2016年 · 第39卷第12期

How to evaluate the academic value of a document? How to evaluate a scholar's academic influence? This is a focus concerning the vital interests of scholars, and it is also a difficult point which is widely concerned by the society. Therefore, in recent years, a variety of different views have emerged, such as "Sci-only theory". Professor Liu Youning, the editor-in-chief of this magazine, questioned the stipulation that "only academicians deserve to be first-class professors" in the column of "Essays of the Editor-in-Chief". Professor Liu believes that "the most important criteria for evaluating professors should be their teaching achievements, the number of students trained and the size of students' academic achievements", while academicians "mainly take creativity and scientific research achievements as the main evaluation criteria". The two emphasize different criteria and should not be mixed and matched.

Since about 2007, non-military teaching-related units began to formally rate professors, and linked them to salaries, pensions and other benefits. I don't know where the imperial edict came from, and I don't know why, but the cold reality is that only academicians can become first-class professors. In other words, no matter how old you are, how big your contributions are, how far-reaching your influence is, how outstanding you are in your job, and how many outstanding students you have trained, if you can't get to the threshold of academicians, don't expect to be the highest-level professor.

At present, the prevalence rate of OSAHS in China is about 4%, and the actual prevalence rate is higher than 4%. With the increasing number of obese people, the prevalence rate will increase accordingly. OSAHS is when a patient repeatedly experiences apnea and hypopnea during sleep. The clinical manifestations are moderate and severe snoring with uneven snoring, patients consciously hold their breath, or even repeatedly wake up, often accompanied by increased nocturia, headache, dizziness and oropharyngeal dryness in the morning. Due to the repeated cerebral cortex awakening and wake response at night, the normal sleep structure and rhythm are destroyed, sleep efficiency is significantly reduced, sleepiness that is difficult to suppress during the day, memory function decreases, cognitive dysfunction and abnormal behavior appear in severe cases. Due to repeated apnea and hypopnea at night, chronic intermittent hypoxia, carbon dioxide retention, increased sympathetic excitability and enhanced systemic oxidative stress response can lead to a series of serious cardiovascular and cerebrovascular diseases, metabolic disorders and aggravation of type 2 diabetes and insulin resistance. At present, it is generally believed that OSAHS is a systemic disease, and it is the source of many chronic diseases. At the same time, it is also an important cause of sudden death and traffic accidents, and it is a widespread social problem.

The aerosol inhalation has the advantages of direct action, low dosage, quick onset of action, low systemic drug concentration and high local drug concentration, and few adverse reactions^[1,2]。 The lesions of chronic obstructive pulmonary disease (COPD) are located in small airways, and the utilization rate of inhaled drugs is mainly related to the proportion of drugs inhaled into the lungs and their deposition rate in the peripheral lungs. By observing the proportion of nebulized drugs inhaled into the lungs and the proportion of nebulized drugs reaching the peripheral lungs under different breathing patterns and different nebulizing devices before and after education, the influence of breathing patterns and devices on the utilization rate of nebulized drugs was discussed.

Iatrogenic injury is the main cause of subglottic stenosis^[1]。 Because the "subglottis" is located between the lower edge of the vocal cord and the lower edge of the cricoid cartilage, surgery cannot completely remove the stenosis and easily leads to bilateral recurrent laryngeal nerve paralysis^[2]However, the efficacy of bronchoscopic interventional therapy is different, which is one of the difficult problems in clinical treatment. Among them, T-type silicone stent is also one of the methods for treating subglottic stenosis^[3,4]The previous T-shaped silicone stent was made of domestic materials, and its application was insufficient due to various factors. In 2014, Montgomery T-type silicone stent (referred to as "T-tube") was introduced in China. At present, there are only case reports of T-tube treatment of subglottic stenosis in China, and there is a lack of systematic reports on early postoperative complications^[5]。 This study summarizes the early complications of subglottic stenosis treated with a rigid bronchoscope-assisted T-silicone stent in a total of 13 cases in 12 patients.

Silicone stents refer to airway stents made of silicone rubber materials, which are mainly used to treat central airway stenosis and can also be used to treat tracheoesophageal fistulas. DUMON silicone stent (NovaTech, France) was listed in China in March 2014. At present, it is the only silicone stent that can be used in airways in China. There is still a lack of experience and related reports on the use of silicone stent in China. The purpose of this study was to summarize the efficacy and safety of DUMON silicone stent in domestic application.

Recently, one patient with fatal massive hemoptysis was successfully rescued by bronchial artery embolization after closing the bleeding airway on the affected side with a stone removal balloon in our hospital, which is reported as follows.

pulmonary alveolar proteinosis (PAP) is a rare pulmonary disease. The main pathophysiological basis is the excessive deposition of surfactant proteins and lipids with periodic acid-Schiff (PAS) staining positive in the alveoli and bronchioles. The literature reported that the incidence rate of this disease was 0.36~0.49/1 million to 3.7~6.2/1 million, the median age of onset was 39 years old, and the ratio of male to female was about 2.1:1^[1,2]。 PAP includes three types: congenital, idiopathic and secondary. High titers of anti-granulocyte-monocyte colony-stimulating factor (GM-CSF) autoantibodies were detectable in the sera of approximately 90% of PAP patients^[3]It is known as idiopathic PAP (iPAP) or autoimmune PAP. iPAP patients often present with dyspnea, some may be combined with bursting sound, clubbing fingers and cyanosis, serum biochemistry shows increased lactate dehydrogenase, lung function mainly manifests as restrictive ventilatory dysfunction and decreased diffusion function, almost 100% of patients have high titer anti-GM-CSF IgG antibody^[3,4]。 Chest CT showed bilateral diffuse pulmonary involvement, with extensive mosaic ground glass shadows and characteristic polygonal interlobular septal thickening forming a typical "paving stone" or "frost flower" pattern. Most of the lesions had clear boundaries and showed "map signs". A substantial proportion of patients did not involve the peripheral part of the lung field, including the costophrenic angle, apex, and subpleura, which is called "narrow zona pellucida". Typically, BALF is opaque milk-like, and precipitate and translucent supernatant can appear after standing. After centrifugation, the supernatant is colorless and transparent with white precipitate. BALF contains phospholipids and surface active proteins A, B and D, and the ratio of lecithin and phosphatidylglycerol is low. Cytological examination and PAS staining are necessary for diagnosis. Large foamy macrophages containing eosinophilic particles were observed in the lavage fluid, and there were homogeneous spherical transparent substances with PAS positive, mucus card red and Alcin blue staining negative outside the cells^[1]。 TBLB or surgically obtained biopsy is the gold standard for diagnosing PAP^[5,6]。 However, because PAP is not involved in the whole lung, false negative results may occur. A more common method for assessing the severity of disease was proposed in a cohort study in Japan, based on "symptoms and PaO₂"Perform a disease severity score (disease severity score, DSS)^[2,7]。

There is a group of patients with chronic cough who can't find a clear cause, and the treatment effect is poor. It was once called "unxplained chronic cough", "refractory chronic cough", isolated chronic cough, idiopathic chronic cough, etc. High sensitivity of cough reflex may be its important pathogenesis. Some scholars put forward the concept of "chronic cough hypersensitivity syndrome (CCHS)" in 2010^[1,2,3]The prevalence of CCHS is estimated to be more than 6%^[4]An epidemiological survey in South Korea showed that older women accounted for about 69.1% of adult patients^[5]。 CCHS are non-homogeneous diseases, but all of them have high sensitivity to cough reflex. They can be stimulated by various chemicals, odors and other environmental irritants to produce respiratory syndrome with cough as the main manifestation, and can be induced by capsaicin extracted from red pepper. transient receptor potential vanniloid receptor 1 (TRPV1) TRPV1 is an important molecule in the highly sensitive regulatory pathway of cough reflex discovered in recent years. It is a member of the transient receptor ion channel protein family. It is expressed on the peripheral and central C fibers of airways, lungs, etc. It is a nociceptor and an integrator that receives different stimuli. It is regulated by heat, acid and various endogenous peptides, and can be specifically activated by capsaicin, further activating the protein kinase family and causing Ca^2＋Ion channels open, prompting the synaptic vesicles to release neuropeptides that continue to signal to the center and along the cough reflex pathway, resulting in cough^{[6,7,8,9,10,11,12,13]}。 Therefore, some researchers have conducted intervention studies on the TRPV1 cough reflex pathway to try to find treatment strategies for chronic cough hypersensitivity syndrome.

1967 Ashbaugh et al.^[1]The concept of ARDS was proposed for the first time. In recent years, protective ventilation, fluid management, extracorporeal membrane oxygenation and other treatment strategies have been successfully applied in clinic. The mortality rate of patients has been reduced to some extent, but the mortality rate of patients with moderate and severe ARDS is still higher than 40%^[2]。 The clinical manifestations of ARDS lack specificity, and it is difficult to differentiate from cardiogenic pulmonary edema and severe pneumonia. Therefore, early accurate diagnosis and early intervention are very important to reduce mortality and improve prognosis. The "Berlin Standard" proposed in 2012^[3]The diagnosis of ARDS has a high accuracy rate, and according to the oxygenation index, ARDS is divided into three grades: mild, moderate and severe. The clinical stratification has a good correlation with pathophysiological mechanisms such as pulmonary edema and alveolar-capillary barrier damage, which can accurately reflect the severity of the patient's disease. But Thille et al.^[4]By analyzing the autopsy results of 712 cases from 1991 to 2010, it was found that the sensitivity of "Berlin criteria" in diagnosing ARDS was 89%, but the specificity was only 63%, and it was difficult to differentiate from cardiogenic pulmonary edema. In order to better diagnose and evaluate the prognosis of ARDS, attention has been turned to biomarkers related to the pathogenesis of ARDS.

Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disease that can involve large and small airways, pulmonary parenchyma and pulmonary blood vessels. It is characterized by incomplete reversible airflow restriction and is also recognized as a heterogeneous disease. Its heterogeneity is reflected in clinical manifestations, etiology, imaging, treatment response, lung function changes and prognosis, etc. In the past, the results of pulmonary function tests were mainly used to distinguish the severity of the disease and give graded treatment. However, the results of recent studies have shown that patients with the same degree of pulmonary function impairment can also have significantly different clinical symptoms and imaging manifestations, and patients with similar symptoms can also have significant differences in the treatment response of the same drug. Pulmonary function tests alone can no longer fully reflect the complexity of COPD. The phenotype of chronic obstructive pulmonary disease (COPD) has been a hot spot in clinical research in recent years. Patients with the same phenotype have similar biological or pathological mechanisms, so their clinical manifestations and treatment responses are also similar. At present, they are mainly divided into COPD-bronchial asthma (asthma) overlap syndrome, frequent acute exacerbation of COPD, emphysema COPD and systemic inflammatory COPD. With the continuous development of treatment methods, phenotypic classification of COPD according to disease characteristics can better guide the clinical formulation of targeted individualized treatment plans.

tuberous sclerosis complex (TSC) is closely related to lymphangioleiomyomatosis (LAM). TSC is a hereditary disease, and the patient's skin, nerves, lungs, abdominal organs and other places are involved. In terms of pulmonary manifestations, TSC patients mainly develop two pathological changes, namely multifocal micronodular pneumocyte hyperplasia (MMPH) and pulmonary lymphangioleiomyomatosis (PLAM), or tuberous sclerosis complex associated LAM (TSC-LAM)^[1]。 However, there are also sporadic cases, called sporadic LAM (S-LAM), which is not linked to genetics.

A 61-year-old male was admitted to the hospital on March 30, 2015 mainly because of "more than one year after upper lobectomy of the right lung and repeated holding breath for one year". The patient underwent right upper lobectomy more than 1 year ago due to a mass in the upper lobe of the right lung (14 February 2014), and the postoperative pathology confirmed that he was poorly differentiated squamous cell carcinoma. One month after operation, there was holding breath after activity, no fever, cough, expectoration, etc. Bronchoscopy performed in an outside hospital showed granulomatous hyperplasia of the right middle bronchus, and no tumor cells were found in pathology. After intermittent bronchoscopic granuloma resection and cryo-and balloon dilatation treatment, the symptoms could only be relieved for 2 to 3 weeks after each operation. Three months ago (December 2014), a metal stent (10 mm ×40 mm) was placed in the right main and middle bronchus in an external hospital, and the patient's symptoms were not relieved after operation. One month ago (Feb. 26, 2015), the patient saw scar stenosis of the right middle bronchial opening under bronchoscopy in an external hospital, and the granulation tissue embedded the stent severely (Figure 1), the local area can't handle it, and it is transferred to our hospital. After admission, the patient underwent interventional treatment with rigid bronchoscopy under general anesthesia on 2 April 2014. The Storz 8.5 rigid bronchoscope was inserted. During the operation, the trachea was patent, the mucosa was smooth, the left main bronchus and the bronchial lumen of each lobe segment were patent, and the right main bronchus was completely occluded at about 1 cm of the opening. The stent was all covered with hyperplastic granuloma tissue, and the stent was not visible. Using a rigid bronchoscope cryoprobe to freeze-cut and attempt to open the bronchus, turbid bloody secretion was seen to flow out, and the stent was still not visible. A holmium (Ho: YAG) laser (1.2 J, 10 Hz) was used to gently ablate the granulation tissue at the upper edge of the stenotic segment, exposing part of the upper edge of the scaffold. An annular cautery was performed along the upper edge of the stent, gradually exposing the entire upper edge of the stent. The upper edge of the stent was gently stripped using a rigid bronchoscopic biopsy forceps, but the stent could not be stripped due to severe granulation hyperplasia in the stent. An attempt was made to remove the granulation tissue in the stent using the tip of the Storz 8.5 rigid bronchoscope barrel because the lumen was too small to access. Switching to a Storz 6.5 rigid bronchoscope barrel, most of the granulation tissue in the stent was successfully removed. Holmium laser was used to remove the residual granulation tissue in the stent to fully expose the middle section of the stent. Switch to a Storz 8.5 rigid bronchoscope barrel, insert the upper edge of the stent into it, then rotate the barrel and gradually push it downward to completely separate the metal stent from the bronchial wall and remove it. After removal, the structural disorder of the right main bronchus and the distal bronchus, a large amount of granulation tissue in the tube wall, and stenosis of the opening of the middle and lower lobes were seen (Figure 2Scan the QR code to watch the surgical video). The procedure went smoothly with a small amount of bleeding. The patient's breath-holding symptoms were relieved after surgery, and the bedside chest X-ray examination on the same day (compared with before surgery) showed that the right lung was recruited (Figure 3，Figure 4)。 Patients were re-examined 2 weeks and 3 weeks after stent removal, and were re-treated with cryotherapy and balloon dilatation. One year later, the patient was followed up by telephone, and there was no obvious aggravation of breathlessness, and no further consultation was made.

The patient was a 31-year-old male. He was admitted to hospital on November 5, 2012 for the main reasons of "fever, chest pain for 15 days and hemoptysis for 1 day". The patient developed fever without obvious trigger 15 days ago, with a maximum body temperature of 37.8 ℃, accompanied by bilateral needle-like pain in the chest and back. Self-administered oral roxithromycin showed no improvement in symptoms. Five days ago, the patient's chest pain was worsened, and the blood routine in the emergency department of our hospital showed that the white blood cells were 13.4×10⁹/L, neutrophils 0.88, X-ray chest radiograph showed patchy high-density shadow of right lower lung (Figure 1)。 Diagnosis of pneumonia, intravenous infusion of cefuroxime (2.25 g/time, 2 times/d), fever and chest pain were not relieved. Hemoptysis occurred 1 d ago, bright red in color, about 5 ml in volume, accompanied by chest tightness, shortness of breath after activity, and chest CT showed double lower lung consolidation (Figure 2，Figure 3), was admitted for further diagnosis and treatment. Past physical fitness. Physical examination: Body temperature was 37.6 ℃, no rash, joint redness, swelling and deformity, superficial lymph nodes were not palpable and swollen, and a few wet rales could be heard in both lower lungs. Heart rate was 96 beats/min, P₂>A₂No murmur was heard in each valve area. The abdomen was flat and soft, without tenderness, the liver and spleen were not palpable under the costs, and there was no edema in both lower limbs. Initial diagnosis of admission: community-acquired pneumonia (CAP).

The 6th Beijing Young Respiratory Scholars Salon in 2016 was held on August 25th, 2016. The theme of this salon was "Re-understanding of Multiple (Diffuse) Cystic Lesions of the Lung (DCLD)", which was presided over by Dr. Huang Hui, Department of Respiratory Medicine, Peking Union Medical College Hospital. In order to make everyone have a perceptual understanding of DCLD, this salon first discusses 2 typical DCLD cases, and then introduces the consensus literature on DCLD in the past 2 years to standardize the clinical diagnosis and treatment process of DCLD.

Airway remodeling in bronchial asthma (asthma) involves immune, inflammatory responses and changes in airway structure, and ultimately leads to irreversible airflow restriction, increased airway resistance and aggravation of airway hyperresponsiveness, which is the pathological basis of refractory asthma. The transformation of fibroblasts (FB) to myofibroblasts (MF) is one of the important steps in airway remodeling in asthma. In the renin-angiotensin system (RAS), angiotensin converting enzyme (ACE) -angiotensin Ⅱ (AngⅡ) -angiotensin type Ⅰ receptor AT1 receptor axis can promote collagen formation, and whether the new branch of RAS antagonizing it, ACE2-Ang- (1-7) -Mas axis, can effectively inhibit the conversion of FB to MF, and down-regulate the levels of key proteins such as transforming growth factor β 1 (TGF-β 1), α-smooth actin (α-SMA) and collagen type Ⅰ (Col-Ⅰ), thus delaying the occurrence and development of asthmatic airway remodeling is still unclear. The purpose of this study was to investigate the role of Ang- (1-7) in the transformation of FB to MF induced by Ang Ⅱ.