Objective To investigate the predictive value of serum adiponectin level on morbidity of acute myocardial infarction, and to evaluate its impact on prognosis in patients with acute myocardial infarction after percutaneous coronary intervention (PCI). Methods We prospectively recruited patients with acute ST segment elevation myocardial infarction (STEMI) who had underwent primary PCI. Their serum adiponectin levels were measured. The TIMI blood flow classification of culprit vessel was recorded after PCI. Echocardiography was performed in 24 h after PCI to evaluate left ventricular ejection fraction (LVEF). Major adverse cardiac events (MACE) were recorded including cardiac death, recurrent nonfatal myocardial infarction, target vessel reascularization, and readmission for heart failure after 18 months′ followed-up. Results 108 consecutive patients with STEMI and 38 control patients without coronary artery stenosis were recruited. The serum adiponectin level in STEMI group was significantly lower than that in control: (1 413.9 ± 218.8) ng/L vs.(1 756.3 ± 205.5) ng/L (P<0.01). STEMI patients with LVEF < 50% had lower serum adiponectin level compared with LVEF ≥50%: (1 334.1 ± 226.3) ng/L vs. (1 453.0 ± 213.8) ng/L , P<0.01. The serum adiponectin level in the TIMI 0-2 group after PCI was significantly lower than that in the TIMI 3 group:(1 350.7 ± 214.9) ng/L vs. (1 430.6 ± 218.5) ng/L, P < 0.01. Multiple logistic regression analysis revealed that lower serum adiponectin level was an independent predictor of STEMI ( OR=0.992, 95% CI 0.987-0.996, P<0.01). MACE occurred in 22 patients (20.4% ). Cox regression analysis revealed that lower serum adiponectin level remained an independent predictor of MACE ( OR=0.996, 95% CI 0.993-0.999, P < 0.01). Conclusions Lower serum adiponectin level is significantly associated with morbidity of STEMI and adverse prognosis in patients with acute myocardial infarction.

OBJECTIVETo investigate the effect of 17-AAG combined with paclitaxel (PTX) on the proliferation and apoptosis of esophageal squamous cell carcinoma cell line Eca-109 in vitro.

METHODSEca-109 cells were treated with 17-AAG and PTX either alone or in combination. The proliferation of Eca-109 cells was detected by MTT assay, and the cell cycle changes and cell apoptosis were determined by flow cytometry.

RESULTSCompared with the control group, both 17-AAG and PTX significantly inhibited the proliferation of Eca-109 cells. A combined treatment of the cells with 0.5 µmol/L PTX and 0.625 µmol/L 17-AAG produced an obviously stronger inhibitory effect on the cell proliferation than either of the agents used alone (P<0.01). Flow cytometry showed that, 17-AAG and PTX used alone caused Eca-109 cell cycle arrest in G2/M phase and S phase, respectively, and their combined use caused cell cycle arrest in both G2/M and S phases. The cell apoptosis rates of Eca-109 cells treated with 17-AAG, PTX and their combination were 4.52%, 10.91%, and 29.88%, respectively, all significantly higher than that in the control group (1.32%); the combined treatment resulted in a distinct apoptotic peak that was significantly higher than that caused by either of the agents alone.

CONCLUSION17-AAG and PTX can inhibit cell proliferation and promote apoptosis of Eca-109 cells, and their combination produces stronger effects in inhibiting cell proliferation and increasing cell apoptosis.

Apoptosis ; Benzoquinones ; pharmacology ; Carcinoma, Squamous Cell ; pathology ; Cell Cycle Checkpoints ; Cell Line, Tumor ; drug effects ; Cell Proliferation ; Esophageal Neoplasms ; pathology ; Humans ; Lactams, Macrocyclic ; pharmacology ; Paclitaxel ; pharmacology

Objective To evaluate the clinical value of epithelial vessel branch detected by non-magnifying narrow-band imaging ( NM-NBI ) in diagnosis of early esophageal cancer. Methods A retrospective analysis was performed on data of 59 patients, who underwent endoscopy with NM-NBI and iodine staining to screen early esophageal cancer in PLA General Hospital from January 2013 to May 2015. The final diagnosis for all lesions were determined by pathology. The diagnostic accuracy, sensitivity and specificity of NM-NBI and iodine staining for early esophageal cancer were compared. Results The accuracy, sensitivity and specificity of NM-NBI on the epithelial vessel branch in diagnosis of early esophageal cancer were 83. 1％ (49/59), 91. 3％ (21/23) and 77. 8％ (28/36), respectively, and the corresponding statistical values of iodine staining were 55. 9％ ( 33/59) , 95. 7％ ( 22/23) and 30. 6％ ( 11/36), respectively. The accuracy (χ2=1. 45, P=0. 028) and specificity (χ2=21. 4, P=0. 000) of epithelial vessel branch by NM-NBI were significantly higher than those of iodine staining, and there was no significant difference in the sensitivity between the two methods (χ2=22. 3, P=1. 000) . Conclusion The observation of epithelial vessel branch using NM-NBI was useful and reliable in diagnosis of early esophageal cancer with high accuracy and specificity, and can be possible for application in the clinic.

Objective To investigate the effect of 17-AAG combined with paclitaxel (PTX) on the proliferation and apoptosis of esophageal squamous cell carcinoma cell line Eca-109 in vitro. Methods Eca-109 cells were treated with 17-AAG and PTX either alone or in combination. The proliferation of Eca-109 cells was detected by MTT assay, and the cell cycle changes and cell apoptosis were determined by flow cytometry. Results Compared with the control group, both 17-AAG and PTX significantly inhibited the proliferation of Eca-109 cells. A combined treatment of the cells with 0.5μmol/L PTX and 0.625μmol/L 17-AAG produced an obviously stronger inhibitory effect on the cell proliferation than either of the agents used alone (P<0.01). Flow cytometry showed that, 17-AAG and PTX used alone caused Eca-109 cell cycle arrest in G2/M phase and S phase, respectively, and their combined use caused cell cycle arrest in both G2/M and S phases. The cell apoptosis rates of Eca-109 cells treated with 17-AAG, PTX and their combination were 4.52%, 10.91%, and 29.88%, respectively, all significantly higher than that in the control group (1.32%); the combined treatment resulted in a distinct apoptotic peak that was significantly higher than that caused by either of the agents alone. Conclusion 17-AAG and PTX can inhibit cell proliferation and promote apoptosis of Eca-109 cells, and their combination produces stronger effects in inhibiting cell proliferation and increasing cell apoptosis.

Objective To investigate the mechanism by which heat shock protein 90 (HSP90) regulates 26S proteasome in hyperthermia. Methods Hyperthermic HepG2 cell models established by exposure of the cells to 42 ℃ for 3, 6, 12, and 24 h were examined for production of reactive oxygen species (ROS) and cell proliferation, and the changes in Hsp90α and 26S proteasome were analyzed. Results ROS production in the cells increased significantly after hyperthermia (F=28.958, P<0.001), and the cell proliferation was suppressed progressively as the heat exposure time extended (F=621.704, P<0.001). Hyperthermia up-regulated Hsp90α but decreased the expression level (F=164.174, P<0.001) and activity (F=133.043, P<0.001) of 26S proteasome. The cells transfected with a small interfering RNA targeting Hsp90α also showed significantly decreased expression of 26S proteasome (F=180.231, P<0.001). Conclusion The intracellular ROS production increases as the hyperthermia time extends. Heat stress and ROS together cause protein denature, leading to increased HSP90 consumption and further to HSP90 deficiency for maintaining 26S proteasome assembly and stability. The accumulation of denatured protein causes unfolded protein reaction in the cells to eventually result in cell death.

Objective To investigate the effect of 17-AAG combined with paclitaxel (PTX) on the proliferation and apoptosis of esophageal squamous cell carcinoma cell line Eca-109 in vitro. Methods Eca-109 cells were treated with 17-AAG and PTX either alone or in combination. The proliferation of Eca-109 cells was detected by MTT assay, and the cell cycle changes and cell apoptosis were determined by flow cytometry. Results Compared with the control group, both 17-AAG and PTX significantly inhibited the proliferation of Eca-109 cells. A combined treatment of the cells with 0.5μmol/L PTX and 0.625μmol/L 17-AAG produced an obviously stronger inhibitory effect on the cell proliferation than either of the agents used alone (P<0.01). Flow cytometry showed that, 17-AAG and PTX used alone caused Eca-109 cell cycle arrest in G2/M phase and S phase, respectively, and their combined use caused cell cycle arrest in both G2/M and S phases. The cell apoptosis rates of Eca-109 cells treated with 17-AAG, PTX and their combination were 4.52%, 10.91%, and 29.88%, respectively, all significantly higher than that in the control group (1.32%); the combined treatment resulted in a distinct apoptotic peak that was significantly higher than that caused by either of the agents alone. Conclusion 17-AAG and PTX can inhibit cell proliferation and promote apoptosis of Eca-109 cells, and their combination produces stronger effects in inhibiting cell proliferation and increasing cell apoptosis.

Objective To investigate the mechanism by which heat shock protein 90 (HSP90) regulates 26S proteasome in hyperthermia. Methods Hyperthermic HepG2 cell models established by exposure of the cells to 42 ℃ for 3, 6, 12, and 24 h were examined for production of reactive oxygen species (ROS) and cell proliferation, and the changes in Hsp90α and 26S proteasome were analyzed. Results ROS production in the cells increased significantly after hyperthermia (F=28.958, P<0.001), and the cell proliferation was suppressed progressively as the heat exposure time extended (F=621.704, P<0.001). Hyperthermia up-regulated Hsp90α but decreased the expression level (F=164.174, P<0.001) and activity (F=133.043, P<0.001) of 26S proteasome. The cells transfected with a small interfering RNA targeting Hsp90α also showed significantly decreased expression of 26S proteasome (F=180.231, P<0.001). Conclusion The intracellular ROS production increases as the hyperthermia time extends. Heat stress and ROS together cause protein denature, leading to increased HSP90 consumption and further to HSP90 deficiency for maintaining 26S proteasome assembly and stability. The accumulation of denatured protein causes unfolded protein reaction in the cells to eventually result in cell death.

Objective:To explore whether left ventricular interstitial fibrosis is associated with left atrial enlargement and left atrial dysfunction in patients of hypertrophic cardiomyopathy(HCM) with preserved ejection fraction.Methods:From October 2018 to September 2021, 59 HCM including 30 with enlarged maximal left artrial volume index (LAVI max), 29 with normal LAVI max and 28 age-and gender-matched controls were retrospectively enrolled. Imaging protocol included cine sequence, late gadolinium enhancement and T 1 mapping.The relationships between left ventricular mass index (LVMI), quantitative myocardial fibrosis and left atrial-related indexes were analyzed. One-way analysis of variance with Bonferroni post hoc correction or Kruskal-Wallis was performed for continuous variables. Categorical variables were assessed using the Chi-square test or Fisher′s exact test. Pearson or Spearman analysis was used for linear or monotonic nonlinear correlations. Results:The left ventricular end-diastolic volume index, left ventricular end-systolic volume index, left ventricular cardiac output and LVMI of HCM with enlarged LAVI max group were higher than HCM with normal LAVI max group and control group( P<0.05).Correlation analysis showed that LVMI correlated positively with LAVI max( r=0.780, P<0.001) and minimal left artrial volume index (LAVI min) ( r=0.816, P<0.001), extracellular volume correlated positively with LAVI max( r=0.462, P<0.001) and LAVI min( r=0.483, P<0.001),%LGE was correlated positively with LAVI max( r=0.311, P<0.05) and LAVI min( r=0.327, P<0.05),left ventricular index interstitial volume was correlated negatively with left atrial ejection fraction of reservoir ( r=-0.669, P<0.001),left atrial ejection fraction of conduit ( r=-0.472, P<0.001),left atrial ejection fraction of pump ( r=-0.518, P<0.001)and left atrial expansion index( r=-0.626, P<0.001). Conclusion:There is association between LVMI and fibrosis and left atrial enlargement and phases dysfunction in HCM with preserved ejection fraction.

Arnebiae Radix is used widely in TCM external treatment. It has obvious curative effect on skin diseases， wound infection and local inflammation， and is used to treat water and fire burns， skin ulcers， eczema， psoriasis， vitiligo and atopic dermatitis， etc. The clinical and commercial preparations mainly include ointment， liniment and suppository. Modern research has proved that microcapsules， nano-micelles， nanofiber membranes， nanogels and other novel nanoformulations can significantly improve the stability of drug-effective substances， improve local drug concentration and targeting， and perform sound drug release properties in vitro. This paper reviews the variety and application of Arnebiae Radix traditional preparations for external use and the research progress of novel nanoformulations of Arnebiae Radix， from which we prospect to provide some valuable references for the future application and development of Arnebiae Radix external preparations.

OBJECTIVE To analyze the dose-adjusted concentrations of Posaconazole oral suspension in patients undergoing hematopoietic stem cell transplantation （HSCT） and their influential factors. METHODS Data were collected from hospitalized HSCT patients admitted to the First Affiliated Hospital of Shandong First Medical University （Shandong Provincial Qianfoshan Hospital） from January 2021 to April whtwhm@yeah.net 2023 who took Posaconazole oral suspension for the prevention of invasive fungal disease （IFD） and received blood concentration of posaconazole. The rate of concentration attainment and clinical failure rate of posaconazole for the prevention of IFD were evaluated， and one-way and multiple linear regression analyses were performed for the influential factors of dose-adjusted concentrations （C0/D） of posaconazole. RESULTS A total of 44 patients were enrolled； the mean C0 of posaconazole in patients was （0.99±0.94） µg/mL， and 20 patients had a C0≥0.7 μg/mL， with a concentration attainment rate of 45.45% for the prevention of IFD； 13 cases were clinical failures， with a clinical failure rate of 29.55%. Of 24 patients who did not achieve C0/D of posaconazole for IFD prophylaxis， one patient was a clinical failure despite timely dose adjustment of posaconazole in seven patients； seven of the thirteen patients who did not undergo dose adjustment were clinical failures； and the remaining four patients were switched to other antifungal agents. The results of univariate analysis showed that gender， body mass index （BMI）， renal function， combined use of sodium phenytoin， omeprazole and metoclopramide had a significant effect on the C0/D of posaconazole （P＜0.05）； the results of multivariate linear regression analysis showed that gender， BMI and combined use of sodium phenytoin were the independent factors affecting the C0/D of posaconazole （P＜0.05）. CONCLUSIONS Significant individual differences are reflected in the blood concentration of Posaconazole oral suspension； gender， BMI and combined use of sodium phenytoin are independent factors affecting the C0/D of posaconazole.