A simple dirac prescription for two-loop anomalous dimension matrices.

A novel method to treat effects from evanescent operators in next-to-leading order (NLO) computations is introduced. The approach allows, besides further simplifications, to discard evanescent-to-physical mixing contributions in NLO calculations. The method is independent of the treatments of and can therefore be combined with different renormalization schemes.

Computing tools for effective field theories: SMEFT-Tools 2022 Workshop Report, 14-16th September 2022, Zürich.

In recent years, theoretical and phenomenological studies with effective field theories have become a trending and prolific line of research in the field of high-energy physics. In order to discuss present and future prospects concerning automated tools in this field, the SMEFT-Tools 2022 workshop was held at the University of Zurich from 14th-16th September 2022. The current document collects and summarizes the content of this workshop.

Confronting the vector leptoquark hypothesis with new low- and high-energy data.

In light of new data we present an updated phenomenological analysis of the simplified -leptoquark model addressing charged-current -meson anomalies. The analysis shows a good compatibility of low-energy data (dominated by the lepton flavor universality ratios and ) with the high-energy constraints posed by Drell-Yan data. We also show that present data are well compatible with a framework where the leptoquark couples with similar strength to both left- and right-handed third-generation fermions, a scenario that is well-motivated from a model building perspective.

Dissertation Topics in Nursing.

Background: Few quantitative studies have documented the types of research topics most commonly employed by nursing PhD students and whether they differ by program delivery (in-person vs. online/hybrid programs).

Objectives: We examined a large set of publicly available PhD dissertation abstracts to (a) describe the relative prevalence of different research topics and methods and (b) test whether the primary topics and methods used differed between online or hybrid and in-person PhD programs.

Fibromyalgia: A clinical update.

Fibromyalgia (FM) is a chronic pain disorder commonly encountered by advanced practice registered nurses in primary and specialty care. Knowing how to recognize FM and its multiple pain and nonpain symptoms facilitates diagnosis. We propose a four-step approach to diagnosis that can reduce costly referrals and treatment delays, and describe evidence-based interventions.

Chronic Pain Clinical and Prescriptive Practices in the Cannabis Era.

Background: To explore how health care providers in the United States are adapting clinical recommendations and prescriptive practices in response to patient use of medical cannabis (MC) for chronic pain symptoms.

Design: Literature searches queried MeSH/Subject terms "chronic pain," "clinician," "cannabis," and Boolean text words "practice" and "analgesics" in EBSCOHost, EMBASE, PubMed, and Scopus, published 2010-2021 in the United States. Twenty-one primary, peer-reviewed studies met criteria.

Which symptoms best distinguish fibromyalgia patients from those with other chronic pain disorders?

Rationale, Aims And Objectives: The primary purpose of this study was to test both classic and novel FM pain and non-pain symptoms to determine their practical efficacy in aiding clinicians to distinguish FM pain from other chronic pain disorders.

Methods: 158 pain patients from two primary care clinics were evaluated with history, physical exam, chart review, and a questionnaire containing 26 exploratory symptoms (10 from the Symptom Impact Questionnaire (SIQR) and 16 from the FM literature)). The symptoms were rated on a 0-10 VAS for severity by those patients reporting pain over the past week.

Validating the revised Symptom Impact Questionnaire with a proposed fibromyalgia phenotype using experimentally-induced pain and patient self-reports.

Objectives: The Symptom Impact Questionnaire (SIQR), now used for over a decade, has strong psychometric properties based on patients' subjective questionnaire data and correlations with other general measures of severity. However, the construct validity of the SIQR in assessing the central features of fibromyalgia (FM) has not been tested specifically with more objective measures. This study examined the construct validity of the SIQR using clinical examination of prominent features of FM, as well as patient questionnaire data.

in the Standard Model at the Dawn of the 2020s.

We reanalyse the ratio in the Standard Model (SM) using most recent hadronic matrix elements from the RBC-UKQCD collaboration in combination with most important NNLO QCD corrections to electroweak penguin contributions and the isospin-breaking corrections. We illustrate the importance of the latter by using their latest estimate from chiral perturbation theory (ChPT) based on the approximation for lowest-lying mesons and a very recent estimate in the scheme that takes into account the contribution of . We find and , respectively.

A simple screening test to recognize fibromyalgia in primary care patients with chronic pain.

Rationale, Aims, And Objectives: Primary care providers are increasingly expected to recognize and treat fibromyalgia (FM) without significant interaction with rheumatologists. The purpose of this study was to evaluate the potential usefulness of 3 simple measures (tenderness to digital pressure, BP cuff-evoked pain, and a single patient question) as a screening test for possible FM in a patient with chronic pain.

Methods: A total of 352 patients (mean age 50 ± 16.

Dysregulated miRNA biogenesis downstream of cellular stress and ALS-causing mutations: a new mechanism for ALS.

Interest in RNA dysfunction in amyotrophic lateral sclerosis (ALS) recently aroused upon discovering causative mutations in RNA-binding protein genes. Here, we show that extensive down-regulation of miRNA levels is a common molecular denominator for multiple forms of human ALS. We further demonstrate that pathogenic ALS-causing mutations are sufficient to inhibit miRNA biogenesis at the Dicing step.

SOD1 silencing in motoneurons or glia rescues neuromuscular function in ALS mice.

Objective: Amyotrophic lateral sclerosis is an incurable disorder mainly characterized by motoneuron degeneration. Mutations in the superoxide dismutase 1 (SOD1) gene account for 20% of familial forms of the disease. Mutant SOD1 exerts multiple pathogenic effects through the gain of toxic properties in both neurons and glial cells.

Somatic and axonal LIGHT signaling elicit degenerative and regenerative responses in motoneurons, respectively.

A receptor-ligand interaction can evoke a broad range of biological activities in different cell types depending on receptor identity and cell type-specific post-receptor signaling intermediates. Here, we show that the TNF family member LIGHT, known to act as a death-triggering factor in motoneurons through LT-βR, can also promote axon outgrowth and branching in motoneurons through the same receptor. LIGHT-induced axonal elongation and branching require ERK and caspase-9 pathways.

Cerebrospinal fluid-targeted delivery of neutralizing anti-IFNγ antibody delays motor decline in an ALS mouse model.

Amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative disorder characterized by the selective and gradual loss of motoneurons in the brain and spinal cord. A persistent inflammation, typified by the activation of astrocytes and microglia, accompanies the progressive degeneration of motoneurons. Interferon gamma (IFNγ), a potent proinflammatory cytokine that is aberrantly present in the spinal cord of ALS mice and patients, has been proposed to contribute to motoneuron death by eliciting the activation of the lymphotoxin-β receptor (LT-βR) through its ligand LIGHT.

Death Receptors in the Selective Degeneration of Motoneurons in Amyotrophic Lateral Sclerosis.

While studies on death receptors have long been restricted to immune cells, the last decade has provided a strong body of evidence for their implication in neuronal death and hence neurodegenerative disorders such as amyotrophic lateral sclerosis (ALS). ALS is a fatal paralytic disorder that primarily affects motoneurons in the brain and spinal cord. A neuroinflammatory process, associated with astrocyte and microglial activation as well as infiltration of immune cells, accompanies motoneuron degeneration and supports the contribution of non-cell-autonomous mechanisms in the disease.

Olesoxime delays muscle denervation, astrogliosis, microglial activation and motoneuron death in an ALS mouse model.

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease. The pathology is mimicked to a striking degree in transgenic mice carrying familial ALS-linked SOD1 gene mutations. Olesoxime (TRO19622), a novel neuroprotective and reparative compound identified in a high-throughput screen based on motoneuron (MN) survival, delays disease onset and improves survival in mutant SOD1(G93A) mice, a model for ALS.

Elevated levels of IFNγ and LIGHT in the spinal cord of patients with sporadic amyotrophic lateral sclerosis.

Background: Amyotrophic lateral sclerosis (ALS) is a paralytic and fatal neurodegenerative disorder caused by the gradual loss of both upper and lower motoneurons. There is compelling evidence from ALS experimental models that neuroinflammation actively contributes to motoneuron damage. We recently proposed that interferon gamma (IFNγ), a potent proinflammatory cytokine, induces motoneuron death by eliciting the activation of the lymphotoxin beta receptor (LT-βR) through its ligand LIGHT.

Necdin protects embryonic motoneurons from programmed cell death.

NECDIN belongs to the type II Melanoma Associated Antigen Gene Expression gene family and is located in the Prader-Willi Syndrome (PWS) critical region. Necdin-deficient mice develop symptoms of PWS, including a sensory and motor deficit. However, the mechanisms underlying the motor deficit remain elusive.

IFNγ triggers a LIGHT-dependent selective death of motoneurons contributing to the non-cell-autonomous effects of mutant SOD1.

Amyotrophic lateral sclerosis (ALS) is an incurable neurodegenerative disease that primarily affects motoneurons in the brain and spinal cord. Dominant mutations in superoxide dismutase-1 (SOD1) cause a familial form of ALS. Mutant SOD1-damaged glial cells contribute to ALS pathogenesis by releasing neurotoxic factors, but the mechanistic basis of the motoneuron-specific elimination is poorly understood.

AAV-mediated expression of wild-type and ALS-linked mutant VAPB selectively triggers death of motoneurons through a Ca2+-dependent ER-associated pathway.

A dominant mutation in the gene coding for the vesicle-associated membrane protein-associated protein B (VAPB) was associated with amyotrophic lateral sclerosis, a fatal paralytic disorder characterized by the selective loss of motoneurons in the brain and spinal cord. Adeno-associated viral vectors that we show to transduce up to 90% of motoneurons in vitro were used to model VAPB-associated neurodegenerative process. We observed that Adeno-associated viral-mediated over-expression of both wild-type and mutated form of human VAPB selectively induces death of primary motoneurons, albeit with different kinetics.

Loneliness among homebound older adults: implications for home healthcare clinicians.

As the population continues to age, the problems of loneliness become more apparent among older adults. Isolation and quietness take over in environments that once were lively with children, pets, and neighbors in the hustle and bustle of everyday life.

Plasma kinetics of lutein, zeaxanthin, and 3-dehydro-lutein after multiple oral doses of a lutein supplement.

Background: Adequate intake of lutein is postulated to reduce the risk of age-related macular degeneration, but kinetic information for developing a dosing regimen is sparse.

Objective: The objective was to characterize lutein plasma kinetics in a multiple dosing design and to assess the effects of lutein intake on concentrations of other plasma carotenoids.

Design: After a run-in period of 7 d, 19 healthy volunteers were assigned to receive daily oral doses of 4.

[Pirbuterol and salbutamol aerosol for exercise-induced bronchoconstriction].

Exercise-induced bronchoconstriction was produced in 12 asthmatic patients after a 6 minutes run on a 10% steep treadmill ergometer. FEV1 decreased by 12-73% (average 27%) of the control value measured before the run. The rather severe exercise-induced bronchoconstriction remained constant for 10-20 minutes after the run.