351 research outputs found

    Marriage and Family Therapy Education and Training: The Development of a Competency-Based Model

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    The turn of the century saw a shift from input-based to outcome-based education in Marriage and Family Therapy (MFT) training. An attempt was also made to establish core competencies that practitioners of MFT should attain to provide effective client care. These developments had a significant impact on version 11.0 and 12.0 of the Commission on Accreditation for Marriage and Family Therapy Education (COAMFTE) Accreditation Standards. Since then, MFT educators have used these standards and guidelines to transition their programs from input-based to competency-based education. The MFT program at a West Coast University was the first COAMFTE accredited program to propose an alternative competency model requiring the completion of 300 direct client contact hours instead of 500 h for all students in the program, when it went through the process of reaccreditation in 2019. The program was granted renewal of accreditation in May 2020. Since then, version 12.5 of the COAMFTE Accreditation Standards have been released and this University’s competency model is aligned with these new standards. This article provides an overview of the competency model used by the MFT program at this University which can serve as an example for other MFT programs. Trends and future directions in competency-based MFT education are also discussed

    No ψ\psi-epistemic model can fully explain the indistinguishability of quantum states

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    According to a recent no-go theorem (M. Pusey, J. Barrett and T. Rudolph, Nature Physics 8, 475 (2012)), models in which quantum states correspond to probability distributions over the values of some underlying physical variables must have the following feature: the distributions corresponding to distinct quantum states do not overlap. This is significant because if the distributions do not overlap, then the quantum state itself is encoded by the physical variables. In such a model, it cannot coherently be maintained that the quantum state merely encodes information about underlying physical variables. The theorem, however, considers only models in which the physical variables corresponding to independently prepared systems are independent. This work considers models that are defined for a single quantum system of dimension dd, such that the independence condition does not arise. We prove a result in a similar spirit to the original no-go theorem, in the form of an upper bound on the extent to which the probability distributions can overlap, consistently with reproducing quantum predictions. In particular, models in which the quantum overlap between pure states is equal to the classical overlap between the corresponding probability distributions cannot reproduce the quantum predictions in any dimension d3d \geq 3. The result is noise tolerant, and an experiment is motivated to distinguish the class of models ruled out from quantum theory.Comment: 5+5 page

    A Bayesian spatio-temporal framework to identify outbreaks and examine environmental and social risk factors for infectious diseases monitored by routine surveillance

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    Spatio-temporal disease patterns can provide clues to etiological pathways, but can be complex to model. Using a flexible Bayesian hierarchical framework, we identify previously undetected space-time clusters and environmental and socio-demographic risk factors for reported giardiasis and cryptosporidiosis at the New Zealand small area level. For giardiasis, there was no seasonal pattern in outbreak probability and an inverse association with density of dairy cattle (β^₁= -0.09, Incidence Risk Ratio (IRR) 0.90 (95% CI 0.84, 0.97) per 1 log increase in cattle/km²). In dairy farming areas, cryptosporidiosis outbreaks were observed in spring. Reported cryptosporidiosis was positively associated with dairy cattle density: β^₁= 0.12, IRR 1.13 (95% CI 1.05, 1.21) per 1 log increase in cattle/km2 and inversely associated with weekly average temperature: β^₁=-0.07, IRR 0.92 (95% CI 0.87, 0.98) per 4°C increase. This framework can be generalized to determine the potential drivers of sporadic cases and latent outbreaks of infectious diseases of public health importance

    CRISPR Knockout of the HuR Gene Causes a Xenograft Lethal Phenotype.

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    Pancreatic ductal adenocarcinoma (PDA) is the third leading cause of cancer-related deaths in the United States, whereas colorectal cancer is the third most common cancer. The RNA-binding protein HuR (ELAVL1) supports a pro-oncogenic network in gastrointestinal (GI) cancer cells through enhanced HuR expression. Using a publically available database, HuR expression levels were determined to be increased in primary PDA and colorectal cancer tumor cohorts as compared with normal pancreas and colon tissues, respectively. CRISPR/Cas9 technology was successfully used to delete the HuR gene in both PDA (MIA PaCa-2 and Hs 766T) and colorectal cancer (HCT116) cell lines. HuR deficiency has a mild phenotype

    Posttranscriptional regulation of PARG mRNA by HuR facilitates DNA repair and resistance to PARP inhibitors

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    The majority of pancreatic ductal adenocarcinomas (PDAC) rely on the mRNA stability factor HuR (ELAV-L1) to drive cancer growth and progression. Here, we show that CRISPR-Cas9–mediated silencing of the HuR locus increases the relative sensitivity of PDAC cells to PARP inhibitors (PARPi). PDAC cells treated with PARPi stimulated translocation of HuR from the nucleus to the cytoplasm, specifically promoting stabilization of a new target, poly (ADP-ribose) glycohydrolase (PARG) mRNA, by binding a unique sequence embedded in its 30 untranslated region. HuR-dependent upregulation of PARG expression facilitated DNA repair via hydrolysis of polyADP-ribose on related repair proteins. Accordingly, strategies to inhibit HuR directly promoted DNA damage accumulation, inefficient PAR removal, and persistent PARP-1 residency on chromatin (PARP-1 trapping). Immunoprecipitation assays demonstrated that the PARP-1 protein binds and posttranslationally modifies HuR in PARPi-treated PDAC cells. In a mouse xenograft model of human PDAC, PARPi monotherapy combined with targeted silencing of HuR significantly reduced tumor growth compared with PARPi therapy alone. Our results highlight the HuR–PARG axis as an opportunity to enhance PARPi-based therapies. ©2017 AACR

    Case Report: A Case of Wood-Smoke–Related Pulmonary Disease

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    CONTEXT: Biomass serves as a major fuel source for > 50% of the world’s population. The global burden of disease attributed to indoor air pollution from biomass combustion accounts for approximately 3% of worldwide disability-adjusted life-years lost. This is due to pneumonia in children and chronic obstructive pulmonary disease and lung cancer in women. CASE PRESENTATION: A 53-year-old man from Mexico was referred to the pulmonary clinic for evaluation of chronic productive cough and pulmonary nodules. In his youth, he worked at a charcoal plant in Mexico, where he burned wood and was exposed to massive amounts of smoke. His evaluation revealed thickened bronchovascular bundles with nodules on thoracic computed tomography, dark black plaques in large airways on bronchoscopy, and carbon-laden macrophages and fibrotic scars on lung biopsy. DISCUSSION: The patient was diagnosed with “hut lung,” a term that refers to the noninfectious, nonmalignant respiratory manifestations of chronic, high-level exposures to biomass smoke. This is the first reported case of hut lung associated with charcoal production. This case highlights that histopathologic abnormalities of the lung parenchyma may be present in patients with only mild symptoms and that clinical progression is likely a function of both the duration and intensity of exposure. RELEVANCE TO CLINICAL PRACTICE: As residents of lesser developed countries continue to be exposed to high levels of biomass smoke at work or at home and continue to immigrate to developed countries, it is important that health care providers in developed countries be aware of biomass-smoke–related pulmonary disease

    Posttranscriptional Upregulation of IDH1 by HuR Establishes a Powerful Survival Phenotype in Pancreatic Cancer Cells.

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    Cancer aggressiveness may result from the selective pressure of a harsh nutrient-deprived microenvironment. Here we illustrate how such conditions promote chemotherapy resistance in pancreatic ductal adenocarcinoma (PDAC). Glucose or glutamine withdrawal resulted in a 5- to 10-fold protective effect with chemotherapy treatment. PDAC xenografts were less sensitive to gemcitabine in hypoglycemic mice compared with hyperglycemic mice. Consistent with this observation, patients receiving adjuvant gemcitabine (n = 107) with elevated serum glucose levels (HgbA1C \u3e 6.5%) exhibited improved survival. We identified enhanced antioxidant defense as a driver of chemoresistance in this setting. ROS levels were doubled in vitro by either nutrient withdrawal or gemcitabine treatment, but depriving PDAC cells of nutrients before gemcitabine treatment attenuated this effect. Mechanistic investigations based on RNAi or CRISPR approaches implicated the RNA binding protein HuR in preserving survival under nutrient withdrawal, with or without gemcitabine. Notably, RNA deep sequencing and functional analyses in HuR-deficient PDAC cell lines identified isocitrate dehydrogenase 1 (IDH1) as the sole antioxidant enzyme under HuR regulation. HuR-deficient PDAC cells lacked the ability to engraft successfully in immunocompromised mice, but IDH1 overexpression in these cells was sufficient to fully restore chemoresistance under low nutrient conditions. Overall, our findings highlight the HuR–IDH1 regulatory axis as a critical, actionable therapeutic target in pancreatic cancer

    Digitalisation and COVID-19: The Perfect Storm

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    \u201cA ship in the harbour is safe, but that is not what ships are built for,\u201d observed that sage 19th century philosopher William Shedd. In other words, technology of high potential is of little value if the potential is not exploited. As the shape of 2020 is increasingly defined by the coronavirus pandemic, digitalisation is like a ship loaded with technology that has a huge capacity for transforming mankind\u2019s combat against infectious disease. But it is still moored safely in harbour. Instead of sailing bravely into battle, it remains at the dockside, cowering from the storm beyond the breakwaters. Engineers and fitters constantly fine-tune it, and its officers and deckhands perfect their operating procedures, but that promise is unfulfilled, restrained by the hesitancy and indecision of officialdom. Out there, the seas of the pandemic are turbulent and uncharted, and it is impossible to know in advance everything of the other dangers that may lurk beyond those cloudy horizons. However, the more noble course is for orders to be given to complete the preparations, to cast off and set sail, and to join other vessels crewed by valiant healthcare workers and tireless researchers, already deeply engaged in a rescue mission for the whole of the human race. It is the destiny of digitalisation to navigate those oceans alongside other members of that task force, and the hour of destiny has arrived. This article focuses on the potential enablers and recommendation to maximise learnings during the era of COVID-19
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