Objective To evaluate the effects of different target effect-site concentrations (Ces) of sufentanil on the minimum alveolar concentration of desflurane inhibiting stress responses to skin incision (MACsAR) in 50％ of patients undergoing abdominal surgery.Methods Eighty-three patients,aged 20-60 yr,scheduled for elective abdominal surgery with an expected incision longer than 10 cm,were enrolled in the study.All the patients were randomly allocated to one of three groups using a random number table:control group (group C,n =28),sufentanil with target Ce of 0.1 ng/ml group (group S1,n =27),and sufentanil with target Ce of 0.3 ng/ml group (group S2,n =28).After tracheal intubation,desflurane inhalation was started,and sufentanil was infused at the preset target Ces in S1 and S2 groups.The initial end-tidal concentration of desflurane was 9.0％ in group C,and 6.0％ in S1 and S2 groups.The target concentration was maintained at least for 15 min.The modified up-and-down method was used to perform the test.The end-tidal concentration of desflurane was adjusted in the next patients according to the response to skin incision.The MACBAR and 95％ confidence interval of desflurane was calculated according to the up-and-down method.Mean arterial pressure and heart rate were monitored and recorded and rate-pressure product was calculated.Results The MACBAR (95％ confidence interval) ofdesflurane was 11.2％ (11.1％-11.3％),7.8％ (7.7％-7.9％),and 4.2％ (4.1％-4.3％) in C,S1 and S2 groups,respectively.MACBAR and rate-pressure product of desflurane were significantly lower in S1 and S2 groups than in C group,and in S2 group than in S1 group (P ＜ 0.05 or 0.01).Conclusion The optimum target Ce of sufentanil is 0.3 ng/ml when combined with desflurane in the patients undergoing abdominal surgery.

Objective To investigate the effect of allergen-specific immunotherapy on FEV1 and airway responsiveness in patients with idiopathic asthma.Methods 90 patients with idiopathic asthma from January 2013 to August 2015 in Deqing City People's Hospital were selected and randomly divided into control group and study group with 45 cases in each group.Control group were treated with anti-infection, relieving cough and eliminating phlegm, relieving spasm and relieving asthma, the study group was treated with allergen specific immunotherapy based on the control group, and a total of 3 months for a course of treatment.Blood samples were used to measure inflammatory mediators , airway sensitivity index, pulmonary function and airway responsiveness, at the same time, the clinical efficacy and complications were compared.Results Compared with before treatment, the levels of FVC, PEF, FEV1 and FEV1/FVC in the two groups increased, levels of AI, AO, T and WA decreased, levels of serum IL-4 decreased, levels of IL-10, IFN-γincreased, levels of serum IgE, SIgE, TIgE and EOS decreased, the difference was statistically significant (P<0.05), compared with the control group, the levels of FVC, PEF, FEV1 and FEV1/FVC in the study group were higher, the levels of AI, AO, T and WA were lower, serum IL-4 levels were lower after treatment, levesls of IL-10, IFN-γwere higher, levels of serum IgE, SIgE, TIgE and EOS were lower, the difference was statistically significant (P<0.05), and the effective rate in the control group (71.11%) was lower than the study group (88.89%), the difference was statistically significant(P <0.05).Conclusion Allergen-specific immunotherapy was effective for cough variant asthma, it can improve pulmonary function, inflammation and airway sensitivity.

To cultivate high-quality medical talents,Shanghai Jiao Tong University School of Medicine established a multidisciplinary and comprehensive basic medical practical integration curriculum Medical Functional Experiment.Over several years' exploration and renovation,insisting on student-centered,this course has established a modular experiment teaching system with emphasis on foundation,combina-tion with clinical and focusing on innovation.Integration curriculum adopts four-stage teaching pattern which is suitable for medical students,and implements diversified teaching method and evaluation system.And meanwhile,the paper explores the ideas and approaches to further deepen the construction of teaching staff,expand experimental teaching techniques,strengthen the construction of curriculum materials,and strengthen the cultivation of teachers' innovative ability.

Objective:To analyze the related factors of acute stress disorder (ASD) in patients with brain injury and discuss its nursing countermeasures.Methods:Totally 326 patients with brain injury hospitalized in Yongkang First People's Hospital from February 2018 to March 2019 were selected. ASD diagnosis was made using the Stanford Acute Stress Response Questionnaire (SASRQ) , and the factors affecting the occurrence of ASD in patients were subjected to univariate and multivariate Logistic regression analysis. Related nursing strategies were thus summarized.Results:Among the 326 patients with brain injury, 133 were complicated with ASD, accounting for an ASD incidence of 40.80%. Logistic regression analysis showed that gender, headache degree, hemiplegia, and sleep quality entered the regression model, which were independent risk factors for ASD in patients with brain injury ( P<0.05) . Conclusions:The incidence of ASD is higher in patients with brain injury. Women, severe headache, poor sleep quality, and hemiplegia are important factors affecting the incidence of ASD. Nursing staff should take targeted measures to prevent ASD in the patients.

Lung adenocarcinoma (LUAD) is a global malignancy with significant chemoresistance impacting patient prognosis. The pro-tumorigenic role of hyaluronan-mediated motility receptor (HMMR) in LUAD is recognized. This study was designed to investigate the underlying mechanisms by which HMMR affects chemoresistance in LUAD. Bioinformatics presented the expression patterns of HMMR in LUAD patients and the association between HMMR levels and patient survival, followed by qRT-PCR to verify HMMR expression in LUAD tissues and cells. Further, bioinformatics was leveraged to identify the signaling pathways enriched by HMMR and its relevance to glycolytic genes, we also analyzed changes in the glycolytic activity of LUAD cells by manipulating HMMR expression. Stemness was evaluated through cell aggregation assays and Western blot, and drug responsiveness was gauged using CCK-8 assays, alongside flow cytometry for apoptosis analysis. HMMR was highly expressed in LUAD tissues and cells, and this overexpression correlated with poorer prognoses in patients. GSEA showed that HMMR was notably enriched in the glycolysis and gluconeogenesis pathways, correlating positively with the expression of key glycolytic genes. Cellular experiments confirmed that HMMR knockdown notably suppressed aerobic glycolysis in LUAD cells. Moreover, overexpression of HMMR could further enhance the stemness and cisplatin resistance of LUAD cells by stimulating glycolysis. In brief, this study has validated that high levels of HMMR in LUAD are predictive of poor patient prognosis, and that overexpression of HMMR can catalyze aerobic glycolysis, thus promoting stemness and chemoresistance in LUAD cells. Thus, HMMR could be a target for improving chemosensitivity in LUAD.

Lung adenocarcinoma (LUAD) is a global malignancy with significant chemoresistance impacting patient prognosis. The pro-tumorigenic role of hyaluronan-mediated motility receptor (HMMR) in LUAD is recognized. This study was designed to investigate the underlying mechanisms by which HMMR affects chemoresistance in LUAD. Bioinformatics presented the expression patterns of HMMR in LUAD patients and the association between HMMR levels and patient survival, followed by qRT-PCR to verify HMMR expression in LUAD tissues and cells. Further, bioinformatics was leveraged to identify the signaling pathways enriched by HMMR and its relevance to glycolytic genes, we also analyzed changes in the glycolytic activity of LUAD cells by manipulating HMMR expression. Stemness was evaluated through cell aggregation assays and Western blot, and drug responsiveness was gauged using CCK-8 assays, alongside flow cytometry for apoptosis analysis. HMMR was highly expressed in LUAD tissues and cells, and this overexpression correlated with poorer prognoses in patients. GSEA showed that HMMR was notably enriched in the glycolysis and gluconeogenesis pathways, correlating positively with the expression of key glycolytic genes. Cellular experiments confirmed that HMMR knockdown notably suppressed aerobic glycolysis in LUAD cells. Moreover, overexpression of HMMR could further enhance the stemness and cisplatin resistance of LUAD cells by stimulating glycolysis. In brief, this study has validated that high levels of HMMR in LUAD are predictive of poor patient prognosis, and that overexpression of HMMR can catalyze aerobic glycolysis, thus promoting stemness and chemoresistance in LUAD cells. Thus, HMMR could be a target for improving chemosensitivity in LUAD.

Lung adenocarcinoma (LUAD) is a global malignancy with significant chemoresistance impacting patient prognosis. The pro-tumorigenic role of hyaluronan-mediated motility receptor (HMMR) in LUAD is recognized. This study was designed to investigate the underlying mechanisms by which HMMR affects chemoresistance in LUAD. Bioinformatics presented the expression patterns of HMMR in LUAD patients and the association between HMMR levels and patient survival, followed by qRT-PCR to verify HMMR expression in LUAD tissues and cells. Further, bioinformatics was leveraged to identify the signaling pathways enriched by HMMR and its relevance to glycolytic genes, we also analyzed changes in the glycolytic activity of LUAD cells by manipulating HMMR expression. Stemness was evaluated through cell aggregation assays and Western blot, and drug responsiveness was gauged using CCK-8 assays, alongside flow cytometry for apoptosis analysis. HMMR was highly expressed in LUAD tissues and cells, and this overexpression correlated with poorer prognoses in patients. GSEA showed that HMMR was notably enriched in the glycolysis and gluconeogenesis pathways, correlating positively with the expression of key glycolytic genes. Cellular experiments confirmed that HMMR knockdown notably suppressed aerobic glycolysis in LUAD cells. Moreover, overexpression of HMMR could further enhance the stemness and cisplatin resistance of LUAD cells by stimulating glycolysis. In brief, this study has validated that high levels of HMMR in LUAD are predictive of poor patient prognosis, and that overexpression of HMMR can catalyze aerobic glycolysis, thus promoting stemness and chemoresistance in LUAD cells. Thus, HMMR could be a target for improving chemosensitivity in LUAD.

Lung adenocarcinoma (LUAD) is a global malignancy with significant chemoresistance impacting patient prognosis. The pro-tumorigenic role of hyaluronan-mediated motility receptor (HMMR) in LUAD is recognized. This study was designed to investigate the underlying mechanisms by which HMMR affects chemoresistance in LUAD. Bioinformatics presented the expression patterns of HMMR in LUAD patients and the association between HMMR levels and patient survival, followed by qRT-PCR to verify HMMR expression in LUAD tissues and cells. Further, bioinformatics was leveraged to identify the signaling pathways enriched by HMMR and its relevance to glycolytic genes, we also analyzed changes in the glycolytic activity of LUAD cells by manipulating HMMR expression. Stemness was evaluated through cell aggregation assays and Western blot, and drug responsiveness was gauged using CCK-8 assays, alongside flow cytometry for apoptosis analysis. HMMR was highly expressed in LUAD tissues and cells, and this overexpression correlated with poorer prognoses in patients. GSEA showed that HMMR was notably enriched in the glycolysis and gluconeogenesis pathways, correlating positively with the expression of key glycolytic genes. Cellular experiments confirmed that HMMR knockdown notably suppressed aerobic glycolysis in LUAD cells. Moreover, overexpression of HMMR could further enhance the stemness and cisplatin resistance of LUAD cells by stimulating glycolysis. In brief, this study has validated that high levels of HMMR in LUAD are predictive of poor patient prognosis, and that overexpression of HMMR can catalyze aerobic glycolysis, thus promoting stemness and chemoresistance in LUAD cells. Thus, HMMR could be a target for improving chemosensitivity in LUAD.

Lung adenocarcinoma (LUAD) is a global malignancy with significant chemoresistance impacting patient prognosis. The pro-tumorigenic role of hyaluronan-mediated motility receptor (HMMR) in LUAD is recognized. This study was designed to investigate the underlying mechanisms by which HMMR affects chemoresistance in LUAD. Bioinformatics presented the expression patterns of HMMR in LUAD patients and the association between HMMR levels and patient survival, followed by qRT-PCR to verify HMMR expression in LUAD tissues and cells. Further, bioinformatics was leveraged to identify the signaling pathways enriched by HMMR and its relevance to glycolytic genes, we also analyzed changes in the glycolytic activity of LUAD cells by manipulating HMMR expression. Stemness was evaluated through cell aggregation assays and Western blot, and drug responsiveness was gauged using CCK-8 assays, alongside flow cytometry for apoptosis analysis. HMMR was highly expressed in LUAD tissues and cells, and this overexpression correlated with poorer prognoses in patients. GSEA showed that HMMR was notably enriched in the glycolysis and gluconeogenesis pathways, correlating positively with the expression of key glycolytic genes. Cellular experiments confirmed that HMMR knockdown notably suppressed aerobic glycolysis in LUAD cells. Moreover, overexpression of HMMR could further enhance the stemness and cisplatin resistance of LUAD cells by stimulating glycolysis. In brief, this study has validated that high levels of HMMR in LUAD are predictive of poor patient prognosis, and that overexpression of HMMR can catalyze aerobic glycolysis, thus promoting stemness and chemoresistance in LUAD cells. Thus, HMMR could be a target for improving chemosensitivity in LUAD.

Na?ve CD4 + T cells differentiate into a variety of T helper (Th) subsets that secrete various cytokines to exert biological effects. Th22 cells, a novel identified CD4 + T cell subset, are distinct from Th1, Th2 and Th17 cell subsets. Th22 cells express chemokine receptors CCR4, CCR6 and CCR10, and secrete multiple cytokines such as IL-22, IL-13 and TNF-α, but not IL-17, IL-4 IFN-γ; and IL-22 is considered as major effector cytokine of Th22. The understanding on functions and differentiation mechanisms of Th22 cells have been constantly improved, and Th22 cells play important roles in human common viral infections. The article reviews the current advances about the characteristics, function, differentiation of Th22 cells, the roles of Th22 cells and the key molecules in several human common viral infections, which would provide novel immune strategies for the prevention and treatment of human viral infection.