Assessing the Efficacy of the ARMOR Tool-Based Deprescribing Intervention for Fall Risk Reduction in Older Patients Taking Fall Risk-Increasing Drugs (DeFRID Trial): Protocol for a Randomized Controlled Trial.

Background: Falls in older patients can lead to serious health complications and increased health care costs. Fall risk-increasing drugs (FRIDs) are a group of drugs that may induce falls or increase the tendency to fall (ie, fall risk). Deprescribing is the process of withdrawal from an inappropriate medication, supervised by a health care professional, with the goal of managing polypharmacy and improving outcomes.

Performance in a Balance Test and Prediction of All-Cause Mortality in Community-Dwelling Elderly Ambulatory Individuals: A Systematic Review and Meta-analysis.

This systematic review and meta-analysis was performed to evaluate the association between an inability to perform a static balance test and mortality in community-dwelling older ambulatory individuals. PubMed, Embase, and Scopus were searched for relevant cohort studies. Hazard ratios (HR) were pooled (random-effect model).

Endothelial-specific loss of IKKβ disrupts pulmonary endothelial angiogenesis and impairs postnatal lung growth.

Pulmonary angiogenesis drives alveolarization, but the transcriptional regulators directing pulmonary angiogenesis remain poorly defined. Global, pharmacological inhibition of nuclear factor-kappa B (NF-κB) impairs pulmonary angiogenesis and alveolarization. However, establishing a definitive role for NF-κB in pulmonary vascular development has been hindered by embryonic lethality induced by constitutive deletion of NF-κB family members.

Pharmacological Exploration of Phenolic Compound: Raspberry Ketone-Update 2020.

Raspberry ketone (RK) is an aromatic phenolic compound naturally occurring in red raspberries, kiwifruit, peaches, and apples and reported for its potential therapeutic and nutraceutical properties. Studies in cells and rodents have suggested an important role for RK in hepatic/cardio/gastric protection and as an anti-hyperlipidemic, anti-obesity, depigmentation, and sexual maturation agent. Raspberry ketone-mediated activation of peroxisome proliferator-activated receptor-α (PPAR-α) stands out as one of its main modes of action.

Transforming Growth Factor-induced Protein Promotes NF-κB-mediated Angiogenesis during Postnatal Lung Development.

Pulmonary angiogenesis is a key driver of alveolarization. Our prior studies showed that NF-κB promotes pulmonary angiogenesis during early alveolarization. However, the mechanisms regulating temporal-specific NF-κB activation in the pulmonary vasculature are unknown.

RNA editing of Filamin A pre-mRNA regulates vascular contraction and diastolic blood pressure.

Epitranscriptomic events such as adenosine-to-inosine (A-to-I) RNA editing by ADAR can recode mRNAs to translate novel proteins. Editing of the mRNA that encodes actin crosslinking protein Filamin A (FLNA) mediates a Q-to-R transition in the interactive C-terminal region. While FLNA editing is conserved among vertebrates, its physiological function remains unclear.

Distinct roles for IκB kinases alpha and beta in regulating pulmonary endothelial angiogenic function during late lung development.

Pulmonary angiogenesis is essential for alveolarization, the final stage of lung development that markedly increases gas exchange surface area. We recently demonstrated that activation of the nuclear factor kappa-B (NFκB) pathway promotes pulmonary angiogenesis during alveolarization. However, the mechanisms activating NFκB in the pulmonary endothelium, and its downstream targets are not known.

Tracheoesophageal Fistula following Endotracheal Intubation for Organophosphorus Poisoning.

Tracheoesophageal fistula (TEF) is an abnormal communication between the trachea and esophagus. Iatrogenic TEF can be due to endotracheal intubation, rigid bronchoscopy or tracheostomy. Tracheostomy tube cuff volumes and pressures require constant monitoring to avoid tracheal injury.

Loss of PPARγ in endothelial cells leads to impaired angiogenesis.

Tie2-promoter-mediated loss of peroxisome proliferator-activated receptor gamma (PPARγ, also known as PPARG) in mice leads to osteopetrosis and pulmonary arterial hypertension. Vascular disease is associated with loss of PPARγ in pulmonary microvascular endothelial cells (PMVEC); we evaluated the role of PPARγ in PMVEC functions, such as angiogenesis and migration. The role of PPARγ in angiogenesis was evaluated in Tie2CrePPARγ(flox/flox) and wild-type mice, and in mouse and human PMVECs.

Activation of the nuclear factor-κB pathway during postnatal lung inflammation preserves alveolarization by suppressing macrophage inflammatory protein-2.

A significant portion of lung development is completed postnatally during alveolarization, rendering the immature lung vulnerable to inflammatory stimuli that can disrupt lung structure and function. Although the NF-κB pathway has well-recognized pro-inflammatory functions, novel anti-inflammatory and developmental roles for NF-κB have recently been described. Thus, to determine how NF-κB modulates alveolarization during inflammation, we exposed postnatal day 6 mice to vehicle (PBS), systemic lipopolysaccharide (LPS), or the combination of LPS and the global NF-κB pathway inhibitor BAY 11-7082 (LPS + BAY).

Differential proteomic and behavioral effects of long-term voluntary exercise in wild-type and APP-overexpressing transgenics.

Physical exercise may provide protection against the cognitive decline and neuropathology associated with Alzheimer's disease, although the mechanisms are not clear. In the present study, APP/PSEN1 double-transgenic and wild-type mice were allowed unlimited voluntary exercise for 7months. Consistent with previous reports, wheel-running improved cognition in the double-transgenic mice.

The urea decomposition product cyanate promotes endothelial dysfunction.

The dramatic cardiovascular mortality of patients with chronic kidney disease is attributable in a significant proportion to endothelial dysfunction. Cyanate, a reactive species in equilibrium with urea, is formed in excess in chronic kidney disease. Cyanate is thought to have a causal role in promoting cardiovascular disease, but the underlying mechanisms remain unclear.

Acyl chain-dependent effect of lysophosphatidylcholine on endothelium-dependent vasorelaxation.

Previously we identified palmitoyl-, oleoyl-, linoleoyl-, and arachidonoyl-lysophosphatidylcholine (LPC 16:0, 18:1, 18:2 and 20:4) as the most prominent LPC species generated by endothelial lipase (EL). In the present study, we examined the impact of those LPC on acetylcholine (ACh)- induced vascular relaxation. All tested LPC attenuated ACh-induced relaxation, measured ex vivo, using mouse aortic rings and wire myography.

Oral cancer: enduring characteristics and emerging trends.

Oral cancer is arguably the most serious condition that dental providers may encounter in their practice. The relatively poor prognosis associated with oral cancer highlights the importance of the dental team's awareness of the disease. While many characteristics of oral cancer have endured over time, new research is revealing trends that are changing the way we approach its screening, diagnosis and treatment.

Oral cancer: enduring characteristics and emerging trends.

Oral cancer is arguably the most serious condition that dental providers may encounter in their practice. The relatively poor prognosis associated with oral cancer highlights the importance of the dental team's awareness of the disease. While many characteristics of oral cancer have endured over time, new research is revealing trends that are changing the way we approach its screening, diagnosis and treatment.

A survey of glioblastoma genomic amplifications and deletions.

Glioblastoma Multiforme (GBM) is a malignant brain cancer that develops after accumulating genomic DNA damage that often includes gene amplifications and/or deletions. These copy number changes can be a critical step in brain tumor development. To evaluate glioblastoma genomic copy number changes, we determined the genome-wide copy number alterations in 31 GBMs.

Biochemical changes induced in liver and serum of diplodiatoxin (Stenocarpella maydis) treated male and female rats.

Present study was conducted to investigate the acute and sub-acute toxic effect of diplodiatoxin with special reference to biochemical membrane bound enzymes like aspartate aminotransferase (ASAT), alanine aminotransferase (ALAT) and RBC acetylcholinesterase (AChE) in male and female rats. For acute study, rats were treated with a single oral dose of 5.7 mg/kg of diplodiatoxin, whereas for sub-acute study, the rats received 0.

Effect of diplodiatoxin (Stenocarpella maydis) on some enzymatic profiles in male and female rats.

Acute and subacute effects of diplodiatoxin were monitored with special reference to biochemical target enzymes like acid phosphatase (AcP), alkaline phosphatase (AkP), and acetylcholinesterase (AChE) in male and female rats. For acute toxicity study the rats were treated with single oral dose of 5.7 mg/kg of diplodiatoxin, whereas for subacute toxicity study the rats were orally treated with 0.