An investigation has been conducted on the pilot projects of community health services in Chang zhou City and an analysis made of several issues hindering the full functioning of the services. The following sugges tions are then put forward. ① Leadership in community health services should be strengthened in real earnest. ② Methods of compensating funds for commmunity health services should be further improved. ③An effective management system and operating mechanism should be established and perfected. ④The building of a contingent of community health services personnel should be enhanced. ⑤Educational campaigns should be conducted at various levels. ⑥A good job should be done of community health services along the lines of reform.

Objective To determine whether peritoneal mesothelial cells express CD40 and to investigate potential mechanism by which CD40-CD40 ligand(CD40L) interaction may be involved in the inflammation of peritoneal membrane. Methods Rat peritoneal mesothelial cells (MC) were harvested from peritoneal cavity and maintained under defined in vitro conditions. Expression of CD40 on MC under normal culture or stimulation with interferon-?(IFN-?), tumor necrosis factor-?(TNF-?), interleukin(IL)-1 was examined by RT-PCR and FACS analysis. After activation with CD40 mAb, the expression of intercellular adhesion molecule-1 (ICAM-1) on MC was analyzed by FCAS. Results MC cultured in vitro expressed CD40 constitutively. The expression of CD40mRNA and CD40 protein up-regulated markedly following the stimulations with IFN-?, but not with IL-1, TNF-?. The expression of ICAM-1 on MC was significantly increased after activation of CD40 with IFN-? and CD40mAb. Conclusions MC functionally expresses CD40. The interaction of CD40 on MC and CD40L+ cells in peritoneal cavity may play an important role in peritoneal local defense and may be involved in the inflammation process of peritoneum.

Objective To observe the changes of four quantitative indexes of diabetic macular edema by using optical coherence tomography.Methods Eighty-nine patients (155 eyes) with diabetic retinopathy were included in this project and were divided into two groups according to the present of diabetic macular edema:Negative group (56 cases,100 eyes) and positive group(33 cases,55 eyes).In addition,23 cases (42 eyes) of normal volunteers constituted the normal control group.All the objects accepted an optical coherence tomography examination and the indexes including central retinal thickness (CRT),subfoveal choroidal thickness (SFCT) and integrity of external limiting membrane(ELM) as well as inner/outer segment (IS/OS) were measured and analyzed.Results The average CRT of positive group (219.048 ± 16.798) μm was significantly thicker than that of control group(217.775 ± 26.866) μm and negative group (280.418 ±74.187) μm (P ＜0.001).Mean SFCT among control group (312.893 ±140.559) μm,negative group (302.080 ± 125.287) μm and positive group (293.745 ±140.517) μm had no statistical significance (P =0.781).There were 3 eyes with disrupted ELM layer in the negative group and 8 eyes in the positive group.Difference between them was proved to be significant (P =0.019).Similarly,the integrity of IS/OS layer had significant difference between negative group (5 eyes disrupted) and positive group (19 eyes disrupted) (P ＜ 0.001).Conelusion CRT of patients with diabetic macular edema is always increased and the integrity of ELM or (and) IS/OS can be disrupted in many cases.Indexes including CRT and the integrity of ELM or (and) IS/OS can be used to evaluate the severity of diabetic macular edema quantificationally.

OBJECTIVE:To explore the effects and safety of atorvastatin combined with probucol on the vascular elasticity in patienits with hypertension. METHODS:246 hypertensive patients were randomly divided into control group and observation group,123 cases in each group. All patients received conventional antigypertensive treatment,based on it,control group was given 10 mg Atorvastatin tablet,qd;observation group was additionally given 0.25 g Probucol tablet,qd,on the basis of control group. They were treated for 1 year. Clinical efficacy,lipid levels(total cholesterol,triglyceride,low density lipoprotein cholesterol,high density lipoprotein cholesterol),cystatin C (Cys-C),C-reactive protein (CRP),elastic parameters of common carotid artery and lower limb artery(stiffness,pressure-strain elastic modulus,compliance,augmentation index,pulse wave velocity)before and af-ter treatment in 2 groups were observed,and the incidence of adverse reactions was compared. RESULTS:Before treatment,there were no significant differences in lipid levels,Cys-C,CRP and elastic parameters of common carotid artery and lower between 2 groups (P>0.05);after treatment,the above-mentioned indexes were significantly improved,and the improvement degree in ob-servation group was superior to control group,the differences were statistically significant(P<0.05). And there were no severe ad-verse reactions during treatment in both 2 groups. CONCLUSIONS:Atorvastatin combined with probucol can improve lipid level and elasticity of common carotid artery and lower limb artery,with good safety.

Objective To investigate the association of T help (Th) lymphocyte and heart rate variability (HRV) in congestive heart failure (CHF) patients. Methods Ninety-six patients with CHF and thirty healthy persons were enrolled in the study. Time-domain HRV analysis was performed based on 24 hour Holter Electrocardiogram (ECG) monitoring. Interferon-γ (IFN-γ) was used as markers for the differentiation of Th1 subsets and interleukin-10 (IL-10) for the Th2 subsets. IFN-γand IL-10 in CD4 + T lymphocytes were quantified by 3-color flow cytometry. Results The frequency of IL-10-Producing T Cells in the CHF group was significantly lower than those in the healthy control ( ( 16.4 ± 5.8 ) % vs. ( 26.8 ± 3.7 ) %, t = 9. 243, P ＜ 0. 001 ). The frequency of IFN-γ in the CHF group ( ( 18.4 ± 7.3 )% ) was significantly lower than that in the healthy controls ( (7.3 ±4.6) % ,t =7. 917, P ＜ 0. 001 ). The following index of HRV in the CHF groups were all significantly lower than those in the healthy controls: (98. 6 ± 21.3) ms vs. ( 145. 1 ± 42. 6) ms for SDNN, (83. 9 ± 22.4) ms vs.(136.5 ±39.6)ms for SDANN, (40.6 ± 14.5) ms vs. (55.8 ± 17.9) ms for SDNNI, (20. 7 ± 12.9) ms vs.(29.1 ± 12.6) ms for RMSSD, (5.6 ± 3.7 ) % vs. ( 11.8 ± 4.4) % for PNN50 ( Ps ＜ 0.05 ). In CHF patients, the frequency of IL-10 were positively associated with SDNN, SDANN, SDNNI, RMSSD and PNN50 ( r = 0. 49,0. 57,0. 58,0.47 and 0. 52 ,respectively,Ps ＜ 0.01 ). In the CHF patients, the frequency of IFN-γand IFN-γ/IL-10 ratio were negatively associated with SDNN ,SDANN ,SDNNI, RMSSD and PNN50 ( r = - 0. 49, - 0. 54, - 0. 57, - 0.52,- 0.53, - 0. 52, - 0.64, - 0.57, - 0. 58, - 0. 67, Ps ＜ 0. 01 ). Conclusions Autonomic nervous system is involved in the regulation of the balance of Th1/Th2 in patients with CHF. Sympathetic nerve system enhances the effect of Th1 ,whereas parasympathetic nervous system enhances the effect of Th2.

AIM: The aim of this study was to reveal the regulatory role of glutathione (GSH) in the transcriptional activity of activating transcription factor-2 (c-Jun/ATF-2) and nuclear factor-?B (NF-?B) of macrophages induced by angiotensin Ⅱ(AngⅡ). METHODS: Macrophage intracellular GSH was determined by fluorophotometry, and buthionine-[S,R]-sulfoximine(BSO)was used for depletion of intracellular GSH. The phosphorylation of c-Jun/ATF-2 and expression of NF-?B p65 were determined by immunoblot, and the activity of NF-?B was determined by electrophoresis mobility shift assay (EMSA). The c-Jun/ATF-2 was also determined by Immunohistochemical staining. RESULTS: The GSH content in the macrophage was decreased in cells that were lipid-peroxidized with AngⅡ (1.0 (?mol/L)) for 30 min and 60 min, respectively, followed by an adaptive GSH increase in the presence of AngⅡ (1.0 (?mol/L)) for longer time. In parallel, exposure to AngⅡfor 60 min also decreased macrophage GSH content in a dose-dependent manner. The GSH of RAW 264.7 cells were depleted by BSO, a specific inhibitor of GSH synthesis, and incubation for 18 h with 0.5 mmol/L BSO was sufficient for complete depletion of intracellular GSH. The phosphorylation of c-Jun/ATF-2 could be induced by the AngⅡ (1.0 (?mol/L)), whereas it did not occur in glutathione-depleted RAW 264.7 macrophages. The activation of NF-?B could also be induced by the AngⅡ (1.0 (?mol/L)), but it did not occur in glutathione-depleted RAW 264.7 macrophages. CONCLUSION: These data provide evidences that the intracellular glutathione redox may participate in the regulation of transcription activity of c-Jun/ATF-2 and NF-?B in macrophages. [

ated acute peritonitis induced by LPS in rats.

Objective To investigate the effects of angiotensin Ⅱ (Ang Ⅱ) on the expression of TLR4 and its role in lipopolysaccharide (LPS)-induced NF-κB activation and CD40 expression in rat peritoneal mesothelial cells (RPMCs). Methods RPMCs were harvested from Spragne-Dawley rat peritoneal cavity and maintained under defined in vitro condition. The cells were treated with Ang Ⅱ at different concentrations (10-9, 10-8, 10-7, 10-6 mol/L) and exposed to Ang Ⅱ (10-7 mol/L) for different times (1, 2, 4, 8, 12, 24, 48 h for mRNA and 6, 12, 24, 36, 48 h for protein, respectively). Meanwhile, the influence of AT1 receptor antagonist (AT1R, losartan, 10-5 mol/L) and AT2 receptor blocker (AT2R, PD123177, 10-5 mol/L) on the TLR4 induced by Ang Ⅱ was observed. After synchronization for 24 hours, the cells were randomly assigned to four groups: the control group, the Ang Ⅱ (10-7 tool/L) group, the LPS (1 mg/L) group, the Ang Ⅱ (10-7 mol/L) plus LPS (1 mg/L) group, which were used to investigate the effects of Ang Ⅱ on the NF-κB activation and CD40 expression induced by LPS. The mRNA expression of TLR4 and CD40 was measured by RT-PCR and the protein abundance of TLR4, NF-κB p65, phospho-p65, IKBα and phospho-IκBα were analyzed by Western blot. Immunofluorescence was performed to determine the subcellular localization of p65 subunit of NF-κB. Results (1) Treatment of RPMCs with Ang Ⅱ resulted in a concentration-dependent increase in the expression of TLR4. Ang Ⅱ at 10-9, 10-8, 10-7 and 10-6 mol/L increased TLR4 mRNA expression by 70.5%, 89.5%, 102.9%, and 121.9%, respectively and protein expression by 12.1%, 27.7%, 51.2%, and 41.6%, respectively (P<0.01). Treatment of RPMCs with 10-7 mol/L Ang Ⅱ resulted in a time-dependent increase in the expression of TLR4, with the peak of mRNA expression at 8 and 12 h (P<0.01) and the protein expression at 12 and 24 h (P<0.01). (2) Losartan antagonized Ang Ⅱ-stimulated expression of TLR4 by 33.5% (P<0.05), PD123177 had no such effect (P0.05). (3) Treatment of RPMCs with LPS (1 mg/L) for 60 rain significantly increased the ratio of phospho-IκBα to IκBα by 362.6% (P< 0.01) , phospho-p65 to p65 by 67.4% (P<0.05), and LPS (1 mg/L) for 4 h significantly increased the expression of CD40 mRNA by 299.9% (P<0.01) compared to the control group. In comparison to the LPS (1 mg/L) group, preincubation of RPMCs with AngⅡ (10-7 mol/L) for 24 h then treated with LPS (1 mg/L) for 60 rain significantly increased the ratio of phospho-IκBα to IκBα by 49.1% (P<0.01), phospho-p65 to p65 by 29.3%(P<0.05), and LPS (1 mg/L) for 4 h significantly increased the expression of CD40 mRNA by 56.8%(P<0.01). (4) The p65 subunit of NF-κB was dominantly distributed in the cytoplasm in the control and Ang Ⅱ group. Following exposure to LPS for 60 min, p65 subunit labeling was upregulated and translocated into the nuclei. A significantly increased nuclear staining of p65 in ceils treated with Ang Ⅱ plus LPS were observed. Conclusions Ang Ⅱ induces the expression of TLR4 in dose- and time-dependent manner in RPMCs, resulting in enhanced NF-κB signaling and induction of CD40 expression, Locally produced Ang Ⅱ in the peritoneum may play an amplified role in LPS-induced peritoneal inflammation.

Objective To investigate the role of C-Jun N-terminal kinase (JNK) in epithelial mesenchymal transition (EMT) induced by transforming growth factor β1 (TGF-β1) in rat peritoneal mesothelial cells(RPMCs). Methods RPMCs were harvested from the peritoneum of male Sprague-Dawley rats, then cultured in DMEM/F12 medium with 15% (V/V) FBS. After stimulation with TGF-β1, the expression of a-smooth muscle actin (α-SMA), E-cadherin and collagen I were detected in RPMCs. In some groups, the ceils were pretreated with SP600125, a specific inhibitor of JNK, for 4 hours before incubation with TGF-β1. The protein expression of phosphorylated JNK was detected by Western blotting. The mRNA and protein expression ofα-SMA, E-cadherin and collagen I were examined with RT-PCR and Western blotting, respectively.The intracellular distribution and expression of α-SMA was determined by indirect immunofluorescence. Results TGF-β1 could significantly increase the expression of α-SMA and collagen I, and decrease the expression of E-cadherin in RPMCs. TGF-α1 could stimulate the expression of phosphorylated JNK at 5 minutes with the peak at 10 minutes (P<0.01). The addition of SP600125 effectively inhibited TGF-β1-induced high expression of α-SMA and collagen I (P<0.05), and prevented TGF-β1-induced down-regulation of E-cadherin expression in RPMCs (P<0.05). The indirect immunofluorescence showed that the expression of intracellular α-SMA in RPMCs stimulated by TGF-β1 for 48 h increased significantly, which could be inhibited by SP600125. Conclusions JNK regulates epithelial mesenchymal transition induced by TGF-β1 in rat peritoneal mesothelial cells. JNK inhibitor may be used as a novel therapeutic agent for peritoneal fibrosis.

Objective To explore the effects of peroxisome proliferator-activated receptorγ (PPARγ) agonist rosiglitazone and 15-deoxy-delta-12,14-prostaglandin J2 (15d-PGJ2) on the expression of PPARγ, toll-like receptor 4 (TLR4) and the activation of STAT1 as well as the local inflammation reaction of abdominal cavity in sprague dawley (SD) rats with peritoneal dialysis- related acute peritonitis induced by lipopolysaccharide (LPS). Methods Twenty-four male SD rats were equally randomized to four groups(n=6 each): control group, injected with 4.25% dextrose peritoneal dialysate (PDF) via abdominal cavity(90 ml/kg); LPS group, injected with LPS(1 mg/kg) via abdominal cavity 4 hours later follewed by PDF injection; rosiglitazone plus LPS group (Rosi group), preconditioned with rosiglitazone (20 mg·kg-1·d-1) by intragastric way for 3 days, then injected with LPS and PDF via abdominal cavity; 15d-PGJ2 plus LPS group (15d-PGJ2 group), preconditioned with 15d-PGJ2 (0.3 mg·kg-1·d-1)via abdominal cavity injection for 3 days, then injected with LPS and PDF via abdominal cavity. The rats were killed 4 hours after PDF injection, IL-6 level in abdominal dropsy was determined by ELISA. Peritoneum tissue was stained by Masson. Leucocyte count in abdominal dropsy was performed. The mRNA expression of PPARγ and TLR4 in peritoneum tissue was determined by RT-PCR; the protein expression of PPARγ, TLR4, p-STAT1 and STAT1 in peritoneum tissue was analyzed by Western blot. Results IL-6 level of abdominal dropsy in LPS group [median 268.53 (range 201.87-335.19) ng/L] was significantly higher than that of control group [median 147.62 (range 130.60-164.64) ng/L] (P<0.01). The IL-6 level of abdominal dropsy in Rosi group [median 110.20 (range 77.60-142.80) ng/L] was significantly lower than that of LPS group (P<0.05). Compared to that of control group, the edematous degree of peritoneum in LPS group was significantly severer, meanwhile, mRNA and proteins expression of PPARγ and TLR4 in rat peritoneum were also significantly higher (P<0.05, P<0.01). Compared to that of LPS group, the edematous degree of peritoneum in Rosi group was lighter, the expression of PPARγ and TLR4 mRNA was significantly up-regulated (P<0.05), meanwhile their proteins expression was down-regulated (P<0.05); and in 15d-PGJ2 group, the edematous degree of peritoneum, the expression of PPARγ mRNA and protein was also decreased (P<0.05), but TLR4 mRNA expression was up-regulated (P<0.01), however, its protein expression was down-regulated (P<0.05). There were no significant differences in leucocyte count of abdominal dropsy among the four groups. The p-STAT1 expression in the rats peritoneum induced by LPS was markedly increased by both rosiglitazone and 15d-PGJ2 (P<0.01). Conclusions Both rosiglitazone and 15d-PGJ2 can down-regnlate the inflammatory reaction in rat peritonitis induced by LIPS, which may be involved in modulating the expression of associated functional protein during LPS signal pathway.