Objective To analyze the current situation of applying case-based learning (CBL) to the education of acupuncture-moxibustion by investigating the published literatures involving CBL in medical education.Method The literatures published between 2001 and 2015 were retrieved from VIP, CNKI, CBM, and WanFang databases, and the manuscripts about the application of CBL in the education of acupuncture-moxibustion were classified and analyzed.Result The related literatures involving the application of CBL in the education of acupuncture-moxibustion were rather limited, not enough for revealing the action and significance of CBL in the education of acupuncture-moxibustion.Conclusion CBL accords with the strong practicality of acupuncture-moxibustion, and is worth promotion; however, there are some shortcomings in the compiling of cases, students grouping, evaluation of study results, and the capability of teachers, which expect further standardization of teaching process and comprehensive use of advanced teaching methods, for cultivating elites in acupuncture-moxibustion.

OBJECTIVEAtherosclerotic lesions occur preferentially in the arterial branches, bifurcations and curvatures where shear stress is low. We aimed to study the possible mechanisms involved in low shear stress (LSS)-induced oxidative damage in vascular endothelial cells.

METHODSHuman umbilical vein endothelial cells (HUVECs) exposed for 60 min to simulated LSS using a parallel-plate flow chamber were examined for intracellular reactive oxygen species (ROS) and cell apoptosis with chemiluminescence assay and TUNEL staining, respectively. Western blotting was used to determine the levels of endothelial nitric oxide synthase (eNOS), P38, extracellular signal-regulate kinase (ERK) and c-Jun as well as their phosphorylation in cells with LSS exposure for different time lengths. To investigate the signaling pathway involved in LSS-induced oxidative damage, the cells were treated with P38, ERK and c-Jun inhibitors and examined for the expression of eNOS-Thr495 that negatively regulated eNOS.

RESULTSExposure to LSS for 1 h resulted in markedly increased ROS accumulation and apoptosis in HUVECs. LSS exposure time-dependently enhanced the phosphorylation of eNOS, P38, ERK and c-Jun but did not significantly affect their total protein expressions. Inhibition of ERK with PD98059 deactivated eNOS-Thr495 and restored super oxide dismutase (SOD) activity, while inhibition of either p38 with SB202190 or c-Jun with SP600125 did no produce such effects.

CONCLUSIONLSS-induced oxidative damage is partly due to activated mitogen-activated protein kinases (MAPK), among which ERK contributes to decreased NO release in endothelial cells.

Apoptosis ; Cells, Cultured ; Flavonoids ; Human Umbilical Vein Endothelial Cells ; cytology ; metabolism ; Humans ; MAP Kinase Signaling System ; Nitric Oxide Synthase Type III ; metabolism ; Oxidative Stress ; Phosphorylation ; Reactive Oxygen Species ; metabolism ; Stress, Mechanical ; p38 Mitogen-Activated Protein Kinases ; metabolism

Objective Atherosclerotic lesions occur preferentially in the arterial branches, bifurcations and curvatures where shear stress is low. We aimed to study the possible mechanisms involved in low shear stress (LSS)-induced oxidative damage in vascular endothelial cells. Methods Human umbilical vein endothelial cells (HUVECs) exposed for 60 min to simulated LSS using a parallel-plate flow chamber were examined for intracellular reactive oxygen species (ROS) and cell apoptosis with chemiluminescence assay and TUNEL staining, respectively. Western blotting was used to determine the levels of endothelial nitric oxide synthase (eNOS), P38, extracellular signal-regulate kinase (ERK) and c-Jun as well as their phosphorylation in cells with LSS exposure for different time lengths. To investigate the signaling pathway involved in LSS-induced oxidative damage, the cells were treated with P38, ERK and c-Jun inhibitors and examined for the expression of eNOS-Thr495 that negatively regulated eNOS. Results Exposure to LSS for 1 h resulted in markedly increased ROS accumulation and apoptosis in HUVECs. LSS exposure time-dependently enhanced the phosphorylation of eNOS, P38, ERK and c-Jun but did not significantly affect their total protein expressions. Inhibition of ERK with PD98059 deactivated eNOS-Thr495 and restored super oxide dismutase (SOD) activity, while inhibition of either p38 with SB202190 or c-Jun with SP600125 did no produce such effects. Conclusion LSS-induced oxidative damage is partly due to activated mitogen-activated protein kinases (MAPK), among which ERK contributes to decreased NO release in endothelial cells.

Objective Atherosclerotic lesions occur preferentially in the arterial branches, bifurcations and curvatures where shear stress is low. We aimed to study the possible mechanisms involved in low shear stress (LSS)-induced oxidative damage in vascular endothelial cells. Methods Human umbilical vein endothelial cells (HUVECs) exposed for 60 min to simulated LSS using a parallel-plate flow chamber were examined for intracellular reactive oxygen species (ROS) and cell apoptosis with chemiluminescence assay and TUNEL staining, respectively. Western blotting was used to determine the levels of endothelial nitric oxide synthase (eNOS), P38, extracellular signal-regulate kinase (ERK) and c-Jun as well as their phosphorylation in cells with LSS exposure for different time lengths. To investigate the signaling pathway involved in LSS-induced oxidative damage, the cells were treated with P38, ERK and c-Jun inhibitors and examined for the expression of eNOS-Thr495 that negatively regulated eNOS. Results Exposure to LSS for 1 h resulted in markedly increased ROS accumulation and apoptosis in HUVECs. LSS exposure time-dependently enhanced the phosphorylation of eNOS, P38, ERK and c-Jun but did not significantly affect their total protein expressions. Inhibition of ERK with PD98059 deactivated eNOS-Thr495 and restored super oxide dismutase (SOD) activity, while inhibition of either p38 with SB202190 or c-Jun with SP600125 did no produce such effects. Conclusion LSS-induced oxidative damage is partly due to activated mitogen-activated protein kinases (MAPK), among which ERK contributes to decreased NO release in endothelial cells.

Objective To explore the influence of MiniQuest teaching model on improving critical thinking ability of nurses in Department of Orthopedics. Methods From January to May 2017, 76 nurses in Orthopedics Department from 4 Class Ⅲ hospitals of one province were selected as the research objects. The nurses of 2 hospitals were set up as the observation group by drawing method of head nurse, and the nurses of the other 2 hospitals were set as the control group, with 36 cases in the observation group and 40 in the control group. The nurses in the control group were taught by routine department work. The observation group was trained with MiniQuest teaching method, and the Critical Thinking Ability Scale was used to compare the critical thinking of 2 groups of nurses. Results The fact finding, open thinking, analytical ability, systematic ability, critical thinking self-confidence, cognitive maturity and total score of the Critical Thinking Ability Scale of the observation group were higher than those of the control group, the differences were statistically significant (P<0.05). There was no significant difference in the score of dimension of thirst for knowledge between the two groups of nurses (P>0.05). Conclusions MiniQuest teaching model can improve the critical thinking ability of nurses in department of orthopedics, and it is worthy of popularizing.

Objective:To investigate the clinical features of IgD multiple myeloma (MM) and the effect and prognosis of daratumumab-based combination therapy.Methods:The clinicopathological data of a IgD MM patient with disease progression and extramedullary infiltration treated with daratumumab in the Affiliated Hospital of Qingdao University in December 2019 were retrospectively analyzed.Results:The 74-year-old woman was diagnosed as IgD MM by bone marrow aspiration and immunofixation electrophoresis. The patient was given VD (bortezomib, dexamethasone), RD (lenalidomide, dexamethasone) and ID (ixazomib, dexamethasone) regimens. In June 2020, the patient developed multiple subcutaneous nodules, and she was assessed as progressive disease with extensive extramedullary infiltration. After treated with daratumumab-PAD (liposomal doxorubicin, bortezomib, dexamethasone) regimen, the patient's subcutaneous nodules were significantly reduced and partially disappeared, and the general condition was significantly improved. But the patient was in a cachexia state and finally died of the irregular treatment and disease progression.Conclusions:IgD MM has a low incidence and a short survival period, and there is no uniform standard treatment. The early application of daratumumab combined with proteasome inhibitors, immunomodulators, cytotoxic drugs and hematopoietic stem cell transplantation may improve the overall survival of patients.