Correlation Between Family Functioning and Health Beliefs in Patients with Stroke in Beijing, China.

Objective: To explore the relationship between family functioning and health beliefs in patients with stroke. Methods: A total of 253 patients with stroke were selected from Beijing Luhe Hospital, Capital Medical University from May 2021 to November 2021. All patients were of Chinese nationality, and 240 valid questionnaires were obtained. The Family Assessment Device and Champion's Health Belief Model Scale were used to collect patients' family functioning and health beliefs information, and correlation analysis was used to analyse it. Results: The total score for family functioning in patients with stroke was 130.5 (22). The highest mean score was 2.46 for behaviour control, and the lowest score was 2.00 for total function. The items were ranked from high to low in this order: behaviour control, emotional response, role, communication, emotional intervention, problem solving and total function. The total score of the patients' health beliefs was 116 (33), The items were ranked from high to low in this order: were self-efficacy, health motivation, perceived benefit, susceptibility, severity and perceived impairment. The scores for family functioning were negatively correlated with the total scores for health beliefs (P < 0.05). Discussion: Stroke can reduce the self-care ability of the patients and aggravate the burden of family care. This can lead to abnormal function roles for patients and their families, emotional reactions in patients with stroke and weaker levels of family functioning. Conclusion: The health beliefs scores of patients with stroke were at the middle level, and family functioning was at the general level. There was a negative correlation between the family functioning score and the total score for health beliefs in patients with stroke.

Mediating Role of Teamwork in the Influence of Team Role on Team Performance.

Objective: As an important hospital task, the quality and efficiency of nursing practice directly affect the medical quality and sustainable development of the hospital. Increasing attention is now paid by managers to nursing teamwork. From the level of the nursing team, this study explored the relationship between team roles, using teamwork as the intermediate variable, and team performance to provide a theoretical foundation for the human resource management of nursing managers. Methods: Taking 29 general inpatient areas of a tertiary general hospital in Beijing as research objects, a questionnaire survey was used to collect basic information on nursing staff, teamwork, team roles and team performance. The collected data were analysed. A pathway analysis based on a multiple regression analysis was used to interpret the effect of each team role on teamperformance. Results: ①The mean and maximum value of emotional type (Teamworker and Finisher) were the largest in the role combination of nursing team. In the team role combination, the average value of emotional type was 12.58 ± 1.48, with significant difference (P<0.001). ② The average level of emotion, thinking and decision of team role combination is positively correlated with work performance; The average level and maximum value of emotion have a positive correlation with team cooperation; The average level of willingness was negatively correlated with team cooperation, job performance and satisfaction (P<0.05). ③ Teamwork plays a certain intermediary role in the mean value of emotion to improve level of team satisfaction and performance. Conclusion: This study identified the important roles of different types of nursing staff in work performance and used a pathway analysis to create a path showing each role. Increasing the emotional-type nursing staff in a team can not only improve the mean level of team emotion but also effectively improve both teamwork and work performance.

RNA helicase DDX5-induced circPHF14 promotes gastric cancer cell progression.

As a well-established member of a strongly conserved protein family, DDX5 binds to RNA helicase in a specific manner, which can regulate mRNA transcription, protein translation and synthesis and precursor messenger RNA processing or alternative splicing. The effects of DDX5 on carcinogenesis and cancer progression are increasingly evident. Circular RNAs (circRNAs), a novel group of functionally non-coding RNAs (ncRNAs) with disordered expression, are associated with various pathological processes (e.g., tumors). circRNA pattern and its function regulated by DDX5 have not yet been determined. According to our findings, DDX5 was dramatically upregulated for stomach cancer tissues, and its overexpression contributed to the cell growth and invasion of GC cells. Based on the analysis of genome-wide circRNAs conducted with circRNA sequencing, DDX5 induces a large number of circRNAs. Further to screen several circRNAs from PHF14 for function, it was found that circPHF14 was essential for the growth and tumorigenesis of DDX5-positive gastric cancer cells. These findings suggest that in addition to the messenger RNA and microRNA patterns, DDX5 also effects a circRNA pattern, as demonstrated by circPHF14. DDX5-induced circRNAs have been found to be of crucial importance for the growth of DDX5-positive gastric cancer cells, providing a new therapeutic target.

Development and Reliability Testing of the Stroke Patient Protection Motivation Scale.

Objective: A scale for evaluating the protective motivation of patients who had suffered a stroke was developed to preliminarily verify the reliability of the scale and provide scientific measurement tools for clinical professionals. Methods: A descriptive research design method was adopted. First, an initial draft of the questionnaire was formed by conducting a literature review supplemented by semi-structured interviews and modified using the Delphi method. A total of 287 patients who had suffered a stroke were selected for the formal survey using the convenience sampling method. Further item screening was performed using an item analysis and an exploratory factor analysis, and reliability testing was also performed. Results: The scale consisted of 34 entries in the following 6 dimensions: severity, susceptibility, internal and external rewards, response efficacy, response cost and self-efficacy. The overall Cronbach's alpha coefficient was 0.935, with correlation coefficients between dimensions and total scale scores ranging from 0.604 to 0.805 (P < 0.05) and correlation coefficients between dimensions ranging from 0.154 to 0.537 (P < 0.05). Conclusion: The protective motivation scale prepared in this study was tested and had good reliability, so this scale can be used as a scientific tool to evaluate the implementation of secondary prevention strategies for protective motivation of patients who have suffered a stroke.

Homocysteine induces the expression of C-reactive protein via NMDAr-ROS-MAPK-NF-κB signal pathway in rat vascular smooth muscle cells.

OBJECTIVE: Homocysteine (Hcy) is known as an independent risk factor for atherosclerosis. C-reactive protein (CRP) directly participates in initiation and progression of atherosclerosis. However, there is no direct evidence to demonstrate pro-inflammatory effect of Hcy on vascular smooth muscle cells (VSMCs) through CRP. In the present study, we examined the effect of Hcy on CRP expression and investigated the related mechanism in VSMCs. METHODS AND RESULTS: Protein expression and secretion were detected by Western blot and ELISA, respectively. mRNA expression was detected by RT-PCR. Superoxide anion was detected by lucigenin chemiluminometry and the immunofluorescence staining was observed by a fluorescence microscope. The results revealed that Hcy significantly induced mRNA and protein expressions of CRP in VSMCs both in vitro and in vivo, and anti-IL-1ß or anti-IL-6 neutralizing antibody alone or in combination partially reduced Hcy-induced CRP expression. Hcy increased the expression of NR1 subunit of N-methyl-d-aspartate receptor (NMDAr), and MK-801 alleviated Hcy-induced CRP expression in VSMCs. Further studies showed that Hcy-stimulated superoxide anion generation in VSMCs. Nevertheless, pretreatment of the cells with MK-801, TTFA and DPI significantly reduced Hcy-stimulated superoxide anion generation, and antioxidant NAC decreased Hcy-induced CRP expression in VSMCs. Additionally, PD98059, SB205380 or PDTC antagonized Hcy-induced CRP expression, and MK-801, NAC, PD98059 or SB205380 inhibited Hcy-activated phosphorylations of ERK1/2 and p38. CONCLUSION: The present study demonstrates that Hcy is able to initiate an inflammatory response in VSMCs by stimulating CRP production, which is mediated through NMDAr-ROS-ERK1/2/p38-NF-κB signal pathway. These findings provide new evidence for a role of Hcy in pathogenesis of atherosclerosis.

Nicotine induces the expression of C-reactive protein via MAPK-dependent signal pathway in U937 macrophages.

Atherosclerosis is an inflammatory disease in the vessel wall. Nicotine, a major component of cigarette smoke, is an independent risk factor for cardiovascular diseases including atherosclerosis. As an inflammatory molecule, C- reactive protein (CRP) participates in atherogenesis. Although it has been confirmed that CRP level in smoking patient is significantly higher than non-smokers and cigarette withdrawal, it is unknown whether nicotine induces CRP expression in macrophages. The present study was to observe effect of nicotine on CRP production and the related signal pathway in U937 macrophages. The results showed that nicotine significantly increased mRNA and protein expression of CRP in U937 macrophages in time- and concentration-dependent ways. Nicotinic acetylcholine receptor (nAChR) blocker hexamethonium, MEK1/2 inhibitor PD98059, p38 MAPK inhibitor SB203580 and NF-κB inhibitor PDTC almost completely abolished nicotineinduced CRP expression in mRNA and protein levels in U937 macrophages. The further study indicated that hexamethonium, PD98059, and SB203580 significantly inhibited ERK1/2 and p38 MAPK phosphorylation. These demonstrate that nicotine has ability to induce CRP expression in macrophages through nAChR-ERK1/2/p38 MAPK-NF-κB signal pathway, which contributes to better understanding of the pro-inflammatory and pro-atherosclerotic effects of nicotine in cigarette smokers.

Epigallocatechin-3-gallate inhibits angiotensin II and interleukin-6-induced C-reactive protein production in macrophages.

BACKGROUND: Consumption of green tea has been associated with health benefits against multiple diseases including cardiovascular diseases. However, the action mechanisms of green tea and its major ingredient epigallocatechin-3-gallate (EGCG) against cardiovascular diseases are still unclear. Emerging evidence has suggested a common role for C-reactive protein (CRP) in the pathogenesis of inflammation and atherosclerosis. Therefore, the effect of EGCG on angiotensin II (Ang II)- and interleukin-6 (IL-6)-induced CRP production in U937 macrophages and the possible mechanisms were observed. METHODS: U937 macrophages were cultured, and Ang II and IL-6 were used as stimulants for generation of CRP. U937 macrophages were preincubated with EGCG at 1, 3, 10 µM for 1 h prior to the stimulation. mRNA expression and protein level were determined by RT-PCR and ELISA, respectively. ROS production was observed by a fluorescence microscope. RESULTS: Pretreatment of macrophages with EGCG prior to the stimulation concentration-dependently inhibited Ang II- and IL-6-induced expression of CRP both in protein and mRNA levels. Meanwhile, EGCG reduced Ang II- and IL-6-stimulated generation of ROS in macrophages. CONCLUSION: EGCG is able to inhibit Ang II- and IL-6-stimulated CRP expression in macrophages to produce an anti-inflammation by interfering with ROS generation. The finding is helpful to update understanding of anti-atherosclerotic effects of EGCG.

Rosiglitazone inhibits angiotensin II-induced C-reactive protein production in human aortic endothelial cells through regulating AT(1)-ROS-MAPK signal pathway.

OBJECTIVE: Atherosclerosis is an inflammatory disease. As an inflammatory molecule, C-reactive protein (CRP) plays a direct role in atherogenesis. Our previous study confirmed that angiotensin II (Ang II) is capable of inducing CRP generation in human aortic endothelial cells (HAECs). The present study observed the effect of rosiglitazone on Ang II-induced CRP expression in HAECs and molecular mechanisms. METHODS: HAECs were cultured, and Ang II (10(-6) M) was used as a stimulant for the generation of CRP and reactive oxygen species (ROS). HAECs were preincubated with rosiglitazone at 1, 10, 100 µM for 18 h prior to the stimulation. mRNA and protein expressions were identified by reverse transcription polymerase chain reaction and Western blot, respectively. ROS production was observed by a fluorescence microscope. RESULTS: Pretreatment of HAECs with rosiglitazone prior to Ang II stimulation markedly downregulated Ang II-induced mRNA and protein expressions of CRP (maximal inhibition of 55.2 and 99.1 %, P < 0.001 vs. Ang II alone) and AT(1) (maximal inhibition of 66.4 and 90.5 %, P < 0.001 vs. Ang II alone) in a concentration-dependent manner, inhibited Ang II-stimulated ROS production (P < 0.01 vs. Ang II alone), and attenuated Ang II-induced phosphorylation of ERK1/2 and JNK (P < 0.001 vs. Ang II alone). Meanwhile, AT(1) receptor blocker losartan also reduced Ang II-stimulated ROS generation in HAECs (P < 0.001 vs. Ang II alone). CONCLUSIONS: Rosiglitazone at the concentrations used in the present experiment is able to inhibit Ang II-induced CRP generation in HAECs by regulating AT(1)-ROS-MAPK signal pathway. These results strengthen our understanding of the anti-inflammatory and anti-atherosclerotic effects of rosiglitazone.

Angiotensin II induces the expression of c-reactive protein via MAPK-dependent signal pathway in U937 macrophages.

Atherosclerosis is an inflammatory disease in the vessel wall. As an inflammatory molecule, C-reactive protein (CRP) participates in all stages of atherosclerotic process. Although angiotensin II (Ang II) can stimulate the vascular cells to produce CRP, it is unknown whether Ang II induces CRP expression in macrophages. The present study was to observe effect of Ang II on CRP production and the related signal pathway in U937 macrophages so as to provide more evidence for the proinflammatory action of Ang II. The results showed that Ang II significantly increased mRNA and protein expression of CRP in U937 macrophages in time- and concentration-dependent manners. AT(1) receptor blocker losartan blocked Ang II -induced CRP expression in mRNA and protein levels in U937 macrophages. Losartan and complex II inhibitor TIFA decreased Ang II -stimulated reactive oxygen species (ROS) generation, and antioxidant NAC completely abolished Ang II -induced CRP expression in U937 macrophages. The further study indicated that losartan, NAC, MEK1/2 inhibitor PD98059, p38MAPK inhibitor SB203580 obviously inhibited ERK1/2 and p38MAPK phosphorylation, and PD98059, SB203580 and NF-κB inhibitor PDTC reduced Ang II -induced mRNA and protein expression of CRP in U937 macrophages. These demonstrate that Ang II is capable of inducing CRP generation in macrophages via AT(1)-ROS-ERK1/2/p38MAPK-NF-κB signal pathway, which contributes to better understanding of the proinflammatory and proatherosclerotic actions of Ang II.

[Mechanism of Dahuang Zhechong pill against atherosclerosis induced by balloon angioplasty in rabbits].

OBJECTIVE: To study the mechanism of Dahuang Zhechong pill (DHZCP) against atherosclerosis induced by balloon angioplasty in rabbits. METHODS: Atherosclerosis model was established by the combination of balloon angioplasty-induced endothelial injury and high cholesterol feeding in rabbit. Male New Zealand rabbits were divided into six groups randomly: normal control, sham, model, positive control and two doses of DHZCP-treated groups. Rabbits in DHZCP-treated groups were intragastrically administered 0.9 and 1.8 g/kg DHZCP for 60 days respectively,and rabbits in positive control group were given 0.5 g/kg Danshen. MDA, NO levels and SOD activity in serum, and MPO activity in the vascular wall were determined with spectrophotometry. Expressions of proliferating cell nuclear antigen (PCNA) and BCL-2 in the vascular wall were detected by SP immuohistochemical technique. RESULTS: Compared with the model group, DHZCP significantly reduced serum MDA level and MPO activity in the vascular wall, increased serum NO level and SOD activity,and inhibited PCNA and BCL-2 expressions in the vascular wall. CONCLUSION: DHZCP inhibits the formation and development of atherosclerosis through anti-oxidative action, protecting endothelium from injury,inhibiting proliferation and promoting apoptosis of vascular smooth muscle cells.

Angiotensin II induces C-reactive protein expression through ERK1/2 and JNK signaling in human aortic endothelial cells.

BACKGROUND: Atherosclerosis is an inflammatory disease in the vessel. As an inflammatory cytokine, C-reactive protein (CRP) participates in atherogenesis. Although angiotensin II (AngII) is known to evoke inflammatory response in vascular endothelial cells (VECs), there is no direct evidence to demonstrate the proinflammatory effect of AngII on VECs through CRP. The present study focused on effect of AngII on CRP expression and the signal pathway in human aortic endothelial cells (HAECs). METHODS AND RESULTS: mRNA and protein expression was identified by RT-PCR and Western blot, respectively. Reactive oxygen species (ROS) were observed by a fluorescence microscope. The results showed that AngII significantly increased mRNA and protein expression of CRP in HAECs in time- and concentration-dependent ways. Anti-IL-1beta and anti-IL-6 neutralizing antibodies did not affect AngII-induced CRP expression. Losartan reduced AngII-induced CRP expression in mRNA and protein levels in HAECs. Losartan and TIFA decreased AngII-stimulated ROS generation, and antioxidant NAC completely abolished AngII-induced CRP expression in HAECs. The further study indicated that losartan, NAC, PD98059, SP600125 significantly inhibited ERK1/2 and JNK phosphorylation, and PD98059, SP600125, PDTC completely antagonized AngII-induced CRP expression in HAECs. CONCLUSIONS: The present study demonstrates that AngII has ability to induce CRP expression in HAECs through AT(1)-ROS-ERK1/2 and JNK-NF-kappaB signal pathway, which strengthens understanding of the proinflammatory and proathroscerotic actions of AngII.

[Progress in signal transduction pathways mediating effects of angiotensin II in endothelial cells].

Angiotensin II (Ang II) not only mediates the effects of vasoconstriction and blood pressure regulation, but is also implicated in inflammation, endothelial dysfunction, atherosclerosis, hypertension and congestive heart failure. Ang 1I activates pathways of MAPK, NADPH and ROS, non-receptor tyrosine kinases and receptor tyrosine kinases via AT1 receptor to produce various effects involved in regulation of endothelial functions, endothelial dysfunction and vascular inflammation response.

[Protection of vascular endothelial cells from ox-LDL induced injury by protocatechualdehyde].

OBJECTIVE: To observe the protective effects of protocatechualdehyde on the human umbilical vein endothelial cells (CRL-1730) induced injury by ox-LDL. METHODS: The CRL-1730 were induced injury by ox-LDL, and then treated with protocatechualdehydes for 24 hours. The cytoactive of CRL-1730 was assessed by colorimetry of MTr, the NO level and NOS activity in the cell culture fluid were observed by colorimetry, and the expression of CD40 protein was determined by flow cytometry. RESULTS: Compared with the ox-LDL group, protocatechualdehyde increased,the number of CRL-1730 and the level of NO and NOS in cell culture fluid. Besides, protocatechualdehyde decreased the expression of CD40 protein, which was increased by ox-LDL. CONCLUSION: Protocatechualdehyde has protective effect on the CRL-1730 induced injury by ox-LDL and its mechanism of action may be related to the CD40/CD40L pathway.

Fenofibrate inhibits tumor necrosis factor-alpha-induced expression of CD40 and matrix metalloproteinase in human vascular endothelial cells.

OBJECTIVE: To investigate the regulatory effects of fenofibrate on TNF-alpha-induced CD40 expression and matrix metalloproteinase (MMP) activity in human vascular endothelial cells (HUVECs). METHODS: Quantitative RT-PCR and flow cytometry were employed to evaluate the effect of fenofibrate on TNF-alpha-induced CD40 mRNA and cell surface CD40 expression in HUVECs, and gelatin zymography was used to determine the effect of fenofibrate on the gelatinolytic activities of MMP-2 and MMP-9 in TNF-alpha-stimulated HUVECs. RESULTS: Fenofibrate at the concentrations of 5x10(-5), 1x10(-4) and 2x10(-4) mol/L significantly reduced TNF-alpha-induced increment of CD40 mRNA and cell surface CD40 expressions (P<0.01), with the maximal inhibition achieved at the concentration of 1x10(-4) mol/L. Fenofibrate at 2x10(-4) mol/L did not further decrease CD40 expression induced by TNF-alpha. Fenofibrate significantly inhibited the stimulatory effect of TNF-alpha on MMP-2 and MMP-9 activities in HUVECs. CONCLUSION: Fenofibrate reduces TNF-alpha-induced increment of CD40 expression and MMP-2 and MMP-9 activities in HUVECs.

Protective effect of tanshinone IIA on human umbilical vein endothelial cell injured by hydrogen peroxide and its mechanism.

Tanshinone IIA (Tan IIA) is isolated from Salvia miltiorrhiza, the root of which is widely used as a traditional Chinese medicine to treat atherosclerosis. The aim of the present study was to evaluate the putative protective effect of Tan IIA in a human umbilical vein endothelial cell line (ECV-304) injured by hydrogen peroxide in vitro and the mechanism of its protection. The percentage of cell viability was evaluated by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl tetrazolium bromide (MTT) assay. The endothelial cell apoptosis and expression of cluster of differentiation 40 (CD40) were detected by flow cytometric analysis. Preincubation with Tan IIA significantly increased the viability of ECV-304 cell injured by hydrogen peroxide, which was accompanied with the increased nitric oxide level and superoxide dismutase activity in a dose-dependent manner. Moreover, cell apoptosis and CD40 expression were decreased in a dose-dependent manner. In conclusion, our data suggests that Tan IIA protects ECV-304 cell damage induced by hydrogen peroxide through its anti-oxidant effect and CD40 anti-inflammatory approach.

Lovastatin reduces apoptosis and downregulates the CD40 expression induced by TNF-alpha in cerebral vascular endothelial cells.

Inflammation may be one of the independent risk factors contributing to many neurological diseases. Moreover, there is an emerging body of data indicating that statins may have neuroprotective action. Recent studies suggest that CD40-CD40 ligand (CD40L) system is proven to be an important mediator of several auto-immune and chronic inflammation diseases. To address whether lovastatin produces neuroprotection as a potential novel anti-inflammatory pathway through the inhibition of CD40 expression, we examined the possible effects of lovastatin on expression of CD40, apoptosis, level of nitric oxide (NO) and nitric oxide synthase (NOS) activity induced by tumor necrosis factor alpha (TNF-alpha) in the cerebral vascular endothelial cells (CVECs) involved in cerebrovascular diseases. Preincubation with lovastatin (10(-7), 10(-6) and 10(-5) mol/l) for 24 hours (h) protected CVECs from TNF-alpha-induced decrease of cellular viability. Further, lovastatin inhibited the TNF-alpha-induced increases of NO level, NOS activity, apoptotic cells and CD40 expression in a dose-dependent manner, and anti-CD40 antibody also inhibited the cellular apoptosis induced by TNF-alpha. In conclusion, our data provide evidence to support a direct pro-inflammatory effect of CD40-CD40L signaling pathway in CVECs, and lovastatin possesses an anti-inflammatory effect independent of its lipid-lowering action involved in the cerebrovascular diseases.