Volume 98  ·  Issue 34  ·  2018

At present, new technologies represented by artificial intelligence have brought profound changes to people's production and life, and kicked off the prelude to the fourth industrial revolution^[1]。 The application of artificial intelligence in the medical field will bring medicine into a new era-the era of intelligent medicine. Intelligent medicine, as the name implies, is the "medicine" of "intelligence". Intelligence is the means and medicine is the purpose. At present, there is no clear definition of intelligent medicine. Combining the current development trend of artificial intelligence and medical field, the concept of intelligent medicine is put forward: intelligent medicine, that is, the science of assisting or replacing human beings in medical behavior through artificial intelligence.

1967, Ashbaugh et al.^[1]Twelve patients with dyspnea of acute onset are described, all presenting with hypoxemia difficult to correct with conventional oxygen therapy accompanied by reduced respiratory compliance and diffuse exudative lesions on chest X-ray, later this series of clinical manifestations became known as acute respiratory distress syndrome (ARDS). Fifty years have passed since ARDS was first proposed.

With the gradual deepening of the cognition of the pathophysiology of acute respiratory distress syndrome (ARDS), in order to correct severe hypoxia and promote the recovery of collapsed alveoli, experts in the field of critical illness have successively put forward the views of lung opening, lung protective ventilation and prone ventilation, but the clinical application is constantly questioned. According to the guidelines or expert consensus recommendation, the implementation of ventilation strategy not only fails to benefit some patients, but often produces opposite results or even serious complications, endangering patients' lives. This is because the establishment of artificial airway and positive pressure ventilation itself can effectively improve the ventilation and partial ventilation function, and because it is contrary to negative pressure respiration in human physiological state, it will inevitably cause damage to alveoli due to excessive positive pressure level, and even lead to alveolar rupture and serious complications such as mediastinal emphysema and pneumothorax, that is, mechanical ventilation-related lung injury (VILI). In addition, the pathogenic factors of ARDS vary widely, the heterogeneity of ARDS and the polymorphism of lung lesions also suggest that a single mechanical ventilation strategy is not suitable for all patients, so individualized pulmonary protective ventilation should be performed according to pathophysiological characteristics^[1,2,3]。 The importance of individualized mechanical ventilation has also been recognized in ARDS mechanical ventilation guidelines/expert consensus published in recent two years at home and abroad^[4,5,6]。

The mortality of acute respiratory distress syndrome (ARDS) is extremely high, which is a serious threat to the life of patients^[1]。 For many years, studies related to respiratory support in ARDS only protective lung ventilation strategies^[2]and prone position ventilation^[3]Extracorporeal membrane oxygenation (ECMO) can be used as a salvage measure to replace or partially replace cardiopulmonary function in patients with extremely severe ARDS who cannot be maintained by conventional mechanical ventilation strategies, and can also help reduce the incidence of ventilator-related lung injury (VILI). In 2009, the successful experience of intravenous-intravenous ECMO (VV-ECMO) in the treatment of extremely severe ARDS caused by novel influenza A (H1N1) virus inspired its application in this field^[4,5,6,7]； Some of the main results of the concurrent CESAR study and the newly published EOLIA study also confirm the advantages of ECMO in treating patients with extremely severe ARDS^[8,9]。 This will undoubtedly promote the widespread application of this technology in China. The pathophysiology, indication grasp and key process management of VV-ECMO are described below.

Acute respiratory distress syndrome (ARDS) is a clinical syndrome characterized by diffuse infiltrative lesions and progressive hypoxemia in both lungs caused by many etiologies. Its main pathophysiological manifestation is diffuse inflammatory alveolar epithelial cells and pulmonary capillary endothelial cells damage. In recent years, with the continuous deepening of research on ARDS, especially the discovery of inflammatory phenotype of ARDS in 2014, we have a further understanding of the pathophysiological characteristics of ARDS^[1]Although ARDS has common characteristics, the pathophysiological characteristics of ARDS are different due to the differences in pathogenesis caused by different risk factors. At the same time, its pathophysiological manifestations are also different at different stages of ARDS.

Acute respiratory distress syndrome (ARDS) is a complex clinical disease caused by many factors inside and outside the lung (such as pneumonia, sepsis, severe trauma, inhalation). Under the action of these injury factors, the inflammatory response in the lungs and the whole body is out of control, resulting in changes in alveolar capillary endothelial cells and alveolar epithelial cells, and increased capillary permeability, thus causing a large amount of fluid to seep into the alveoli and alveolar interstitium to cause pulmonary edema. Clinically, ARDS mainly manifests as progressive respiratory distress and refractory hypoxemia. In adults, the incidence of ARDS is approximately (17.6 to 64.0) per 100,000 per year, and in intensive care units the incidence is even higher than 10%^[1]。 Currently, the treatment of ARDS is still supportive treatment based on mechanical ventilation. Low tidal volume ventilation, positive end-expiratory pressure (PEEP), prone position ventilation, and neuromuscular blockers have been shown to be effective in a selection of patients with ARDS in clinical trials. Despite this, the mortality rate in hospital is still 20% ~50% at present^[1]。 Uncontrolled infection and extrapulmonary organ failure are the leading causes of death in patients with ARDS. In addition, survivors of ARDS may be complicated by chronic lung diseases such as pulmonary fibrosis, and neuromuscular diseases such as cognitive deficits and post-traumatic stress disorder, and their long-term prognosis is still poor. Therefore, on the basis of further understanding the pathogenesis of ARDS, it is an urgent requirement and challenge for basic and clinical workers to seek more effective drug therapy and biological therapy methods to improve the prognosis of patients with ARDS. The problems of drugs and biological therapy for ARDS are described.

To investigate the clinical features, diagnosis and therapy of hepatic perivascular epithelioid neoplasms (PEComa).

The clinical data of eleven patients with hepatic PEComa who received surgical treatment at Shengjing Hospital Affiliated to China Medical University from April 2012 to October 2017 were collected. The clinical manifestations, imaging features, diagnostic and therapeutic strategies, pathologic features, prognosis were analyzed.

The patients aged from 35 to 55 years (mean: 47 years , 3 males and 8 females). Two patients had epigastric pain, the others rarely had any clinical symptom. Hepatitis C virus (HCV) infection was present in one patient 9.09%(1/11), the rate of correct diagnosis by imageological examination before operation was only 9.09%(1/11). All patients received a surgical resection, the final diagnosis of hepatic PEComa was made with pathology and immunohistochemistry. The antibodies used for immunohistochemistry varied from patient to patient. The positive rates of Melan A, HMB45, smooth muscle actin and S-100 were 100%(10/10), 90%(9/10), 77.8%(7/9)and 33.3%(3/9) respectively, the Ki-67 positive index was 1%-10%. One patient died after surgery because of hemorrhage, other ten patients received long-term follow-up(5-71 months), and no recurrence or metastasis was observed.

Hepatic PEComa is a rare mesenchymal neoplasm which expresses both melanocytic and myogenic markers. Middle aged females are susceptive to hepatic PEComa, and patients rarely have any specific clinical presentation. It′s difficult to make a correct diagnosis before operation. The diagnosis finally depends on the pathological examination. Surgical resection and close follow-up are the principal methods for the management of hepatic PEComa.

To investigate the efficacy and safety of prophylactic use of pegylated recombinant human granulocyte colony-stimulating factor(PEG-rhG-CSF) in breast cancer receiving docetaxel as adjuvant chemotherapy.

A total of 58 patients with breast cancer receiving adjuvant chemotherapy with docetaxel were included between January 2014 to October 2017. Prophylactic use of PEG-rhG-CSF was administered.Patients were further divided into two groups according to the frequency of PEG-rhG-CSF use: frequent use group (≥3 cycles) and non-frequent use group (<3 cycles).

There were significant differences in the incidence rates of grade 3/4 neutropenia between the prophylactic group and non-prophylactic group in cycle 1-3(P<0.05). Less febrile neutropenia (FN) was also noted in the prophylactic group compared with the non-prophylactic group in cycle 1 and cycle 3 (P<0.05). Grade 3/4 neutropenia and FN were less in the frequent use of group compared with the non-frequent use group(P<0.001). The most common side effects of PEG-rhG-CSF included fatigue (10.2%), bone joint pain(50.8%), and 2 patients (3.4%) refused further treatment because of bone joint pain.

PEG-rhG-CSF should be prophylactically used for preventing neutropenia and febrile neutropenia in breast cancer patients receiving adjuvant chemotherapy with docetaxel regimen.

To analyze the clinical characteristics and prognosis of newly diagnosed localized head and neck rhabdomyosarcoma.

Cases of newly diagnosed localized head and neck rhabdomyosarcoma between January 2006 and December 2016 were analyzed retrospectively. The clinical features of the patients were described. The Kaplan-Meier method was used to analyze the survival rate under different combined modality therapy and the survival rate with or without chemotherapy. The prognostic factors were analyzed by Cox model.

A total of 46 patients were included in this study. Among them, the median follow-up time was 77 months and the median relapse free survival time was 13 months. The relapse free survival time of 5 cases with inadequate local treatment and without combined chemotherapy was 5 months as control, and it was 7 months (P=0.110) in 11 cases with adequate local treatment without combined chemotherapy. Then in 7 cases with inadequate local treatment combined with chemotherapy and 23 cases with adequate local treatment combined with chemotherapy, it was 13 months (P=0.007) and 21 months (P<0.001), respectively. The median relapse-free survival time of chemotherapy patients was significantly longer than that of those without chemotherapy (21 vs 6 months,P=0.018). The effect of combined modality therapy was evaluated according to the adequacy of local treatment and whether to receive systemic chemotherapy, and the combined modality therapy degree was the independent prognostic factor in Cox′s proportional hazards regression model (P=0.004).

Rhabdomyosarcoma in head and neck is a highly malignant tumor with high relapse rate and easy metastasis. In patients with tolerable condition, systemic chemotherapy and adequate combined modality therapy are recommended to improve relapse-free survival.

To summarize the clinical characteristics of silent paraganglioma.

A total of 247 pheochromocytoma cases in Peking University First Hospital between January 1993 and December 2015 were analyzed retrospectively.The cases were divided into two groups according to whether they had hypertension: non-silent group (193 cases) and silent group (53 cases), then the clinical characteristics between the groups were compared, and the clinical features of silent pheochromocytoma were reviewed.

There were 53 silent pheochromocytoma cases in this study, which accounted for 21.5% (53/247), and imaging was the main way to find the tumor. Forty-one in 53 cases (77.4%) located in adrenal gland, in which 31 cases (75.6%) were benign and 2.3-8.0 cm in diameter, while 10 cases (24.4%) were malignant and 3.5-12.0 cm in diameter. Twelve in 53 cases (22.6%) located in extra-adrenal tissue, in which 4 cases were benign and 2.0-5.5 cm in diameter, while 8 cases were malignant and 5.0-10.5 cm in diameter. With the tumor diameter increased, the malignant rate increased: 1 in 8 cases in diameter<3 cm, 2 in 12 cases in diameter 3-5 cm, 15 in 33 cases in diameter>5 cm were malignant. There was no significant difference in age, sex, tumor location, benign or malignant rate between the two groups (allP>0.05). Compared with the non-silent group, the proportion of tumor size≥5 cm in silent group was significantly higher (62.3% vs 45.9%,P=0.034), and the incidence of hyperglycemia and the concentrations of norepinephrine and epinephrine were lower (all P<0.05) in silent group.Misdiagnosis was common in silent group, and up to 35.8% (19/53) had not been diagnosed correctly before operation. Twenty-one in 53 (39.6%) silent pheochromocytoma cases occured severe intra-operative blood pressure fluctuation.

Silent pheochromocytoma was not uncommon and imaging was the main way to find it. The tumor size was always big and misdiagnosis was common, especially extra-adrenal tumors. Therefore, regardless of the adrenal or extra-adrenal tumors, especially in diameter>3.0 cm but with normal blood pressure, the possibility of silent pheochromocytoma should be considered. In order to reduce misdiagnosis and intra-operative blood pressure fluctuations, preoperative diagnosis and preparation, as well as intra-operative monitoring should be fully made.

To compare the effect of cold snare and hot snare on the resection of small colorectal polyps, and to explore the clinical value of cold snare technique in removing colorectal polyps.

From September 1, 2017 to January 31, 2018, 206 cases of patients with colorectal polyp resection in the Department of Gastroenterology of Peking University International Hospital were studied. During this period, according to the standard, 103 cases of patients (158 polyps) were in the cold snare group, and 103 patients (180 polyps) were randomly selected as control group from patients of the hot snare group. The related clinical data were analyzed retrospectively. The location, shape, size, polypectomy time, pathological type, complete resection rate, specimen recovery rate, complications and related costs of the two groups of polyps were compared.

The polypectomy time of the cold snare group was shorter than that of the hot snare group.The difference was statistically significant (Z=-11.727, P<0.001). The related cost of the perioperative period of the cold snare group was lower than that of the hot snare group.The difference was statistically significant (Z=-12.680, P<0.001). There were no statistically significant differences in the number of polyps/case, size, shape, pathological classification, complete resection rate, specimen recovery rate, and perioperative complications of the patients in the two groups(P>0.05).

The operation time of cold snare technique in colorectal polyps (6-9 mm in diameter) is shorter and the cost is lower, which is worthy of clinical promotion.

To investigate the association between kinase insertion region receptor (KDR) gene genetic variation and the efficacy of bevacizumab in patients with advanced colorectal cancer(CRC) were investigated in this study.

118 patients with advanced colorectal cancer who were treated by bevacizumab based first line regimens were included in this study. Peripheral blood and the biopsy tissue specimens of the CRC patients were collected for the genotyping of genetic variation and KDR gene expression, respectively. The univariate analysis of genotypes and prognosis was carried out by Kaplan-Meier survival analysis, and multivariate were adjusted by Cox regression analysis.

Located in the coding region, the prevalence of 889 C>T in KDR among the study population were as follows: CC genotype 86 cases (72.88%), CT genotype 30 cases (25.42%), TT genotype 2 cases (1.70%), minor allele frequency of 889 C>T is 0.14. The distribution of three genotypes in accordance with Hardy-Weinberg Equilibrium (P=0.737). There were no statistical differences in the distribution of the genotypes in baseline clinical data. TT and CT genotype patients were merged in the comparison of clinical outcomes. The clinical outcomes analysis of patients with different genotypes found that the objective response rates (ORR) of CT/TT genotypes were 34.38% and 43.02% (P=0.395), respectively. And the median progression free survival (PFS) of patients with CT/TT genotype and CC genotype were 7.5 and 9.7 months respectively, which was statistically significant (P=0.009). In terms of overall survival (OS), the median OS of the two genotypes were 19.3 and 20.1 (P=0.025), respectively. Adjusted in multivariate Cox regression analysis of PFS, CT/TT genotypes were an independent factor for PFS (OR=1.88, P=0.023). Additionally, of the 57 biopsy tissue specimens, gene expression analysis was conducted. And the results showed that the expression of KDR in cancer tissues of the patients with CT/TT genotypes were significantly higher than those of the CC genotype patients (P<0.001).

Among advanced colorectal cancer patients treated by bevacizumab, the polymorphism 889 C>T of KDR may impact the clinical outcomes of bevacizumab first line treatment by influencing the mRNA expression of KDR.

To investigate the effects of Toll-like receptor 4 (TLR4)-phosphatidylinositol 3-kinase (PI3K) -Ras-related C3 botulinum toxin 1 (Rac1) signaling pathway on macrophage cytoskeleton rearrangement and phagocytosis.

Mouse macrophage cell line RAW264.7 was divided into blank group, negative control group and TLR4-RNA interference (RNAi) group. The lentivirus carrying TLR4 short hairpin RNA (shRNA) and nonsense control sequence were respectively transfected into TLR4-RNAi group and negative control group. The cells in blank group were not transfected. The silencing efficiency of TLR4 was detected by Western blot. Real-time fluorescence quantitative PCR was used to detect the expression of PI3K and Rac1 mRNA in each group. The expressions of PI3K, p-Rac1 and Rac1 protein were detected by Western blot. Cytoskeleton was observed by laser scanning confocal microscopy. Mean fluorescence intensity (MFI) and the percentage of cells phagocytosing flurescein inothiocyanate-labeled Eseherichina coli (FITC-E.coli) (Phagocytosed cell %) were detected by flow cytometry.

The RAW264.7 cells can be successfully transfected by TLR4-shRNA lentivirus, and the transfection efficiency ranged from 80% to 90%. The silencing efficiency of TLR4 gene was (63±4)%. After silencing the TLR4 gene, the relative expression of TLR4 mRNA and protein (0.20±0.03, 0.37±0.04), PI3K mRNA and protein (0.64±0.06, 0.75±0.06), Rac1 mRNA, protein and p-Rac1 protein (0.75±0.04, 0.76±0.01, 0.74±0.05) in TLR4-RNAi group were significantly lower than those in negative control group and blank group (all P<0.01). The change of cytoskeleton: after silencing the TLR4 gene, the celluar pseudopods were short and stiff, with the impaired capacity of phagocytosing FITC-E.coli. Cells in blank group and negative control group extended good pseudopodia, and the capacity of phagocytosing FITC-E.coli was normal. The MFI and Phagocytosed cells % of TLR4-RNAi group[(7 453±564), (70.20±2.27)%]were significantly lower than those in the blank group and the negative control group (all P<0.01). Positive correlations were existed between mRNA, protein expression of TLR4, PI3K, Rac1 and MFI, Phagocytosed cells% (allP<0.05) in all groups.

TLR4-PI3K-Rac1 pathway involves in the cytoskeleton rearrangement and impairs the phagocytosis of macrophages.

To investigate the effect and mechanism of microRNA-146a (miR-146a) on Toll-Like Receptor 4 (TLR4) inflammatory signal pathway in the lung tissues of rats with mechanical ventilator-induced lung injury.

Thirty-two healthy male Sprague-Dawley rats were randomly divided into 4 groups (n=8 each): group A, normal control group, no mechanical ventilation, spontaneous breathing; group B, mechanical ventilation injury; group C, mechanical ventilation injury plus no-load virus transfection; group D, mechanical ventilation injury plus virus transfection; in group B, C, and D, mechanical ventilation were performed, respiratory rate was controlled at 80 beats/min, tidal volume was 40 ml/kg, inhaled oxygen concentration (FiO₂) was 21%, inhalation/expiration ratio was 1∶2, positive end expiratory pressure ventilation (PEEP) was 0, each group were ventilated 4 hours daily, 7 days continuously to establish ventilator induced lung injury (VILI) rat model. Paraffin-embedded sections of lung tissue were stained with HE, the morphology and damage of lung tissue were observed under microscope. The lungs wet and dry ratio (W/D), the levels of inflammatory cytokines interleukin (IL)-1β, IL-2 and tumor necrosis factor (TNF)-α were determined. Real-time PCR was used to detect the expression of TLR4 mRNA. The level of TLR4 protein was determined by Western blot.

The levels of lung tissue W/D and lung injury scores in group B (6.41±0.10, 11.38±0.92), group C (6.45±0.19, 11.75±1.04), group D (5.95±0.14, 7.53±4.78) were significantly increased than those in group A (4.33±0.08, 0.25±0.46), and in group D they were significantly decreased than group C (all P<0.01). The levels of IL-1β, IL-2, TNF-α in group B[(36.07±4.28) pg/ml, (5.02±0.63) ng/ml, (382.57±35.41) ng/ml], group C[(35.82±5.47) pg/ml, (4.98±0.71) ng/ml, (375.13±36.95) ng/ml], group D[(27.01±3.18) pg/ml, (3.96±0.82) ng/ml, (297.56±39.08) ng/ml]were significantly increased than those in group A[(21.46±3.15) pg/ml, (2.45±0.17) ng/ml, (195.92±18.07) ng/ml], and in group D they were significantly decreased than group C (allP<0.01). The relative expression levels of TLR4 mRNA and TLR4 proteins in group B (29.57±5.10, 0.75±0.110), group C (27.27±4.72, 0.77±0.130), group D (12.89±2.58, 0.48±0.057) were significantly increased than those in group A (1.02±0.13, 0.18±0.025), and in group D they were significantly decreased than group C (allP<0.01). There was no significant difference of all the above indicators between group B and C (allP>0.05).

MiR-146a can reduce acute lung inflammation and TLR4 expression in lungs of rats with mechanical ventilator-induced lung injury. MiR-146a may inhibit the inflammatory response through TLR4 signaling pathway.

To explore the influence of patatin-like phospholipase domain containing-3 (PNPLA3) wild type 148I/I and mutant type 148M/M on HepG2 cell proliferation and the relative mechanisms.

HepG2 cell line stably overexpressing PNPLA3 148I/I, 148M/M and negative control (NC) were set up. Cell counting kit-8 (CCK8) assay was used to measure cell viability. Edu assay was used to determine the ability of cell proliferation. Western blot was used to detect the protein levels in the phosphatidylinositol 3-kinases (PI3K) pathway. Enzyme-linked immunosorbent assay (ELISA) was used to detect proliferation-related PNPLA3 metabolites[arachidonic acid (AA) and lysophosphatidic acid (LPA)]. Quantitative real-time PCR was used to detect the expression level of prostaglandin G/H synthase 2 (PTGS2) and proliferator-activated receptor gamma coactivator 1-alpha (PGC1α) associated with PNPLA3.

The cell viability of overexpression of PNPLA3 148M/M group was about 1/3 times higher than that of overexpression of PNPLA3 148I/I group, and the difference was statistically significant[(98.02±1.29)% vs (71.51±2.89)%, P<0.001]. There was no significant difference between overexpression of PNPLA3 148M/M group and negative control group[(98.02±1.29)% vs (100±2.61)%,P=0.181]. The proliferative activity of overexpression of PNPLA3 148M/M group was about 1/3 times higher than that of overexpression of PNPLA3 148I/I group, and the difference was statistically significant(46.46±1.83 vs 35.96±2.65, P=0.001). There was no significant difference between overexpression of PNPLA3 148M/M group and negative control group(46.46±1.83 vs 46.64±7.33, P=0.965). The PGC1α mRNA expression, total PI3K, P_Thr-308AKT, P_Ser2448-mammalian target of rapamycin (P_Ser2448-mTOR) and PGC1α protein expression levels in the overexpression of PNPLA3 148M/M group were higher than those in the overexpression of PNPLA3 148I/I group, but there were no significant differences in AA and LPA levels, as well as PTGS2 mRNA expression levels.

PNPLA3 148M/M cell proliferation was stronger than PNPLA3 148I/I.

To study the mortality and death-related risk factors of patients hospitalized for asthma exacerbation in Chinese urban areas.

A retrospective study was carried out in 29 hospitals of 29 provinces throughout mainland China. Patients hospitalized for asthma exacerbation during 2013—2014 in each hospital were included. For each patient, information about demography, admission time, comorbidities, severity of diseases, intense care unit (ICU) admission, use of mechanical ventilation and the outcome was obtained. The mortality of patients hospitalized for asthma exacerbation was calculated, and the basic information and causes of death of the patients who died were summarized. The death-related risk factors and numbers of comorbidities were compared between the patients who survived and those who died during hospitalization.

A total of 3 240 patients (median age 57.0) were included and among them 8 patients (median age 68.5) died. The mortality of patients hospitalized for asthma exacerbation was 0.25%. All the patients who died were admitted during the winter and spring. One patient died of acute myocardial infarction, one of cardiac shock, one of tension pneumothorax, one of sudden death, one of respiratory failure and three of unknown causes. The average number of comorbidities of patients who died was 1.10, larger than that of patients who survived (0.83) (P>0.05). More patients had diabetes, coronary artery diseases and hypertension as comorbidities in the patients who died (2/8) than those who survived[7.6% (246/3 232), 7.6% (246/3 232), 22.6% (731/3 232), respectively](allP>0.05).

The in-hospital mortality of patients hospitalized for asthma exacerbation of China in this study is low. The patients who died are much older, and with more comorbidities, and a higher percentage of comorbidities such as diabetes, coronary artery diseases, and hypertension.

A 58-year-old male was admitted to hospital on May 18, 2015 due to "lymph node enlargement for more than 1 year, cough and fever for more than 4 months". The patient was found to have multiple lymph nodes swollen in the neck, axilla and groin in May 2014. The local hospital had given isoniazid, rifampicin and ethambutol anti-tuberculosis treatment for half a year without significant improvement. In January 2015, I developed a cough, cough of yellow and white phlegm, fever, and shortness of breath after activity. The local hospital gave a variety of antibiotics to treatment with poor results. After 10 days of treatment with imipenem and cilastatin sodium, the symptoms improved, and the lymph nodes shrank slightly, which increased again after discontinuation. In March of the same year, he went to the First Affiliated Hospital of Guangxi Medical University for treatment. Check white blood cells 19.2×10⁹/L, hemoglobin 90 g/L, neutrophils 15.3×10⁹/L. CT of the chest showed a large dense shadow of the right lung, effusion in the right pleural cavity, and swollen mediastinal lymph nodes. Cervical lymph node pathology showed granuloma formation, Langerhans giant cells and caseous necrosis, acid-fast staining positive bacteria, PAS staining (-), no fungi (FIG. 1A，FIG. 1B)； Negative pathogenic culture. After admission, he was treated with cefoperazone, tazobactam, moxifloxacin and fluconazole, and was treated with isoniazid, rifampicin, ethambutol, pyrazinamide and streptomycin for antituberculosis. The upper symptoms improved after treatment. Continuation of pentagrammatic anti-tuberculosis therapy outside the hospital. One month later, multiple rash and itching on the trunk and limbs appeared, cough, expectoration and fever recurred, and the lymph nodes on the left neck and axilla gradually swelled, and then he was admitted to the First Affiliated Hospital of Guangxi Medical University again. Spontaneous weight loss of 5 kg. Had shingles 1 year ago.

The patient, a 73-year-old male, was admitted to the Department of Urology, First Hospital of Jilin University on January 21, 2018 because the right kidney cyst was found in physical examination for 4 years and enlarged for 10 days after reexamination. Four years ago, the patient underwent color ultrasound during physical examination in the local hospital and found a right kidney cyst with a diameter of about 4 cm. It was not treated. After reexamination of color ultrasound 10 days ago, it was found that the cyst was enlarged. He came to our hospital for further diagnosis and treatment. Suffering from hypertension for 30 years, taking captopril tablets orally and measuring blood pressure at ordinary times 140/90 mmHg (1 mmHg =0.133 kPa). Diabetic history for 3 years, oral metformin, usual fasting blood glucose 7.0 mmol/L. Deny family history of tumor, deny history of exposure to carcinogens.

A series of anatomical and physiological changes in digestive tract organs caused by aging, coupled with high Helicobacter pylori infection rate, smoking, stress and the use of non-steroidal anti-inflammatory drugs and antithrombotic drugs, make the risk of acid-related diseases in the elderly significantly increased. At the same time, comorbidities and their concomitant multimedication are important characteristics of elderly patients, and therefore, the combination of proton pump inhibitors with common comorbidity-related drugs is very common in elderly patients. Combination of drugs will inevitably lead to drug interactions. Pharmacokinetic interactions can occur in four stages: absorption, distribution, metabolism and excretion, among which metabolic drug-drug interactions (MDDI) have the highest incidence. When two or more drugs are administered simultaneously or sequentially, the interference of the action in the metabolic link can enhance the curative effect or even produce toxic side effects, or cause the curative effect to weaken or even fail the treatment. In view of the high use rate of proton pump inhibitors in elderly patients with comorbidities, this paper intends to briefly explain the metabolic interactions between proton pump inhibitors and common concomitant drugs, in order to provide reference for the safe, effective and rational application of proton pump inhibitors.

Acquired von Willebrand syndrome (AvWS) is a class of hemorrhagic coagulation disorders caused by secondary von Willebrand factor (vWF) structural or functional disorders. Patients often present with unexplained gastrointestinal bleeding, the etiology is easily overlooked, or misdiagnosed as von Willebrand disease (vWD)^[1]。 Common secondary causes of AvWS include lymphoproliferative disorders (48%), cardiovascular disorders (21%), myeloid proliferative disorders (15%), other neoplastic disorders (5%) and autoimmune disorders (2%)^[1]。 Among them, AvWS secondary to cardiovascular disease are associated with hemodynamic abnormalities, and their etiology is the deletion of high molecular weight (HMW) vWF multimers. AvWS may be present in approximately 79% of patients with aortic stenosis (AS)^[2]90% of patients with severe AS and 50% of patients with moderate to severe AS may have AvWS, and severe massive bleeding can be seen in about 30% to 48% of patients with severe calcified AS^[3]Such patients can also present with chronic blood loss and anemia^[4]。 In addition, AvWS associated with hemodynamic abnormalities can also be seen in other valvular heart diseases^[5]Multiple congenital heart diseases^[6]Pulmonary hypertension type I^[7]Hypertrophic obstructive cardiomyopathy^[8]and receiving left ventricular assist device therapy^[9,10]Or receive extracorporeal membrane oxygenation system therapy^[11]of patients.

On July 27-29, 2018, the 15th China International Congress of Vascular Medicine and the 15th Anniversary Celebration were held in Beijing International Convention Center. It was sponsored by the Organizing Committee of China International Congress of Vascular Medicine, China Branch of International Vascular Health Society, Chinese Medical Education Association, and the Vascular Disease Community Prevention and Treatment Center of Peking University School of Medicine, and jointly organized by Shougang Hospital of Peking University, Basic Medical School of Peking University and Vascular Medicine Professional Committee of Chinese Medical Education Association. Professor Wang Hongyu, Vice President and Director of Vascular Medicine Department of Shougang Hospital of Peking University, Director of Vascular Disease Community Prevention and Treatment Center of Peking University School of Medicine, and Chairman of Vascular Medicine Professional Committee of Chinese Medical Education Association, served as the chairman of the conference. The theme of the 2018 conference is "Artificial Intelligence and Human Heart and Vascular Health".