A Psychometric Evaluation of the Staff-Reported EOLD-CAD Measure Among Nursing Home Residents With Cognitive Impairment.

Objectives: The End-of-Life Dementia-Comfort Assessment in Dying (EOLD-CAD) scale is one of the few outcome instruments designed to capture symptom burden and well-being among nursing home residents with dementia; however, psychometric evaluations of the EOLD-CAD are limited. Although the instrument is often used to assess outcomes prospectively, it was originally developed and tested as a postmortem assessment. The purpose of this study is to evaluate the instrument properties of the EOLD-CAD using staff reports from a large sample of nursing home residents with cognitive impairment prior to death.

Human GBP1 facilitates the rupture of the containing vacuole and inflammasome activation.

Inflammasomes are essential for host defense against intracellular bacterial pathogens like , as they activate caspases, which promote cytokine release and cell death to control infection. In mice, interferon (IFN) signaling promotes inflammasome responses against bacteria by inducing a family of IFN-inducible GTPases known as guanylate-binding proteins (GBPs). Within murine macrophages, IFN promotes the rupture of the -containing vacuole (LCV), while GBPs are dispensable for this process.

Using Palliative Leaders in Facilities to Transform Care for People with Alzheimer's Disease (UPLIFT-AD): protocol of a palliative care clinical trial in nursing homes.

Background: Palliative care is an effective model of care focused on maximizing quality of life and relieving the suffering of people with serious illnesses, including dementia. Evidence shows that many people receiving care in nursing homes are eligible for and would benefit from palliative care services. Yet, palliative care is not consistently available in nursing home settings.

Lipid A Variants Activate Human TLR4 and the Noncanonical Inflammasome Differently and Require the Core Oligosaccharide for Inflammasome Activation.

Detection of Gram-negative bacterial lipid A by the extracellular sensor, myeloid differentiation 2 (MD2)/Toll-like receptor 4 (TLR4), or the intracellular inflammasome sensors, CASP4 and CASP5, induces robust inflammatory responses. The chemical structure of lipid A, specifically its phosphorylation and acylation state, varies across and within bacterial species, potentially allowing pathogens to evade or suppress host immunity. Currently, it is not clear how distinct alterations in the phosphorylation or acylation state of lipid A affect both human TLR4 and CASP4/5 activation.

Unexpected cell type-dependent effects of autophagy on polyglutamine aggregation revealed by natural genetic variation in C. elegans.

Background: Monogenic protein aggregation diseases, in addition to cell selectivity, exhibit clinical variation in the age of onset and progression, driven in part by inter-individual genetic variation. While natural genetic variants may pinpoint plastic networks amenable to intervention, the mechanisms by which they impact individual susceptibility to proteotoxicity are still largely unknown.

Results: We have previously shown that natural variation modifies polyglutamine (polyQ) aggregation phenotypes in C.

HSP-4/BiP expression in secretory cells is regulated by a developmental program and not by the unfolded protein response.

Differentiation of secretory cells leads to sharp increases in protein synthesis, challenging endoplasmic reticulum (ER) proteostasis. Anticipatory activation of the unfolded protein response (UPR) prepares cells for the onset of secretory function by expanding the ER size and folding capacity. How cells ensure that the repertoire of induced chaperones matches their postdifferentiation folding needs is not well understood.

Multiple Molecular Mechanisms Rescue mtDNA Disease in C. elegans.

Genetic instability of the mitochondrial genome (mtDNA) plays an important role in human aging and disease. Thus far, it has proven difficult to develop successful treatment strategies for diseases that are caused by mtDNA instability. To address this issue, we developed a model of mtDNA disease in the nematode C.

Natural genetic variation determines susceptibility to aggregation or toxicity in a C. elegans model for polyglutamine disease.

Background: Monogenic gain-of-function protein aggregation diseases, including Huntington's disease, exhibit substantial variability in age of onset, penetrance, and clinical symptoms, even between individuals with similar or identical mutations. This difference in phenotypic expression of proteotoxic mutations is proposed to be due, at least in part, to the variability in genetic background. To address this, we examined the role of natural variation in defining the susceptibility of genetically diverse individuals to protein aggregation and toxicity, using the Caenorhabditis elegans polyglutamine model.

Lumbar repositioning deficit in a specific low back pain population.

Study Design: A cross-sectional observational design study was conducted to determine lumbar repositioning error in 15 subjects who had chronic low back pain with a clinical diagnosis of lumbar segmental instability and 15 asymptomatic participants.

Objective: To determine whether individuals with lumbar segmental instability have a decreased ability to reposition their lumbar spine into a neutral spinal position.

Summary Of Background Data: Proprioception of the lumbar spine has been investigated in individuals who have low back pain with variable results.