Microfold cells or membraneous cells(M cell)are special differentiated cells of follicle associated epithelium(FAE) covered underlining lymphoid follicle,called organ-associated lymphoid tissue(OALT).M cells in the GI transport transcellularly antigens or organism selectively from the gut lumen and trigger the immune reaction.As doorkeepers,they manipulate the function channel of intestinal barrier.The features,and the important role in intestinal barrier of M cells are reviewed.

Objective To explore the differences of resistin level between Mongol and Han population in patients with metabolic syndrome and to analyze its related factors.Methods According to the diagnostic criterion of metabolic syndrome,30 patients with metabolic syndrome in Mongol population (group 1) and 28 patients with metabolic syndrome in Han population(group 2) were randomly selected from health examination population.Radioimmunoassay kit was used to examine the serum resistin level in patients with metabolic syndrome.At the same time,their weight,height,blood pressure,blood glucose,blood lipid [high density lipoprotein (HDL),low density lipoprotein (LDL),total cholesterol (TC),glycerin three greases (TG)],blood uric acid (UA),leptin,insulin were measured,and body mass index(BMI) and insulin resistance index(HOMA-IR) were counted and compared.Results There were significant differences in systolic pressure,leptin,resistin,blood insulin and HOMA-IR between the two groups(all P ＜ 0.05).There were no significant differences in age,diastolic pressure,BMI,HDL,LDL,TG,TC,UA and blood glucose between the two groups(all P ＞0.05).The increase of resistin level in group 1 was associated with UA,systolic pressure and HOMA-IR(r =0.357,0.427,0.582,all P ＜ 0.05).Conclusion The serum resistin level of patients with metabolic syndrome in Mongol population is correlated with UA,systolic pressure and insulin resistance index,and maybe play an important role in the development of metabolic syndrome.

Objective To investigate the differences of leptin (LEP) between Mongol and Han population with metabolic syndrome (MS) and its related factors.Methods According to the diagnostic criterion of MS,291 people with MS were selected as subjects,of which,146 were Han nationality(A group) and 145 were Mongol(B group).Radioimmunoassay kit was used to measure the serum leptin level.At the same time,the indices including weight,height,blood pressure,blood glucose,blood lipid,Serum uric acid (sUA),insulin (Fins),body mass index (BMI) and insulin resistance index (HOMA-IR) were measured.Results The following indices in B group including fasting plasma glucose (FPG),Low-density lipoprotein cholesterol (LDL-C),leptin,blood insulin,insulin resistance index were (6.2 ± 1.5) mmol/L,(3.1 ± 0.8) mmol/L,(4.3 ± 2.0) μg/L,(22.4-± 16.0) mU/L and (6.5 ± 0.5) respectively,significantly differed from that of A group ((6.7 ±1.7) mmol/L,(2.7 ±0.7) mmol/L,(3.4 ± 1.5) μg/L,(18.8 ±14.0) mU/L,(4.7 ±3.6)respectively;t =2.04,2.84,3.47,2.18,4.82 ;P ＜ 0.01 or P ＜ 0.05).There was no significant difference in terms of age((46.9 ±9.8) vs.(46.3 ± 8.4)),systolic blood pressure (SBP) ((146.8 ± 17.0) mm Hg vs.(149.1 ±19.2) mm Hg),diastolic blood pressure (DBP) ((90.5 ± 11.6) mm Hg vs.(92.5 ± 13.1) mm Hg),BMI ((27.4 ± 2.9) kg/m2 vs.(27.9 ± 3.2) kg/m2),total cholesterol (TC) ((5.5 ± 1.0) mmol/L vs.(5.5 ±0.9) mmol/L),triacylglycerol (TG) ((2.3 ± 1.4) mmol/L vs.(2.3 ± 1.4) mmol/L),high density lipid cholesterol (HDL-C) ((1.3 ±0.3) mmol/L vs.(1.2 ±0.4) mmol/L),and sUA (((320.7 ±93.6)μmol/L) vs.(308.7 ±86.9) μmol/L) between the patients with metabolic syndrome in Mongol population and in Han population(t =0.47,0.90,1.15,1.15,0,0,1.00,0.94 respectively,P ＞ 0.05).The increase of leptin level in the patients with metabolic syndrome in B group was associated with blood glucose,blood insulin and insulin resistance index (r =0.108,0.146,0.183 ; P ＜ 0.05).BMI,blood insulin and insulin resistance index may be the factors due to the higher of serum leptin levels.Conclusion The serum leptin of patients with metabolic syndrome in Mongol population are correlated with blood glucose,blood insulin and insulin resistance index,which plays an important role in the development of metabolic syndrome.

BACKGROUND:Presently,cartilage defect is mainly treated by autologous cartilage transplantation,which cannot be accepted by patients.With development of tissue engineering,mesenchymal stem cells have been a hot focus in research.Most scholars believed that dynamic stress,hypoxia and some growth factors are advantageous factors for differentiation of bone marrow mesencymal stem cells into chondrocytes,which suggest microenvironment of the joint cavity.OBJECTIVE:To establish a method for isolating bone marrow mesenchymal stem cells,to found a microenvironment of the joint cavity,and to observe outcome of injure repair by transplanting autologous bone marrow mesenchymal stem cells into cartilage injured region of rabbits,which is covered by periosteum.DESIGN,TIME AND SETTING:The randomized,controlled animal experiment was performed at the Laboratory of Department of Orthopaedics,Second Hospital,Shanxi Medical University from July 2005 to July 2007.MATERIALS:A total of 24 New Zealand rabbits were selected for creating models of articular cartilage injury.METHODS:Rabbit bone marrow mesenchymal stem cells were collected and purified using density gradient centrifugation,and amplified by in vitro adherence method.Twenty-four rabbits were randomly assigned into three groups(n=8).In the non-induced bone marrow mesenchymal stem cells + periosteal flap group,bone marrow mesenchymal stem cells were implanted into articular cartilage defects of rabbit knees and covered by autologous periosteal flap.In the periosteal flap group,periosteal flap was used to cover the injured region.Rabbits in the blank control group were left intact.MAIN OUTCOME MEASURES:Repair tissues of rabbits were examined at 6 and 12 weeks after surgery.RESULTS:In the non-induced bone marrow mesenchymal stem cells + periosteal flap group,the defects were filled with hyaline-like cartilage at 6 weeks.Cartilage and the subchodral bone were remodeled at 12 weeks after surgery.The expression of type Ⅱ collagen in the repair tissues was verified by immunohistochemistry.In the periosteal flap group,the defects were partly filled with chondrocytes-like in the surface and basement.In the blank control group,fibrous tissue repair was presented,with a few cartilage-like cells in the basement.CONCLUSION:Following comparison of results from three groups,in vitro cultured rabbit bone marrow mesenchymal stem cells and periosteal transplantation can enhance repair of articular cartilage injury.This method can be an effective way for repairing injured articular cartilage,presently.

Objective To survey and analyze the etiology of pericardial effusion in different age patients. Methods The data of 450 patients who were diagnosed as pericardial effusion were studied retrospectively. The pathogenesis of pericardial effusion were analyzed and compared among the five age groups : juvenile group (0-19 years),young group (20-39 years),middle age group (40-59 years), aged group (60-79 years) and existed advanced age group (≥80 years). Results The different pathogenesis of pericardial effusion existed in different age groups. The first three causes are tumor, tuberculous, heart failure in all patients. As a pathogeny, cardiopulmonary insufficiency induced pericardial effusions constitute the majority (about 50%) in the advanced age group. Tumor, heart failure are the main causes in aged group. In middle age group, tumor and tuberculous are the most frequent pathogenesis, while the tuberculous is the principal causes in juvenile and young groups. Conclusions The rate of tumor, heart failure, lung infection raised along with the age increasing in the patients with pericardial effusion, meanwhile the cases of tuberculoses declined. Attention should be given to this tendency on the diagnosis and treatment of the patients with pericardial effusions.

ObjectiveTo determine the effect of unfractionated heparin (UFH) on lipopolysaccharide (LPS)-induced expression of granulocyte colony-stimulating factor (G-CSF), and the role of Toll-like receptor 4 (TLR4) signaling pathway in this process.Methods Human pulmonary microvascular endothelial cells (HPMECs) were cultured in vitro, and the cells between passages 3 and 5 were used in the experiments. ExperimentⅠ: the cells were divided into four groups as follows: control group, LPS stimulation group (LPS 10μg/mL), LPS+ 0.1 U/mL UFH group, and LPS+ 1 U/mL UFH group. HPMECs in UFH groups were treated with 0.1 U/mL or 1 U/mL UFH 15 minutes before LPS stimulation, and HPMECs in control group were treated with an equal volume of phosphate-buffered saline (PBS) instead. The concentrations of interleukin-6 (IL-6) and G-CSF in cell culture supernatants were determined by enzyme linked immunosorbent assay (ELISA) 24 hours after LPS challenge to detect the effect of UFH on HPMECs. ExperimentⅡ: HPMECs were treated with 5μg/mL of rhodobacter sphaeroides LPS (LPS-RS, antagonist for TLR4) 4 hours before the addition of PBS or LPS. The concentrations of IL-6 and G-CSF in cell culture supernatants were determined 24 hours after LPS stimulation to detect the effect of TLR4 on LPS-induced HPMEC injury. ExperimentⅢ: HPMECs were divided into four groups as before: control group, LPS stimulation group, LPS+ 0.1 U/mL UFH group, LPS+ 1 U/mL UFH group. Treatments to cells were the same as experimentⅠ. The protein expression of TLR4 in HPMECs was determined by Western Blot 1 hour after LPS stimulation to detect the effect of UFH on TLR4.Results① Compared with control group, the levels of IL-6 and G-CSF in LPS stimulation group were increased [IL-6 (ng/L): 655.9±58.3 vs. 75.5±18.2, G-CSF (ng/L): 388.7±36.2 vs. 35.3±12.6, both P< 0.05]. Compared with those of LPS stimulation group, in LPS+ 0.1 U/mL UFH group and LPS+ 1 U/mL UFH group, the levels of IL-6 and G-CSF were significantly decreased [IL-6 (ng/L): 518.2±64.6, 489.1±75.6 vs. 655.9±58.3, G-CSF (ng/L): 298.8±41.0, 273.4±33.2 vs. 388.7±36.2, allP< 0.05]. The results indicated that 1 U/mL UFH had better results, though there was no statistical significance between the results of two UFH groups.② LPS-induced up-regulation of IL-6 and G-CSF levels was prevented by LPS-RS [IL-6 (ng/L): 139.1±37.6 vs. 655.9±58.3, G-CSF (ng/L): 73.7±19.7 vs. 388.7±36.2, bothP< 0.05]. LPS-RS alone had no effect on cytokines [IL-6 (ng/L):118.2±42.1 vs. 75.5±18.2, G-CSF (ng/L): 48.4±26.8 vs. 35.3±12.6, bothP> 0.05].③ Compared with control group, the protein expression of TLR4 (grey value) in LPS stimulation group was significantly upregulated after 1 hour (0.87±0.23 vs. 0.36±0.12,P< 0.05). UFH with 0.1 U/mL and 1 U/mL lowered TLR-4 protein expression induced by LPS (0.68±0.18, 0.62±0.26 vs. 0.87±0.23, bothP< 0.05).ConclusionsThe expressions of IL-6 and G-CSF were increased obviously in LPS treated HPMECs. UFH might take its therapeutic effect through TLR4-dependent pathway.

Objective To study the in vitro larvicidal activity of nitric oxide (NO) to the juvenile Schistosoma japoni-cum. Methods Macrophages were induced by LPS or LPS + IFN-? to produce NO, schistosomula obtained mechanically from cercariae were added to the medium with activated macrophages, the larvicidal activity was observed within 48 h . In order to further confirm the effect of NO, an inhibitor of iNOS,L-NNA (N?-nitro-L-arginine), was used to inhibit the production of NO, larvicidal activity was measured by the same methods and the difference of dead larvae ratio was compared between the inhibited and uninhibited groups. Results LPS and LPS + IFN-? can induce macrophages effectively, with the NO production of (109.96?3.70)?mol/L and (113.50?7.38) ?mol/L respectively, accordingly the larvicidal effect reached to 91.07% ?2.92% and 96.86%?2.36% respectively. This activity can be inhibited by L-NNA. NO production and dead larvae ratio were reduced significantly in the inhibited group than in the uninhibited one. Conclusion NO produced by activated macrophages can kill schistosomula of Schistosoma japonicum.

Objective To study the expression of inducible nitric oxide synthase (iNOS) in livers of mice infected with Schistosoma japonicum. Methods The livers of NMRI mice infected with S. japonicum were collected on day 21, 28, 38, 45 post infection(p.i.), total RNA of livers were extracted and kinetics of the mRNA expression of iNOS were detected by RT-PCR, the protein expression of iNOS was then confirmed by Western blotting and the distribution of iNOS in the infected liver was determined by immunohistochemical methods. Results The mRNA expression of iNOS was not detectable in the uninfected liver, iNOS mRNA expression was detected on day 21 p.i, the expression increased on day 28 p.i and peaked on day 38 p.i, then decreased slightly on day 45 p.i. Western blotting showed an iNOS expression in the livers only on day 38, 45 p.i. IFA test showed that the expression of iNOS was maily distributed in the granuloma of the livers. Conclusion S. japonicum infection can induce the expression of iNOS in a time-dependent manner in the liver of the host,and eggs may be the main factor in inducing the expression.

Objective To evaluate the efficacy and safety of emergency percutaneous coronary intervention(PCI) in patients with non-ST-segment elevation acute coronary syndrome(ACS).Methods A total of 233 patients(emergency group) were treated with emergency PCI within 48 h of heart attack and another 152 patients(delayed group) were treated with PCI after 3-14 days of medical therapy.All culprit lesions were treated.Procedural success rate,the time from admission to angina relief,the length of hospital stay and cardiac events incidence in 30 days were observed.Results The procedural success rates for the emergency group and the delayed group were similar(98.1% vs 95.5%),but cardiac events incidence in 30 days was significantly lower in the emergency group than that of the delayed group(2.9% vs 14.1%,P

Objective To study the efficacy and safety of naftopidil,a new ? 1-adrenoceptor antagonist for treatment of benign prostatic hyperplasia(BPH). Methods A randomized,double-blind,double-simulant,parallel-controlled,multicentral clinical trial was conducted in 224 patients with BPH.Patients of treatment group received naftopidil (25 mg,once a day) and the controls received tamsulosin (0.2 mg,once a day). Results After 6-week therapy,IPSS,quality of life (QOL) score,maximum urinary flow rate (Qmax) and average urinary flow rate(Qave) were significantly improved both in naftopidil group and tamsulosin (control) group.In naftopidil group,IPSS was averagely decreased by 11.03 (P0.05).The clinical adverse event rate was 2.68% in naftopidil group, which was significantly lower than that in tamsulosin group (8.93%,P