Our results indicate that prenatal exposure to AgNP can compromise neonatal rats' postnatal development, especially the reproductive features. We present here data on Gram-negative rods bacteremia (GNRB) rates, risk factors and associated mortality. Data on GNRB episodes were prospectively collected in 65 allo-/67 auto-HSCT centers in 24 countries (Europe, Asia, Australia). In patients with and without GNRB, we compared demography, underlying disease, HSCT-related data, center` fluoroquinolone prophylaxis (FQP) policy and accreditation status, and involvement of infection control team (ICT). The GNRB cumulative incidence among 2818 allo-HSCT was pre-engraftment (pre-eng-allo-HSCT), 8.4 (95% CI 7-9%), post-engraftment (post-eng-allo-HSCT), 5.8% (95%CI 5-7%); among 3152 auto-HSCT, pre-eng-auto-HSCT, 6.6% (95%CI 6-7%), post-eng-auto-HSCT, 0.7% (95%CI 0.4-1.1%). GNRB, especially MDR, was associated with increased mortality. Multivariate analysis revealed the following GNRB risk factors (a) pre-eng-allo-HSCT south-eastern Europe center location, underlying diseases not at complete remission, and cord blood source; (b) post-eng-allo-HSCT center location notin northwestern Europe; underlying non-malignant disease, not providing FQP and never accredited. (c) pre-eng-auto-HSCT older age, autoimmune and malignant (vs. plasma cell) disease, and ICT absence. Benefit of FQP should be explored in prospective studies. Increased GNRB risk in auto-HSCT patients transplanted for autoimmune diseases is worrying. Infection control and being accredited are possibly protective against bacteremia. GNRB are associated with increased mortality. Benefit of FQP should be explored in prospective studies. Increased GNRB risk in auto-HSCT patients transplanted for autoimmune diseases is worrying. Infection control and being accredited are possibly protective against bacteremia. GNRB are associated with increased mortality.In emergency situations, such as during the coronavirus disease 2019 (COVID-19) pandemic, medical community looks for quick answers and guidance. Under these circumstances, experts instead of admitting ignorance, feel obliged to give an answer, often pressurized by political or other authorities, even when such an answer is unavailable. Under these circumstances, publications based on fallacious reasoning are virtually unavoidable. In the present review, we summarize examples underlying fallacious reasoning recommendations regarding treatment with Renin-Angiotensin-Aldosterone inhibitors (RAASi) in the COVID-19 context. Most scientific societies emphasize that RAASi use is safe and that these agents should not be discontinued, based mainly on the results of observational studies (OSs) and occasionally preprints, as relevant randomized controlled trials (RCTs) are currently lacking. However, over the past 4 decades, results from successful RCTs have repeatedly proved that practices based on OSs were wrong. Lack of RCTs results in uncertainty. In this setting, the physician's wisdom and knowledge related to pathophysiologic mechanisms and effect of pharmacologic agents become even more important as they may limit fallacies. Based on these principles, in diseases (e.g., mild, or moderate arterial hypertension, etc.) where equally effective alternative therapies to RAASi are available, these therapies should be applied, whereas in diseases (e.g., heart failure, diabetic kidney disease, etc.), where equally effective alternative therapy compared to RAASi is not available, RAASi should be used. Admittedly this strategy, like all the other recommendations, is not based on solid evidence but is intended to be individualized and follows the Hippocratic "Primum non nocere".Alzheimer's disease (AD) represents the most common form of dementia among old age subjects, and despite decades of studies, the underlying etiopathogenetic mechanisms remain unsolved, and no cure is available. The amyloid hypothesis has been recently questioned due to the failure of amyloid-centered treatments. The fact that cognitively normal old age subjects have substantial amyloid deposition in the brain comparable to the levels observed in AD patients suggests that amyloid accumulation may enter into the normal process of aging and what really triggers neuronal death and clinical manifestation is the loss of function due to an energetic failure. With this viewpoint article, we aim to challenge the traditional view of amyloid as the leading cause of AD. Conversely, we propose the core feature of aging, that is the progressive brain energy decline, as the main risk factor for dementia in older persons. Thus, a bioenergetic deficit secondary to mitochondrial dysfunction may lead to progressive neuronal death and clinical expression of dementia. The optimization of brain energetics should become a key component in future strategies for preventing and treating dementia.Neurodegenerative diseases (NDs) cause progressive loss of neurons in nervous system. NDs are categorized as acute NDs such as stroke and head injury, besides chronic NDs including Alzheimer's, Parkinson's, Huntington's diseases, Friedreich's Ataxia, Multiple Sclerosis. The exact etiology of NDs is not understood but oxidative stress, inflammation and synaptic dysfunction are main hallmarks. Oxidative stress leads to free radical attack on neural cells which contributes to protein misfolding, glia cell activation, mitochondrial dysfunction, impairment of DNA repair system and subsequently cellular death. Neural stem cells (NSCs) support adult neurogenesis in nervous system during injuries which is limited to certain regions in brain. NSCs can differentiate into the neurons, astrocytes or oligodendrocytes. Impaired neurogenesis and inadequate induction of neurogenesis are the main obstacles in treatment of NDs. https://www.selleckchem.com/products/cc-99677.html Protection of neural cells from oxidative damages and supporting neurogenesis are promising strategies to treat NDs. Nuclear factor-erythroid 2-related factor 2 (Nrf2) is a transcriptional master regulator that maintains the redox homeostasis in cells by provoking expression of antioxidant, anti-inflammatory and cytoprotective genes. Nrf2 can strongly influence the NSCs function and fate determination by reducing levels of reactive oxygen species in benefit of NSC survival and neurogenesis. In this review we will summarize the role of Nrf2 in NSC function, and exogenous and endogenous therapeutic strategies in treatment of NDs.