The prevalence of comorbidity of eating disorders(ED)and bipolar disorder(BD)is high,and patients with comorbid conditions often have a high risk of suicide and poor prognosis.Exploring the pathogenesis of BD comorbid with ED is of great significance for improving clinical efficacy and adverse prognosis in patients.The mechanisms underlying BD comorbid ED remain unclear,involving multifaceted neurobiological factors such as serotonin system dysfunction,dopamine reward pathway disruption,abnormal immune system activation,fluctuations in sex hormone levels,and functional and structural abnormalities in brain regions associated with emotional control and reward system pathways.Therefore,this article provides ideas for the research direction of BD comorbid with ED by analyzing the roles of genetic metabolism,neurobiochemistry,immune,and imaging changes in the comorbidity mechanism.

The prevalence of comorbidity of eating disorders(ED)and bipolar disorder(BD)is high,and patients with comorbid conditions often have a high risk of suicide and poor prognosis.Exploring the pathogenesis of BD comorbid with ED is of great significance for improving clinical efficacy and adverse prognosis in patients.The mechanisms underlying BD comorbid ED remain unclear,involving multifaceted neurobiological factors such as serotonin system dysfunction,dopamine reward pathway disruption,abnormal immune system activation,fluctuations in sex hormone levels,and functional and structural abnormalities in brain regions associated with emotional control and reward system pathways.Therefore,this article provides ideas for the research direction of BD comorbid with ED by analyzing the roles of genetic metabolism,neurobiochemistry,immune,and imaging changes in the comorbidity mechanism.

ObjectiveTo study the correlation between Vimentin and hepatocellular carcinoma （HCC） and the mechanism of Jianpi Yiqi prescription against HCC through Vimentin. MethodCorrelation between Vimentin and HCC was analyzed based on the cancer genome atlas（TCGA）， clinical proteomic tumor analysis consortium（CPTAC）， STRING， and Cytoscape. SD rats were randomized into normal group （normal saline， ig， once/day， 4 weeks）， model group （normal saline， ig， once/day， 4 weeks）， low-dose， medium-dose， and high-dose （5.25， 10.5， 21 g·kg^-1， ig， once/day， 4 weeks） JianpiYiqi prescription groups， signal transducer and activator of transcription 3 （STAT3） inhibition group （C188-9， 4.5 mg·kg^-1， ip， once/day， 4 weeks）， and glycoprotein 130 （gp130） inhibition group （SC144， 4.5 mg·kg^-1， ip， once/day， 4 weeks）， 10 rats in each group. Diethylnitrosamine （DEN， 70 mg·kg^-1 body weight， ip） was injected in rats except the normal group to induce HCC. After the modeling， administration began. After last administration， Real-time polymerase chain reaction（Real-time PCR） was performed to determine Vimentin mRNA level in rat liver tissue. Caspase-3 activity in liver tissue was detected by colorimetry， and expression of Rho kinase （ROCK）1， ROCK2， aurora kinase B （AURKB）， Zinc-finger protein 148 （ZNF148）/zinc-binding protein-89 （ZBP-89）， STAT3， p-STAT3， total Vimentin， and phosphorylated （p）-Vimentin in liver tissue and Vimentin in liver tissue nucleus detected by Western blot. Serum Vimentin concentration was measured by enzyme-linked immunosorbent assay （ELISA）. ResultVimentin mRNA level was high in tissues from HCC patients with different cancer stages （stage Ⅰ-Ⅳ）， different pathological grades （G₁-G₃）， no regional lymph node metastasis （N0）， and different subtypes （P<0.01）. Vimentin mRNA expression was higher in tissues from patients with lymph node metastasis than in patients without lymph node metastasis and normal samples. Vimentin protein level was decreased in HCC tissues （P<0.01）. Vimentin gene has 4 mutations which can induce change in the primary structure of Vimentin protein and patients with Vimentin gene mutation had short disease free survival time （P<0.01）. The mRNA expression of Vimentin was negatively associated with HCC cell purity （P<0.01） but was positively associated with the infiltration levels of cancer-associated fibroblasts， M2 macrophages， myeloid dendritic cell and other immune cells in tumor microenvironment （P<0.01）. Association analysis results showed that the expression of Vimentin was correlated with the STAT3 expression in HCC tissues （P<0.01）. As for the animal experiment， Vimentin mRNA level and protein levels of total Vimentin and p-Vimentin in liver tssue， Vimentin protein level in liver tissue nucleus， Vimentin in rat serum， ROCK2， AURKB， STAT3 and p-STAT3 in liver tissues were up-regulated （P<0.01） and protein level of negative regulator ZBP-89 was reduced in the model group （P<0.01） compared with those in the normal group. Activity of Caspase-3 in liver tissue increased and the ROCK1 protein level was increased in the model group compared with those in the normal group. STAT3 inhibitor， gp130 inhibitor， and medium-dose and high-dose Jianpi Yiqi prescription all can reduce the secretory Vimentin protein in serum， protein levels of total Vimentin and p-Vimentin in liver tissues， and Vimentin in liver tissue nucleus， and the protein levels of STAT3/Vimentin signaling pathway-related molecules， such as STAT3， p-STAT3， ROCK2， and AURKB and up-regulate the protein level of negative regulator ZBP-89 and activity of Caspase-3 （P<0.05， P<0.01）. Effect of medium-dose or high-dose Jianpi Yiqi prescription on Vimentin mRNA expression， STAT3 protein expression， ZBP-89 protein expression， ROCK2 protein expression， AURKB protein expression and Caspase-3 activity was not significantly different from that of STAT3 inhibitor. ConclusionVimentin， an important inflammatory molecule， is closely related to the occurrence and development of HCC and its expression， subcellular location and function may be affected by cancer-associated fibroblasts， M2 macrophages， myeloid dendritic cell， and IL-6/STAT3 signaling pathway， particularly by STAT3 molecule. Jianpi Yiqi prescription may exert therapeutic effect on HCC via regulating Vimentin through the STAT3/Vimentin signaling pathway.

OBJECTIVE：To explore the therap eutic effects and its mech anism of Jianpi yiqi decoction on diethylnitrosamine （DEN）induced liver cancer model rats. METHODS ：Totally 80 male SD rats were divided into normal group ，model group ， Nod-like receptor family 3（NLRP3）inhibition group （MCC950，4.5 mg/kg），caspase-1 inhibitory group （VX-765，4.5 mg/kg）， Jianpi yiqi decoction low-dose ，medium-dose and high-dose groups （5.25，10.5，21 g/kg），with 10 rats in each group except for 20 rats in model group （10 of them were only used to judge whether modeling was successful ）. Rats in each group were intraperitoneally injected with DEN （70 mg/kg）to induce liver cancer model ，except for the rats in normal group which were replaced by normal saline. After modeling ，normal group and model group were given normal saline intragastrically ；inhibitor groups were given relevant medicine intraperitoneally ；Jianpi yiqi decoction groups were given relevant medicine intragastrically ， once a day ，for consecutive 4 weeks. After last administration ，histopathological morphology of liver tissue was observed. The contents of serum inflammatory factors TNF-α and IL-1β were detected. The expression of NLRP3 and programmed cell necrosis associated protein （ASC，pro-caspase-1，RIP1，RIP3 and MLKL ）in liver tissue were detected. RESULTS ：Compared with the normal group ，the hepatocytes of model group showed varying， degrees of steatosis ，enlarged nuclei ，lumpy，bleeding and necrosis，accompanied by proliferative foci and nodules. Liver 198086， tissue injury index ，serum content of TNF-α and IL-1β as well as the protein expression of NLRP 3，ASC，pro-caspase-1，RIP1，RIP3 and MLKL in liver tissue were significantly increased （P＜0.05 or P＜0.01）. Compared with model 防治。E-mail：sherwin_zhuo@126.com group，there were still a large number of inflammatory cell infiltration in the liver tissue of rats in Jianpi yiqi decoction low-dose and medium dose groups ，while the inflammatory cell infiltration of rats in high-dose group and inhibitor groups decreased significantly ；the liver tissue injury index and above indexes levels in serum and liver tissue were decreased significantly （P＜0.05 or P＜0.01）. CONCLUSIONS ：Jianpi yiqi decoction shows therapeutic effect on liver cancer model rats ，the mechanism of which may be associated with down-regulating the expression of NLRP3 inflammasome and inhibiting programmed cell necrosis.

OBJECTIVE：To study the effects of ferulic acid on t he proliferation ，invasion and apoptosis of HepG 2 hepatocelluar carcinoma cells. METHODS ：CCK-8 assay was used to screen the concentration of ferulic acid. Western blot assay was adopted to screen the optimal concentration of interleukin 6（IL-6）to induce HepG 2 cell model with high expression of phosphorylated signal transduction protein and activator 3（p-STAT3）protein. HepG 2 cell were divided into blank control group ， model group ，ferulic acid group （0.5 mmol/L）and positive control group （p-STAT3 inhibitor C 188-9，10 μmol/L）. Except for blank control group ，model group treated with IL- 6，while administration groups were treated with IL- 6 and relevant drugs. Cell survival rate ，invasion and apoptosis rate in early and late stage were detected by CCK- 8 assay，Transwell assay and Annexin V-FITC/PI double staining ，respectively. Western blot assay was used to detect the expression of p-STAT 3，caspase-3，ZBP-89 and vimentin proteins in each group. On the basis of the PDB protein database ，using 1BG1，a highly similar crystal structure of STAT3，as docking template ，using the region around Tyr 705 as the putative binding pocket ，the docking analysis of ferulic acid with STAT 3 protein was carried out. RESULTS ：It is selected to use 0.5 mmol/L ferulic acid intervention for 48 h as the follow-up experimental condition ；50 ng/mL IL- 6 was selected as the modeling condition. Compared with blank control group ，the number of cell invasion ，p-STAT3/STAT3 ratio and protein expression of vimentin were increased significantly in model group （P＜0.05 or P＜0.01），while late apoptosis rate and protein expression 20 of caspase- 3 were decreased significantly （P＜0.05 or P＜ 0.01）. Compared with model group ，cell survival rate ，the number of cell invasion ，p-STAT3/STAT3 ratio and protein expression of vimentin were d ecreased significantly in ferulic acid group and positive control group （P＜0.05 or P＜0.01）；early apoptotic rate （except for ferulic acid group ），late apoptotic rate，the protein expression of caspase- 3 and ZBP- 89（except for positive control group ）were increased significantly （P＜0.05 or P＜0.01）. The results of molecular docking showed that the carboxylic groups of ferulic acid could interact with 1.9 Å hydrogen bond of Asn 581 and 2.0 Å hydrogen bond of Lys 591，with binding energy of －4.4 kcal/mol. CONCLUSIONS ：Ferulic acid may inhibit the activity of p-STAT 3 by directly binding to the phosphorylation site of STAT 3；it may up-regulate the protein expression of caspase- 3 via STAT 3 dependent pathway ，or up-regulate the protein expression of ZBP- 89 via STAT 3 independent pathway and then down-regulate the protein expression of vimentin ，so as to inhibit the proliferation ，invasion and apoptosis of HepG 2 cells.

STAT3, a member of the signal transducer and activator of transcription family, is abnormally activated in chronic inflammation-related tumors including liver cancer. As a key signal molecule in the microenvironment of liver cancer and inflammation, STAT3 not only participates in the inflammation-cancer transformation during the development of liver cancer, but also promotes the proliferation, invasion, and metastasis of hepatoma cells through many ways, and therefore, it may be a potential target for the treatment of liver cancer. This article reviews the recent advances in the association between STAT3 and liver cancer.

Objective: To evaluate the cost-effectiveness of intervention and management of the patients with dyslipidemia in some districts in Shenzhen and provide health economic basis for prevention and control of dyslipidemia. Methods: We conducted a comprehensive community intervention among patients for dyslipidemia management, enrolling 204 cases of dyslipidemia in the intervention group and 200 cases in the control group through multi-stage cluster random sampling. We collected baseline and intervention data, such as the cost of institutional intervention (labor costs, office expenses, material expenses, loss of low-value consumables, service costs, and depreciation of fixed assets), patient costs (direct and indirect medical costs), effect indicators (lipid control rate, lipid improvement rate, and lipid exacerbation rate) to analyze cost-effectiveness. Results: After 12 months of the comprehensive community intervention, the total cost for the intervention group was 1 321.62 yuan per capita; the cost per patient was 973.33 yuan; and per capita institutional cost was 348.29 yuan. Total cholesterol, triglyceide, and high-density lipoprotein cholesterol of intervention group decreased by 0.43 mmol/L, 0.16 mmol/L, and 0.42 mmol/L, respectively, after the intervention, and there was a significant difference before and after the intervention (P<0.05). After intervention, the intervention group lipid control rate was 17.6%, the lipid improvement rate was 48.0%, and the lipid exacerbation rate was 7.4%, whereas those of the control group were 10.5%, 22.5%, and 16.0%, respectively. The lipid control rate and improvement rate in the intervention group were higher than those in the control group, and the lipid exacerbation rate was lower than that of the control group. The difference between the two groups was statistically significant (χ²=43.774, P<0.001). Patients in the control group had a unit cost of 81.17 yuan for 1% of blood lipid control rate and 37.88 yuan for one unit of blood lipid improvement rate. The corresponding per capita cost of the intervention group was 74.87 yuan and 27.51 yuan, respectively. The intervention group's cost-effect ratio was lower than that of the control group and had good cost-effectiveness. Conclusions The comprehensive community intervention and management of patients with dyslipidemia was effective in terms of health economics and it is worth the long-term implementation and promotion in the community health service center.

Objective To study the effects of salt and cooking oil intervention among hypertensive patients on knowledge-attitude-practice. Method Three thousand hypertensive patients from 20 community health service centers in Shenzhen were chosen by multi-stage cluster random sampling method. Salt measuring spoons and scaled oil pots were provided during six-month health intervention. Before and after the six-months health intervention, 2 976 and 2 864 valid questionnaires were collected respectively. After intervention, 40 families were randomly selected to perform an investigation of cooking oil and salt weighing during 3 d 24 h. Result Before the intervention, the rates of awareness on the intake of salt and cooking oil were 29.94% and 16.23% respectively. After intervention, the rates increased to 88.58% (P<0.000 1) and 84.29%(P<0.000 1) respectively. The rates of restriction on the intake of salt and cooking oil were 62.97% and 59.07%, respectively, after the intervention, the rates were 97.14% and 96.79% (P<0.000 1), respectively. By using the salt measuring spoons and scaled oil pots, the intake of cooking oil and salt reached the recommended amount in Chinese dietary guideline. Conclusion The implementation of health education combined with appropriate tools could promote the knowledge and behavior of the salt and cooking oil consumption.

Objective To realize the bacterial contamination on uniforms of health care workers(HCWs)in a gen-eral hospital,and put forward the corresponding management measures.Methods In May-October 2012,a total of 360 specimens of 120 uniforms of HCWs in departments of respiratory internal medicine,general surgery,gynecolo-gy,and pediatrics were taken on the first,third and seventh day of wearing,bacterial counts on uniforms were mo-nitored,compared and analyzed.Results Bacterial counts of uniforms at different wearing time were statistically differ-ent.The longer time of uniforms were worn,the more bacteria could be detected.Bacterial contamination of nurses’uni-forms was more serious than doctors ([0.65±3.38]CFU/cm2 vs [7.68±2.99]CFU/cm2 ),contamination of uniforms of HCWs in surgical departments was more serious than non-surgical departments([10.43±4.12 ]CFU/cm2 vs [8.60± 3.01]CFU/cm2 )(U=5.06,2.78,respectively,both P<0.01),over standard rate of different sites of HCWs’uniforms were significantly different(χ2 =33.12,P<0.01));over standard rates of bacteria on the cuffs,abdomen and chest sites was 73.33%,58.33% and 36.67% respectively.Conclusion The management of cleaning system of HCWs’uniforms needs to be strengthened,the change cycle of uniforms is suggested twice a week,and the frequency needs to be increased in high contamination departments.

Objective To analyze a potential outbreak mechanism 0f Pseudomonas eruginosa by investigating the homology of pan-drug resistance isolates(PDR)isolated in four hospitals of Guangzhou from March 2005 to March 2007.Methods The pulse-field gel lectrophoresis(PFGE)was used to detectl34 strains of pan-drug resistant Pseudomonas eruginosa in four hospitals,and determined whether they were derived from the same clone.Results 1 34 strains were classified into 56 types based on PFGE pattern. Type A Was the commonest clone among four hospitals,45 strains belonged to type A,mainly spreaded in hospital A. The rest strains were identified:7 for type B,6 for type C,6 for type D,which were isolated from hospital B to hospital D,respectively.There were 40 strains classified for individual types.General comparison showed there Was no a large clone existing in all four hospitals,though type Q clone appeared in hospital B and hospital D.One strain from hospital B and one strain from hospital C had 80%homology with type A from hospital A.The environment survey showed there was no clonal strain of type A found in hospital A,although various samples from respiratory therapy equipment,bronchoscopes and medical erosols were collected and cultivated for three times during the period.However,six patients arrying type A Pseudomonas aeruginosa had been admitted to the same ICU of hospital A for many times.Analysis of antimicrobial resistance of the common clone from four hospitals revealed that 42 of 43 type A of Pseudomonas aernginosa produced IMP-9 metallo β-lactamase.The strains of type B,type C and type D didn't produced metallo B. 1actamase.Conclusions The various degree of clonal spread of pan-drug resistance Pseudomonas aeruginosa had occurred in four hospitals individually in two years.There Was also clonal spread among some hospitals. It is important to monitor the patients colonized with epidemic clones to prevent clonal spread.