Objective:To explore the role and related mechanism of myeloid related differentiation markers (MYADM) in lung adenocarcinoma metastasis induced by high cholesterol diet.Methods:(1) Cell experiments: Using lung adenocarcinoma A549 and H1975 cells, the cells were treated with 0.8 mg/ml cholesterol and then transfected with a lentivirus to knock down MYADM. The overexpression of MYADM was achieved by transfecting the cells with an overexpression plasmid. Western blotting was used to detect the expression levels of MYADM, E-cadherin, β-catenin, MMP-2, MMP-9, and vimentin in the cells. The proliferation ability of the cells was assessed using the plate clonal formation assay, while the migration and invasion ability were evaluated using the Transwell assay. Western blot was used to determine the effects of MYADM knockdown or overexpression on these proteins. Western blot and immunofluorescence assays were conducted to investigate the impact of Akt phosphorylation on the expression of MYADM and Rac1 in cholesterol-treated lung adenocarcinoma cells, as well as the phosphorylation of c-Myc. Western blot was also used to assess the effect of c-Myc knockdown on the expression of MYADM and MCT1 in lung adenocarcinoma cells. Chromatin immunoprecipitation (ChIP) assays were performed to investigate the impact of cholesterol on the binding between c-Myc and the promoters of MYADM and MCT1 in lung adenocarcinoma cells. (2) Animal experiment: A549 cells or A549 cells with MYADM knockdown were intravenously inoculated into BALB/c nude mice, which were then divided into a normal diet group and a high cholesterol diet group. Using a live imaging system, the growth and metastasis of tumors in the mice were monitored. After 42 days, lung tissues were collected for immunohistochemical staining to detect changes in relevant proteins.Results:After cholesterol treatment, the expression level of MYADM in A549 cells increased from 1.00±0.18 to 3.28±0.28 ( P<0.001), and in H1975 cells, it increased from 1.00±0.06 to 2.03±0.10 ( P<0.001). Compared with the control group, the expression of E-cadherin in lung adenocarcinoma cells after MYADM knockdown increased ( P<0.01), while the expressions of β-catenin, MMP-2, MMP-9, and vimentin decreased (all P<0.01). After MYADM knockdown, the number of clonal plates decreased in A549 cells (203±23 vs 60±18, t=8.48, P=0.001) and H1975 cells (298±64 vs 137±51, t=3.41, P=0.271). The number of invasive cells also decreased in A549 cells (212±18 vs 99±34, t=5.09, P=0.007) and H1975 cells (268±34 vs 134±14, t=6.31, P=0.003). Additionally, the number of migratory cells decreased in A549 cells (353±37 vs 124±29, t=8.44, P=0.001) and H1975 cells (279±41 vs 79±19, t=7.67, P=0.002). In the lung adenocarcinoma cells overexpressing MYADM, the expression of E-cadherin decreased ( P<0.01), while the levels of β-catenin, MMP-2, MMP-9, and vimentin increased (all P<0.01). The number of plate clonal colonies formed by lung adenocarcinoma cells overexpressing MYADM increased significantly in A549 cells, (94±26 vs 298±34, t=8.26, P=0.001) and H1975 cells (83±13 vs 331±24, t=15.74, P<0.001). The number of invasive A549 cells also increased (118±17 vs 193±24, t=4.41, P=0.012) and (156±19 vs 321±12, t=12.72, P<0.001). Additionally, the number of migrating cells increased in A549 cells (171±22 vs 284±15, t=7.35, P=0.002) and in H1975 cells (178±7 vs 263±12, t=10.6, P<0.001). Experiments related to the molecular mechanism showed that overexpression of MYADM promotes the expression of MCT1 in lung adenocarcinoma cells (all P<0.01). Cholesterol not only enhances the expression of MYADM in lung adenocarcinoma cells, but also boosts the expression of Rac1 and MCT1, as well as the phosphorylation of Akt and c-Myc (all P<0.05). Immunoprecipitation experiments revealed that in A549 cells treated with cholesterol, MYADM-Rac1 interaction levels increased from (100.0±15.9)% to (191.0±26.7)% ( P=0.007), while in H1975 cells, the levels increased from (100.0±18.2)% to (170.0±27.5)% ( P=0.021). ChIP confirmed that cholesterol treatment enhances the binding of c-Myc to the promoters of MYADM and MCT1. In vivo experiments demonstrated that a high-cholesterol diet promotes the metastasis of lung adenocarcinoma cells in mice, inducing the expression of MYADM, MCT1, and Rac1, as well as the phosphorylation of Akt and c-Myc in mouse lung tissue. Conversely, knocking down MYADM inhibits the metastasis of lung adenocarcinoma cells in mice, suppressing the expression of MYADM, MCT1, and Rac1, as well as the phosphorylation of Akt and c-Myc in mouse lung tissues. Conclusion:Cholesterol may induce lung adenocarcinoma cells proliferation and metastasis by regulating the MYADM/Rac1/Akt/c-Myc/MCT1 axis.

Objective:To explore the role and related mechanism of myeloid related differentiation markers (MYADM) in lung adenocarcinoma metastasis induced by high cholesterol diet.Methods:(1) Cell experiments: Using lung adenocarcinoma A549 and H1975 cells, the cells were treated with 0.8 mg/ml cholesterol and then transfected with a lentivirus to knock down MYADM. The overexpression of MYADM was achieved by transfecting the cells with an overexpression plasmid. Western blotting was used to detect the expression levels of MYADM, E-cadherin, β-catenin, MMP-2, MMP-9, and vimentin in the cells. The proliferation ability of the cells was assessed using the plate clonal formation assay, while the migration and invasion ability were evaluated using the Transwell assay. Western blot was used to determine the effects of MYADM knockdown or overexpression on these proteins. Western blot and immunofluorescence assays were conducted to investigate the impact of Akt phosphorylation on the expression of MYADM and Rac1 in cholesterol-treated lung adenocarcinoma cells, as well as the phosphorylation of c-Myc. Western blot was also used to assess the effect of c-Myc knockdown on the expression of MYADM and MCT1 in lung adenocarcinoma cells. Chromatin immunoprecipitation (ChIP) assays were performed to investigate the impact of cholesterol on the binding between c-Myc and the promoters of MYADM and MCT1 in lung adenocarcinoma cells. (2) Animal experiment: A549 cells or A549 cells with MYADM knockdown were intravenously inoculated into BALB/c nude mice, which were then divided into a normal diet group and a high cholesterol diet group. Using a live imaging system, the growth and metastasis of tumors in the mice were monitored. After 42 days, lung tissues were collected for immunohistochemical staining to detect changes in relevant proteins.Results:After cholesterol treatment, the expression level of MYADM in A549 cells increased from 1.00±0.18 to 3.28±0.28 ( P<0.001), and in H1975 cells, it increased from 1.00±0.06 to 2.03±0.10 ( P<0.001). Compared with the control group, the expression of E-cadherin in lung adenocarcinoma cells after MYADM knockdown increased ( P<0.01), while the expressions of β-catenin, MMP-2, MMP-9, and vimentin decreased (all P<0.01). After MYADM knockdown, the number of clonal plates decreased in A549 cells (203±23 vs 60±18, t=8.48, P=0.001) and H1975 cells (298±64 vs 137±51, t=3.41, P=0.271). The number of invasive cells also decreased in A549 cells (212±18 vs 99±34, t=5.09, P=0.007) and H1975 cells (268±34 vs 134±14, t=6.31, P=0.003). Additionally, the number of migratory cells decreased in A549 cells (353±37 vs 124±29, t=8.44, P=0.001) and H1975 cells (279±41 vs 79±19, t=7.67, P=0.002). In the lung adenocarcinoma cells overexpressing MYADM, the expression of E-cadherin decreased ( P<0.01), while the levels of β-catenin, MMP-2, MMP-9, and vimentin increased (all P<0.01). The number of plate clonal colonies formed by lung adenocarcinoma cells overexpressing MYADM increased significantly in A549 cells, (94±26 vs 298±34, t=8.26, P=0.001) and H1975 cells (83±13 vs 331±24, t=15.74, P<0.001). The number of invasive A549 cells also increased (118±17 vs 193±24, t=4.41, P=0.012) and (156±19 vs 321±12, t=12.72, P<0.001). Additionally, the number of migrating cells increased in A549 cells (171±22 vs 284±15, t=7.35, P=0.002) and in H1975 cells (178±7 vs 263±12, t=10.6, P<0.001). Experiments related to the molecular mechanism showed that overexpression of MYADM promotes the expression of MCT1 in lung adenocarcinoma cells (all P<0.01). Cholesterol not only enhances the expression of MYADM in lung adenocarcinoma cells, but also boosts the expression of Rac1 and MCT1, as well as the phosphorylation of Akt and c-Myc (all P<0.05). Immunoprecipitation experiments revealed that in A549 cells treated with cholesterol, MYADM-Rac1 interaction levels increased from (100.0±15.9)% to (191.0±26.7)% ( P=0.007), while in H1975 cells, the levels increased from (100.0±18.2)% to (170.0±27.5)% ( P=0.021). ChIP confirmed that cholesterol treatment enhances the binding of c-Myc to the promoters of MYADM and MCT1. In vivo experiments demonstrated that a high-cholesterol diet promotes the metastasis of lung adenocarcinoma cells in mice, inducing the expression of MYADM, MCT1, and Rac1, as well as the phosphorylation of Akt and c-Myc in mouse lung tissue. Conversely, knocking down MYADM inhibits the metastasis of lung adenocarcinoma cells in mice, suppressing the expression of MYADM, MCT1, and Rac1, as well as the phosphorylation of Akt and c-Myc in mouse lung tissues. Conclusion:Cholesterol may induce lung adenocarcinoma cells proliferation and metastasis by regulating the MYADM/Rac1/Akt/c-Myc/MCT1 axis.

OBJECTIVE To provide a reference for the standardized treatment of chronic obstructive pulmonary disease （COPD） and the adjustment of therapeutic drugs for COPD in the national essential medicine list. METHODS Relevant clinical experts， pharmaceutical experts and medical insurance experts were invited to sort out the COPD treatment drugs involved in the domestic and foreign COPD clinical guidelines， the national essential medicine list， the WHO standard list of essential medicine， the national medical insurance catalogue， and comparatively analyzed the COPD treatment drugs. RESULTS & CONCLUSIONS Compared with domestic clinical guidelines， foreign clinical guidelines included an additional COPD triple preparation， while involving fewer types of expectorants and antioxidants； there were only 12 kinds of COPD treatment drugs included in the WHO standard list of essential medicine， while there were 18 kinds in the national essential medicine list in China， and more theophylline drugs， expectorants and antioxidants were included. In addition， 15 kinds of COPD treatment drugs were found in both the national clinical guidelines and the national medical insurance catalogue， but not in the national essential medicine list， including terbutaline， levalbuterol hydrochloride， salmeterol， formoterol， indacaterol， beclometasone， mometasone furoate， salbutamol ipratropium， glycopyrronium formoterol， umeclidinium vilanterol， indacaterol glycopyrronium， beclometasone formoterol， budesonide/glycopyrrolate/formoterol fumarate， fluticasone furoate/vilanterol/umeclidinium， and fudosteine， which were mainly long-acting beta 2-agonists and COPD triple preparations. These drugs had certain evidence-based medicine evidence， their efficacy and economy had certain advantages， and their impact on the budget of the medical insurance fund was controllable. Therefore， it is suggested that the aforementioned drugs should be included in the essential medicines list in the subsequent update.

The data of a case of congenital subglottic stenosis (C-SGS) who underwent slide laryngotracheoplasty in the Center for Respiratory Intervention, Children′s Hospital Affiliated to Shandong University in December 2021 was analyzed retrospectively.The patient was a girl aged 2 months and 15 days.She visited the hospital 23 days after tracheotomy due to dyspnea for more than 2 months.The bronchoscopy and annular cartilage B ultrasound results suggested subglottic stenosis and no scar hyperplasia.Based on the medical history, the child was diagnosed with C-SGS.Slide laryngotracheoplasty was performed 2 weeks after admission, and the tracheotomy tube was removed after surgery.The child was followed up 2 months after surgery, and she recovered well with no dyspnea.The study results suggest that early and safe slide laryngotracheoplasty after definite diagnosis can provide immediate and sufficient airway space for C-SGS patients, and protect their voice and swallowing function.

Eosinophil extracellular traps (EETs), an important pathway of eosinophil to exert its effects, are composed of DNA fibers, histone and eosinophil granule proteins. Recently, many researches have shown that EETs play an important role in the genesis and development of respiratory diseases including asthma, allergic bronchopulmonary aspergillosis and chronic obstructive pulmonary disease. EETs can directly damage airway epithelial cells, promote airway inflammation and airway hypersecretion, increase the stickiness of secretions and induce the generation of autoantibody, helping eosinophils and their products participate in a cascade of events leading to inflammation and disease. Researches on EETs can also be helpful in investigating new targets for the treatment of chronic airway diseases.

Objective To compare the anesthetic effects of interscalene brachial plexus combined with ulnar nerve and axillary brachial plexus block guided by nerve stimulator. Methods Eighty patients belonging to ASA ⅠorⅡ and undergoing replantation of severed palm or wrist were divided randomly into 2 groups, Each group had 40 patients. Nerve stimulator guided nerve block. Patients in groupⅠreceived interscalene brachial plexus combined with ulnar nerve block, and those in groupⅡreceived axillary brachial plexus block. The onset time, hold time, tourniquet tolerance of radial nerve, median nerve and ulnar nerve of two groups was recorded. The phrenic nerve block, Horner′s syndrome and recurrent laryngeal nerve block was compared between two groups. Results The onset time of radial nerve, median nerve and ulnar nerve in group Ⅰwas (5.13 ± 0.76), (7.13 ± 1.04), (3.23 ± 0.62) min , in group Ⅱ was (9.23 ± 1.61), (12.35 ± 1.76), (8.83 ± 1.13) min, and there were significant differences (P<0.05). The excellent rates of sensory block of radial nerve, median nerve and ulnar nerve in group Ⅰ were 90.0%(36/40), 85.0%(34/40), 97.5%(39/40), in group Ⅱ were 72.5%(29/40), 65.0%(26/40), 70.0%(28/40), and there were significant differences (P<0.05). The full rates of motor block of radial nerve, median nerve and ulnar nerve in groupⅠwere 75.0%(30/40), 37.5%(27/40), 80.0%(32/40), in groupⅡ were 47.5%(19/40), 40.0%(16/40), 45.0%(18/40), and there were significant differences (P < 0.05). The tourniquet tolerance rate in group Ⅰwas significantly higher than that in groupⅡ:90.0%(36/40) vs. 62.5%(25/40) , P<0.05. In groupⅠ, phrenic nerve block occurred in 2 patients, and Horner syndrome occurred in 1 patient. None had laryngeal recurrent nerve block in both group. Conclusions The interscalene brachial plexus combined with ulnar nerve block guided by nerve stimulator is more suitable for a long time microsurgery of the palm or wrist, because it takes action faster, has better sensory and motor block effects, improves the rate of tourniquet tolerance without increasing untoward reaction.

Hematologic Neoplasms ; Hepatitis E virus ; Humans

Objective: To explore the efifcacy and safety of sildenaifl for treating the patients of congenital heart disease (CHD) with severe pulmonary hypertension in plateau area.
Methods: A total of 50 CHD patients combining severe pulmonary hypertension treated in our hospital from 2010-01 to 2013-10 were studied. The patients were randomly divided into 2 groups, n=25 in each group. Control group, the patients received conventional treatment and Sildenaifl group, based on conventional treatment, the patients received additional sildenaifl medication. The hemodynamic, blood gas, routine and biochemistry were recorded and compared between 2 groups.
Results: Compared with Control group, Sildenaifl group had more reduction of pulmonary artery pressure, increased arterial pressure of oxygen, left ventricular output, cardiac index and oxygenation index, all P<0.05. The patients’ arterial pressure, blood routine and biochemistry were similar between 2 groups, P>0.05. There was no obvious adverse reaction observed in Sildenaifl group.
Conclusion: Based on conventional treatment, Sildenafil may effectively reduce the pulmonary artery pressure in CHD patients combining pulmonary hypertension in plateau area, it improving the cardiac function without adverse reaction.

Three cases of Good's syndrome with pulmonary lesions in our hospital from June 1,2010 to June 1,2013 were retrospective analyzed and relevant literatures were reviewed.Clinical manifestation,characteristics of pulmonary lesions,diagnosis and treatment were summarized.Abnormality of lymphocyte subpopulation to varying degrees in peripheral blood was detected in all 3 cases.However none showed hypogammaglobulinemia.If thymoma patients developed recurrent respiratory infections,Good's syndrome should be considered.Pulmonary manifestations of Good's syndrome have lesions similar to those of diffuse panbronchiolitis or interstitial lung disease.Early screening of immune competency and treatment for immunodeficiency may improve prognosis.

Objective To investigate the diagnosis and treatment of serous cystadenoma of the pancreas. Methods The clinical data of 18 patients with serous cystadenoma of the pancreas which were admitted into the First Affiliated Hospital of China Medical University from October 1999 to October 2010 were retrospectively analyzed. Results There were 15 females(83.3%) and 3 males (16.7%).Tumors were present in the pancreatic body and tail in 12 cases ( 66. 7% ), in the pancreatic head in 3 cases ( 16. 7% ) and in the pancreatic neck in 3 cases( 16. 7% ). The mean maximum diameter of the tumor was 6. 5 cm. No specific clinical features were indentified. The size of the tumor was significantly correlated with clinical symptoms. CT was main examination with correct diagnosing rate of 61.1%. All 18 patients received surgical resection. Pancreaticoduodenectomy was performed in 3 patients, distal pancreatectomy in 5 cases,spleen-preserving distal pancreatectomy in 5 cases, middle pancreatectomy in 3 cases, and tumor enucleation in 2 cases. Postoperative pancreatic fistula developed in 10 cases (55.6%);Fistula was healed by conservative therapy in all these 10 cases. Postoperative followed up from 6 to 125 months (mean,48. 3months) found no recurrence or metastasis. Conclusions CT was main imaging examination for serous cystadenoma of the pancreas. Surgical resection should be adopted for serous cystadenoma of the pancreas with clinical symptoms but uncertain malignancy.