Pain Management Strategies in Nursing

In the second phase, a digital questionnaire was devised to gauge the perceived regularity and effectiveness of various strategies. Content from the PAIN-SP scale was showcased to an independent cohort of professionally trained nurses at the baccalaureate, masters, and doctorate levels who were actively engaged in clinical practice. These practitioners offered insights regarding the clarity and pertinence of the material in relation to their professional duties, triggering adjustments. These revised iterations underwent a trial run with the same demographic, followed by further refinements. Subsequently, the PAIN-SP scale was subjected to an additional pilot test among the designated demographic: nurses who provide care for adult patients in high-acuity environments. A structured critique of the tool ensued and is elucidated in the subsequent segments. In the initial step, behavioral markers for five pain relief tactics, previously elaborated in the American Nurses Association (ANA) protocols, were pinpointed. These protocols underline the essential process of evaluation, intervention, and reevaluation to maintain or enhance patient well-being. Embedded within each tactic is a sequence of evaluation, corresponding relief measures, and follow-up assessments. Dual Delphi inquiries were executed to ascertain both the relevance and lucidity for the nursing cadre. Seasoned nursing specialists and active nurse practitioners offered their evaluations and commentary until a collective agreement was formulated. This empirical, quantitative study sought to evaluate the practicality of the Pain Management Strategies in Nursing Practice (PAIN-SP) scale. The tool, meticulously designed to chronicle the frequency and perceived potency of pain relief approaches employed by nurses in the treatment of hospitalized adults confronting medical issues that necessitate pain and discomfort management, was put to the test

Regulation of cellular contractile force, shape and migration of fibroblasts by oncogenes and Histone deacetylase 6

The capacity of cells to adhere to, exert forces upon and migrate through their surrounding environment governs tissue regeneration and cancer metastasis. The role of the physical contractile forces that cells exert in this process, and the underlying molecular mechanisms are not fully understood. We, therefore, aimed to clarify if the extracellular forces that cells exert on their environment and/or the intracellular forces that deform the cell nucleus, and the link between these forces, are defective in transformed and invasive fibroblasts, and to indicate the underlying molecular mechanism of control. Confocal, Epifluorescence and Traction force microscopy, followed by computational analysis, showed an increased maximum contractile force that cells apply on their environment and a decreased intracellular force on the cell nucleus in the invasive fibroblasts, as compared to normal control cells. Loss of HDAC6 activity by tubacin-treatment and siRNA-mediated HDAC6 knockdown also reversed the reduced size and more circular shape and defective migration of the transformed and invasive cells to normal. However, only tubacin-mediated, and not siRNA knockdown reversed the increased force of the invasive cells on their surrounding environment to normal, with no effects on nuclear forces. We observed that the forces on the environment and the nucleus were weakly positively correlated, with the exception of HDAC6 siRNA-treated cells, in which the correlation was weakly negative. The transformed and invasive fibroblasts showed an increased number and smaller cell-matrix adhesions than control, and neither tubacin-treatment, nor HDAC6 knockdown reversed this phenotype to normal, but instead increased it further. This highlights the possibility that the control of contractile force requires separate functions of HDAC6, than the control of cell adhesions, spreading and shape. These data are consistent with the possibility that defective force-transduction from the extracellular environment to the nucleus contributes to metastasis, via a mechanism that depends upon HDAC6. To our knowledge, our findings present the first correlation between the cellular forces that deforms the surrounding environment and the nucleus in fibroblasts, and it expands our understanding of how cells generate contractile forces that contribute to cell invasion and metastasisis

Chlorhexidine versus Povidone-Iodine for the prevention of ‎Surgical Site ‎Infections: A review.‎

BackgroundSurgical Site Infections (SSIs) are the third most frequently reported health care-associated ‎infection‎ and it remain a major clinical problem despite improvements in prevention, as they ‎are associated with ‎significant mortality and morbidity. Prevention strategies for SSIs are based ‎on reducing the risk of infection by bacteria, So many antiseptic agents are ‎used, the most ‎common one are Chlorhexidine and Povidone-Iodine.‎AimsTo discuss the ‎findings of RCTs that compare Chlorhexidine versus Povidone-Iodine in the prevention of ‎Surgical ‎Site ‎Infections (SSIs).‎Methods This systematic review was carried out, including PubMed, Google Scholar, and EBSCO that ‎examining randomized trials of Chlorhexidine and Povidone-Iodine to summarize the major ‎RCT that compare Chlorhexidine versus Povidone-Iodine in the prevention of Surgical Site ‎Infections (SSIs).‎Results The review included six randomized studies that compare between Chlorhexidine and Povidone-‎Iodine for the prevention of SSIs. The findings showed that many studies prefer using ‎Chlorhexidine over Povidine-Iodine to reduce SSIs, few studies prefer using PVI as antiseptic ‎and other studies reported that there is no significant difference between both. ConclusionMajority of results prefer using Chlorhexidine than Povidone-Iodine‎ as antiseptics but ‎there were few findings prefer ‎PVI and other studies reported that there was no significant ‎difference between using them as ‎antiseptics.

DataSheet1_Regulation of cellular contractile force, shape and migration of fibroblasts by oncogenes and Histone deacetylase 6.docx

The capacity of cells to adhere to, exert forces upon and migrate through their surrounding environment governs tissue regeneration and cancer metastasis. The role of the physical contractile forces that cells exert in this process, and the underlying molecular mechanisms are not fully understood. We, therefore, aimed to clarify if the extracellular forces that cells exert on their environment and/or the intracellular forces that deform the cell nucleus, and the link between these forces, are defective in transformed and invasive fibroblasts, and to indicate the underlying molecular mechanism of control. Confocal, Epifluorescence and Traction force microscopy, followed by computational analysis, showed an increased maximum contractile force that cells apply on their environment and a decreased intracellular force on the cell nucleus in the invasive fibroblasts, as compared to normal control cells. Loss of HDAC6 activity by tubacin-treatment and siRNA-mediated HDAC6 knockdown also reversed the reduced size and more circular shape and defective migration of the transformed and invasive cells to normal. However, only tubacin-mediated, and not siRNA knockdown reversed the increased force of the invasive cells on their surrounding environment to normal, with no effects on nuclear forces. We observed that the forces on the environment and the nucleus were weakly positively correlated, with the exception of HDAC6 siRNA-treated cells, in which the correlation was weakly negative. The transformed and invasive fibroblasts showed an increased number and smaller cell-matrix adhesions than control, and neither tubacin-treatment, nor HDAC6 knockdown reversed this phenotype to normal, but instead increased it further. This highlights the possibility that the control of contractile force requires separate functions of HDAC6, than the control of cell adhesions, spreading and shape. These data are consistent with the possibility that defective force-transduction from the extracellular environment to the nucleus contributes to metastasis, via a mechanism that depends upon HDAC6. To our knowledge, our findings present the first correlation between the cellular forces that deforms the surrounding environment and the nucleus in fibroblasts, and it expands our understanding of how cells generate contractile forces that contribute to cell invasion and metastasisis.</p