Objective To investigate the best application time and effect of the prevention and treatment of postpartum hemorrhage caused by uterine atony. Methods A total of 168 women with bleeding tendency were treated in our hospital from October 2014 to October 2016. They were randomly divided into three groups, 56 cases each. Among them, A group was used immediately after delivery, and group B was suffering from uterine atony, which was the use of hemabate, and C group did not use hemabate. The blood loss and the amount of postpartum hemorrhage in the three groups were compared and analyzed. Results Compared with group B and C, the amount of bleeding, the amount of bleeding in the 2 hours postpartum and the amount of 24 hours postpartum hemorrhage in group A were significantly lower than that in group(P<0.05). The 2 hours postpartum bleeding volume and 24 hours postpartum hemorrhage in group B were significantly lower than that in group C(P<0.05). The incidence of postpartum hemorrhage in group A was 3.57％, significantly lower than that in group B, group 14.28％ and group C, 30.36％(P<0.05). The incidence of postpartum hemorrhage in group B was 14.28％, significantly lower than that in group C (30.36％) (P<0.05). Conclusion To prevent and treat uterine atony postpartum hemorrhage, it is effective to prevent and treat postpartum hemorrhage. And the best application for the immediate use of fetal labor, can further reduce the amount of postpartum hemorrhage, to ensure maternal safety.

Pulmonary infections in the immunocompromised patients have become common problem in clinical work along with the immunocompromised ones increased.The pathogens in those patients were complex.The clinical manifestations were always atypical and may be covered up with immunosuppressors.The state of this illness can deteriorate in many patients.In recent years,many pathogen survey technique and therapy have been developed,and give a positive impact on clinical diagnosis and treatments.It is important to find out the current diagnosis and therapy in the pulmonary infections in immunocompromised patients,and pay more attention to clinical pathway for improving the outcome and reducing complications in those patents. Abstract:Summ ary:Pu lmonary infections in the immunocomprom ised patients have becom e common prob lem in c lin icalwork along w ith the immunocomprom ised ones increased.The pathogens in those patients were comp lex.The c lin ical m an ifestations were always atyp ical and m ay be covered up w ith immunosuppressors.The state of th is illness can deteriorate in m any pa-tients.In recent years,m any pathogen survey techn ique and therapy have been developed,and give a positive impact on c lin ical d iagnosis and treatm ents.It is important to find out the current d iagnosis and therapy in the pu lmonary infections in immunocomprom ised patients,and pay more attention to c lin ical pathway for improving the outcom e and reduc ing com-p lications in those patents.

Airway Remodeling ; drug effects ; Cholinergic Antagonists ; therapeutic use ; Humans ; Pulmonary Disease, Chronic Obstructive ; drug therapy ; immunology ; metabolism ; Scopolamine Derivatives ; therapeutic use ; Tiotropium Bromide

Since 2005,guidelines for the management of adults with CAP or HAP were updated in United States,Europe and Japan,respectively.In these new CAP guidelines,severity-of-illness scores could be used to decide site of care.Routine diagnostic tests to identify an etiologic diagnosis were optional for outpatients with CAP.Empirical antibiotic therapy regimen,time to first antibiotic dose and duration of antibiotic therapy were all detailed explained.In new HAP guidelines,prevention was still emphasized.In order to prevent VAP,measures should be taken to reduce the risk of aspiration,including subglottic drainage and maintenance of stable optimal endotracheal tube cuff pressure.Cultures of lower respiratory secretions have diagnostic value for VAP.The diagnostic accuracy of blind sampling was similar to that of bronchoscopy-directed methods.Much more attention was paid on multidrug resistant bacteria infections.

Objective:To assess the genetic relationship of clinical isolates of carbapenem-resistant A.baumannii (resistant to both imipenem and meropenem) from January 2007 to March 2008 in Peking University Third Hospital for measures to decrease the isolates; to investigate the characteristics of patients with carbapenem-resistant A. baumannii colonization or infection and to evaluate antibiotic treatment for health care-associated infections caused by carbapenem-resistant A. baumannii. Methods: The medical records of patients with carbapenem-resistant A. baumannii colonization or infection were reviewed. Antibiotic susceptibilities of the isolates were determined by the standardized disk-diffusion method and the clonal relationship of the isolates was analyzed by pulsed-field gel electrophoresis. Results: A total of 49 carbapenem-resistant A. baumannii strains were isolated from the 49 patients hospitalized during the study period and pulsed-field gel electrophoresis typing yielded 7 different patterns. A total of 45 (91.8%)genotyped strains showed clonal relationship. The most frequently identified predisposing factors were intensive care unit stay, invasive procedures, and hypoalbuminemia. Chronic obstructive pulmonary disease (12 cases) and cerebrovascular disease (10 cases) were the most common comorbid conditions.The mortality of patients with carbapenem-resistant A. baumannii infection was 38. 1% (8 of 21 patients), and the acute physiology and chronic health evaluation Ⅱ score, initial antibiotic therapy failure rate and the presence of hypoalbuminemia were significantly increased in the death group. Combination therapy regimens had higher success rates than monotherapy regimens (11/13, 84. 6% vs. 3/17,17.6%). Conclusion: There has been clonal spread of carbapenem-resistant A. baumannii strains among patients in our hospital since 2007. Intensive care unit stay, invasive procedures, hypoalbuminemia, chronic obstructive pulmonary disease and cerebrovascular disease were common in patients with carbapenem-resistant A. baumannii colonization or infection. Antibiotic combination therapy may be effective for carbapenem-resistant A. baumannii infection.

Objective To study clinical characteristics and diagnostic methods of lymphoma with chest invovement. Methods Twenty-five lymphoma patients with chest involvement were retrospectively analysed, they were all diagnosed in Peking University Third Hospital during 2000 to 2007. The data were collected including clinical manifestations, blood examinations, chest X-ray and CT scan, diagnostic methods and pathologic diagnosis. Results The median age of the 25 patients was 46 years old. Pyrexia(13 cases), weight loss over 10 percent in 6 months(11 cases), cough(10 cases), shortness of breath(9 cases) and painless enlargement of the peripheral lymph nodes(16 cases) were common manifestations. Erythrocyte sedimentation rate and serum lactate dehydrogenase(LDH) level were increased in 72.7% and 81% patients, respectively. The enlargement of mediastinum lymph nodes(16 cases, 64%) was the most common presentation of chest radiography, followed by pulmonary involvement(15 cases, 60%) including infiltration or pulmonary consolidation, mass, multiple nodules, diffuse ground-glass shadow, miliary lesion. There were also presentations of pleural effusion(10 cases, 40%), pericardial effusion(4 cases, 16%), chest wall mass(2 cases, 8%). Eighteen patients(72%) had at least two kinds of these presentations. The appearance of pleural effusion were yellow turbid, bloody or chyliform. Rivaha tests were all positive. The median value of plearal effusion examinations were listed as follows: specific gravity 1.031, total cells 9800×10~6/L, WBC 6.72×10~9/L, lymphocyte 86%, neutrophil 14%, protein 31.4 g/L, LDH 296 U/L,adenosine deaminase (ADA) 67.4 U/L Most patients(16 cases) were diagnosed by surgical biopsy,especialy peripheral lymph nodes biopsy (12 cases). Other patients were diagnosed by ultrasound or CT-guided biopsy (5 cases), video-assisted thoracoscopic pleural biopsy (1 case), video-mediastinoscopic mediastinum lesion biopsy(1 case), bronchial mucosa biopsy through bronchoscope(1 case), bone marrow examination(1 case). All the cases were non-Hodgkin lymphoma except one. Conclusions There was no specific clinical manifestation for lymphoma with chest involvement, but in almost half of patients there were enlargement of not only peripheral but also mediastinum lymph nodes. And there were some characteristics in serum, pleural effusion, chest X-ray and CT scan. Surgical biopsy of peripheral lymph nodes was a simple and convenient method for diagnosis. Micro-invasive biopsy had good diagnostic value for lymphoma with chest involvement, including ultrasound-or CT-guided biopsy for superficial mass, pleura, lung, liver, spleen and deep lymph nodes, video-assisted thoracoseopic and video-mediastinoscopic biopsy for pleura, lung and mediastinum lesions. But bronchial mueosa and lung biopsy during bronchoscopy had a low diagnostic rate for lymphoma.

Objective To explore the molecular mechanism of inhibition of LPS-induced inflammation by fenoterol, a β2 adrenoceptor agonist in monocyte. Methods Concentrations of interleukin 1β (IL-1β), tumor necrosis factor α (TNF-α) and MCP-1 from cell supernatants from THP-1 cells and wild type or MyD88- / - mice peritoneal macrophages stimulated by LPS in the presence or absence of fenoterol were determined by use of an ELISA system. Expression of MyD88 (myeloid differentiation factor 88) stimulated by LPS in the presence or absence of fenoterol were determined by Western blot. Results Fenoterol inhibited LPS-induced activation of MyD88 and secretion of inflammatory cytokines (TNF-α, MCP-1, and IL-1β). The reaction of MyD88- / - mice peritoneal macrophages to LPS was much lower than that of the wild type mice peritoneal macrophages. Conclusions MyD88 plays an important role in inflammation induced by LPS. The inhibition of LPS-induced expression of MyD88 by fenoterol is associated with its anti-inflammatory effect.

Objective To investigate the effect of pioglitazone (PIO) on the expression of peroxisome proliferators-activated receptor γ (PPARγ),nuclear factor-κB (NF-κB) c-Rel and anti-apoptosis factor Bcl-xL in cultured Wistar rat cortical neurons after oxygen-glucose deprivation/reoxygenation (OGD/R).Methods The rat cerebral cortical neurons were primarily cultured in vitro and a model of OGD/R was induced.The rats were divided into 7 groups:normal,OGD 4 h/R 6 h,OGD 4 h/R 12 h,OGD 4 h/R 6 h + PIO,OGD 4 h/R 6 h + PPARγ inhibitor T0070907 (TIO),OGD 4 h/R 12 h + PIO,and OGD 4 h/R 12 h + TIO groups.Western blot was used to detect the expression of PPARγ and NF-κB c-Rel protein in neurons.Reverse transcriptionpolymerase chain reaction assay was used to detect the expression of Bcl-xL mRNA in neurons.Results Western blot analysis showed that the expression levels of PPARγ and NF-κB c-Rel proteins after OGD/R were increased significantly compared to those of the normal group (P ＜0.01).After giving PIO,the expression levels of PPARγ and NF-κB c-Rel proteins were further increased,and they were significantly higher than those in the OGD 4 h/R 6 h and OGD 4 h/R 12 h groups (P ＜0.01),and after giving TIO,the expression levels of PPARγ and NF-κB c-Rel proteins were decreased,and they were significantly lower than those in the OGD/R group (P ＜0.05) and the corresponding PIO group (P ＜0.01).Reverse transcription-polymerase chain reaction analysis showed that the expression level of Bcl-xL mRNA in the OGD 4 h/R 6 h group was significantly higher than that in the normal group (P ＜0.01).The expression level of Bcl-xL mRNA in the PIO group was significantly higher than that in the OGD 4 h/R 6 h and OGD 4 h/R 12 h groups (P ＜0.01).After giving TIO,the expression of Bcl-xL mRNA was decreased.It was significantly lower than that in the OGD/R and corresponding PIO groups (P ＜ 0.05 and P ＜ 0.01).Conclusions PIO can upregulate the expression of PPARγ protein in cultured cortical neurons after OGD/R,and then increase the expression of anti-apoptotic factor Bcl-xL mRNA of NF-κB c-Rel regulation.This may be the part mechanism of PPARγ neuroprotective effect.

Objective:To express hTRAIL_ 41～281 protein using E.coli and refold it into a functional form.Methods:The expression of protein was induced by IPTG,protein was purified by Ni-NTA chromatography column,and refolded by dialysis ,protein purified was determined by SDS-PAGE and Western blot.Antitumor activity of hTRAIL_ 41～281 protein was measured by DNA fragmentation electropherogram.Results:Results of SDS-PAGE and Western blot proved that the 30.5 kD protein purified were hTRAIL_ 41～281 protein,the purity of protein was more than 90%.After refolding,DNA fragmentation electropherogram showed that hTRAIL_ 41～281 protein had good antitumor activity.Conclusion:hTRAIL_ 41～281 protein with antitumor activity was successfully expressed with E.coli and purified by Ni-NTA chromatography column,refolded by dialysis.

AIM:To study the effect of acyl coenzyme A:cholesteryl acyltransferase 1(ACAT1)antisense oligonucleotides on the formation of foam cells(FC).METHODS:THP-1 cells were cultured and differentiated into macrophages(MP)by phorbol myristate acetate(PMA).Over-expressing ACAT1 gene THP-1 cells were constructed.The ACAT1 antisense and missense oligonucleotides conducted by LipofectamineTM 2000 were incubated with above cells.Ac-LDL was added 6 h later and incubated for 24 h.The expression of ACAT1 protein was detected by Western blotting.The ACAT activity was measured by quantifying the incorporation of 1-14C oleoyl CoA into cholesteryl esters.The formation of foam cells was detected by oil red O staining.RESULTS:The ACAT1 antisense oligonucleotides inhibited the activity of ACAT in macrophages and over-expressing ACAT1 gene THP-1 cells.It also inhibited the formation of foam cell in macrophages and over-expressing ACAT1 gene THP-1 cells with lipid loading.The missense oligonucleotides did not show the inhibitory effects.CONCLUSION:The ACAT1 antisense oligonucleotides inhibit the activity of ACAT and the formation of foam cells.