22 research outputs found
Prolonged Mechanical Ventilation Induces Cell Cycle Arrest in Newborn Rat Lung
Rationale: The molecular mechanism(s) by which mechanical ventilation disrupts alveolar development, a hallmark of bronchopulmonary dysplasia, is unknown. Objective: To determine the effect of 24 h of mechanical ventilation on lung cell cycle regulators, cell proliferation and alveolar formation in newborn rats. Methods: Seven-day old rats were ventilated with room air for 8, 12 and 24 h using relatively moderate tidal volumes (8.5 mL.kg-1). Measurement and Main Results: Ventilation for 24 h (h) decreased the number of elastin-positive secondary crests and increased the mean linear intercept, indicating arrest of alveolar development. Proliferation (assessed by BrdU incorporation) was halved after 12 h of ventilation and completely arrested after 24 h. Cyclin D1 and E1 mRNA and protein levels were decreased after 8-24 h of ventilation, while that of p27Kip1 was significantly increased. Mechanical ventilation for 24 h also increased levels of p57Kip2, decreased that of p16INK4a, while the levels of p21Waf/Cip1 and p15INK4b were unchanged. Increased p27Ki
Risk of chronic kidney disease after cancer nephrectomy.
The incidence of early stage renal cell carcinoma (RCC) is increasing and observational studies have shown equivalent oncological outcomes of partial versus radical nephrectomy for stage I tumours. Population studies suggest that compared with radical nephrectomy, partial nephrectomy is associated with decreased mortality and a lower rate of postoperative decline in kidney function. However, rates of chronic kidney disease (CKD) in patients who have undergone nephrectomy might be higher than in the general population. The risks of new-onset or accelerated CKD and worsened survival after nephrectomy might be linked, as kidney insufficiency is a risk factor for cardiovascular disease and mortality. Nephron-sparing approaches have, therefore, been proposed as the standard of care for patients with type 1a tumours and as a viable option for those with type 1b tumours. However, prospective data on the incidence of de novo and accelerated CKD after cancer nephrectomy is lacking, and the only randomized trial to date was closed prematurely. Intrinsic abnormalities in non-neoplastic kidney parenchyma and comorbid conditions (including diabetes mellitus and hypertension) might increase the risks of CKD and RCC. More research is needed to better understand the risk of CKD post-nephrectomy, to develop and validate predictive scores for risk-stratification, and to optimize patient management
The surgical pathology of pulmonary infarcts: diagnostic confusion with granulomatous disease, vasculitis, and neoplasia
Measurement of vertebral bone marrow lipid profile at 1.5-T proton magnetic resonance spectroscopy and bone mineral density at dual-energy X-ray absorptiometry: correlation in a swine model
Environmental Pollution Policies in Light of Biotechnological Assessment: Organisation for Economic Cooperation, United Kingdom, and European Economic Council Perspectives
The effect and mechanism of YH0618 granule on chemotherapy- induced hair loss in patients with breast cancer: study protocol for a randomized, double-blind, multi-center clinical trial
Determinants and regulating processes in bronchial hyperreactivity
textabstractBronchial hyperresponsiveness (BHR) can be considered as a feature of asthma, although only a loose relationship is present with symptoms and severity of the disease. Epidemiology of BHR may inform about determining factors in BHR and its role as a risk factor. BHR is found already at a young age, mostly diminishes with age, and increases in many asthmatic patients after midlife. Genetic determinants are suggested by familial segregation and twin studies. Allergy, respiratory infections, and cigarette smoking are found to induce increase in BHR and to modify its degree at the long run. The mechanisms in BHR are being unraveled gradually. A chronic inflammation with an important role for eosinophils, mast cells, and others, is thought to modify bronchial mechanisms, such as smooth muscle, epithelium, and autonomic systems. Growing evidence supports that T lymphocytes are implicated and may determine many of the inflammatory cells, such as eosinophils, neutrophils, and mast cells