The incidence of atypical pneumonia is pretty high throughout the world,accounting for 15%-50% of the community-acquired pneumonia.Epidemiological studies have revealed that Mycoplasma pneumoniae (MP) ranks the top among the pathogens which are most likely to cause atypical pneumonia,while Chlamydia pneumoniae (CP) ranks the second and Legionella pneumophila (LP) the lowest.However,LP may induce outbreak of pneumonia with the highest mortality.Q fever pneumonia is also one type of atypical pneumonia,which is not commonly seen in clinic and rarely reported.Definite diagnosis of atypical pneumonia remains a difficult problem since specific clinical presentations are unavailable,with difficulties in culturing etiological agents,and low value of serum tests for diagnosis.Nevertheless,PCR assay seemed to be an important technique for early diagnosis of atypical pneumonia,provided that false positive rate was effectually reduced by strict quality control.Regarding to the therapeutic drugs,macrolides and quinolones are the most effective ones for the treatment of atypical pneumonia.Those drugs covering atypical pneumonia related pathogens are recommended for initial treatment for patients with community-acquired pneumonia.Moreover,patients who are suspected to have Legionella pneumophila infection are recommended to take quinolones to decrease mortality.

We observed the pulmonary responses and changes in TXB2 and 6-keto-PGF1a concentrations in plasma and lung lymph in endotoxin induced lung injury. The typical pulmonary responses appeared after the injury. The TXB2 concentrations in plasma and lung lymph increased by 24.5 and 30.7 times and those of 6-keto-PGFla by 10.6 and 15.7 times, respectively, as compared with baseline. The TXB2 and 6-keto-PGF1a concentrations in lymph were 68 and 75 percent higher than those in plasm a respectively. The results indicated that TXA2 and-PGI2 synthesis increased in the lung after injury and that TXA2 and PGI2 were important media in the lung injury.

The purpose of this study was to determine the role of lipid peroxidation by measuring the induced-chemiluminescence (ICL) of plasma and lung lymph in endotoxin-induced acute lung injury in awake sheep. The ICL of aortic plasma and lung lymph were significantly increased, but the ICL of venous plasma was not significantly increased after endotoxin infusion. The peak level of ICL was increased and its time was delayed after endotoxin. We conclude that lipid peroxidation plays an important role in endotoxin-induced acute lung injury, and ICL of arterial plasma is a sensitive marker in reflecting oxidant damage in lung.

Background and purpose:Endostatin can effectively inhibit angiogenesis,it could slow down tumor growth in heterogenic transplantation model by given ES systematically.This study was to evaluate the inhibition of endostatin on tumor growth and metastasis of lung cancer of the thoracic cavity implant model in nude mouse.Methods:H460 cells were inoculated subcutaneously into the thoracic cavity of nude mouse,and the mice were randomized into ES group(ESG)and control group(CG).At the fi rst day,the ESG was given 20 mg/kg of endostatin s.c.qd,the CG was treated daily s.c.with equal volumes of PBS for 20 days.The weight of the animal and the transplantation tumor,mice life span,MMP2 of blood were observed.Results:The rate of tumor formation was 100%,and the thoracic cavity implant models gradually had metastasis.The transplantation tumor weights were(1.54?0.14)in ESG group that was less than that(0.9?0.3)in CG group(t=-3.163,P=0.005);the comparison of the change value of weight on day 1 and day 21 between CG(1.9?2.8)and ESG(-0.8?2.8)was statistically different(t=-2.156,P=0.045).The average survival time of the ESG was longer than that of the CG.Conclusion:The results demonstrate that endostatin could inhibit the growth and metastasis of H460 cell in athymic mouse,and one of the important mechanisms involves was inhibition of the MMPs expression.The thoracic cavity implant model was easier to obtain metastasis,and provided a reliable research tool for the study of endostatin inhibition on tumor growth and metastasis of lung cancer.

Objective To research the portable electron video equipment for tracheal intubatton in first aid. Methods According to the attributes of physiological bend and specialty of windpipe and gular of image, a horniness endoscopic of "C" model was designed with optical interface, CCD image transducer and small crystal display. It could quickly and visually lead tracheal intubatton through nonnasality. Results It was portable, visual, easily-operated. The rate of successful leading of tracheal intubatton is 97.8% . Conclusion It is especially suited to field battle, first aid, abrupt affairs, etc.

Objective To investigate the protective and cure effects of dexamethasone on bleomycin-induced pulmonary fibrosis.Methods32 rats were randomly divided into the control group (C-group, n=8), injury group (I-group, n=12) and dexamethasone group (D-group, n=12). The acute pulmonary model was established by intratracheal injection of bleomycin with rats of the I-group and D-group; while rats of the C-group injected with distilled water. After that, rats of the D-group were injected with dexamethasone sodium phosphate in intraperitoneal every day, those of the C-group and I-group were injected with saline. The animals were killed on the 3rd, 7th, 14th, and 27th days after treatment, and tests of bronchoalveolar lavage fluid (BALF), total lung collagen content and lung tissue processing were performed.ResultsPathological evidence of the I-group rats demonstrated that the alveolar compartment companied with massive inflammatory cell invasion and a number of myofibroblast proliferation became more thick. However, lung injury in the D-group rats got better than that in the I-group. Neutrophil percentage achieved peak in both I-group and D-group on the 7th day. But the neutrophil ratio in the D-group was significantly lower than that of the I-group on the 7th day ( P<0.05) and the 14th day ( P<0.01). Total lung collagen content achieved peak on the 14th day both in I-group and D-group, but that of the I-group was significantly higher than that of the C-group ( P<0.01) and the D-group was significantly lower than the I-group ( P<0.01).ConclusionDexamethasone plays a protective and cure role in lung fibrosis by efficiently inhibiting the gather and invasion of neutropils and restraining the increase of collagen secreted by proliferous fibroblasts.

BACKGROUND:Contraction of three-dimensional collagen gels has been used as a model for the contraction which characterizes both normal wound healing and the development of fibrosis in the tissue. Several factors and cytokines,such as tumor necrosis factor alpha (TNF-α), interleukin-1, prostaglandin E2 and insulin have been proved to play important roles in collagen remodeling in vitro as well as serum extravasation during the fibrotic progress.OBJECTIVE: To observe extracellular collagen matrix contraction and apoptosis of fetal lung fibroblasts in TNF-α,interleukin-1, insulin, prostaglandin E2, albumin and globum under three-dimensional culture, and investigate the effects of cytokines, insuin, serum and serum protein on the remodeling and fibrotic formation of lung tissue.DESIGN: A randomized controlled experiment.SETTING: Department of Respiratory Medicine, Lanzhou General Hospital of Lanzhou Military Area Command of Chinese PLA.MATERIALS: The experiment was carried out The experiments were carried out in the respiratory laboratory of Lanzhou General Hospital of Lanzhou Military Area Command of Chinese PLA from August 2005 to January 2006. Human fetal lung fibroblasts (American Type Culture Collection), Dulbecco's modified Eagle's medium (DMEM) and fetal bovine serum, insulin, transforming growth factor (TGF) (R&D), prostaglandin E2, type Ⅰ collagen was extracted from rat-tail tendons.METHODS: In order to investigate the effect of initial collagen concentration in the gels on the contractility of fibroblasts,the appropriate amount of collagen was mixed with distilled water, four fold-concentrated DMEM, and cells were suspended so that the mass concentration was 0.75-2.0 g/L, with a physiological ionic strength and the desired cell concentration. In order to investigate the effect of cell number in the gels on the contraction, the cellular concentration fibroblasts in the gels were prepared to 0.2×107-4×107 L-1. The areas of floating gels were measured daily and the contraction was calculated by contrasting the initial size (％ of initial area). Different serum concentrations (0.01％-0.5％)in the medium were prepared, the serum albumin (0.1％) or globulin (0.1％) were added to the serum-free culture medium to observe the gel contraction. TGF (10 mg/L), interleukin-1 (10 mg/L), insulin (1 mg/L) and prostaglandin E2 (0.1 μmol/L) were added to observe the effects of cytokines and insulin on fibroblasts-mediated collagen gel contraction.The DNA content and cellular survivability in gels in collagen were determined.MAIN OUTCOME MEASURES: Effect of lung fibroblasts on collagen contraction with or without the presence of cytokines in three-dimensional culture; Effect of collagen with different concentration on the proliferation and apoptosis.RESULTS: ① Collagen gel contraction showed a dependence on the number of fibroblasts. ② Collagen gel contraction was augmented by increasing serum concentration in culture medium, and albumin increased the contraction dramatically. ③TGF and insulin significantly increased the contraction, whereas prostaglandin E2 and interleukin-1 significantly inhibited the gel contraction. ④ The lower the initial collagen concentration was, the more gel contracted and smaller final size were observed, and cell apoptosis increased.CONCLUSION: During the fibrotic process, fibroblast population migrated into the injured lung tissue may play an important role in the development of pulmonary fibrosis and serum infiltrating into injury lung tissue may play an role in stimulating the fibrotic progress. Infiltrating fluids and edema result in the dilution of the collagen concentration in the pulmonary interstitial which may lead to stronger contraction and serious fibrosis. In the dense fibrosis area, cells were hard to survive. In consequence, the final structure of fibrotic lung could not been changed and lung fibrosis progressed.