Objective To compare the clinical efficacy and safety of thrombolysis with anticoagulation therapy for patients with acute sub-massive pulmonary thromboembolism. Methods The clinical data of 84 patients with acute sub-massive pulmonary thromboembolism were analyzed retrospectively, mainly focusing on the in-hospital efficacy and safety of thrombolysis and/ or anticoagulation. The efficacy was evaluated based on 6 grades: cured, markedly improved, improved, not changed, deteriorated and died. Results Among the 84 patients,49 patients received thrombolysis and sequential anticoagulation therapy( thrombolysis group) , 35 patients received anticoagulation therapy alone( anticoagulation group) . As compared with the anticoagulation group, the thrombolysis group had higher effective rate( defined as patients who were cured, markedly improved or improved, 81. 6% versus 54. 3%, P = 0. 007) , lower critical event occurrence ( defined as clinical condition deteriorated or died, 2. 0% versus 14. 3% , P = 0. 032) . There was no significant difference in bleeding rates between the two groups ( thrombolysis group 20. 4% versus anticoagulation group 14. 3% , P gt; 0. 05) . No major bleeding or intracranial hemorrhage occurred in any of the patients. Conclusions Thrombolysis therapy may be more effective than anticoagulation therapy alone in patients with acute sub-massive pulmonary thromboembolism, and thus warrants further prospective randomized control study in large population.
Objective To construct the mouse NF-κB P65 subunit expression plasmid, and identify its biological activity. Methods NF-κB P65 siRNA retrovirus expression vectors were reconstructed by molecular clone technology. Recombinant vectors were transfected into 293E package cells and virus suspension was collected. RT-PCR was used to detect the expression level of NF-κB P65 mRNA and TNF-α mRNA at different time-point of LPS stimulation. Western blot was performed to analyze the protein level of NF-κB P65. ELISA was applied to detect the expression level of TNF-α released by LPS-stimulated J774A.1. Results NF-κB P65 siRNA retrovirus expression vectors of mouse were successfully constructed. From2 hours after the stimulation of LPS, the expression level of NF-κB P65 mRNA of the siRNA group was obviously lower than the scramble control group ( 0.91 ±0.03 vs. 1.02 ±0.02, Plt;0.01) . At24,36, 48 and 72 hours after the LPS stimulation, the expression level of NF-κB P65 protein of the siRNA group was significantly decreased compared with the scramble control group ( 0.97 ±0.02 vs. 1.01 ±0.01, 0.94 ± 0.01 vs. 1.02 ±0. 01,0.94 ±0.02 vs. 1.02 ±0.01, 0.93 ±0.01 vs. 1.00 ±0.02, Plt;0. 05) . At 2, 6, 12, 24 hours after the LPS stimulation, both the expression level of TNF-α mRNA and the content of TNF-α in the culture medium supernatant of the siRNA group were lower than the scramble control group ( Plt;0. 01) . Conclusions The construction of NF-κB P65 siRNA retrovirus expression vectors is feasible. Inflammation factors in mouse monocyte-macrophages are significantly inhibited after NF-κB expression is depressed by RNA interference technology, which may be applied to prevent and treat excessive inflammatory reaction in acute lung injury.
侵袭性真菌感染(IFI)不仅可发生在恶性血液病、恶性肿瘤、器官移植和AIDS等经典免疫功能缺陷患者中，近年来ICU的重症患者由于严重的基础疾病、外科手术指征和范围的扩大、各种导管的体内介入与留置，以及广谱抗生素和糖皮质激素的广泛应用等，IFI发病率也迅速增加。据统计，IFI占医院获得性感染的8％-15％。IFI病情进展快速、凶险，已13益成为导致ICU危重病患者死亡的重要原因之一。引起ICU IFI的病原体包括念珠菌、曲霉、隐球菌、镰刀霉、接合菌、肺孢子菌等，其中以念珠菌和曲霉最多见，占90％ 以上。由于ICU危重症患者多数属非经典IFI高危人群，临床表现缺乏特异性，临床诊治极为困难。本文就ICU内侵袭性念珠菌感染(Ic)和侵袭性曲霉感染(IA)的流行病学、诊断和治疗进展进行阐述，以期对临床有所裨益。
ObjectiveTo explore the role of osteopontin (OPN) in hyperoxia-induced acute lung injury and its relationship with nuclear factor-κB (NF-κB),matrix metalloproteinase 2 and 9 (MMP-2,MMP-9). MethodsNinety-six mice were randomly divided into a phosphate buffer solution intranasal inhalation group (PBS group) and a recombinant OPN intranasal inhalation group. The mice were exposed in sealed cages >95% oxygen for 24-72 hours to induce lung injury or room air as control. The severity of lung injury was evaluated. The expression of NF-κB,MMP-2,MMP-9,TIMP-1 and TIMP-2 mRNA in lung tissue at 24,48 and 72 hours under hyperoxia were examined by reverse transcript-polymerase chain reaction (RT-PCR). Immunohistochemistry (IHC) was performed for detection of NF-κB protein in lung tissue. ResultsPBS group mice developed more severe acute lung injury at 72 hours under hyperoxia.TIMP-1 and TIMP-2 mRNA expressions were significantly increased in r-OPN group than their matched PBS group when exposed to hyperoxia. IHC study showed higher expression of NF-κB protein in lung tissue of PBS group at 72 hours of hyperoxia. ConclusionOPN can protect against hyperoxia-induced lung injury by inhibiting the expressions of NF-κB,MMP-2 and MMP-9.
ObjectiveTo identify the expression functions of human NF-κBp65 nuclear localization signals' deletion mutant plasmids(namely pcDNA3.1(+)-NF-κBp65ΔNLS, NF-κBp65ΔNLS, for short) and the changes of proliferation, migration and adhesion ability of A549 lung cancer cells with low expression of NF-κBp65 (namely A549/NF-κBp65 shRNA cells). MethodsHuman A549/NF-κBp65 shRNA cells were cultivated and divided into a control group, a transfection pcDNA3.1 (+) group, and a transfection NF-κBp65ΔNLS group. Indirect immunofluorescence, real-time fluorescent quantitative PCR and Western blot techniques were used to detect the NF-κBp65 intracellular localization and the change of NF-κBp65 mRNA and protein expression level. MTT, Transwell and cell adhesion experiments were used to analyze the changes of proliferation, migration and adhesion ability of A549/NF-κBp65 shRNA cells. ResultsThe human NF-κBp65ΔNLS eukaryotic expression plasmid was successfully constructed. Compared with the control group and the transfection pcDNA3.1(+) group, NF-κBp65 mRNA expression level in A549/NF-κBp65 shRNA cells was increased in the transfection NF-κBp65ΔNLS group(10.63±0.84 vs. 1.04±0.21 and 1.23±0.22, P < 0.01) and NF-κBp65 protein expression level was also increased (1.07±0.06 vs. 0.53±0.02 and 0.59±0.04, P < 0.01). NF-κBp65 protein mainly located in the cytoplasm, and did not significantly transferred into the nucleus after stimulated by TNF-α. At the same time, A549/NF-κBp65 shRNA cells' proliferation, migration and adhesion ability were enhanced compared with the control group and the transfection pcDNA3.1(+) group. ConclusionsThrough gene mutation technology to build the human NF-κBp65ΔNLS eukaryotic expression plasmid and transfect into A549/NF-κBp65 shRNA lung cancer cell lines, both mRNA and protein expression levels of NF-κBp65 were increased significantly, and NF-κBp65 protein mainly located in the cytoplasm. The overexpressed NF-κBp65 in cytoplasm can obviously enhance the A549/NF-κBp65 shRNA cell's proliferation, migration and adhesion ability. It suggests that NF-κBp65 stranded in the cytoplasm can still regulate biological behavior of lung cancer cells by influencing the NF-κB signaling pathway related proteins.
Objective To investigate the pathogen distribution and drug resistance in ICU patients, provide reference for prevention of severe infection and empirical antibacterial treatment. Methods The patients admitted in ICU between January 2013 and December 2014 were retrospectively analyzed. The pathogenic data were collected including bacterial and fungal culture results, the flora distribution and drug resistance of pathogenic bacteria. Results A total of 2088 non-repeated strains were isolated, including 1403 (67.2%) strains of Gram-positive bacteria, 496 (23.8%) strains of Gram-negative bacteria, and 189 (9.0%) strains of fungus. There were 1324 (63.42%) strains isolated from sputum or other respiratory specimens, 487 (23.33%) strains from blood specimens, 277 (13.27%) strains from other specimens. The bacteria included Acinetobacter baumannii (17.2%), Klebsiella pneumoniae (14.8%), Pseudomonas aeruginosa (9.9%), C. albicans (6.3%), E. coli (5.6%), E. cloacae (5.4%), Epidermis staphylococcus (5.0%) and Staphylococcus aureus (4.7%). There were 15 strains of penicillium carbon resistant enterobacteriaceae bacteria (CRE) accounting for 2.3%, including 5 strains of Pneumonia klebsiella, 4 strains of E. cloacae. In 117 strains of E. coli, drug-resistant strains accounted for 86.4% including 85.5% of multiple drug-resistant strains (MDR) and 0.9% of extremely-drug resistant (XDR) strains. In 359 strains of Acinetobacter baumannii, drug-resistant strains accounted for 75.2% including 72.1% of XDR strains and 3.1% of MDR strains. MDR strains accounted for 10.6% in Pseudomonas aeruginosa. Detection rate of methicillin resistant Staphylococcus aureus (MRSA) and methicillin resistant coagulase-negative Staphylococci (MRCNS) was 49.0% and 95.5%, respectively. There were 4 strains of vancomycin resistant Enterococcus faecalis. There were 131 (69.3%) strains of C. albicans, 23 (12.2%) strains of smooth candida. C. albicans was sensitive to amphotericin and 5-fluorine cytosine, and the resistance rate was less than 1% to other antifungle agents. The resistance rate of smooth ball candida was higher than C. albicans and nearly smooth candida, but still less than 15%. Conclusions The predominant pathogens in ICU was gram-negative bacteria. The top eight pathogenic bacteria were Acinetobacter baumanni, Klebsiella pneumoniae, Pseudomonas aeruginosa, C. albicans, E. coli, E. cloacae, Epidermis staphylococcus and S. aureus. Sputum and blood are common specimens. CRE accounts for 2.3%. Drug-resistant strains are most common in E. coli mainly by MDR, followed by Acinetobacter baumannii mainly by XDR, and least in Pseudomonas aeruginosa. C. albicans is the most common fungus with low drug resitance.
Objective To study the clinical features and prognosis of recurrent pneumonia associated with myotonic dystrophy. Methods A case of recurrent pneumonia related to myotonic dystrophy was retrospectively analyzed and the related literatures were reviewed. Results The patient was a 32-year-old man with recurrent fever, cough and expectoration for more than 10 years. He was diagnosed as " pneumonia” in the local hospital at every relapse, and improved after antibiotic therapy. Nine months ago, the symptoms of fever, cough and expectoration aggravated. The chest X-ray examination showed consolidation in right middle and lower lobe. After 2-month antibiotic treatment, the symptoms relieved. Then he was admitted to Beijing Anzhen Hospital for further diagnosis and treatment. Physical examination revealed " hatchet-faced” appearance with neck muscles atrophy and slightly flexion. Bilateral sternocleidomastoid muscle symmetrically rised. Few moist rales of bilateral lower lung were found. Lateral elbow and femoral quadriceps muscles symmetrically rised. The muscle strength of his four distal limbs became weakness, and the squat and standing movement was difficult. Chest CT showed pathy effusion and consolidation in right middle lobe and the lower left lobe. Electromyography showed myogenic damage in left extensor digitorum, left deltoid, right anterior tibial muscle, femoral quadriceps muscle, and left sternocleidomastoid, and spontaneous myotonic discharges in left extensor digitorum, right anterior tibial muscle and left sternocleidomastoid. Pathologic examination of left femoral quadriceps muscle showed inflammatory myopathy. The final diagnosis was myotonic dystrophy associated recurrent pneumonia. Two articles revolving 2 cases were retrieved in English literature. No case was reported in Chinese literature. Conclusion The possibility of myotonic dystrophy should be considered in the case of recurrent pneumonia complicated with muscle atrophy, weakness and myotonia.
Objective To investigate the clinical characteristics and drug sensitivity of patients with Gram-negative bacilli infection, and evaluate the risk factors related to infection, so as to provide a theoretical basis for clinical prevention and treatment of hospital-acquired infection. Methods The complete medical records of 181 patients with Gram-negative bacilli infection in the Department of Respiratory and Critical Care Medicine of Beijing Anzhen Hospital from January 2018 to September 2021 were retrospectively collected. They were divided into a Carbapenem-resistant Gram-negative bacillus (CR-GNB) group and a Carbapenem-sensitive Gram-negative bacillus (CS-GNB) group according to their different sensitivities to carbapenems. Results A total of 238 strains of Gram-negative bacilli were detected, including 108 strains of CR-GNB and 130 strains of CS-GNB. Acinetobacter baumannii was the most common, followed by Pseudomonas aeruginosa, Klebsiella pneumoniae, Enterobacter cloacae, Escherichia coli and Serratia marcescens. Univariate analysis showed that the risk factors of CR-GNB infection were heart disease and cerebrovascular disease, receiving invasive mechanical ventilation, deep venous catheterization and indwelling catheter, hypoproteinemia, renal insufficiency, pre-infection exposure to tigecycline, carbapenems, vancomycin, polymyxin, and combined use of antibiotics. Hypoproteinemia and deep venous catheterization were independent risk factors for CR-GNB infection. The resistance rates of CR-GNB to cefepime, ceftazidime, levofloxacin and ciprofloxacin were 88.0%, 88.0%, 86.1% and 75.0%, respectively. The resistance rate to cefuroxime, amika, ceftriaxone, gentamicin and cotrimoxazole was low, and the resistance rate to ceftazidime avibactam was the lowest (3.7%). Except tetracycline, tigecycline, cefuroxime, polymyxin, cefazolin and ampicillin, the drug resistance rates of CR-GNB group to other antibacterial drugs were higher than those of CS-GNB group, and the differences were statistically significant (P<0.05). The all-cause mortality in CR-GNB group (42.4%) was significantly higher than that in CS-GNB group (6.3%), and the difference was statistically significant (P<0.05). Conclusions The disease burden caused by CR-GNB infection is becoming heavier and heavier, which has a serious impact on the prognosis of hospitalized patients. The increase of antibiotic resistance leads to poor efficacy of antimicrobial therapy. Therefore, early identification of high-risk groups of infection and reasonable and prudent application of antimicrobial therapy can achieve the purpose of reducing the mortality of infection and improving the prognosis of hospitalized patients.