The results of analysing 179 patients with pulmonary heart disease (PHD) show an acid-base disorder just before death.Acid-base disorder,chronic respiratory acidosis is the most commoa Triple acid-base disorder,chronic respiratory acidosis plus metabolic acidosis and chronic respiratory acidosis plus metabolic alkalosis are in succession.Chronic respiratory alkalosis ( CRA),CRA plus metabolic alkalosis and metabolic acidosis are seldom.The major cause of death in patients with PHD is supper gastrointestinal hemorrhage,the next is acid-base disorder,especially triple acid-base disorders.

Acute lung injury(ALI) and acute respiratory distress syndrome(ARDS) are commonly encountered serious diseases.The pathogenesis of ALI and ARDS remains unclear at present.The mortality rate of ALI and ARDS remains high due to the Absence of sensitive method for early diagnosis and specific and effective therapy.The present paper will focus on the latest developments of diagnosis and treatment for ALI and ARDS.Diagnosis:Althongh theoretically it is possible to look for the diagnostic markers and target of injury by painstaking study of its pathogenesis,but as yet an ideal pathognomonic marker with due sensitivity and specificity remains unavailable.Diffuse alveolar injury is a major pathological feature and may act as a reliable parameter for the diagnosis of ALI and ARDS.However,it is difficult to obtain the lung tissues from living patients with ALI/ARDS,and dynamic monitoring of arterial blood gas,combined with clinical symptoms,is still the main criterion for early diagnosis of API and ARDS in clinical setting.Therapy:The use of corticosteroids to subdue rampant inflammatory reaction had not given a promising result in clinical study,so it is not recommended for routine use,however short-term corticosteroids may be considered for allergy-or aspiration-induced ALI in early stage.With the treatment of primary diseases as the main strategy,the main therapeutic measures for ALI/ARDS should be integrated treatment of multiple targets and correction of hypoxia.Mechanical ventilation is the main substitutive therapy for correction of hypoxia.Protective ventilation with adequate tidal volume and positive end-expiratory pressure(PEEP) are recommended.Briefly,management of primary disease,correct use of mechanical ventilation,nutritional support and specific treatment for pathological changes and clinical manifestation are important for ALI and ARDS patients.Hereafter,emphasis should be placed on seeking the methods for early diagnosis and effective therapies for diffuse alveolar injury and massive inflammation.

Acute lung injury/acute respiratory distress syndrome (ALI/ARDS) refers to acute progressive respiratory failure with stubborn hypoxemia induced by different predisposing factors except cardiogenic causes. The definition of ALI/ARDS have been renewed and standardized in recent years, thus there is a new understanding in the pathogenesis of ALI/ARDS. The new diagnostic criteria and the combining therapeutic measures of ALI/ARDS have been proposed. With the progress in research pertaining to ALI/ARDS and the new insight into the pathogenesis of intractable systemic inflammation, new therapeutic measures directing at controlling and regulating inflammatory responses may be expected to achieve a breakthrough in the treatment of ALI/ARDS.

Background and Purpose:To analyse the chromosome of peripheral lymphocytes and tissue samples of lung cancer for the long term survival patients after surgery,which could provide the rationale for the screening of relative genes of carcinogenesis and clinical treatment of lung cancer.Methods:Twenty patients with over 5 year survival after operation were defined as long term survival group.There were 9 patients with squamous cell carcinoma,6 with adenocarcinoma and 5 with small cell carcinoma in the long term survival group.The control group was defined as the samples from the patients with lung cancer who had surgery within one year and had to be randomly chosen,8 patients were histologically proven as squamous cell carcinoma,7 as adenocarcinoma and 5 as small cell carcinoma in the control group.The samples from healthy donors were defined as the normal group.The chromosome variations of peripheral lymphocytes in all these 3 groups were analyzed by routine methods.The comparative genomic hybridization of the embed-paraffin tissue sample of lung carcinoma was done by the DeVries methods.Results:In the long term survival group,the chromosome variations rate of lymphocytes was 3.15%,which was lower than that of the control group(3.15% vs 10.85%,P

Objective To construct human eukaryotic expression system expressing T cell surface molecule CD40L and identify the expression product in SCCL cell line h446. Methods The expression vector pcDNA3.1-CD40L was constructed by recombinant DNA technology, then transfected into h446 cell line of SCCL by lipidosome methods, and the expressed membrane protein was identified by flow cytometry. Results The pcDNA3.1(+)-CD40L was constructed successfully and the coding region was inserted into the vector correctly. The membrane protein was observed by flow cytometry on transfected h446 cell line of SCCL. Conclusion Human CD40L was expressed successfully in eukaryotic system, which is very important in the anti-tumor vaccination study with a recombinant human CD40L in clinic.

The major problem in lung cancer chemotherapy is the emergence of inherent and acquired drug resistance of the cancer cells. The cancer becomes resistant not only to the drugs used initially, but also to those to which it has not yet been exposed, This condition is known as multidrug resistance (MDR). MDR has been found to be related to three members of the ABC-superfamily of membrane transport proteins (transporters) and one member of the non-ABC-superfamily of transporter. The formers are P-glycoprotein (P-gp), multidrug resistance-associated protein (MRP), and breast cancer resistance pro-tein (BCRP). The latter is lung resistance-related protein (LRP). These findings provided new molecular targets to predict drug resistance, and an atraumatic detection method by using Tc-99m methoxyisobutyl isonitrile ( 99m Tc-MIBI ) SPECT has been developed for predicting MDR in lung cancer. Based on these transporters, different strategies are tried attempting to reverse drug resistance in lung cancer. Encouraging results have been acquired, but further research is necessary.

AIM: To explore the changes of L-selectin expression on peripheral blood polymorphonuclear leukocytes (PMNs) and their significance in rats with acute lung injury (ALI). METHODS: ALI model in rat was established by intravonous injection of E. coli endotoxin (ET). The expression of L-selectin on peripheral blood PMNs was measured by immunofluorescence and flow cytometry.RESULTS: The contribution of L-selectin fluorescence signal was on the surface of PMNs membrane. The expression of L-selectin on poeripheral blood PMN was significantly lower at 5 min after injection of ET and the lowest during 15 min to 30 min, then gradually increased, but the expression of L-selectin on PMN was lower at 60 min after injection of ET than that of control animal.CONCLUSION: In physiological state, L-selectin were expressed on the surface of PMN membrane. The protein expression of L-selectin on PMNs reduced rapidly after injection of ET and the lowest at 15 min, then gradually increased. L-selectin may play a role in the development of ALI.

Objective To observe the effects of mouse indoleamine 2,3-dioxygenase (IDO) gene on CD4+ T cells by transfecting an eukaryotic expression vector containing mouse IDO gene fused with enhanced green fluorescent protein (pEGFP-N1). Methods The immature dendritic cells (imDCs) derived from mouse bone marrow were cultured in vitro and morphologically identified by transmission electron microscope, scanning electron microscope and flow cytometry. The immature dendritic cells were transfected by DOTAP liposome, and the expression of green fluorescence protein was confirmed with inverted fluorescence microscope. The spleen-derived CD4+ T lymphocytes from mice were isolated and purified in vitro, and then carried to mixed lymphocyte reaction (MLR) with 3H-TdR incorporation. The effect of IDO gene on the proliferation of spleen-derived CD4+ T lymphocytes of the allergized mouse challenged by ovalbumin was assayed by 3H-TdR MLR incorporation, and the apoptosis of spleen-derived CD4+ T lymphocytes was assayed by TUNEL. Results The proliferation of spleen-derived CD4+ T lymphocytes of the allergized mouse challenged by ovalbumin were inhibited by the imDCs transfected with IDO gene, the number of CD4+ T lymphocytes treated with the imDCs transfected pEGFP-N1-IDO eukaryotic expression vector decreased significantly compared with that in control group (P

Objective To establish a multidrug-resistant cell subline NCI-H446/CDDP of human small cell lung cancer and characterize its biological properties. Methods The cell subline NCI-H446/CDDP was derived from human small cell lung cancer cell line NCI-H446 by exposing it to high concentration first followed by being cultured with gradually increasing dose of cisplatin, which used to be the first-line chemotherapeutic drug for lung cancer. The cell growth curve and the doubling time were determined by cell counting. The chemosensitivities of NCI-H446/CDDP and NCI-H446 to cisplatin, hydroxycamptothecine, vincristin, 5-fluorouracil and topotecan were tested and IC 50 measured by MTT. Changes in cellular morphology and ultrastructure were observed under inverted-microscope, scanning electron microscope and transmission electron microscope, respectively. Results Multidrug-resistant cell subline (NCI-H446/CDDP) of human small cell lung cancer was established successfully after culturing NCI-H446 in a high concentration of cisplatin first, followed by subjecting it to increasing concentrations of CDDP until they could stably grow in the culture medium containing 0.5?g/mL CDDP. The rate of cell proliferation of NCI-H446/CDDP was similar to that of NCI-H446, but the number of the former cells exhibiting S phase increased (20.24% vs 18.42% P

BACKGROUND: Chronic obstructive pulmonary disease(COPD) is characterized of chronic inflammation in airway, pulmonary parenchyma and pulmonary vessels. The mechanism of the increment and activity changes of these inflammatory cells is unclear at present.OBJECTIVE: To study the apoptotic character of peripheral blood polymorphonuclear neutrophils(PMNs) and its relationship with COPD to provide a reference for early intervention and function surveillance for COPD patients.DESIGN: An observatory comparative study based on COPD patients and healthy population as controls.SETTING: Department of pulmonary medicine in a military medical university of Chinese PLA affiliated hospital.PARTICIPANTS: Totally 98 COPD patients were admitted by the Department of Pulmonary Medicine, Research Institute of Surgery, Daping Hospital, Third Military Medical University of Chinese PLA between February 2003 and December 2003 due to COPD acute attack. Eighteen patients including 12 males and 6 females aged between 48 and 70 years old [mean of(56 ± 7) years old]were randomly selected into COPD group according to random number table.Totally 14 healthy adults including 10 males and 4 females aged between 50 and 70 years old [mean of (59 ± 8) years old] who were individuals came for physical check up in our hospital were selected in control group.METHODS: PMNs were separated from peripheral blood by density gradient centrifugation. The dynamic changes of PMNs apoptosis in peripheral blood was observed by flow cytometer and TUNEL method.MAIN OUTCOME MEASURES: Comparison of PMNs apoptotic rate in peripheral blood among groupsRESULTS: As indicated by flow cytometric analysis, PMNs apoptotic rate at early apoptotic phase in COPD patients at paracmasis was(8.5 ± 1.3)%,which was significantly lower than(12.5 ± 1.8)% of normal control group( t=6.25, P ＜ 0. 01); PMNs apoptotic rate was(5.1 ±0.6)% at acute aggravation stage, which was significantly lower than that of paracmasis group ( t =5.66, P ＜001). As indicated by TUNEL analysis, PMNs apoptotic rate at paracmasis was(12.42 ±2.7)% , which was significantly lower than (21.5±4.8)% of normal control group(t=5.76, P ＜ 0.01); PMNs apoptotic rate was(4. 9 ±0.4)% at acute aggravation stage, which was significantly lower than that of paracmasis group( t = 6. 12, P ＜ 0. 01 ) . PMNs changes at the late phase of apoptosis/necrosis had a contrary tendency, i. e.,PMNs rate at late apoptotic phase/necrosis was(2. 8 ± 0.5)% in COPD patients at paracmasis, which was significantly higher than(1. 3 ±0.4)% of normal control group ( t= 6. 37, P ＜ 0. 01 ); PMNs rate was (3.7 ± 0. 3) % at acute aggravation stage, which was significantly higher than that of paracmasis group(t=5.81, P ＜0.01).CONCLUSION: PMNs abnormal apoptosis might be an important reason that induces PMNs aggregation in airway and lung tissues in COPD. This process might have an important significance in the generation and development of chronic airway inflammation, which provides an etiologic basis for the primary rehabilitative intervention of COPD.