2010年 · 第33卷第04期

The role of cigarettes in the pathogenesis of COPD has been highly valued^[1,2]。 However, 25% to 45% of COPD patients never smoke^[3]In addition to smoking, indoor and outdoor air pollution, occupational dust exposure, and history of lower respiratory tract infections in childhood also play an important role in the pathogenesis of COPD^[4]。

A large number of research results fully prove that smoking is the most important environmental factor leading to COPD, but not all long-term smokers will eventually suffer from COPD, and there are obvious differences in the susceptibility of COPD among different individuals among smokers. Fletcher and Peto^[1]It was pointed out 30 years ago that only those who are sensitive to tobacco effects among smokers have accelerated lung function decline, while the rate of lung function decline in insensitive people is not different from that of non-smokers. The research on the difference of COPD susceptibility among smokers has at least two important significances: (1) It is helpful to further elucidate the etiology and pathogenesis of COPD; (2) It is helpful to improve the efficiency of COPD prevention and treatment. If we can find markers of COPD-prone patients that are practical in clinical and epidemiological research work, so that we can prospectively and accurately find COPD-prone individuals among smokers, and carry out targeted intervention work, we can achieve more significant intervention effect. The author thinks that the research work in the following three fields should be further strengthened.

Looking back on the course of prevention and treatment of COPD, the prevention and treatment of COPD in China has gone through the following stages: in the 1970s, the focus of disease prevention and control was chronic pulmonary heart disease, and in the 1980s, most patients with chronic respiratory failure were treated. Since then, with the application of antibiotics and the progress of mechanical ventilation technology, the clinical treatment level of COPD has been greatly improved. In the 1990s, although the prevention and treatment of COPD has moved forward to the treatment of patients with acute exacerbation and stable stage, the economic burden brought by COPD to patients and the pain of disease are still heavy.

COPD is one of the diseases with high disability and mortality rates in the world. Acute exacerbation of COPD (AECOPD) is closely related to accelerated loss of pulmonary function, decreased quality of life and increased mortality. AECOPD results in repeated hospitalizations of patients and constitutes a major part of the cost of illness^[1,2]。 However, the definition of AECOPD and its severity lacks objective indicators and is mainly based on the patient's subjective symptoms and the doctor's judgment^[3]。 Therefore, it is necessary to search for one or more plasma biomarkers that are easily measurable to provide objective evidence of AECOPD. An ideal biomarker not only helps to distinguish the stable phase of COPD from AECOPD, but can also predict the severity of the condition. Most AECOPD are associated with acute respiratory bacterial and viral infections. AECOPD caused by pathogens and various irritants aggravates pulmonary and systemic inflammation, and this aggravation of inflammation suggests that it is possible to explore systemic biomarkers induced by inflammatory mediators.

COPD is a disease characterized by airflow restriction, which is not completely reversible and progressively developed, and is associated with abnormal inflammation of the lungs to harmful gases or particles such as cigarette smoke, which involves all levels of airways, pulmonary parenchyma and pulmonary blood vessels. It is generally believed that chronic pulmonary inflammation plays a major role in the formation of COPD and emphysema. Recent studies have shown that T cell-mediated inflammatory response is involved in the occurrence and development of COPD and emphysema, and it is related to the severity of the disease, suggesting that immune response may play an important role in it.

At present, there have been many studies on the etiology of COPD, but the influence of nasal diseases such as nasal cavity and sinus on COPD is little known. Available findings suggest that patients with COPD are often accompanied by nasal symptoms or nasal inflammatory diseases^{[1,2,3,4,5,6]}The presence of nasal symptoms can significantly reduce the quality of life of COPD patients^[7]And correlated with the exacerbation and deterioration of COPD patients^[8]。 In order to draw attention to the effect of nasal disease on COPD among respiratory physicians, we have conducted a review of relevant studies.

COPD is a chronic respiratory disease characterized by progressively developing, incompletely reversible airflow obstruction. The prevalence of COPD among people over 40 years old in China is 8.2%^[1]。 COPD is a polygenic disease with the interaction of genetic factors and environmental factors, and has a tendency to family aggregation. Smoking is the most important environmental risk factor for COPD, and people with genetic predisposition who smoke or have smoked can significantly decrease their lung function. The genetic susceptibility to COPD is one of the current research hotspots. We summarize its research progress as follows.

At present, BCG is the only tuberculosis vaccine that can be applied to human body, but its protective efficiency against adult tuberculosis is very low. DNA, polypeptide and virus subunit vaccines can enhance the immune protection effect of BCG or recombinant BCG vaccines, which is considered as one of the important directions of tuberculosis vaccine research^[1,2]。 Compared with DNA vaccine and polypeptide vaccine, the recombinant live TB subunit vaccine can continuously express MTB-specific antigen in vivo, which makes it efficient and economical. Recombinant Ag85A attenuated vaccinia virus vaccine can stimulate antigen-specific CD₄⁺T cell activation, especially in people who have been vaccinated with BCG vaccine, can produce long-lasting immune protection^[3]。 Attenuated Typhimurium strains expressing early secretary antigenic target 6000 (ESAT-6) increased pulmonary MTB clearance^[4]。 However, due to the large vector genome and many complications of the above-mentioned subunit vaccine, its further application is limited. The genetic background of adenovirus vector is clear, the virus particles are stable and safe. Therefore, the recombinant MTB secreted protein 64 (MPT64) subunit vaccine was constructed by adenovirus vector in this study, which provides new ideas for the study of new tuberculosis vaccine.

Aptamers screened by systematic evolution of ligands by exponential enrichment (SELEX) technology have the characteristics of in vitro synthesis, high purity, strong stability and easy preservation, and have been used to detect a variety of target substances. Aptamer has been reported to detect the content of interferon gamma in MTB secreted protein 64 (MPT64) and simulated pleural effusion^[1,2]Since MPT64 is one of the important antigens for serological diagnosis of tuberculosis, this study aimed to screen high-affinity aptamers of MPT64 antibody by SELEX technology and use them for serological detection, and conduct preliminary functional evaluation of the obtained aptamers.

Pulmonary thromboembolism (PTE) has a high incidence, disability and mortality rate, which has been paid attention to in clinical work in recent years. The diagnosis of PTE does not mean the end of the diagnosis, and the cause should be further searched and treated to avoid the risk of recurrence of PTE. Many hereditary and acquired risk factors have been identified, but 25% to 50% of PTE patients still have unknown etiology^[1]。 High density lipoprotein cholesterol (HDL-C) has antithrombotic and fibrolytic effects, and the reduction of HDL-C plays an important role in the occurrence of arteriosclerotic diseases. In this study, the correlation between HDL-C and PTE was studied in order to find out some causes of PTE.

sleep apnea hypopnea syndrome (SAHS) is a common and potentially dangerous disease, which can lead to targeted damage to multiple organs including cardiovascular system and urinary system^[1,2,3]However, whether there is organ specificity in its systemic damage is not well understood. By simulating the pathogenic characteristics of SAHS, we established a rat model of high fat combined with chronic intermittent hypoxia, dynamically observed the effects of chronic intermittent hypoxia on the ultrastructure of multiple organ tissues in rats on the basis of lipid metabolism disorder, compared the severity of injury, and explored the possible mechanism of multi-system targeted damage caused by SAHS.

A 57-year-old male was admitted to the hospital on 20 March 2008 due to "repeated cough for more than 2 months". In January 2008, the patient developed paroxysmal cough without obvious trigger, mainly dry cough, occasionally with a small amount of white sticky sputum, no fever, night sweats, no chest pain, and hemoptysis. At that time, no treatment was given. One month later, chest CT examination in another hospital showed nodules in the right upper lung. After one week of anti-infective treatment with penicillin sodium, there was no obvious change in the lesions, so we were admitted to our hospital. The patient had a previous history of diabetes mellitus for 2 years and smoking index of 60 pack years. Physical examination: the superficial lymph nodes of the whole body were unpalpable and enlarged, the breathing sounds of both lungs were clear, no dry and wet rales were heard, the heart rate was 70 beats/min, the heart rhythm was uniform, no pathological murmur was heard in the auscultation area of each valve, the abdomen was flat and soft, the liver and spleen were not palpable under the costs, and there was no edema in both lower limbs. Laboratory test: white blood cells 8.84×10⁹/L, blood neutrophils 0.57, hemoglobin 170 g/L, liver and kidney function normal, ESR, C-reactive protein normal, carcinoembryonic antigen, neuroenolase, SCC squamous cell carcinoma related antigen normal, rheumatic factor and allergen detection negative, immunoglobulin and complement normal. Sputum cancer cells and acid-fast bacilli were negative, sputum smears were found spores twice, sputum culture showed Candida albicans, and serum 1,3-β-D-glucan antigen detection (G test) and serum galactomannan antigen detection (GM test) were negative. Auxiliary examination: Pulmonary function was normal, bone ECT (emission single photon computed tomography) and cranial magnetic resonance examination showed no abnormalities. One week after admission (March 28, 2008), the chest CT examination revealed a nodule of about 3 cm ×2 cm in the posterior segment of the right upper lung, with burrs at the edge, inobvious lobulation, uneven density, and vacuolar sign. After enhancement, the edge of the lesion was enhanced, involved with the visceral pleura, without calcification, and without satellite foci. It was considered that lung cancer was likely (Figure 1，Figure 2，Figure 3，Figure 4，Figure 5，Figure 6)。

The 8th event of Beijing Young Respiratory Scholars Salon in 2009 was held on November 24th, 2009. The event was hosted by Dr. Yang Hui of Respiratory Department of Shougang Hospital of Peking University, and the theme was "Discussion on Related Issues of Home Mechanical Ventilation".

For a long time, the role of smoking in the pathogenesis of COPD has been highly valued, but there are also patients with COPD who never smoke, which indicates that there are other pathogenic factors besides smoking, and biofuel smoke is one of them. Biofuels are the main source of energy for households. About 3 billion people worldwide are exposed to biofuel smoke, which harms far more people than those exposed to cigarette smoke. Therefore, biofuel smoke exposure may be the biggest risk factor for the onset of COPD, which cannot but be of great concern to us. In this issue, Professor Ran Pixin was specially invited to combine the research work of the State Key Laboratory of Respiratory Diseases of Guangzhou Institute of Respiratory Diseases to write a review of "The role of biofuels in the pathogenesis of chronic obstructive pulmonary disease cannot be ignored", and synthesized relevant data at home and abroad to explain the latest research trends, existing problems and future research directions in this field, hoping to attract everyone's attention. Professor Xu Yongjian specially wrote an article for the special written talk column "Strengthening the research on the differences and causes of predisposition to chronic obstructive pulmonary disease among smokers". His predisposition to COPD among smokers has always been concerned by scholars, but there is no conclusion at present. Professor Xu discussed this problem and pointed out the problems, feasible methods and ideas that should be studied, which is very enlightening. Professor Yao Wanzhen discussed "several opinions on promoting the implementation of prevention and treatment strategies of chronic obstructive pulmonary disease" from a macro perspective, and used the past as a metaphor for the present to explain the importance of the concept of tertiary prevention put forward by modern medicine. Professor Yao believes that COPD can be prevented and cured, but it should be prevented and treated early. Intervention should be carried out in the early stage of the disease. In addition to health publicity and education, avoiding exposure to risk factors and vaccination, drug intervention should also be carried out.