Objective To explore the effect and its clinical significance of different dose of glucocorticoids on inflammation mediators in patients with acute exacerbation of chronic obstructive pulmonary diseases.Methods 45 patients admitted to our hospitals from March 2007 to March 2011 were randomly divided into 3 groups:methylprednisolone 40 mg group (methylprednisolone 40mg,iv,qd),methylprednisolone 80 mg group (methylprednisolone 80mg,iv,bid),and control group (without any glucocorticoids).The changes of dyspnea scores,arterial blood gas analysis,clinical symptom scores and serum IL-6,IL-8 and tumor necrosis factor (TNF) levels were detected in patients of each group before and at the 7th day after treatment.The related adverse drug reactions were recorded.Results The improvements in clinical symptom scores,Borg scores,PaCO2,PaO2 after treatment were higher in methylprednisolone 40 mg group and methylprednisolone 80 mg group than in control group (F=3.6747.162 and 42.88,respectively,P＜0.01 or 0.001),and the above improvements was better in methylprednisolone 80 mg group than in methylprednisolone 40 mg group (all P＜0.05).The decreases in levels of serum IL-8,TNF-α,IL-6,C-RP after the treatment were more significant in methylprednisolone 40 mg group and methylprednisolone 80 mg group than in control group (F=12.65,16.17,30.99,respectively,all P＜0.001),and the decrements were more significant in methylprednisolone 80 mg group than in methylprednisolone 40 mg group(all P＜0.05).NO serious adverse drug reactions happened during the course of treatment in the three groups.Conelusions Short-term and moderate dose of glucocorticoid treatment is effective and safe in treating the patients with acute exacerbation of chronic obstructive pulmonary diseases.Methylprednisolone 80 mg injection daily can more obviously improve AECOPD symptoms,and reduce the levels of inflammatory factors better.

AIM: To explore the pathological features of airway inflammation in patients with eosinophilic bronchitis(EB) and compared to those with cough variant asthma(CVA).METHODS: Flexible fibre optic bronchoscopy was performed in 11 patients with EB,10 with CVA,14 with bronchial asthma and 10 normal controls.The mean thickness of the basement membrane was measured by light microscopy.Using immunohistochemical and special staining,the localization and density of inflammatory cells(eosinophils,mast cells,T lymphocytes) were detected in bronchial submucosa in EB and CVA patients.RESULTS: The mean thickness of the basement membrane was significantly increased in the subjects with EB [2.92 ?m(2.10-6.50 ?m)],CVA [5.64 ?m(3.23-8.48 ?m)] and bronchial asthma [9.08 ?m(6.61-11.99 ?m)] rather than that in the normal controls [2.08 ?m(1.62-3.40 ?m)].There were also significant differences among the three groups.The number of mast cells and eosinophils in the bronchial submucosal from subjects with EB [75 cells/mm~2(35-112 cells/mm~2),7 cells/mm~2(0-31(cells/mm~2))] was substantially decreased than those in subjects with CVA [148 cells/mm~2(34-200 cells/mm~2),114 cells/mm~2((1-768 cells/mm~2));P

OBJECTIVETo summarize the clinical features of severe acute respiratory syndrome (SARS) and to discuss diagnosis and management of the disease.

METHODSA retrospective study was conducted on 78 cases of SARS referred to the Guangzhou Institute of Respiratory Diseases(GIRD) between December 22, 2002 and near the end of March 2003. Items reviewed cover all data concerning clinical manifestations, laboratory investigation and radiology.

RESULTSThe patients on the study consisted of 42 males and 36 females, aged 20-75 yrs (mean age 37.5 +/- 11.6 yrs), including 44 affected health-care professionals. Clinical symptoms seen in the group were fever (100.0%), cough (88.5%), and dyspnea (79.5%). There were 12 cases (15.3%) with WBCs < 4.0 x 10(9) /L, 49 cases (62.8%) ranging between (4.0 -10.0) x 10(9) /L and 17 cases (21.8%) over 10.0 x 10(9) /L. The average was (7.58 +/- 4.96) x 10(9) /L, with 0.75 +/- 0.14 (neutrophil) and 0.18 +/- 0.11 (lymphocyte). Chest films and CT scanning revealed changes related to pneumonia. The transmission of the disease was likely via close contact with contagious droplets. The prevalences of acute lung injury (ALI, in 37 cases) and acute respiratory distress syndrome (ARDS, 21 out of 37 cases) were considerably high among the patients. Seven patients who developed ARDS complicated with multiple organs dysfunction syndrome (MODS) died.

CONCLUSIONSA history of close contact, fever, sign of pneumonia by X-ray and normal-to-lowered WBC counts are favorable for the diagnosis of SARS. Recognition of ALI as the important index for critical SARS and comprehensive supportive management are of paramount in decreasing the mortality of the disease.

Adult ; Aged ; Female ; Humans ; Male ; Middle Aged ; Prognosis ; Retrospective Studies ; Severe Acute Respiratory Syndrome ; diagnosis ; therapy

Objective To investigate the effects of “patient-family-community”health promotion mode on patients with impaired glucose regulation(IGR).Methods Using the function of random case samples in SPSS,we randomly chose an experimental village and a control village respectively from all villages in Zhuqiao of Pudong New Area.Altogether 75 IGR patients who met the requirement were filtered in the two villages. According to the villages they belonging to,39 of them were divided into experimental group and 36 to control group.From March 201 4 to August 201 4, subjects in the experimental group were intervened by“patient-family-community”health promotion mode,while participants in the control group used the regular health guidance.We compared the test score of knowledge-attitude-practice (KAP) questionnaire,family APGAR questionnaire and blood glucose between two groups.Results Relevant indexes of the two groups before intervention showed no difference (P >0.05).After intervention,the knowledge(K),attitude(A)and practice (P)test scores of the experimental group were (8.85 ±1 .31 ),(8.87 ±1 .77)and (6.92 ±2.67),higher than (5.86 ±2.37),(6.78 ±2.92)and (3.89 ±3.02)of the control group(Z =-5.1 89,-3.299,-4.042;P <0.05).The APGAR test scores of the experimental group(7.56 ±1 .90)was higher than(6.47 ±1 .77)of the control group(t =2.571 ,P <0.05).The FPG,2hPG and HbA1 c of the experimental group were (5.86 ± 0.50)mmol/L,(8.02 ±0.72)mmol/L and(5.73 ±0.42)%,which were lower than (6.1 1 ±0.45)mmol/L, (8.60 ±0.97)mmol/L and(5.97 ±0.53)% of the control group (t =-2.293,-2.383,-2.1 70;P <0.05).Conclusions Applying “patient-family-community”health promotion mode can improve the KAP, family function of IGR patients,control their blood glucose better and prevent diabetes.

Pien Tze Huang(PZH),a class-1 nationally protected traditional Chinese medicine(TCM),has been used to treat liver diseases such as hepatitis;however,the effect of PZH on the progression of sepsis is un-known.Here,we reported that PZH attenuated lipopolysaccharide(LPS)-induced sepsis in mice and reduced LPS-induced production of proinflammatory cytokines in macrophages by inhibiting the acti-vation of mitogen-activated protein kinase(MAPK)and nuclear factor-kappa B(NF-κB)signalling.Mechanistically,PZH stimulated signal transducer and activator of transcription 3(STAT3)phosphory-lation to induce the expression of A20,which could inhibit the activation of NF-κB and MAPK signalling.Knockdown of the bile acid(BA)receptor G protein-coupled bile acid receptor 1(TGR5)in macrophages abolished the effects of PZH on STAT3 phosphorylation and A20 induction,as well as the LPS-induced inflammatory response,suggesting that BAs in PZH may mediate its anti-inflammatory effects by acti-vating TGR5.Consistently,deprivation of BAs in PZH by cholestyramine resin reduced the effects of PZH on the expression of phosphorylated-STAT3 and A20,the activation of NF-κB and MAPK signalling,and the production of proinflammatory cytokines,whereas the addition of BAs to cholestyramine resin-treated PZH partially restored the inhibitory effects on the production of proinflammatory cytokines.Overall,our study identifies BAs as the effective components in PZH that activate TGR5-STAT3-A20 signalling to ameliorate LPS-induced sepsis.