Objective To evaluate the effect of rocuronium on entropy to endotracheal intubation during anesthesia induction with propofol. Methods Forty patients anesthetized induction with propofol using a target-controlled infusion were randomly divided into two groups: rocuronium group (R group, 20 cases) received 0.6 mg/kg rocuronium or saline group (S group, 20 cases) received saline. 2-3 min later, endotracheal intubation was performed. Response entropy(RE) and state entropy(SE) were recorded during baseline(Ta), at steady state(Tb), 2 min after rocuro nium or saline administration (Tc) and 0, 1, 2 and 3 min after endotracheal intubation (T0, T1, T2, T3). Results At T2, the RE-SE was higher in S group than that in R group. Endotracheal intubation induced increasing in RE and SE. Comparing T2 and T0 values in R group and S group, SE increased from 42 ± 7 to 50 ± 8 and 43 ± 13 to 55 ± 12, and RE increased from 45 ± 6 to 54 ± 9 and 48 ± 16 to 66 ± 15, respectively. At T0, RE and RE-SE were higher in S group. Conclusion Rocuronium affects RE-SE and RE and RE-SE responses to endotracheal intubation and may confound interpretation of entropy monitoring.

Objective To study the changes of lipid levels and body weight during the treatment of bipolar disorder by lithium carbonate combined with olanzapine or lithium. Methods Lipid and body weight was measured in forty-six patients with bipolar disorder in the first six months (treated by lithium carbonate combined with olanzapine) and in the second six months (treated by lithium only). Then the results were compared with the data before the treatment. Results When the first six months was over,the levels of the total cholesterol, triglyceride and apolipoprotein B increased(P＜ 0.05 ) ,and when the second six months was over,the levels of the total cholesterol,triglyceride,low density lipoprotein cholesterol (LDL-C),and apolipoprotein B increased Significantly (P ＜ 0.05 ). The levels of the total cholesterol, triglyceride, LDL-C were more than the normal level,but apolipoprotein B didn't exceed the normal level. When the first six months was over, the body weight was higher than that before treatment [ (68.70 ± 8.35 ) kg vs. (64.85 ±7.52 ) kg, P ＜ 0.05 ]. When the second six months was over, the body weight [ (71.72 ± 7.96 ) kg ] was higher than that at the end of the first six months (P ＜ 0.05 ). Gender difference showed non-statistical significance.Conclusions The lipid levels and body weight will both increase whether treated with lithium carbonate combined with olanzapine or with lithium only. The lipid level changes apparently in treatment with lithium separately, and the risk of coronary heart disease will increase.

Objective:To investigate the association between polymorphisms of FGFR2 and the susceptibility of breast cancer in Han population in Guizhou province.Methods:Genotyping was performed using PCR-sequence-specific primers(PCR-SSP)in 106 histologically confirmed breast cancer cases and 116 cancer-free controls.Results:The genotype frequencies of rs1219648 TT,TC,and CC were 50%,25.47%.and 24.53% in breast cancer cases and 29.31%,48.28%,and 22.41% in the controls.The gene frequencies of T in breast cancer cases and the controls were 62.74% and 53.45%.respectively.The gene frequencies of C were 37.26% and 46.55%.respectively.The distribution of allele and genotype frequencies of FGFR2 rs1219648 was statistically different between breast cancer cases and the controls(P<0.05).Conclusion:FGFR2 rs1219648 polymorphism influences the susceptibility of breast cancer.TT genotype might serve as a risk factor for breast cancer.

OBJECTIVE: To provide anatomic data for cochlear implantation, and to find the method of locating lamina spiralis (LS) on the surface of promontory. METHOD: Microanatomical study was carried out on 30 sides of human temporal bones by observing and measuring lamina spiralis below promontory, including its location, course and adjacent structures. RESULT: (1) The basal turn of lamina spiralis below promontory can be divided into three segments: the hook segment (1.52 +/- 0.16) mm, the anteroinferior round window segment (3.83 +/- 0.37) mm and the forwarding segment (2.70 +/- 0.36) mm by two hinge points of which one was located at anterior of the junction of superior margin and anterior border of RW, and the other was located at anteroinferior of the round window; (2) The plane of round window anteroinferior segment of LS lay (51.00 +/- 5.97) degrees anteroinferior to horizontal segment of the facial nerve and comparative permanently meet posterior margin of'stapes head. Made posterior margin of stapes head as a fixation point and draw a line on promontory lay (51.00 +/- 45.97) degrees anteroinferior to horizontal segment of the facial nerve. This line can be thought as the projection of anteroinferior round window segment of LS on promontory; (3) The width of scala tympani at cochleostomy site on promontory: width of scala tympani at midpoint of superior margin of round window was (0.36 +/- 0.06) mm; width of scala tympani at midpoint of anterior border of round window was (0.97 +/- 0.14) mm; width of scala tympani at 3 mm point of anteroinferior round window segment was (1.24 +/- 0.21) mm. CONCLUSION (1) The basal turn lamina spiralis below promontory can be divided into three segments (the hook segment, the anteroinferior round window segment and the forwarding segment) by two hinge points; (2) The projection of anteroinferior round window segment of LS and the features exhibited in its course provide reference for locating the basal turn scala tympani and offer reliable anatomical basis for minimal invasive intervention during cochlear implantation.
Adult ; Cochlear Implantation ; methods ; Facial Nerve ; anatomy & histology ; surgery ; Humans ; Round Window, Ear ; anatomy & histology ; surgery ; Scala Tympani ; anatomy & histology ; surgery ; Temporal Bone ; anatomy & histology ; surgery

Purpose: Myofibroblastic cancer-associated fibroblasts (myCAFs) are important components of the tumor microenvironment closely associated with tumor stromal remodeling and immunosuppression. This study aimed to explore myCAFs marker gene biomarkers for clinical diagnosis and therapy for patients with bladder cancer (BC). Materials and Methods: BC single-cell RNA sequencing (scRNA-seq) data were obtained from the National Center for Biotechnology Information Sequence Read Archive. Transcriptome and clinical data were downloaded from The Cancer Genome Atlas and the Gene Expression Omnibus databases. Subsequently, univariate Cox and LASSO (Least Absolute Shrinkage and Selection Operator regression) regression analyses were performed to construct a prognostic signature. Immune cell activity was estimated using single-sample gene set enrichment analysis whilst the TIDE (tumor immune dysfunction and exclusion) method was employed to assess patient response to immunotherapy. The chemotherapy response of patients with BC was evaluated using genomics of drug sensitivity in cancer. Furthermore, Immunohistochemistry was used to verify the correlation between MAP1B expression and immunotherapy efficacy. The scRNA-seq data were analyzed to identify myCAFs marker genes. Results: Combined with bulk RNA-sequencing data, we constructed a two-gene (COL6A1 and MAP1B) risk signature. In patients with BC, the signature demonstrated outstanding prognostic value, immune infiltration, and immunotherapy response. This signature served as a crucial guide for the selection of anti-tumor chemotherapy medications. Additionally, immunohistochemistry confirmed that MAP1B expression was significantly correlated with immunotherapy efficacy. Conclusions Our findings revealed a typical prognostic signature based on myCAF marker genes, which offers patients with BC a novel treatment target alongside theoretical justification.

Purpose: Myofibroblastic cancer-associated fibroblasts (myCAFs) are important components of the tumor microenvironment closely associated with tumor stromal remodeling and immunosuppression. This study aimed to explore myCAFs marker gene biomarkers for clinical diagnosis and therapy for patients with bladder cancer (BC). Materials and Methods: BC single-cell RNA sequencing (scRNA-seq) data were obtained from the National Center for Biotechnology Information Sequence Read Archive. Transcriptome and clinical data were downloaded from The Cancer Genome Atlas and the Gene Expression Omnibus databases. Subsequently, univariate Cox and LASSO (Least Absolute Shrinkage and Selection Operator regression) regression analyses were performed to construct a prognostic signature. Immune cell activity was estimated using single-sample gene set enrichment analysis whilst the TIDE (tumor immune dysfunction and exclusion) method was employed to assess patient response to immunotherapy. The chemotherapy response of patients with BC was evaluated using genomics of drug sensitivity in cancer. Furthermore, Immunohistochemistry was used to verify the correlation between MAP1B expression and immunotherapy efficacy. The scRNA-seq data were analyzed to identify myCAFs marker genes. Results: Combined with bulk RNA-sequencing data, we constructed a two-gene (COL6A1 and MAP1B) risk signature. In patients with BC, the signature demonstrated outstanding prognostic value, immune infiltration, and immunotherapy response. This signature served as a crucial guide for the selection of anti-tumor chemotherapy medications. Additionally, immunohistochemistry confirmed that MAP1B expression was significantly correlated with immunotherapy efficacy. Conclusions Our findings revealed a typical prognostic signature based on myCAF marker genes, which offers patients with BC a novel treatment target alongside theoretical justification.

Purpose: Myofibroblastic cancer-associated fibroblasts (myCAFs) are important components of the tumor microenvironment closely associated with tumor stromal remodeling and immunosuppression. This study aimed to explore myCAFs marker gene biomarkers for clinical diagnosis and therapy for patients with bladder cancer (BC). Materials and Methods: BC single-cell RNA sequencing (scRNA-seq) data were obtained from the National Center for Biotechnology Information Sequence Read Archive. Transcriptome and clinical data were downloaded from The Cancer Genome Atlas and the Gene Expression Omnibus databases. Subsequently, univariate Cox and LASSO (Least Absolute Shrinkage and Selection Operator regression) regression analyses were performed to construct a prognostic signature. Immune cell activity was estimated using single-sample gene set enrichment analysis whilst the TIDE (tumor immune dysfunction and exclusion) method was employed to assess patient response to immunotherapy. The chemotherapy response of patients with BC was evaluated using genomics of drug sensitivity in cancer. Furthermore, Immunohistochemistry was used to verify the correlation between MAP1B expression and immunotherapy efficacy. The scRNA-seq data were analyzed to identify myCAFs marker genes. Results: Combined with bulk RNA-sequencing data, we constructed a two-gene (COL6A1 and MAP1B) risk signature. In patients with BC, the signature demonstrated outstanding prognostic value, immune infiltration, and immunotherapy response. This signature served as a crucial guide for the selection of anti-tumor chemotherapy medications. Additionally, immunohistochemistry confirmed that MAP1B expression was significantly correlated with immunotherapy efficacy. Conclusions Our findings revealed a typical prognostic signature based on myCAF marker genes, which offers patients with BC a novel treatment target alongside theoretical justification.

Purpose: Myofibroblastic cancer-associated fibroblasts (myCAFs) are important components of the tumor microenvironment closely associated with tumor stromal remodeling and immunosuppression. This study aimed to explore myCAFs marker gene biomarkers for clinical diagnosis and therapy for patients with bladder cancer (BC). Materials and Methods: BC single-cell RNA sequencing (scRNA-seq) data were obtained from the National Center for Biotechnology Information Sequence Read Archive. Transcriptome and clinical data were downloaded from The Cancer Genome Atlas and the Gene Expression Omnibus databases. Subsequently, univariate Cox and LASSO (Least Absolute Shrinkage and Selection Operator regression) regression analyses were performed to construct a prognostic signature. Immune cell activity was estimated using single-sample gene set enrichment analysis whilst the TIDE (tumor immune dysfunction and exclusion) method was employed to assess patient response to immunotherapy. The chemotherapy response of patients with BC was evaluated using genomics of drug sensitivity in cancer. Furthermore, Immunohistochemistry was used to verify the correlation between MAP1B expression and immunotherapy efficacy. The scRNA-seq data were analyzed to identify myCAFs marker genes. Results: Combined with bulk RNA-sequencing data, we constructed a two-gene (COL6A1 and MAP1B) risk signature. In patients with BC, the signature demonstrated outstanding prognostic value, immune infiltration, and immunotherapy response. This signature served as a crucial guide for the selection of anti-tumor chemotherapy medications. Additionally, immunohistochemistry confirmed that MAP1B expression was significantly correlated with immunotherapy efficacy. Conclusions Our findings revealed a typical prognostic signature based on myCAF marker genes, which offers patients with BC a novel treatment target alongside theoretical justification.

This study examined the effects of flow shear stress on the bio-capacity of the endothelial cells' induced from mesenchymal stem cells (MSCs). After cultivating the SD rat mesenchymal stem cells in vitro, we exposed them under different intensity of flow shear stress and induced these cells to endothelial cells. The variations of total anti-oxidation competence (T-AOC) and quantity of nitrogen monoxide (NO) were tested. The results showed that shear stress has an enhanced effect on the T-AOC and NO of endothelial cells induced from MSCs in an intensity-dependent manner. Flow shear stress could provide a protective action on the in vitro induction of endothelial cells, thus formulating a theoretical foundation for the therapeutics of ischemic heart diseases and vascular tissue engineering.
Animals ; Antioxidants ; metabolism ; Bone Marrow Cells ; cytology ; physiology ; Cell Differentiation ; physiology ; Cells, Cultured ; Endothelial Cells ; cytology ; metabolism ; Female ; Male ; Mesenchymal Stromal Cells ; cytology ; physiology ; Oxidation-Reduction ; Rats ; Rats, Sprague-Dawley ; Stress, Mechanical

Objective To investigate the damage mechanism of typeⅡalveolar epithelial cells (AECⅡ) after hyperoxia exposure by proteomics. Methods The primary AECⅡ of preterm Sprague-Dawley (SD) rats were divided into normoxia and hyperoxia groups, and cultured in room air (21% O2) or hyperoxia (95% O2) condition, respectively. The cell morphology change was observed under an inverted contrast microscope; the protein expressions of Bcl-2 and caspase-3 were detected by Western Blot to ensure a successful model. Total protein in AECⅡ was collected, and mass spectrometry-based tandem mass tag (TMT)-labeled quantitative proteomics were used to detect the change of protein profile. Proteins with changes greater than 1.5-fold and P < 0.05 were considered differentially expressed, and bioinformatics analysis was performed. According to the proteomic results, AECⅡ were divided into three groups:normoxia group, hyperoxia group and hyperoxia+MW167 group (γ-secretase inhibitor MW167 was added to culture medium 30 minutes before they were placed into the chamber). The cell viability was detected by the cell proliferation and toxicity kit (CCK-8), and the expressions of Hes1, Bax mRNA were detected by real-time fluorescence quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Results ① The cells in the normoxia group proliferated and prolonged significantly, and the cytoplasmic particulate matter was abundant. In the hyperoxia group, nucleus pyknosis and cytoplasmic particulate matter decreased significantly. Compared with the normoxia group, the expression of caspase-3 in the hyperoxia group was significantly increased, and the expression of Bcl-2 was significantly decreased (caspase-3/GAPDH: 1.352±0.086 vs. 0.769±0.080, Bcl-2/GAPDH: 0.614±0.060 vs. 1.361±0.078, both P < 0.01).② A total of 162 differentially expressed proteins were identified between normoxia and hyperoxia groups, the proteins up-regulated by hyperoxia were commonly associated with response processes to various stimuli, and located in the extracellular region; the proteins down-regulated by hyperoxia were commonly associated with synthesis of substances, and located in the cellular matrix. KEGG Pathway analyses suggested that metabolism by cytochrome P450, oxidative phosphorylation, and Notch signaling pathway were associated with the mechanism of hyperoxia injury on AECⅡ.③Compared with the normoxia group, the viability of cells in the hyperoxia group was significantly decreased, and the expressions of Hes1 and Bax mRNA were significantly increased [cell viability (A value): 0.060±0.003 vs. 1.058± 0.017, Hes1 mRNA (2-ΔΔCt): 2.235±0.606 vs. 1.144±0.107, Bax mRNA (2-ΔΔCt): 2.210±0.240 vs. 1.084±0.096, all P < 0.05]. Compared with the hyperoxia group, the viability of cells in the hyperoxia+MW167 group was significantly increased, and the expressions of Hes1 and Bax mRNA were significantly decreased [cell viability (A value): 0.271±0.025 vs. 0.060±0.003, Hes1 mRNA (2-ΔΔCt): 0.489±0.046 vs. 2.235±0.606, Bax mRNA (2-ΔΔCt): 1.289±0.041 vs. 2.210±0.240, all P < 0.05]. Conclusion The mechanism of hyperoxia injury on AECⅡ may be related to the metabolism by cytochrome P450, oxidative phosphorylation and activation of Notch signaling pathway.