intestinal barrier and organoid growth.

Objective To explore the molecular mechanism through detecting methylation status in esophageal carcinoma and Barrett's esophagus.Methods The methylation-specific PCR was employed to detect the expressions of RASSF2 in esophageal carcinoma tissues,adjacent tissues from 27 patients after surgery and Barrett's esophagus tissues from 18 patients after gastroscopic biopsy.Results The rate of RASSF2 methylation was much higher in esophageal carcinoma (66.7 ％,18/27) than that in adjacent tissues (22.2 ％,6/27) (P ＜ 0.05),and was more frequently than that in Barrett's esophagus (33.3 ％,6/18) (P ＜ 0.05).However,no significant difference of methylation status was observed between Barrett's esophagus and adjacent tissue (P ＞ 0.05).Conclusion The hypermethylation of RASSF2 may be the molecular mechanism in the development of esophageal carcinoma,and more samples should be used for further experiment in Barrett' s esophagus.

Objective To screen and diagnose obstructive sleep apnea-hypopnea syndrome (OSAHS) in elderly males by obesity index using receiver operating characteristic(ROC) curves. Methods Data of 402 consecutive elderly male patients who underwent polysomnography from 2001 to 2008 were collected. The relationship between apnea hypopnea index(AHI) and obese indexes such as body mass index (BMI), neck circumference (NC), waist circumference (WC) and waist-to-hip ratio (WHR) were analyzed by Pearson's correlation. ROC curves were used to determine the best cutoff values to screen and diagnose OSAHS, and their priority was compared by area under curve (AUC). A two-tailed P value less than 0.05 was considered statistically significant. Statistical analysis was carried out with SPSS version 13.0. Results (1) AHI was positively correlated with BMI (r=0.241,P<0.001), NC(r=0.201,P<0.001), WC(r=0.210,P<0.001) and WHR(r=0. 097,P>0.05)) in elderly male patients. The area under curve (AUC) of BMI, NC, WC and WHR was 0.61, 0.58, 0.51 and 0.45 respectively, and P value was 0.001,0.060,0.840 and 0. 250 respectively. Only BMI was competent in screening and diagnosing OSAHS in elderly male adults; (2) The optimal value of BMI was 22.0 kg/m~2 in screening OSAHS with specificity 90% and rate of missed diagnosis 10%; (3) The optimal value of BMI was 29.0 kg/m~2 in diagnosing OSAHS with specificity 90% and rate of missed diagnosis 10%. Conclusions BMI more than 22.0 kg/m~2 could be the reference standard to screen OSAHS and BMI more than 29.0 kg/m~2 to diagnose OSAHS in elderly men.

Aim To observe the damages induced by hydrogen peroxide in cultured bovine cerebral microvascular endothelial cells (BCMEC) and evaluate the protective effects of hydroxyethylpuerarin on hydrogen peroxide-injured BCMEC. Methods BCMEC were cultured and transferred into modified Eagle medium (MEM). The viability of cells was detected by MTT assay. Cell injury was determined by lactate dehydrogenase (LDH) activity in the extracellular medium. Flow cytometry was employed to observe the occurrence of apoptosis. Morphologic changes of cells were visualized under phase contrast and electron occurrence of apoptosis. Hydroxyethylpuerarin was shown to increase the survival rate and decrease the activity of LDH of BCMEC damaged by hydrogen peroxide. Hydroxyethylpuerarin was also found to protect BCMEC against apoptosis induced by hydrogen peroxide. Conclusion Hydrogen peroxide induces BCMEC injury either by apoptosis or through necrosis. Hydroxyethylpuerarin protects BCMEC against hydrogen peroxide-induced injury in a concentration-dependent manner. Its antioxidant effects might be involved as the mechanism protection.