Sustainability and Impact of a Lung Health Outpatient Resource Center

BACKGROUND: According to the Worldwide Health Organization, worldwide, it is estimated hundreds of millions of people are affected by chronic respiratory diseases. COPD is a leading cause of death in the United States, and imposes an enormous financial burden on our nation\u27s health care system (COPD. NIH.GOV). COPD patients with severe exacerbations requiring emergency visits or hospitalizations per year are at higher risk for all- cause mortality (Soler-Cataluna JJ, et al. Thor-ax.200,60:925-931 ). A multidisciplinary Lung Health Outpatient Resource Center was established as a continuum of care to support our COPD population post discharge. Patients seen in the center showed successful outcomes, which have led to decreasing readmissions and improved cost savings. Therefore, the center expanded its services to include other chronic pulmonary diseases including pneumonia and pleurisy, asthma, bronchitis, and other respiratory infections. METHODS: The multidisciplinary team was headed by the Respiratory Department in con-junction with the Outpatient clinic and included; nurse practitioners (ARNP), respiratory therapist (RT), registered nurses (RN), social worker (SW), pulmonologist and pharmacy. The center incorporates weekly follow up visits during the acute phase post discharge where symptom management, individualized action plans, interpersonal psychosocial and emotional support is provided and created with the patient and family. Pharmacological and non-pharmacological interventions are utilized to optimize the individual\u27s treatment goal. RESULTS: The Lung Health Outpatient Resource Center was established in June 2017. Data was collected from June 2017 to March 2019. Total population referred was 304 patients. Patients seen in the center (150) had an 8% readmission rate, and those not seen (154) had a 12.9% readmission rate. The estimated average variable cost savings for patients seen was of $1,217,206.90 CONCLUSION: Through utilizing an outpatient resource center and adherence to plan of care, hospital readmission rates were decreased and variable cost savings improved. Sustainability by expanding our services to other chronic pulmonary diseases has been shown

Propuesta didáctica innovadora que promueva el aprendizaje significativo del Movimiento Circular Uniforme en los estudiantes de

Esta investigación se dirigió a la estructura de una propuesta didáctica con estrategias que promuevan el aprendizaje significativo del Movimiento Circular Uniforme en los estudiantes de 1

Deaths with leprosy as the underlying cause recorded in Brazil : use of data base linkage to enhance information

O presente estudo objetivou descrever as características dos óbitos que tiveram como causa básica a hanseníase, registrados no Sistema de Informações sobre Mortalidade (SIM), e comparar estas características entre os grupos de óbitos cujos casos foram notificados e não notificados no Sistema de Informação sobre Agravos de Notificação (Sinan). Foram incluídos os óbitos com causa básica hanseníase, ocorridos no Brasil no período 2004-2009, e os casos registrados de hanseníase entre 1975-2010. Realizou-se o relacionamento probabilístico das bases do SIM e Sinan. Dos 1.463 óbitos por hanseníase registrados no SIM, 44,2% não foram encontrados no Sinan. Do total dos óbitos, a maioria foi de homens (72,5%), com 60 ou mais anos de idade (56,6%), ocorridos em hospitais (65,3%) e com assistência (45,8%). Dos 820 óbitos identificados no Sinan, 92% foram multibacilares, 45,2% tinham alta por cura no Sinan e 38,9%, óbito. Foram encontrados óbitos por hanseníase que estão registrados no SIM, mas não foram notificados no Sinan. O relacionamento das bases permitiu identificação de subregistros e inconsistências entre os sistemas.This study sought to describe the characteristics of deaths with leprosy as the underlying cause recorded in the Mortality Information System (SIM) and compare these characteristics with the groups of cases where the cause of death was reported, or failed to be reported, in the National Case Registration Database (Sinan). Deaths with leprosy as the underlying cause occurring in Brazil in the 2004-2009 period, and cases of leprosy from 1975 to 2010 were included. The probabilistic bases of SIM and Sinan were compared. Of the 1,463 deaths from leprosy recorded in SIM, 44.2% were not recorded in Sinan. Of the total number of deaths, the majority were men (72.5%), aged 60 or older (56.6%), occurring in hospitals (65.3%) and with due care (45.8%). Of the 820 deaths identified in Sinan, 92% were patients with multibacillary disease, 45.2% were discharged as cured by Sinan and 38.9% died. Deaths due to leprosy were found on SIM that were not notified to Sinan. The data base linkage enabled identification of ancillary records and inconsistencies between the systems

Dissecting the Shared Genetic Architecture of Suicide Attempt, Psychiatric Disorders, and Known Risk Factors

Background Suicide is a leading cause of death worldwide, and nonfatal suicide attempts, which occur far more frequently, are a major source of disability and social and economic burden. Both have substantial genetic etiology, which is partially shared and partially distinct from that of related psychiatric disorders. Methods We conducted a genome-wide association study (GWAS) of 29,782 suicide attempt (SA) cases and 519,961 controls in the International Suicide Genetics Consortium (ISGC). The GWAS of SA was conditioned on psychiatric disorders using GWAS summary statistics via multitrait-based conditional and joint analysis, to remove genetic effects on SA mediated by psychiatric disorders. We investigated the shared and divergent genetic architectures of SA, psychiatric disorders, and other known risk factors. Results Two loci reached genome-wide significance for SA: the major histocompatibility complex and an intergenic locus on chromosome 7, the latter of which remained associated with SA after conditioning on psychiatric disorders and replicated in an independent cohort from the Million Veteran Program. This locus has been implicated in risk-taking behavior, smoking, and insomnia. SA showed strong genetic correlation with psychiatric disorders, particularly major depression, and also with smoking, pain, risk-taking behavior, sleep disturbances, lower educational attainment, reproductive traits, lower socioeconomic status, and poorer general health. After conditioning on psychiatric disorders, the genetic correlations between SA and psychiatric disorders decreased, whereas those with nonpsychiatric traits remained largely unchanged. Conclusions Our results identify a risk locus that contributes more strongly to SA than other phenotypes and suggest a shared underlying biology between SA and known risk factors that is not mediated by psychiatric disorders.Peer reviewe

Analysis of shared heritability in common disorders of the brain

ience, this issue p. eaap8757 Structured Abstract INTRODUCTION Brain disorders may exhibit shared symptoms and substantial epidemiological comorbidity, inciting debate about their etiologic overlap. However, detailed study of phenotypes with different ages of onset, severity, and presentation poses a considerable challenge. Recently developed heritability methods allow us to accurately measure correlation of genome-wide common variant risk between two phenotypes from pools of different individuals and assess how connected they, or at least their genetic risks, are on the genomic level. We used genome-wide association data for 265,218 patients and 784,643 control participants, as well as 17 phenotypes from a total of 1,191,588 individuals, to quantify the degree of overlap for genetic risk factors of 25 common brain disorders. RATIONALE Over the past century, the classification of brain disorders has evolved to reflect the medical and scientific communities' assessments of the presumed root causes of clinical phenomena such as behavioral change, loss of motor function, or alterations of consciousness. Directly observable phenomena (such as the presence of emboli, protein tangles, or unusual electrical activity patterns) generally define and separate neurological disorders from psychiatric disorders. Understanding the genetic underpinnings and categorical distinctions for brain disorders and related phenotypes may inform the search for their biological mechanisms. RESULTS Common variant risk for psychiatric disorders was shown to correlate significantly, especially among attention deficit hyperactivity disorder (ADHD), bipolar disorder, major depressive disorder (MDD), and schizophrenia. By contrast, neurological disorders appear more distinct from one another and from the psychiatric disorders, except for migraine, which was significantly correlated to ADHD, MDD, and Tourette syndrome. We demonstrate that, in the general population, the personality trait neuroticism is significantly correlated with almost every psychiatric disorder and migraine. We also identify significant genetic sharing between disorders and early life cognitive measures (e.g., years of education and college attainment) in the general population, demonstrating positive correlation with several psychiatric disorders (e.g., anorexia nervosa and bipolar disorder) and negative correlation with several neurological phenotypes (e.g., Alzheimer's disease and ischemic stroke), even though the latter are considered to result from specific processes that occur later in life. Extensive simulations were also performed to inform how statistical power, diagnostic misclassification, and phenotypic heterogeneity influence genetic correlations. CONCLUSION The high degree of genetic correlation among many of the psychiatric disorders adds further evidence that their current clinical boundaries do not reflect distinct underlying pathogenic processes, at least on the genetic level. This suggests a deeply interconnected nature for psychiatric disorders, in contrast to neurological disorders, and underscores the need to refine psychiatric diagnostics. Genetically informed analyses may provide important "scaffolding" to support such restructuring of psychiatric nosology, which likely requires incorporating many levels of information. By contrast, we find limited evidence for widespread common genetic risk sharing among neurological disorders or across neurological and psychiatric disorders. We show that both psychiatric and neurological disorders have robust correlations with cognitive and personality measures. Further study is needed to evaluate whether overlapping genetic contributions to psychiatric pathology may influence treatment choices. Ultimately, such developments may pave the way toward reduced heterogeneity and improved diagnosis and treatment of psychiatric disorders

Cabbage and fermented vegetables : From death rate heterogeneity in countries to candidates for mitigation strategies of severe COVID-19

Large differences in COVID-19 death rates exist between countries and between regions of the same country. Some very low death rate countries such as Eastern Asia, Central Europe, or the Balkans have a common feature of eating large quantities of fermented foods. Although biases exist when examining ecological studies, fermented vegetables or cabbage have been associated with low death rates in European countries. SARS-CoV-2 binds to its receptor, the angiotensin-converting enzyme 2 (ACE2). As a result of SARS-CoV-2 binding, ACE2 downregulation enhances the angiotensin II receptor type 1 (AT(1)R) axis associated with oxidative stress. This leads to insulin resistance as well as lung and endothelial damage, two severe outcomes of COVID-19. The nuclear factor (erythroid-derived 2)-like 2 (Nrf2) is the most potent antioxidant in humans and can block in particular the AT(1)R axis. Cabbage contains precursors of sulforaphane, the most active natural activator of Nrf2. Fermented vegetables contain many lactobacilli, which are also potent Nrf2 activators. Three examples are: kimchi in Korea, westernized foods, and the slum paradox. It is proposed that fermented cabbage is a proof-of-concept of dietary manipulations that may enhance Nrf2-associated antioxidant effects, helpful in mitigating COVID-19 severity.Peer reviewe

Nrf2-interacting nutrients and COVID-19 : time for research to develop adaptation strategies

There are large between- and within-country variations in COVID-19 death rates. Some very low death rate settings such as Eastern Asia, Central Europe, the Balkans and Africa have a common feature of eating large quantities of fermented foods whose intake is associated with the activation of the Nrf2 (Nuclear factor (erythroid-derived 2)-like 2) anti-oxidant transcription factor. There are many Nrf2-interacting nutrients (berberine, curcumin, epigallocatechin gallate, genistein, quercetin, resveratrol, sulforaphane) that all act similarly to reduce insulin resistance, endothelial damage, lung injury and cytokine storm. They also act on the same mechanisms (mTOR: Mammalian target of rapamycin, PPAR gamma:Peroxisome proliferator-activated receptor, NF kappa B: Nuclear factor kappa B, ERK: Extracellular signal-regulated kinases and eIF2 alpha:Elongation initiation factor 2 alpha). They may as a result be important in mitigating the severity of COVID-19, acting through the endoplasmic reticulum stress or ACE-Angiotensin-II-AT(1)R axis (AT(1)R) pathway. Many Nrf2-interacting nutrients are also interacting with TRPA1 and/or TRPV1. Interestingly, geographical areas with very low COVID-19 mortality are those with the lowest prevalence of obesity (Sub-Saharan Africa and Asia). It is tempting to propose that Nrf2-interacting foods and nutrients can re-balance insulin resistance and have a significant effect on COVID-19 severity. It is therefore possible that the intake of these foods may restore an optimal natural balance for the Nrf2 pathway and may be of interest in the mitigation of COVID-19 severity

Genetic Overlap Between Alzheimer’s Disease and Bipolar Disorder Implicates the MARK2 and VAC14 Genes

Background: Alzheimer's disease (AD) and bipolar disorder (BIP) are complex traits influenced by numerous common genetic variants, most of which remain to be detected. Clinical and epidemiological evidence suggest that AD and BIP are related. However, it is not established if this relation is of genetic origin. Here, we applied statistical methods based on the conditional false discovery rate (FDR) framework to detect genetic overlap between AD and BIP and utilized this overlap to increase the power to identify common genetic variants associated with either or both traits. Methods: We obtained genome wide association studies data from the International Genomics of Alzheimer's Project part 1 (17,008 AD cases and 37,154 controls) and the Psychiatric Genetic Consortium Bipolar Disorder Working Group (20,352 BIP cases and 31,358 controls). We used conditional QQ-plots to assess overlap in common genetic variants between AD and BIP. We exploited the genetic overlap to re-rank test-statistics for AD and BIP and improve detection of genetic variants using the conditional FDR framework. Results: Conditional QQ-plots demonstrated a polygenic overlap between AD and BIP. Using conditional FDR, we identified one novel genomic locus associated with AD, and nine novel loci associated with BIP. Further, we identified two novel loci jointly associated with AD and BIP implicating the MARK2 gene (lead SNP rs10792421, conjunctional FDR=0.030, same direction of effect) and the VAC14 gene (lead SNP rs11649476, conjunctional FDR=0.022, opposite direction of effect). Conclusions: We found polygenic overlap between AD and BIP and identified novel loci for each trait and two jointly associated loci. Further studies should examine if the shared loci implicating the MARK2 and VAC14 genes could explain parts of the shared and distinct features of AD and BIP