2011年 · 第34卷第06期

After the reform and opening up, the field of scientific research in China has lifted all kinds of constraints and achieved rapid development, and the number of academic papers has increased in an "explosive" way. Around 1980, there were only about 500 papers collected by SCI in China every year, but by 2009, it had reached more than 110,000 papers, ranking second in the world. Some people expect that it will soon surpass the United States and become the largest paper producer in the world. These achievements are naturally gratifying, but at the same time, some worrying phenomena have followed, such as the low frequency of citations despite the huge number of papers, and occasional reports of papers from mainland China being revoked for academic misconduct. What is even more wary is that due to the wrong guidance of some domestic competent authorities, some units and individuals are obsessed with SCI, and even blindly worship them to the extent that they are regarded as omnipotent gods. Without SCI, you can't be promoted to professional titles, you can't get scientific research awards, and you can't even graduate without a doctorate certificate; In order to win in the comparison and competition between units, many hospital leaders have adopted the extreme incentive policy of rewarding RMB XX (4~5 Arabic digits are omitted here) for every increase in the impact factor of SCI papers. Faced with this situation, most ordinary medical workers are forced to bear tremendous pressure for no reason. Doctors who have worked in the clinical front line all year round and solved the sufferings of countless patients have been treated extremely unfairly only because they have no SCI papers. There are also some people who have been forced to embark on the road of no return of plagiarism and fraud. Faced with the above sad reality, a senior editor of a famous medical journal jokingly called SCI "Stupid Chinese Index"^[1]Of course, this title can't be said to be appropriate, but I think it still makes sense.

Professor Alexander Fleming has long been famous as the discoverer of the world's first antibiotic-penicillin, and British Prime Minister Winston Churchill is even more familiar, but did you know that there is another little-known story between these two men?

Professor Wu Shaoqing (1895-1980) is a famous pulmonologist, medical educator and first-class professor in China, and a pioneer of tuberculosis prevention in China. Professor Wu Shaoqing was born in a rural private school teacher family in Chao County, Anhui Province. He determined to study medicine since childhood. He graduated from Xiangya Medical College in 1921 with a doctorate in medicine. In 1929, he went to the United States for further study. During this period, he became interested in pulmonary department because of tuberculosis, and determined to change the pulmonary department and serve it for the rest of his life.

BACKGROUND AND OBJECTIVES: Guidelines for the treatment of COPD suggest that patients with moderate to very severe COPD should use inhaled long-acting bronchodilators to reduce the risk of symptoms and acute exacerbation, but do not determine whether the drug of choice is long-acting anticholinergic drugs or long-acting beta₂Receptor agonists. The aim of this study was to investigate whether the long-acting anticholinergic drug tiotropium bromide is superior to long-acting beta in preventing acute exacerbations of COPD₂Receptor agonist salmeterol. Methods: In a 1-year randomized, double-blind, double-dummy, parallel-group clinical trial, patients with moderate to very severe COPD with acute exacerbations in the previous year were selected to compare the effects of treatment with tiotropium bromide (18 μ g, once/d) with salmeterol (50 μ g, twice/d) on the incidence of moderate or severe acute exacerbations. Results: A total of 7376 patients were randomly assigned to receive tiotropium (3707) or salmeterol (3669). Compared with salmeterol, tiotropium delayed the time to the first acute exacerbation (187 d and 145 d, respectively) with a 17% risk reduction (hazard ratio 0.83, 95% confidence interval 0.77-0.90,P<0.01)。 Tiotropium bromide also delayed the first severe acute exacerbation (hazard ratio 0.72, 95% confidence interval 0.61-0.85,P<0.001), reducing the annual incidence of moderate or severe acute exacerbations (0.64 and 0.72, respectively, with a rate ratio of 0.89 and a 95% confidence interval of 0.83-0.96,P<0.01), and reduced the annual incidence of severe acute exacerbations (0.09 and 0.13, respectively, with a rate ratio of 0.73 and a 95% confidence interval of 0.66 to 0.82,P<0.01)。 The incidence of serious adverse events and adverse events leading to treatment discontinuation was similar in both groups. Sixty-four (1.7%) patients died in the tiotropium group and 78 (2.1%) in the salmeterol group. Conclusions: Tiotropium bromide is superior to salmeterol in the prevention of acute exacerbations in patients with moderate to extremely severe COPD.

BACKGROUND AND OBJECTIVE: Smoking is associated with pulmonary emphysema and radiological interstitial abnormalities, but we do not know the correlation between pulmonary interstitial abnormalities and decreased total lung volume and extent of emphysema. Methods: 2416 high-resolution CT (HRCT) of the lungs were obtained from a cohort study of smokers, from which smokers with pulmonary interstitial abnormalities were sought; Linear regression was used to evaluate the correlation between pulmonary interstitial abnormalities and total lung volume measured by HRCT and emphysema. Results: Of the 2416 lung HRCT scans evaluated, 8% (194/2416) had pulmonary interstitial abnormalities. In the adjusted statistical pattern, pulmonary interstitial abnormalities and decrease in total lung volume [-0.444 L, 95% CI (95%CI) is-0.596 to-0.292,P<0.01] and decreased degree of emphysema (-3%, 95%CIIs-4 to-2,P<0.01) correlation; Smokers with pulmonary interstitial abnormalities were more likely to have restrictive ventilatory dysfunction than smokers without pulmonary interstitial abnormalities (total lung volume less than 80% of the expected value, odds ratio 2.3, 95%CI1.4 to 3.7,P<0.01), and did not readily meet the diagnostic criteria for COPD (odds ratio 0.53, 95%CI0.37 to 0.76,P<0.01)。 The effect of pulmonary interstitial abnormalities on total lung volume and emphysema depends on the status of COPD (P<0.05)。 Pulmonary interstitial abnormalities were positively associated with greater smoking exposure and current smoking. Conclusions: Pulmonary interstitial abnormalities are associated with decreased total lung volume and decreased degree of emphysema in smokers.

Cryotherapy has been used in the diagnosis and treatment of airway diseases for more than 40 years. In 1968, Gage used a special cryoprobe to treat malignant tumors in the airway, which was the beginning of intra-airway cryotherapy^[1]。 Traditional cryotherapy, commonly referred to as "cryotherapy," directly kills tissue cells by low temperature. This cytotoxic effect is delayed, and it takes several days for local tissues to gradually necrotic and shed. Therefore, bronchoscopy should be performed again 8 to 10 days after freeze-thaw treatment to remove necrotic tissue. This delay makes freeze-thaw therapy unusable alone to treat acute airway obstruction caused by intracavitary tumor obstruction^[1]。 In 2004, Hetzel et al.^[2]With the help of a new type of cryoprobe, the tumor tissue can be directly adhered to and the obstructed airway can be opened quickly. Since then, the concept of cryorecannalization (CR) has been put forward. Since then, many scholars at home and abroad have verified the effectiveness and safety of this technology. Large histological specimens can be obtained during freezing treatment. Further research results found that these specimens are not only large in size, but also have good internal tissue structure integrity, and molecular markers on the cell surface and inside the nucleus are not damaged. Hetzel et al^[3]In 2008, the concept of "cryobiopsy" was formally proposed. Cryobiopsy is developed on the basis of cryo-resection, which is actually two different manifestations of the same technique in the diagnosis and treatment of diseases.

Lung cancer is one of the most common malignant tumors. At present, it is believed that the occurrence and development of lung cancer are regulated by genetics and epigenetics. Epigenetics includes DNA methylation modifications, histone modifications, and non-coding RNA-induced alterations. At present, it has been found that microRNA (miRNA) and DNA methylation have a complex interregulatory mechanism, and it is closely related to the occurrence and development of tumors^[1,2,3]。 The research progress of the interaction between the two in lung cancer is summarized as follows.

Pleural effusion is a common clinical disease or complication, and its immunological mechanism is not fully understood. Inflammatory mediators may be an important link in it. CC chemokines (CCL) 22 and 17 are cell-derived chemotactic mediators, which mobilize immune cells expressing corresponding chemokine receptor (CCR) through receptor-ligand pathway to migrate and reach the lesion to exert immune effect. We examined the pleural effusion and serum levels of CCL22 and CCL17 in patients with malignant and tuberculous pleural effusion to explore their immunological significance in the development of pleural effusion.

OSAHS is a common sleep disorder, which is characterized by recurrent apnea during sleep. chronic intermittent hypoxia (CIH) is considered to be the most important pathophysiological mechanism in the pathogenesis of OSAHS^[1]Its relationship with oxidative stress, inflammatory response and apoptosis has been reported^[2]。 Autophagy is another form of programmed cell death different from apoptosis, which plays an important role in cell growth, development and disease development, and is closely related to hypoxia, oxidative stress, etc^[3]The relationship between OSAHS and autophagy has not been reported. In this experiment, the pathophysiological process of OSAHS was simulated, and the mouse model of chronic intermittent hypoxia was established. At different intervention times (3 d, 1 week, 2 weeks, 3 weeks, 4 weeks), the ultrastructural changes of autophagy bodies in hippocampal CA1 region of chronic intermittent hypoxia mice were observed by transmission electron microscope, and the expression of microtubule-associated protein light chain 3 (LC3) in hippocampal CA1 region was detected. The activation of autophagy in hippocampal CA1 region of chronic intermittent hypoxia mice was observed, and the possible mechanism of autophagy in hippocampal neuronal damage induced by chronic intermittent hypoxia was preliminarily discussed.

In recent years, although the new drugs and methods for the treatment of lung cancer are increasing, lung cancer is still one of the malignant tumors with high mortality rate in China. The main reason is that the early diagnosis of lung cancer is difficult, and more than 1/3 of patients have developed distant metastasis at the time of diagnosis, among which lymph node metastasis is one of the important factors of poor prognosis. The results of animal experiments showed that cyclooxygenase-2 (COX-2) inhibitors could inhibit tumor growth and lymphangiogenesis and prevent lymph node metastasis^[1]。 nimesulide is the first selective COX-2 inhibitor^[2]It has good anti-inflammatory, analgesic and antipyretic effects, and has few gastrointestinal adverse reactions. The results of animal experiments showed that nimesulide could inhibit the growth of pancreatic, colon and lung cancer cells and induce apoptosis of tumor cells^[3,4,5]However, its mechanism of action and clinical dosage are unclear, which limits clinical application. In this study, we established a subcutaneous transplanted tumor model of human lung cancer in nude mice, and intervened the lung cancer model in nude mice with different doses of nimesulide to investigate its effects on the growth of human lung cancer transplanted tumors in nude mice and the effects on the expression of COX-2, vascular endothelial growth factor-C (VEGF-C) and vascular endothelial growth factor receptor-3 (VEGFR-3).

COPD is a polygenic genetic disease, and its molecular mechanism and susceptibility genes have not been fully understood. Transforming growth factor-beta₁(TGF-β₁As one of the relevant candidate genes for COPD, it has attracted much attention in recent years. In this study, TGF-β in Chinese Jiangxi Han nationality population₁The relationship between the polymorphism of gene promoter region (-800G/A and-509C/T) and exon 1 (+869T/C and +915G/C) and COPD susceptibility was discussed in order to provide theoretical basis for early prevention and treatment of COPD.

The patient was a 76-year-old female. Four months ago, there was no obvious trigger to cough, cough a small amount of thin white phlegm, in the local hospital according to "chronic pharyngitis" treatment, "Qingyan pill and amoxicillin" and other drugs, the cough symptoms were not relieved. One month ago, I was given "azithromycin, methylprednisolone and cefoperazone" treatment in the local hospital, but the effect was not good. One week ago, the patient developed inspiratory dyspnea, and the symptoms gradually worsened. Bronchoscopy was performed in a local hospital. Under the microscope, milky white necrosis was seen 4 cm below the glottis, which was attached in a ring shape, with a thickness of about 3 to 5 mm, and local stenosis. Subsequently, the patient's dyspnea was significantly aggravated, accompanied by lip cyanosis, and blood gas analysis showed hypoxia and carbon dioxide retention. He was urgently subjected to tracheal intubation and mechanical ventilation, and was transferred to our hospital for endoscopic treatment. The patient had previous hypertension for 10 years, and 2 years after gastroscopic resection of esophageal carcinoma in situ. He had been given multiple radiotherapy after the operation, and his condition was stable. The history of marriage and childbirth and family history are not special. Admission physical examination: body temperature 36.8 ℃, 20 breaths/min, heart rate 86/min, blood pressure 130/74 mm Hg (1 mm Hg =0.133 kPa). Clear consciousness, coarse breathing sound in the right lung, low breathing sound in the left lung, and no dry and wet rales; The heart boundary is not large, the heart rhythm is uniform, and no pathological murmur is heard; The abdomen was soft without tenderness, and there was no edema in both lower limbs. Auxiliary examination: X-ray chest radiograph showed heavy texture in the right lower lung, patchy blurred shadows near the left hilum, and enlarged and blurred bilateral hilar shadows. CT of the chest showed stenosis of the main airway, heavy texture at the tips of both lungs, some disordered texture, small patchy shadows in the left lower lung, slightly thicker left pleura, and multiple small lymph nodes in the mediastinum.

A 58-year-old male was admitted to the hospital on 16 August 2010 due to "progressive shortness of breath for 20 years, aggravated for 6 months". The patient developed shortness of breath without obvious trigger 20 years ago, which was aggravated after heavy physical activity. 20 years ago, he went to an outside hospital for bronchoscopy and was diagnosed with tracheal amyloidosis without special treatment. Occasionally, cough and white phlegm appear after a cold, accompanied by wheezing. In the past six months, the above symptoms have gradually aggravated, and cough and dyspnea have aggravated when exposed to cold air, oil fume and other peculiar odors. Now I feel shortness of breath when I walk on a flat road. He has smoked for 10 years, smoked an average of 10 cigarettes a day, and has quit smoking for 20 years. Physical examination at admission: body temperature 36 ℃, heart rate 72 beats/min, breathing 18 beats/min, blood pressure 124/96 mm Hg (1 mm Hg =0.133 kPa), no cyanosis of the lips, symmetrical breathing movement of both lungs, voiceless percussion of both lungs, coarse breathing sound at auscultation, and no dry or wet rales. Auxiliary examinations: Blood routine, urine routine, liver and kidney function, blood gas analysis and coagulation time were all normal. Pulmonary function showed variable intrathoracic upper airway obstruction. CT of both lungs and three-dimensional reconstruction of trachea showed that the middle and lower segments of trachea, partial calcification in irregular thickening of the wall, obvious stenosis of the lumen, normal carina and bilateral main bronchus (Figure 1)。 Bronchoscopy: Many places in the middle and lower tracheal walls saw bulges of different sizes protruding into the lumen, and the surface of the bulge showed pale yellow nodules, resulting in diffuse and irregular stenosis of the lumen, and the inner diameter of the narrowest part was less than 1/2 of the inner diameter of the trachea (Figure 2), the carina is sharp, the mucosal surface is smooth, and the size of the left and right main bronchial lumen is basically normal (Figure 3)。 When the nodule on the surface of the bulge was biopsied with a biopsy forceps, the texture felt tough, and there was a small amount of local bleeding after the forceps examination. Pathological examination showed a large amount of powder-stained amyloid deposition, cartilage and ossification under the tracheal mucosa, and Congo red staining (+), which was diagnosed as primary tracheal amyloidosis (Figure 4)。 Bronchoscopic high-frequency cauterization was performed on August 17, 2010 to remove the protruding lumen mass (Figure 5), the lumen was significantly enlarged after treatment, but the lumen was not regular enough (Figure 6)。 On August 25th, high-frequency electric cauterization was performed again, and high-pressure balloon dilation was performed to further enlarge the inner diameter and shape of the trachea. After treatment, the tracheal lumen was slightly more regular than before (Figure 7)。 After operation, the symptoms of shortness of breath were significantly improved after activity, and reexamination of both lungs CT and three-dimensional tracheal reconstruction showed that the stenosis of the lower tracheal lumen was improved compared with the previous one (Figure 8), lung function improved compared with before.

Rosai-Dorfman disease, also known as sinus histiocytosis with giant lymphadenopathy (SHML), was first reported by Rosai and Dorfman in the United States in 1969. It is a rare non-neoplastic histiocytosis with bilateral painless cervical lymph node hyperplasia and low fever, increased ESR, leukocytosis and hypergammaglobulinemia. Extranodal lesions, including skin, orbit, and nasopharynx, were present in approximately 1/3 of patients. Hyperactivation of nuclear factor-κ B (NF-κ B) is strongly associated with inflammation, neoplasms and autoimmune diseases. A case of extremely rare and fatal tracheal SHML without giant lymphadenopathy confirmed by surgery and pathology is reported, and its possible pathogenesis is discussed.

In recent years, the discussion about "SCI" has been rampant, with some praisers and some degraders. Especially in the field of medical research, it is directly linked to the evaluation of academic level, professional title, and even economic benefits. So what does SCI really stand for? Is it the Science Citation Index, or the Stupid Chinese Index? Professor Liu Youning, the editor-in-chief of this journal, who is very familiar with clinical, scientific research and journal work, has something to say about this. He called for "not to absolute SCI", and at the same time put forward pertinent suggestions for the development of this journal, which are worth thinking about.