2015年 · 第38卷第03期

I remember that in 1988, shortly after the author returned from studying abroad at Professor Fishman of the University of Pennsylvania, Corey admitted a well-known patient. The patient suffered from pneumonia accompanied by trance and hyponatremia. The treatment with β-lactam antibiotics was ineffective. He was quickly diagnosed with Legionella pneumonia, and was cured and discharged after targeted treatment. Unexpectedly, a few weeks after discharge, the patient's pneumonia recurred, and the neurological symptoms became more and more obvious. The effect of repeated erythromycin treatment was not obvious. Multiple brain abscesses were found by cranial magnetic resonance examination. Compared with foreign literature pictures, it was highly suspected that it was toxoplasma brain abscess. At this time, we began to suspect that the patient might have AIDS, and then confirmed the diagnosis after T cell subsets and multiple human immunodeficiency virus (HIV) antibody serum-specific tests by designated departments.

In recent years, when the author reviewed the manuscript, it was found that many doctors were not very clear about the anesthesia method and concept of bronchoscopy. In the case reports of painless bronchoscopy, some authors actually used laryngeal mask or tracheal intubation with mechanical ventilation, and used general anesthesia, which had nothing to do with "painless bronchoscopy". The author published "Evaluation of the Application of Sedative and Analgesic Drugs in Bronchoscopy" in the "Interventional Garden" of Chinese Journal of Tuberculosis and Respiratory in 2010^[1]Now, the related issues are further explained.

Pulmonary diffusion function refers to the ability of certain alveolar gas to diffuse from the alveoli to the capillaries to the blood through the alveolar-capillary membrane (consisting of the alveolar epithelium and its basement membrane, the alveolar capillary endothelium and its basement membrane, and the connective tissue between the two basement membranes) and bind to hemoglobin (Hb) in red blood cells. The gas exchanged in the alveolar-capillary membrane is mainly oxygen (O₂) and carbon dioxide (CO₂)。 The method is complicated because it is necessary to measure the mean partial pressure of blood oxygen in pulmonary capillaries directly to calculate the diffusion amount of oxygen; While the binding force of carbon monoxide (CO) to hemoglobin is higher than that of O₂210 times larger, oxygen partial pressure in the physiological range is not a major interfering factor; Except for heavy smokers, the content of carbon monoxide in the plasma of normal people is almost zero, which is convenient to calculate the intake of carbon monoxide in the examination; Moreover, carbon monoxide is rarely dissolved in plasma during transport, so carbon monoxide is an ideal gas for measuring lung diffusion function. 1915, Krogh^[1]According to the principle of diffusion, it was first proposed to measure the amount of lung diffusion (D_LCO).

OSAHS is a form of repeated apnea and hypopnea during sleep caused by partial or complete collapse of the upper airway, resulting in hypoxemia, hypercapnia and structural disorders of sleep^[1]Thus causing a series of clinical syndromes with pathophysiological changes. The purpose of this study was to compare the differences of common cardiopulmonary exercise test indicators in patients with OSAHS under different exercise loads, and to evaluate the early cardiopulmonary function impairment in patients with OSAHS.

acute respiratory distress syndrome (ARDS) is a common critical disease in clinic, and mechanical ventilation is the most important supportive treatment for ARDS patients. Whether spontaneous breathing or mechanical ventilation, the essence of pulmonary ventilation is the mechanical process by which the power of breathing overcomes resistance and drives the movement of the gas. Knowing the respiratory mechanics characteristics of ARDS patients is of great significance for understanding the pathophysiological mechanism of ARDS, grasping the principle of ventilator therapy, guiding the formulation of appropriate lung protective ventilation protocol, and reducing ventilator induced lung injury (VILI) caused by inappropriate mechanical ventilation.

Severe community-acquired pneumonia (CAP) is one of the most common causes of death in patients with infectious diseases, with a mortality rate of up to 30%^[1]The mortality rate of severe CAP after admission to ICU can be as high as 58%^[2]The mortality rate of patients with septic shock can reach more than 50%^[3]。 With the increase of antibiotic resistance rate, the mortality rate increases, and even the application of new antibiotics cannot significantly improve the prognosis of patients, so further research on the application of adjuvant therapy methods is needed^[4]。

In the ICU, the phenomenon of myasthenia in critically ill patients without the basis of acute or chronic neuromuscular disease is attracting attention. This phenomenon is called "intensive care unit – acquired weakness" (ICUAW)^[1]It is an important reason for the increase in mortality of critically ill patients^[2]。 Respiratory muscle weakness as a key part of acquired weakness^[3]The diaphragm is the most important respiratory muscle, and diaphragm dysfunction will lead to prolonged mechanical ventilation time, difficulty offline, and recurrent respiratory failure after extubation, thus increasing the incidence of complications in critically ill patients and occupying a large number of medical resources^[4]。 In the process of diagnosis and treatment of critically ill patients in ICU, critical illness itself (such as sepsis) and its treatment methods (such as mechanical ventilation, drugs, etc.) can have an impact on diaphragm function, which is summarized as follows.

The use of non-invasive assisted ventilation in patients with sleep disordered breathing disorders is well established^[1]However, with the increase of disease awareness and disease complexity, noninvasive assisted ventilation treatment for patients with some special types of sleep apnea, such as central type and complex sleep apnea, is also facing more and more difficulties. In order to better solve the practical clinical problems, the treatment mode of non-invasive assisted ventilation is also constantly improved. In recent years, new noninvasive assisted ventilation modes have emerged for the above-mentioned special nature of apnea. In order to enable clinicians to better understand, master and apply these new technologies, the application of noninvasive assisted ventilation in patients with central and complex apnea is briefly reviewed as follows.

Chronic obstructive pulmonary disease (COPD) is a respiratory disease characterized by chronic inflammation, small airway remodeling, and destruction of lung parenchyma (emphysema). It is estimated that by 2020, COPD will rank fifth in the world for the economic burden of disease and third in the world for the cause of death^[1,2]。 COPD currently affects approximately 10% of people over the age of 45, rising to 50% among heavy smokers^[3]。 In China, the prevalence of COPD in people over 40 years old reaches 8.2%^[4]Seriously aggravate the social and economic burden. Oxidative stress has been recognized as an important contributing factor to the onset of COPD. This paper reviews the mechanisms of oxidative stress involved in the pathogenesis of COPD, including (1) the source of pulmonary reactive oxygen species (ROS) and antioxidant system; (2) COPD and carbonyl stress; (3) oxidative stress and inflammation in the airways; (4) oxidative stress and emphysema; (5) oxidative stress and autoimmune response; (6) Host genetic susceptibility.

Bronchopleural fistula is a common serious disease. Patients are repeatedly complicated with pulmonary infection, empyema, etc., with poor quality of life, high treatment cost and high mortality. At present, the treatment of bronchopleural fistula mainly includes surgical treatment and minimally invasive treatment. The surgical treatment technique is relatively mature and has a high success rate, but it is traumatic and risky. In recent years, the development of interventional respiratory technology has provided many minimally invasive therapeutic approaches for the management of bronchopleural fistula. At present, there are many researches on minimally invasive treatment of bronchopleural fistula at home and abroad, mainly using materials for occlusion, including the following methods: (1) Balloon: Using arterial thrombotic catheter (including balloon) or floating catheter (including balloon) for occlusion^[1,2]。 (2) gelatin sponge, fibrin, autologous blood clot, or tissue glue sealing^[2,3]。 (3) endobronchial valves (EBV) occlusion^[4,5,6]。 (4) Self-expanding bronchial stent occlusion^[7]。 (5) Local injection of silver nitrate. (6) Topical Injection of Polidocanol Hardener^[8]。 (7) Nd: YAG Laser Therapy^[9]。

It is currently known that the main pathophysiological alterations of bronchial asthma (asthma) are chronic inflammation of the airways and dysfunction of the bronchial smooth muscle. However, this alone does not well explain the difference between asthma and other chronic airway inflammatory diseases such as chronic obstructive pulmonary disease (COPD). The author re-examines the existing research results, and tries to explore and explain the unique characteristics of airway lesions of asthma, which are different from other airway diseases, from a new angle.

pneumonia is one of the most common human diseases and is usually divided into community acquired pneumonia (CAP) and hospital acquired pneumonia (HAP) according to the place of infection. However, the actual clinical situation is ever-changing, and it is inevitable to generalize simply by classifying the place of incidence to guide the treatment. The factors influencing the treatment strategy of CAP are briefly described below for readers' reference.

A 27-year-old male, employee of the company, was admitted to the hospital on March 26, 2014 due to "repeated cough, chest pain and shortness of breath for 1 month". The patient developed dry cough after catching a cold in mid-February 2014, persistent chest pain, shortness of breath after climbing the third floor, no fever, hemoptysis, edema and polyuria, etc., and was not treated. On March 3, 2014, an X-ray chest radiograph in a foreign hospital showed "right pneumothorax", and the right lung basically recruited after "chest puncture and pumping"; On March 14, 2014, after severe cough, chest tightness and pain and shortness of breath after activity appeared again. X-ray chest radiograph showed "left pneumothorax", and the symptoms were significantly relieved after "chest puncture and pumping". On March 21, 2014, the above symptoms recurred, and the re-examination of chest X-ray showed "left pneumothorax". For further diagnosis and treatment, he was referred to our hospital on March 26, 2014. Past physical health, denied smoking history. Admission physical examination: normal development, superficial lymph nodes not swollen, mild cyanosis of the lips, no deformity of the thorax, and no rales in both lungs. The heart boundary was normal, the heart rate was 113 beats/min, and the rhythm was uniform. No murmur was heard in the auscultation area of each valve, and no abnormalities were found. Auxiliary examination: Blood gas analysis (inhaled oxygen concentration 35%) on 26 March 2014: partial pressure of carbon dioxide 40 mmHg (1 mm Hg =0.133 kPa), partial pressure of oxygen 61.5 mmHg, pH 7.422, oxygen saturation 92.1%. Blood routine on 27 Mar 2014: white blood cell count 9.54×10⁹/L, neutrophil count 6.19×10⁹/L, hemoglobin 147 g/L. There were no abnormalities in procalcitonin, liver and kidney function, rheumatic factor and immunoglobulin, and anti-nuclear antibody, anti-double stranded DNA antibody, anti-ENA antibody spectrum and anti-neutrophil cytoplasmic antibody were all negative. There were no abnormalities in electrocardiogram, cardiac color ultrasound, CT of abdomen and pelvis and brain, and bone ECT. Pulmonary function: mixed ventilatory dysfunction (FEV₁/FVC was 78.34%, FEV₁28.9% of the estimated value, VC 29.7% of the estimated value), the maximum ventilation volume decreased, the airway resistance was normal, the residual gas and residual total ratio increased, and the diffusion function was severely reduced. Chest CT (Figure 1、Figure 2、Figure 3、Figure 4、Figure 5、Figure 6、Figure 7、Figure 8): Multiple cystic cavities in both lungs, different sizes, partially fused, with the middle and lower lungs as the main, and no swelling of mediastinal lymph nodes.

Dear editor, hello!

First of all, I would like to thank Dr. Lu Ming for his letter and for his endorsement of the concept of "mixed pulmonary aspergillosis (MTPA)"^[1]； For information, responses to several of the questions raised in the letter are given below.

Bronchial asthma (asthma) is a common chronic respiratory inflammatory disease. Chronic inflammation can cause increased airway reactivity, leading to recurrent symptoms such as wheezing, shortness of breath, chest tightness, and/or cough. However, long-term inflammation can also cause airway wall remodeling in some patients. The main pathological manifestations are increased eosinophils, airway wall hyperplasia (basement membrane thickening, smooth muscle hyperplasia and hypertrophy, vascular proliferation and dilation), epithelial damage and shedding, bronchial subepithelial fibrosis, mucous gland hyperplasia causing mucus secretion hyperactivity, etc^[1]。 With the progress of industrialization, the global air, water and soil pollution is becoming more and more serious, and the morbidity and mortality of asthma are increasing year by year in the world, which has become a health problem of global concern^[2]。 mild asthma accounts for more than 50% of asthma patients, including mild intermittent asthma and mild persistent asthma^[3]。

The 7th event of Beijing Young Respiratory Scholars Salon in 2014 was held in Chinese Medical Association on December 25th, 2014. Respiratory doctors from many hospitals in Beijing jointly analyzed and discussed the "problems related to thermoplasty treatment of bronchial asthma". This salon activity was hosted by Dr. Li Nan of Peking University First Hospital.

pulmonary artery hypertension (PAH) is a type of disease characterized by mean pulmonary arterial pressure (mPAP) ≥25 mmHg (1 mmHg =0.133 kPa) at rest. It involves a wide range of diseases, is harmful, and lacks effective treatment means. In recent years, the research on PAH has made great progress, but its pathogenesis is still not very clear. Previous studies of our research group demonstrated that bone morphogenetic protein 4 (BMP4) mediates the upregulation of canonical transient receptor potential (TRPC) in rat pulmonary arterial smooth muscle cells (PASMCs), and this is the main cause of the proliferation of PASMCs. This study focuses on the upregulation of the signal transduction pathway of TRPC by BMP4.

In this study, peroxisome proliferator-activated receptor (PPAR) γ regulates calcium pool-manipulated calcium channel (SOCE) and transient receptor potential type I channel (TRPC) in chronic hypoxia model rats to identify its potential molecular mechanism. Rosiglitazone, a PPAR γ agonist, can alleviate the pathogenesis of chronic hypoxia model rats, inhibit the expression of vascular hypoxia-inducible factor (HIF) -1 α, TRPC1 and TRPC6 in distal pulmonary artery, and reduce the SOCE of smooth muscle cells in distal pulmonary artery of rats. Using RNA interference technique and recombinant adenovirus vectors for gene silencing and overexpression functional analysis, and luciferase double reporter detection based on bioinformatics analysis of the promoter region of TRPC, we confirmed that PPAR γ may exert anti-proliferative, anti-migratory and pro-apoptotic effects in rat pulmonary artery smooth muscle cells by inhibiting calcium pool manipulative calcium influx (SOCC) and TRPC expression, but these effects are inhibited under hypoxia or HIF-1 α accumulation. Under hypoxic conditions, accumulated HIF-1 α can act as upstream of PPAR γ to inhibit its expression level; On the other hand, PPAR γ, as a negative feedback regulator, can also inhibit HIF-1 α expression and HIF-1 α-mediated signaling pathway. PPAR γ may regulate the expression of SOCE and TRPC by inhibiting the expression of HIF-1 α and its signal transduction targeting, and ultimately slow chronic hypoxic pulmonary hypertension.