Effect of Dehydrocostus Lactone on Proliferation of K562 Cells and Its Mechanism / 中国实验血液学杂志

OBJECTIVE@#To explore the inhibitory effect of dehydrocostus lactone on the proliferation of human chronic myeloid leukemia K562 cells and the underlying mechanisms.@*METHODS@#Cell viability was evaluated by CCK-8 assay. Flow cytometry was used to assess the effect of dehydrocostus lactone on the cell cycle and apoptosis of K562 cells. The levels of BCR/ABL-STATs-related molecules were analyzed by using Western blot.@*RESULTS@#The CCK-8 assay showed that dehydrocostus lactone at graded concentration of 4, 6, 8, 10, 12 μmol/L could significantly inhibit the proliferation of K562 cells after exposure for 24 h. The proliferation inhibition rate was (24.32±3.05%), (42.91±3.89%), (46.35±4.93%), (77.06±5.42%) and (89.04±4.25%) respectively, showing statistically significantly different from (2.08±0.27%) in the control (P＜0.05). Also, the treatment with 5 and 10 μmol/L of dehydrocostus lactone induced K562 cell apoptosis, the apoptotic rate of K562 cells was significantly higher than that the control group (P＜0.05), and up-regulated the expression level of BAX and p21. Furthermore, dehydrocostus lactone (5 and 10 μmol/L) also increased the percentage of cells in G2/M [(8.53±1.71)% to (17.42±2.72) and (31.79±4.38%)](P＜0.05). The study results also revealed that dehydrocostus lactone significantly inhibited the expression of BCR/ABL STAT3, STAT5, CyclinB1, CDK1 and BCL-2, and up-regulated the expression level of BAX and p21.@*CONCLUSION@#Dehydrocostus lactone can suppress the proliferation of K562 cells and induce the apoptosis of K562 cells through BCR/ABL-STAT signaling pathways.

Problems in data security and privacy protection of healthcare wearable devices and measures for their solution / 中华医学图书情报杂志

The problems in data collection, data management and data security of healthcare wearable devices were summarized and analyzed with measures proposed for the solution of these problems and for speeding up the sustainable development of healthcare wearable devices from the aspects of technologies, management and laws, such as using multiple data coding technologies, establishing hierarchical data management and control model, adding remote control functions, investigating the responsibility for use of their data, working out law systems for protecting personal healthcare data,beefing up popularization of privacy data protection.

Study of the mechanisms of dyspnea during exercise in COPD / 中国应用生理学杂志

<p><b>AIM</b>To study the relationships between dyspnea and respiratory drive or respiratory muscle function in COPD.</p><p><b>METHODS</b>Thirty-one patients with COPD and 26 normal subjects were involved in the study. Routine pulmonary function, pulmonary diffusing capacity, P0.1, PI(max) were measured at rest. Oxygen consumption (VO2), carbon dioxide production (VCO2), minute ventilation (VE) etc were observed during exercise test. Dyspnea was assessed with Borg Scale (BS) simultaneously. Arterial blood gas measured before and after exercise.</p><p><b>RESULTS</b>(1) PI(max) of COPD (5.33 +/- 1.95) kPa decreased compared with the normal subjects (7.02 +/- 2.53) kPa, P < 0.05, P0.1 of COPD (0.37 +/- 0.12) kPa increased compared with the normal subjects (0.26 +/- 0.09) kPa, P < 0.05, inspiratory drive efficacy (V(T)/P0.1) of COPD (1.6 +/- 0.31) L/kPa decreased than that of the normal subjects (2.1 +/- 0.53) L/kPa, P < 0.05. P0.1/PI(max) of COPD (0.069 +/- 0.021) was higher than that of the normal individuals (0.037 +/- 0.009), P < 0.01. (2) Peak exercise dyspnea was correlated with dyspnea at rest and P0.1/PI(max) (r = 0.41, P < 0.05 and r = 0.48, P < 0.05, respectively), and P0.1/PI(max) was also positively correlated with the change in BS from rest to maximal exercise (deltaBS) (r = 0.44, P < 0.05) in COPD patients.</p><p><b>CONCLUSION</b>In COPD, breathlessness during exercise is not simply related to hyperinflation and the damaged gas exchange, but also to the relatively increased respiratory drive and dysfunction of respiratory muscle.</p>

Protection of artesunate on activation and injury of vascular endothelial cells induced by lipopolysaccharide / 中国中西医结合杂志

<p><b>OBJECTIVE</b>To investigate the protective effects and mechanism of artesunate (AR) on the activation and injury of human umbilical vein endothelial cells (HUVECs) induced by lipopolysaccharide (LPS).</p><p><b>METHODS</b>After HUVECs were cultured and turned to fusion manner, LPS and different concentration of AR (0.04 mg/L, 0.2 mg/L, 1 mg/L, 5 mg/L and 20 mg/L) were added respectively and co-incubated for 24 hrs. The expression of von Willebrand factor (vWF) in the conditioned media was tested by ELISA, the expression of intercellular adhesion molecule (ICAM-1) protein was determined by Western blot method and the expression of tumor necrosis factor alpha (TNFalpha) mRNA was determined by in situ hybridization.</p><p><b>RESULTS</b>After being exposed to 1 microg/ml LPS, vWF and ICAM-1 expression were higher than those in the control group. AR could significantly down-regulate the increased expressions concentration-dependently, significant difference showed as the concentration of AR reached 1 mg/L (P < 0.05). In situ hybridization showed that AR in 0.2 mg/L and 1 mg/L could markedly down-regulate the TNFalpha mRNA expression, showing significant difference as compared with that in LPS group (P < 0.05, P < 0.01).</p><p><b>CONCLUSION</b>AR has protective effect on LPS induced HUVECs activation and injury, which might be related with its inhibition on TNFalpha mRNA expression.</p>

Vascular endothelial injuries and changes of blood coagulation and fibrinolysis indexes in patients with acute respiratory distress syndrome / 中国医学科学杂志(英文版)

<p><b>OBJECTIVE</b>To study endothelial damage by observing changes of circulating endothelial cells (CECs) in blood, coagulation and fibrinolysis index in patients with acute respiratory distress syndrome.</p><p><b>METHODS</b>CECs were separated by isopycnic centrifugation method in 14 patients with acute lung injury (ALI), 7 patients with acute respiratory distress syndrome (ARDS), 10 intensive care unit (ICU) controls, and 15 healthy controls. Plasma prothrombin time (PT), activated partial thromboplastin time (APTT), fibrinogen (FG), fibrin degradation products (FDP), and D-dimer were examined simultaneously. Acute physiology and chronic health evaluation (APACHE) II and lung injury score (LIS) were recorded to evaluate severity of illness and lung injury.</p><p><b>RESULTS</b>(1) The number of CECs in ALI (10.4 +/- 2.3) and ARDS groups (16.1 +/- 2.7) was higher than that in the healthy (1.9 +/- 0.5) (P < 0.01). In both ALI and ARDS, the number of CECs correlated with APACHE II (r = 0.55, P < 0.05 and r = 0.62, P < 0.05, respectively) and LIS (r = 0.60, P < 0.05 and r = 0.53, P < 0.05, respectively). CEC number was negatively correlated with PaO2 in ALI and ARDS (r = -0.49, P < 0.05 and r = -0.64, P < 0.05, respectively). (2) The level of FDP and D-dimer were higher in ALI and ARDS patients than that in ICU and healthy control groups (P < 0.05). The level of FG in ARDS group was significantly higher than in the ICU and healthy control groups (P < 0.05). But in ALI group, the level of FG was significantly higher than only healthy control group (P < 0.05).</p><p><b>CONCLUSIONS</b>Endothelial cell damage occurs in ARDS patients, which may play a major role in the pathophysiology of ARDS. Changes of endothelial cell activation and damage markers, such as CECs, plasma coagulation and fibrinolysis index, to some extent reflect severity of illness and lung injury in ARDS.</p>