Objective To explore the reporting process of our health risk warning system and its long-term effectiveness.Methods A total of 1 168 individuals who were identified as higher risk populations from July 2011 to June 2012 in our Health Mangement Center were served as the control group,and another 973 adults who were identified as higher risk individuals from July 2012 to May 2013 were assigned to the study group.Diagnosis and treatment were based on our health risk reporting process and follow-up system.Paired t test and paired contingency table x2 test were used for data analysis.Results The rate of follow-up (97％ vs 100％,x2=30.503,P＜0.05),consultation (83.48％ vs 93.63％,x2=52.142,P＜ 0.05),mean treatment time ((3.0±0.5) vs (1.5±0.5) d,t=69.12,P＜0.05) and patient satisfaction (87.84％ vs 96.20％,x2=48.361,P＜0.05) were significantly different between the two groups,although no statistically significant difference of incidence of adverse events was found (0.26％ vs 0.10％,x2 =0.102,P＞0.05).Conclusion Our health risk warning system may reduce the time for physical examination and improve disease diagnosis level and patients' satisfaction.Moreover,our health manatement system and health service quality should further be improved in practice.

Objective To observe the relationship between clinical medication and the prognosis in elderly community-acquired pneumonia (CAP).Methods A prospective randomized controlled single-blind study in Tianjin Hospital Internal Medicine.A total of 160 elderly patients with CAP were selected from January 2011 and January 2015.According to the computer,patients were randomly divided into treatment group and control group,80 cases in each group.Treatment group adopted routine treatment and moderate amount of glucocorticoids in combination with a low-dose of diuretic,and the control group only received routine treatment.In two groups of patients,we observed the initial treatment effect,change in pulse oxygen saturation,the rate of invasive test,the incidence of adverse reactions,mortality rate,total hospital stay,etc.Results Compared with control group,the initial treatment was better,the improvement rate in SPO2 was increased,and the rate of invasive test was decreased in treatment group 72 hours after treatment (x2 =6.234,3.906 and 7.059,respectively,P=0.013,0.048 and 0.008).After the overall prognosis and outcome analysis,compared with control group,the percentage of patients transferred to the intensive care unit,the mortality rate was decreased (x2=4.783 and 4.737,P=0.029 and 0.030),hospitalization cost was declined,and the total hospital stay was shorted (x2 =-72.087 and-5.127,both P＜0.0001).There was no statistically significant difference in the incidence of adverse reactions such as electrolyte disorder and mental disorder(both P＞0.05).Conclusions Corticosteroids in combination with a low-dose of diuretic for the auxiliary treatment of elderly CAP can reduce the mortality rate,decrease the rate of invasive test,and shorten the duration of hospitalization,with no obvious increase of adverse events,and it help to improve the prognosis of CAP patients.

AIM:NLRP3 inflammasome was identified as the cellular machinery responsible for activation of inflammatory processes .The present study investigated whether the activation of NLRP 3 inflammasomes contributes to hyperhomocysteinemia ( HHcy)-induced in-flammation and atherosclerosis .METHODS:ApoE-/-mice were fed regular diet , high fat ( HF) diet or HF plus high methionine (HM) diet for 10 weeks.NLRP3 shRNA or scramble shRNA viral suspension was injected twice at the 2nd and the 6th weeks after HFHM treatment.The whole aortas and aortic root sections were stained with Oil Red O for atherosclerotic lesion .Plasma lipids, ho-mocysteine ( Hcy) , IL-1βand IL-18 levels were measured .We also examined the effect of Hcy on NLRP 3 inflammasomes activation in THP-1 differentiated macrophages in the presence or absence of NLRP 3 siRNA, caspase-1 inhibitor Z-WEHD-FMK, or antioxidant N-acetyl-L-cysteine ( NAC) .RESULTS:HFHM treatment induced HHcy in ApoE-/-mice.Increased plasma levels of IL-1βand IL-18, aggravated macrophage infiltration into atherosclerotic lesion , and accelerated development of atherosclerosis were detected in HHcy mice, which were associated with the activation of NLRP 3 inflammasomes.Silencing the NLRP3 gene significantly suppressed NLRP3 inflammasomes activation , reduced plasma levels of proinflammatory cytokines , attenuated macrophage infiltration , and improved HHcy-induced atherosclerosis .Moreover, we found that Hcy activated NLRP3 inflammasomes and promoted subsequent production of IL-1βand IL-18 in macrophages, which were blocked by NLRP3 gene silencing, Z-WEHD-FMK, or NAC.CONCLUSION:These data suggest that the activation of NLRP 3 inflammasomes contributes to HHcy-induced inflammation and atherosclerosis .Hcy activates NLRP3 inflammasomes in reactive oxygen species dependent pathway in macrophages .

Objective:To observe the change of periphery and centra lymphocyte subsets at the crest-time of MOG_(35-55) induced EAE disease in mice,and to explore the alteration of cellular immunity and humoral immunity in the invasion process in EAE.Methods:MOG_(35-55) was used to establish EAE model in femina C57BL/6 mice.The behavioral changes and the histological scores were recorded after the mice were immuned .The changes of CD3~+CD4~+,CD3~+CD8~+,CD4~+CD25~+ and B220~+ on periphery and centra lymphocytes in spleen,brain and spinal cord were analyzed by flow cytometry.Results:The CD3~+CD4~+,CD3~+CD8~+,CD4~+CD25~+ and B220~+ lymphocytes were detected in the brain and spinal cord of EAE group mice,but they were not detected in CFA control group.The CD3~+CD4~+ and CD3+CD8+lymphocytes in the spleen of EAE crest-time group were lower than those in CFA control group(P＜0.05).The B220~+ lymphocytes were obviously higher than in the CFA control group (P＜0.01).And CD4~+CD25~+ lymphocytes were slight higher than the CFA control group.Conclusion:At the crest-time during EAE,the CD3~+CD4~+,CD3~+CD8~+lymphocytes of spleen reduced obviously,B220~+ lymphocytes increased markedly,and the CD4~+CD25~+ lymphocytes just have the increasing trend.It indicates that cellular immunity and humoral immunity coregulated the patho-process at the crest-time of EAE,T lymphocytes and B lymphocytes all played important roles in the pathogenesy of EAE.

BACKGROUND: Cerebrovascular disease often causes dysfunction of the brain nerve, and nerve cel apoptosis is the important factor of cerebral nerve dysfunction. The excessive expression of c-fos can block the transduction of intracelular signal so that producing some apoptosis-promoting factors, which involve in nerve cel apoptosis process after ischemia injury of brain. Bcl-2 is an inhibited factor. It might to be the key to treat ischemic cerebrovascular disease by inhibiting or reducing the apoptosis of nerve cels after ischemia injury. OBJECTIVE: To investigate the therapeutic effect and mechanism of the Total Flavone of Hawthorn Leaf on chronic cerebral ischemia rats. METHODS: A total of 72 healthy male Sprague-Dawley rats were randomly divided into sham surgery group, model group, Total Flavone of Hawthorn Leaf group and ginkgo leaf group. Permanent bilateral carotid artery ligation was used to prepare chronic cerebral ischemia model in the model group, Total Flavone of Hawthorn Leaf group and ginkgo leaf group. Total Flavone of Hawthorn Leaf group and ginkgo leaf group respectively received 140 mg/kg Total Flavone of Hawthorn Leaf and 12.3 mg/kg ginkgo leaf intragastricaly for 36 days from 36 days after model induction. Model group and sham surgery group received 3.5 mL/kg physiological saline intragastricaly. RESULTS AND CONCLUSION: Compared with the model group, the expression of c-fos protein significantly deceased in the Total Flavone of Hawthorn Leaf group (P < 0.01), Bcl-2 expression levels significantly increased (P < 0.01), and Ca2+ content decreased (P < 0.05). Moreover, no significant difference in above indexes was detected between Total Flavone of Hawthorn Leaf group and ginkgo leaf group (P> 0.05). These data indicated that the protective effect of Total Flavone of Hawthorn Leaf on chronic cerebral ischemia was associated with its inhibition of neuronal apoptosis. Its mechanism of anti-apoptosis might be associated with up-regulating expression of Bcl-2, down-regulating expression of c-fos and decreasing Ca2+ content in brain.

Chronic pulmonary aspergillosis (CPA) is a serious fungal infection, which complicates pulmonary tuberculosis, chronic obstructive pulmonary disease and sarcoidosis with high mortality. At present, the treatment of CPA include drug treatment and surgical treatment. The treatment plan should be determined by the type, clinical manifestations and surgical indications of the patients. Nevertheless, there is no standard plan, and more research is needed to improve it. Combined with the current literature reports, this article reviews the current and progress in the treatment of CPA.

OBJECTIVE: To explore the effects of matrine on the proliferation, tumor cell stemness, β-catenin transcriptional activity and AKT/GSK3β/β-catenin signaling pathway in human hepatocellular carcinoma (HCC) HepG2 and Huh7 cells. METHODS: The proliferation and colony formation ability of HepG2 and Huh7 cells treated with 200, 400, and 800 μg/mL matrine were evaluated with MTT assay and colony formation assay, respectively. Real-time quantitative PCR was performed to detect the mRNA expressions of CD90, epithelial cell adhesion molecule (EpCAM) and CD133, and dual-luciferase assay was used to detect the transcriptional activity of β-catenin in the treated cells. The effects of matrine on the expressions of protein kinase B (AKT), P-AKT, GSK-3β, P-GSK-3β, P-β-catenin and β-catenin proteins in the Wnt/β-catenin signaling pathway were assessed using Western blotting. RESULTS: Matrine inhibited the proliferation of the two HCC cell lines in a time- and concentration-dependent manner. The half-inhibitory concentrations of matrine were 2369, 1565 and 909.1 μg/mL at 24, 48 and 72 h in HepG2 cells, respectively, and were 1355, 781.8, and 612.8 μg/mL in Huh7 cells, respectively. Matrine concentrationdependently suppressed colony formation of the HCC cells, producing significant inhibitory effects at 400 μg/mL < 0.01) and 800 μg/mL < 0.001) in HepG2 cells and at 200 μg/mL < 0.05), 400 μg/mL < 0.01), and 800 μg/mL < 0.001) in Huh7 cells. Matrine at 400 and 800 μg/mL significantly inhibited the mRNA expression of CD90, EpCAM and CD133 and the transcriptional level of β-catenin in both HepG2 and Huh7 cells < 0.05 or 0.01). Matrine at 400 and 800 μg/mL also significantly decreased the protein levels of β-catenin, P-AKT and P-GSK-3β and increased the phosphorylation level of β-catenin in both of the cell lines. CONCLUSIONS Matrine inhibits the proliferation, colony formation, and the expressions of tumor stem cell markers CD90, EpCAM and CD133 in both HepG2 and Huh7 cells probably by inhibiting Wnt/β-catenin signaling pathway and the transcriptional activity ofβ-catenin.

Humans ; Thyrotoxicosis/chemically induced* ; Amiodarone