Non-invasive ventilation (NIV) is the mainstay to treat patients who need augmentation of ventilation for acute and chronic forms of respiratory failure. The last several decades have witnessed an extension of the indications for NIV to a variety of acute and chronic lung diseases. Evolving advancements in technology and personalised approaches to patient care make it feasible to prioritise patient-centred care models that deliver home-based management using telemonitoring and telemedicine systems support.
View Article and Find Full Text PDFBackground: The strategic response of nurses in addressing health inequities in marginal sectors led to the conduct of a health leadership governance training program for local chief executives.
Objective: This study aimed to explore and provide a description of the experiences of local chief executives (LCEs) or mayors who participated in the nurse-initiated health training named Municipal Leadership and Governance Program (MLGP).
Methods: A qualitative descriptive design was used through key informant interviews of fifteen mayors or local chief executives (LCE) in the provinces of Bohol and Negros Oriental, Philippines.
Numerous studies have demonstrated that endostatin (ES), a potent angiostatic peptide derived from collagen type XVIII α 1 chain and encoded by , is elevated in pulmonary arterial hypertension (PAH). It is important to note that elevated ES has consistently been associated with altered hemodynamics, poor functional status, and adverse outcomes in adult and pediatric PAH. This study used serum samples from patients with Group I PAH and plasma and tissue samples derived from the Sugen/hypoxia rat pulmonary hypertension model to define associations between /ES and disease development, including hemodynamics, right ventricle (RV) remodeling, and RV dysfunction.
View Article and Find Full Text PDFThe tumor-suppressor p53 is commonly inactivated in colorectal cancer and pancreatic ductal adenocarcinoma, but existing treatment options for p53-mutant (p53) cancer are largely ineffective. Here, we report a therapeutic strategy for p53 tumors based on abnormalities in the DNA repair response. Investigation of DNA repair upon challenge with thymidine analogs reveals a dysregulation in DNA repair response in p53 cells that leads to accumulation of DNA breaks.
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