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BACKGROUND The nurse-physician relationship is important for the stability of collaboration. The COVID-19 pandemic has put unprecedented pressure on the health care system and has placed greater demands on nurse-physician collaboration. Nurses and physicians often struggle to share mutual responsibility and communicate effectively. OBJECTIVE This study aimed to evaluate the relationship between nurses and physicians during the COVID-19 pandemic and construct a new model combining the attitude and behaviors of the 2 groups to assess various factors’ impacts on job satisfaction and confrontational behavior. METHODS We conducted this quantitative cross-sectional study to assess the relationship between nurses and physicians based on the attitudes and behaviors toward nurse-physician collaboration. We first investigated the satisfaction of nurses and physicians with their relationship and how they thought the COVID-19 pandemic had affected that relationship. We used an adapted and modified Jefferson Scale of Attitudes Toward Physician-Nurse Collaboration questionnaire that consisted of 17 items under 5 dimensions. Structural equation modeling was used to assess the relationships between domains. Ordinal logistic regression was used to evaluate the relationship between different domains of the questionnaire and the satisfaction of the current nurse-physician relationship. RESULTS We included a total of 176 nurses and 124 physicians in this study. Compared to 7.2% (9/124) of physicians, 22.7% (40/176) of nurses were dissatisfied with the current nurse-physician relationship. Most physicians (101/124, 81.5%) and nurses (131/176, 74.5%) agreed that the nurse-physician relationship had become better because of the COVID-19 pandemic and that the public had greater respect for them. However, significantly fewer nurses (59/176, 33.5% vs 79/124, 63.7%; Pcaring versus curing (mean 16.27, SD 2.88 vs mean 17.43, SD 2.50; Pphysician’s authority (mean 8.72, SD 3.21 vs mean 7.24, SD 3.32; Pshared education and collaboration subscale had a significantly positive relationship with the nurse’s autonomy subscale (standardized coefficient=0.98; Pshared education and collaboration: Pcaring versus curing: Pnurse’s autonomy: Pconfrontation: P=.01) were significantly associated with the level of satisfaction of the current nurse-physician relationship. CONCLUSIONS This study showed that nurses were more dissatisfied with the current nurse-physician relationship than physicians in Shanghai. Policy makers and managers in the medical and educational system should emphasize an interprofessional collaboration between nurses and physicians. Positive attitudes toward shared collaboration and responsibility may help to improve the relationship between the 2 parties.

This study was aimed to investigate whether ginsenoside Rb1 (GS-Rb1) from the cardioprotective Chinese medicine ginseng can reduce hypoxia-reoxygenation (HR)-induced damage to cardiomyocytes by protecting the mitochondria. Mitochondria-mediated apoptosis plays a key role during myocardial ischemia-reperfusion injury (MIRI). When MIRI occurs, the continuous opening of the mitochondrial permeability transition pore (mPTP) causes mitochondrial damage and ultimately leads to apoptosis. We treated H9c2 cells, derived from rat embryonic cardiomyoblasts, with GS-Rb1, diazoxide, and 5-hydroxydecanoate (5-HD), using HR to simulate MIRI. We found that GS-Rb1 can reduce mPTP by stabilizing the mitochondrial membrane potential (MMP) and by reducing reactive oxygen species (ROS) during HR. This protects the mitochondria by reducing the release of cytochrome c and the expression of cleaved-caspase-3 in the cytoplasm, ultimately reducing apoptosis. During this process, GS-Rb1 and diazoxide showed similar effects. These findings provide some evidence for a protective effect of GS-Rb1 treatment on MIRI.

To investigate the effect of Sini decoction on rats with myocardial fibrosis induced by banding the abdominal aorta, and explore the mechanism underlying its actions on angiotensin ¢ò(Ang ¢ò), transforming growth factor-¦Â1 (TGF-¦Â1) and connective tissue growth factor (CTGF).Forty-eight male Sprague-Dawley rats were randomly divided into sham operation, model, Captopril, and Sini decoction groups. The models were established by the partial banding of the abdominal aorta according to Doering's method. Eight weeks later, heart weight indexes were calculated; hemodynamic changes of the hearts were tested; changes in myocardial tissue morphology were observed by Masson staining; and myocardial collagen volume fraction was calculated. Enzyme-linked immunosorbent assay was used to measure the concentration of Ang ¢ò in serum. The expression of TGF-β1 and CTGF were determined by immunohistochemistry and Western blotting.Compared with the sham operation group, the heart weight index, collagen volume fraction of the myocardium, serum levels of Ang ¢ò and the expression of myocardial TGF-β1 and CTGF in the model group were significantly increased (P0.05). Compared with the model group, the heart weight index, collagen volume fraction of the myocardium, serum levels of Ang ¢ò and the expression of myocardial TGF-β1 and CTGF in all treatment groups were significantly reduced (P0.05).Sini decoction reduced Ang ¢ò level and inhibited the expression of myocardial TGF-β1 and CTGF, which may explain the mechanism of its protective effect on myocardium with fibrosis.

In addition to the known antitumour effects of ursolic acid (UA), increasing evidence indicates that this molecule plays a role in cardiac protection. In this study, the effects of ursolic acid on the heart in mice treated with doxorubicin (DOX) were assessed. The results showed that ursolic acid improved left ventrical fractional shortening (LVFS) and left ventrical ejection fraction (LVEF) of the heart, increased nitrogen oxide (NO) levels, inhibited reactive oxygen species (ROS) production and decreased cardiac apoptosis in mice treated with doxorubicin. Mechanistically, ursolic acid increased AKT and endothelial nitric‐oxide synthase (eNOS) phosphorylation levels, and enhanced eNOS expression, while inhibiting doxorubicin induced eNOS uncoupling through NADPH oxidase 4 (NOX4) down‐regulation. These effects of ursolic acid resulted in heart protection from doxorubicin‐induced injury. Therefore, ursolic acid may be considered a potential therapeutic agent for doxorubicin‐associated cardiac toxicity in clinical practice.

Puerarin, a major isoflavonoid compound isolated from the Chinese herb Kudzu roots, has been a long history and widely used for treatment of cerebral and cardiovascular diseases in China and other Asian countries, including coronary artery disease, heart failure and myocardial infarction. However, the underlying mechanisms by which puerarin inhibits vascular atherogenic diseases are largely unknown. The activated macrophages release of inflammatory cytokines and uptake of oxLDL forming foam cells are critical for the development of atherosclerotic plaque. The present study investigated whether puerarin inhibited atherogenic lipid oxLDL-mediated macrophage activation and foam cell formation in human THP1 macrophage. The Cells were cultured and differentiated into macrophages by pre-incubation with 100 ng/ml PMA. Treatment with oxLDL (50 μg/ml) significantly increased the mRNA expression of proinflammatory cytokines tumor necrosis factor α(TNFα, 160%) and interleukin (IL)1β(13 fold) accompanied by upregulation of toll-like receptor 4 (TLR4, 165%) and the ratio of phospho-I κ Bα/I κ Bα in THP1 macrophage. Puerarin dose-dependently prevented an increase in oxLDL-induced proinflammatory gene expression with downregulation of TLR4 and the ratio of phospho-I κ Bα/I κ Bα. Furthermore, puerarin prevented oxLDL-mediated lipid deposition and foam cell formation associated with downregulation of scavenger receptor CD36. Flow cytometry analysis showed that puerarin reduced the number of early apoptotic cells of macrophages induced by oxLDL. Our results show that puerarin has anti-inflammatory and anti-atherogenic effects in vitro, the underling mechanisms may involve the inhibition of TLR4/NF κ B pathway and downregulation of CD36 expression. The results from the present study provide scientific evidence and may expand our armamentarium to use puerarin for prevention and treatment of cardiovascular and atherosclerotic diseases.

Puerarin, an isoflavone derived from Kudzu roots, has been widely used for treatment of cardiovascular and cerebral vascular diseases in China and other Asian countries. However, the underlying mechanisms are largely unknown. The present study investigated whether puerarin inhibited atherogenic lipid oxLDL-mediated macrophage activation and foam cell formation in human THP1 macrophage. Treatment with oxLDL significantly increased the mRNA expression of proinflammatory cytokines tumor necrosis factorα(TNFα, 160%) and interleukin (IL) 1β(13 fold) accompanied by upregulation of toll-like receptor 4 (TLR4, 165%) and the ratio of phospho-IκBα/IκBαin THP1 macrophage. Puerarin dose-dependently prevented an increase in oxLDL-induced proinflammatory gene expression with downregulation of TLR4 and the ratio of phospho-IκBα/IκBα. Furthermore, puerarin prevented oxLDL-mediated lipid deposition and foam cell formation associated with downregulation of scavenger receptor CD36. Flow cytometry analysis showed that puerarin reduced the number of early apoptotic cells of macrophages induced by oxLDL. Our results show that puerarin has anti-inflammatory and antiatherogenic effects in vitro; the underlying mechanisms may involve the inhibition of TLR4/NFκB pathway and downregulation of CD36 expression. The results from the present study provide scientific evidence and may expand our armamentarium to use puerarin for prevention and treatment of cardiovascular and atherosclerotic diseases.