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The aim of this study was to explore predictors of nurses' willingness to handle abuse of older people. Abuse of older people is a long-discussed healthcare issue worldwide. Although nurses are considered capable of identifying and reporting cases of abuse of older people, no study has been conducted in Taiwan on nurses' willingness to handle abuse of older people. A cross-sectional design was used. The study was conducted from May to June 2019. A convenience sampling was adopted to survey 555 nurses from a medical center in Taiwan. Data were collected using the Knowledge of Abuse of Older People Scale, Attitudes Towards Older People Scale, Attitudes Towards Handling Abuse of Older People Scale, Willingness to Handle Abuse of Older People Scale, and personal characteristics. Pearson correlation coefficient analysis, independent sample t-test, one-way analysis of variance, and multiple linear regression were performed. Participants scored an average of 2.98 out of 4 on the Willingness to Handle Abuse of Older People Scale, indicating that they were inclined to do so. Attitudes towards older people, knowledge, attitudes towards handling abuse of older people, awareness of the hospital's reporting procedure and dissemination of information related to abuse of older people, sex, age, and clinical work experience explained 41.4% of the variance of willingness. Participants' attitudes toward handling abuse of older people was the most important predictor of their willingness to do so. To improve nurses’ willingness to handle cases of abuse of older people, particularly that of male nurses, hospital authorities should provide in-service training and education and disseminate information on the subject matter. Nursing schools should prioritize offering gerontological nursing courses to foster nursing students’ positive attitudes toward older adults and handling abuse of older people. Nurses' attitudes toward handling abuse of older people were the most important predictor of their willingness to handle abuse of older people.

Repair of tissues is a necessary step in restoring tissue function following injury consequent to inflammation. Many inflammatory mediators are capable of modulating not only the activity of \"inflammatory cells\" but also of modulating functions of parenchymal cells that may contribute to repair. Disordered repair is believed to contribute to tissue dysfunction in many inflammatory diseases, including bronchial asthma. The current study evaluated the ability of prostaglandin D(2) (PGD(2)) to modulate fibroblast repair using the in vitro contraction of three-dimensional native collagen gels as a model system. PGD(2) stimulated gel contraction in a concentration- and time-dependent manner. In contrast, the PGD(2) analog BW245C inhibited contraction. Both effects were blocked by a DP-receptor blocker (AH6809). Neither TP receptor blocker SQ29548 nor protein kinase (PK) A antagonist KT5720 hand an effect on PGD(2)-stimulated contraction, suggesting action through a novel prostaglandin D receptor. PKC inhibitor calphostin-C (10(-6) M) blocked the PGD(2) stimulation of gel contraction. A calcium-independent PKC-epsilon inhibitor (Ro31-8220), but not calcium-dependent PKC-alpha and -beta inhibitors, also blocked the PGD(2) effect on contraction, implying a role for a calcium-independent pathway. This study, therefore, supports a role for PGD(2) in tissue repair and remodeling. These effects of PGD(2) appear to be mediated through receptor-signal transduction pathways different from the cAMP-PKA pathways mediating the proinflammatory activity of PGD(2), creating the possibility for selective therapeutic manipulation.

Repair of tissues is a necessary step in restoring tissue function following injury consequent to inflammation. Many inflammatory mediators are capable of modulating not only the activity of \"inflammatory cells\" but also of modulating functions of parenchymal cells that may contribute to repair. Disordered repair is believed to contribute to tissue dysfunction in many inflammatory diseases, including bronchial asthma. The current study evaluated the ability of prostaglandin D(2) (PGD(2)) to modulate fibroblast repair using the in vitro contraction of three-dimensional native collagen gels as a model system. PGD(2) stimulated gel contraction in a concentration- and time-dependent manner. In contrast, the PGD(2) analog BW245C inhibited contraction. Both effects were blocked by a DP-receptor blocker (AH6809). Neither TP receptor blocker SQ29548 nor protein kinase (PK) A antagonist KT5720 hand an effect on PGD(2)-stimulated contraction, suggesting action through a novel prostaglandin D receptor. PKC inhibitor calphostin-C (10(-6) M) blocked the PGD(2) stimulation of gel contraction. A calcium-independent PKC-epsilon inhibitor (Ro31-8220), but not calcium-dependent PKC-alpha and -beta inhibitors, also blocked the PGD(2) effect on contraction, implying a role for a calcium-independent pathway. This study, therefore, supports a role for PGD(2) in tissue repair and remodeling. These effects of PGD(2) appear to be mediated through receptor-signal transduction pathways different from the cAMP-PKA pathways mediating the proinflammatory activity of PGD(2), creating the possibility for selective therapeutic manipulation.

Aim： To investigate whether luteolin, the major polyphenolic components of Lonicerajaponica, has beneficial effects against lipopolysaccharide （LPS）-induced acute lung injury （ALl） and to determine whether the protective mechanism involves anti-inflammatory effects on neutrophils. Methods： ALl was induced with intratracheal instillation of LPS in mice. The level of ALl was determined by measuring the cell count and protein content in bronchoalveolar lavage （BAL） fluid. Neutrophils were stimulated with formyI-Met-Leu-Phe （fMLP） or LPS in vitro. Chemotaxis and superoxide anion generation were measured to evaluate neutrophil activation. The potential involvement of intracellular signaling molecules in regulating neutrophil activation was analyzed by using Western blot. Results： LPS induced ALl in mice, as evidenced with leukocyte infiltration and protein leakage into the lungs. Luteolin attenuated LPS- induced leukocyte infiltration and protein extravasationo In cell studies, luteolin attenuated the fMLP-induced neutrophil chemotaxis and respiratory burst （IC50 0.2±0.1 μmol/L and 2.2±0.8 μmol/L, respectively）, but had a negligible effect on superoxide anion generation during phorbol myristate acetate stimulation. Furthermore luteolin effectively blocked MAPK/ERK kinase 1/2 （MEK）, extracellular signal-regulated kinase （ERK）, and Akt phosphorylation in fMLP- and LPS-stimulated neutrophils. Conclusion： These results indicate that luteolin has beneficial effects against LPS-induced ALl in mice, and the attenuation of neutrophil chemotaxis and respiratory burst by luteolin involves the blockade of MEK-, ERK-, and Akt-related signaling cascades.