Patient-Specific Factors Associated with Surgical Delay in a Large Academic Hospital

The high cost of healthcare is driving the search for more efficient practice, especially in high-stakes locations like the operating room. In addition to financial losses, patients suffer physical and emotional distress, including an increased risk of morbidity or mortality when surgical cases are delayed due to inefficiency. While patient-related causes of delay have been implicated, it is unclear which specific factors are most significant. This study aimed to identify specific patient factors correlated with surgical delay and develop a predictive risk algorithm that describes the relationship between patient-specific factors and surgical delay. A retrospective review of 36,543 patients’ charts who underwent surgery at a large academic hospital over a 5-year period was conducted. Patient-specific factors, including demographics, insurance type, proximity to the hospital, anesthesia type, American Society of Anesthesiologists (ASA) classification, system-specific comorbidities, and medication usage, were identified. Bivariate analysis using chi-square analysis was conducted to determine if any of these factors were significantly correlated with surgical delay. The significant patient-specific factors were entered into a logistic regression model. Black race, ASA =\u3e3, renal failure, insulin, steroid, and several surgical specialties (colorectal, gynecologic oncology, hepatobiliary, neurosurgery, ophthalmology, and plastic surgery) were associated with an increased odds of surgical delay in this sample. Obesity, general anesthesia, and cardiovascular anesthesia were associated with a decreased odds of surgical delay. The model explains approximately 3.8-5.3% of surgical delays in this sample. The overall predictive rate of the model was 57.1%. Despite previous studies attributing a significant amount of surgical delay to patient factors, reasons other than patient factors were responsible for 94-95% of surgical delay in this sample. Further research in other populations or studies using different methods such as a prospective approach are necessary to fully understand the role of patient-specific factors in surgical delay. On the other hand, the power of this study permitted the discovery of seemingly small disparities that are nonetheless clinically significant. This study demonstrates that there are certain types of patients more at risk for surgical delay and therefore a diminished access to care

Diagnostic and therapeutic aspects of recurrent renal stone disease

Recurrent renal stones occur in 7.5% ofCaucasian men and 3% of all women. Even withincreasing urbanisation, renal calculi are reported inless than I% of black South African men and women. Four hundred recurrent stone formers were studied at the metabolic stone clinic using routine and special tests. The appropriate therapy for each subgroup is outlined and studies on various different treatments are presented. In addition, lithogenic risk factors were studied in normal black and white subjects and in black stone formers, in order to clarify the low incidence in the black population.Patients were classified according dietary andmetabolic lithogenic risk factors. 10% of stoneformers had pure dietary factors. The percentage ofstone formers in each of the various metabolicsubgroups was as follows: Renal hypercalciuria 12%, Absorptive hypercalciuria 10%, Mild metabolichyperoxaluria 20%, Hypocitraturia 50%. Successfultherapy in terms of preventing further stoneformation was reported using indapamide, calciumcarbonate and potassium citrate in renal hypercalciuria,mild metabolic hyperoxaluria and hypo-citraturia respectively. Black volunteer subjects hadsignificantly higher 24hr urinary sodium excretionand significantly lower 24hr urinary calcium, citrateand cystine excretion than white volunteer subjects. Twenty-four hours urinary values in black stoneformers were found to be approaching those levelsfound in white.As urbanisation occurs in the black population, the incidence of urolithiasis would be expected to increase. We conclude that a detailed metabolic work-up is essential in the elucidation of the various metabolic risk factors. in so-called "idiopathic" CaOx stone formers. It allows appropriate, specific and highly cost-effective therapy aimed at the prevention of recurrence. [Erratum appears in AJN, 2017; 20(1):200.

Correction: Diagnostic and therapeutic aspects of recurrent renal stone disease

In Table 3 of the original publication of this article [1], the citrate excretion in white subjects is given as 1.39(0.92), which is incorrect. The correct value is 2.39(0.92). Reference1. Meyers A, Whalley N, Martins M. Diagnostic and therapeutic aspects of recurrent renal stone disease. Afr J Nephrol. 1998; 2(1):12-17

Moral Distress in Critical Care Nursing: The State of the Science

Background: Moral distress is a complex phenomenon frequently experienced by critical care nurses. Ethical conflicts in this practice area are related to technological advancement, high intensity work environments, and end-of-life decisions. Objectives: An exploration of contemporary moral distress literature was undertaken to determine measurement, contributing factors, impact, and interventions. Review Methods: This state of the science review focused on moral distress research in critical care nursing from 2009 to 2015, and included 12 qualitative, 24 quantitative, and 6 mixed methods studies. Results: Synthesis of the scientific literature revealed inconsistencies in measurement, conflicting findings of moral distress and nurse demographics, problems with the professional practice environment, difficulties with communication during end-of-life decisions, compromised nursing care as a consequence of moral distress, and few effective interventions. Conclusion: Providing compassionate care is a professional nursing value and an inability to meet this goal due to moral distress may have devastating effects on care quality. Further study of patient and family outcomes related to nurse moral distress is recommended

Decolonial/Anti-Racist interventions in Tibetan/Buddhist Studies – AAR Roundtable, Colorado 2019

This roundtable session held at the 2019 meeting of the American Association of Religious Studies explores how decolonial analytics and praxis can be applied productively in Tibetan/Buddhist Studies. As scholars, it is critical for us to consider how the racialized perceptions of non-Western religious traditions and peoples are tethered to their continued structural dispossession. A decolonizing intervention here means making the material hierarchies among peoples and their knowledge systems legible but also interrogating the politics of knowledge production in light of these overlapping colonial histories. Our discussion explicitly explores how our choices as scholars have effects in the real world, including how we represent Tibet and the Himalayas/Buddhism in our publications and teaching, the current inequalities of access to academic capital for Tibetan and nonwhite students/scholars, etc. We draw from Indigenous Studies approaches that center Indigenous knowledges and voices, given the history of their marginalization and ask how can we better center Tibetan/Himalayan voices/epistemologies in the study of Tibetan Buddhism

Combining natural language processing and metabarcoding to reveal pathogen-environment associations.

Cryptococcus neoformans is responsible for life-threatening infections that primarily affect immunocompromised individuals and has an estimated worldwide burden of 220,000 new cases each year-with 180,000 resulting deaths-mostly in sub-Saharan Africa. Surprisingly, little is known about the ecological niches occupied by C. neoformans in nature. To expand our understanding of the distribution and ecological associations of this pathogen we implement a Natural Language Processing approach to better describe the niche of C. neoformans. We use a Latent Dirichlet Allocation model to de novo topic model sets of metagenetic research articles written about varied subjects which either explicitly mention, inadvertently find, or fail to find C. neoformans. These articles are all linked to NCBI Sequence Read Archive datasets of 18S ribosomal RNA and/or Internal Transcribed Spacer gene-regions. The number of topics was determined based on the model coherence score, and articles were assigned to the created topics via a Machine Learning approach with a Random Forest algorithm. Our analysis provides support for a previously suggested linkage between C. neoformans and soils associated with decomposing wood. Our approach, using a search of single-locus metagenetic data, gathering papers connected to the datasets, de novo determination of topics, the number of topics, and assignment of articles to the topics, illustrates how such an analysis pipeline can harness large-scale datasets that are published/available but not necessarily fully analyzed, or whose metadata is not harmonized with other studies. Our approach can be applied to a variety of systems to assert potential evidence of environmental associations

Epstein-barr virus infected gastric adenocarcinoma expresses latent and lytic viral transcripts and has a distinct human gene expression profile

Abstract Background EBV DNA is found within the malignant cells of 10% of gastric cancers. Modern molecular technology facilitates identification of virus-related biochemical effects that could assist in early diagnosis and disease management. Methods In this study, RNA expression profiling was performed on 326 macrodissected paraffin-embedded tissues including 204 cancers and, when available, adjacent non-malignant mucosa. Nanostring nCounter probes targeted 96 RNAs (20 viral, 73 human, and 3 spiked RNAs). Results In 182 tissues with adequate housekeeper RNAs, distinct profiles were found in infected versus uninfected cancers, and in malignant versus adjacent benign mucosa. EBV-infected gastric cancers expressed nearly all of the 18 latent and lytic EBV RNAs in the test panel. Levels of EBER1 and EBER2 RNA were highest and were proportional to the quantity of EBV genomes as measured by Q-PCR. Among protein coding EBV RNAs, EBNA1 from the Q promoter and BRLF1 were highly expressed while EBNA2 levels were low positive in only 6/14 infected cancers. Concomitant upregulation of cellular factors implies that virus is not an innocent bystander but rather is linked to NFKB signaling (FCER2, TRAF1) and immune response (TNFSF9, CXCL11, IFITM1, FCRL3, MS4A1 and PLUNC), with PPARG expression implicating altered cellular metabolism. Compared to adjacent non-malignant mucosa, gastric cancers consistently expressed INHBA, SPP1, THY1, SERPINH1, CXCL1, FSCN1, PTGS2 (COX2), BBC3, ICAM1, TNFSF9, SULF1, SLC2A1, TYMS, three collagens, the cell proliferation markers MYC and PCNA, and EBV BLLF1 while they lacked CDH1 (E-cadherin), CLDN18, PTEN, SDC1 (CD138), GAST (gastrin) and its downstream effector CHGA (chromogranin). Compared to lymphoepithelioma-like carcinoma of the uterine cervix, gastric cancers expressed CLDN18, EPCAM, REG4, BBC3, OLFM4, PPARG, and CDH17 while they had diminished levels of IFITM1 and HIF1A. The druggable targets ERBB2 (Her2), MET, and the HIF pathway, as well as several other potential pharmacogenetic indicators (including EBV infection itself, as well as SPARC, TYMS, FCGR2B and REG4) were identified in some tumor specimens. Conclusion This study shows how modern molecular technology applied to archival fixed tissues yields novel insights into viral oncogenesis that could be useful in managing affected patients

Genetic Associations and Architecture of Asthma-COPD Overlap

BACKGROUND: Some people have characteristics of both asthma and COPD (asthma-COPD overlap), and evidence suggests they experience worse outcomes than those with either condition alone. RESEARCH QUESTION: What is the genetic architecture of asthma-COPD overlap, and do the determinants of risk for asthma-COPD overlap differ from those for COPD or asthma? STUDY DESIGN AND METHODS: We conducted a genome-wide association study in 8,068 asthma-COPD overlap case subjects and 40,360 control subjects without asthma or COPD of European ancestry in UK Biobank (stage 1). We followed up promising signals (P < 5 x 10(-6)) that remained associated in analyses comparing (1) asthma-COPD overlap vs asthma-only control subjects, and (2) asthma-COPD overlap vs COPD-only control subjects. These variants were analyzed in 12 independent cohorts (stage 2). RESULTS: We selected 31 independent variants for further investigation in stage 2, and discovered eight novel signals (P < 5 x 10(-8)) for asthma-COPD overlap (meta-analysis of stage 1 and 2 studies). These signals suggest a spectrum of shared genetic influences, some predominantly influencing asthma (FAM105A, GLB1, PHB, TSLP), others predominantly influencing fixed airflow obstruction (IL17RD, C5orf56, HLA-DQB1). One intergenic signal on chromosome 5 had not been previously associated with asthma, COPD, or lung function. Subgroup analyses suggested that associations at these eight signals were not driven by smoking or age at asthma diagnosis, and in phenome-wide scans, eosinophil counts, atopy, and asthma traits were prominent. INTERPRETATION: We identified eight signals for asthma-COPD overlap, which may represent loci that predispose to type 2 inflammation, and serious long-term consequences of asthma.Peer reviewe

Analysis of compound heterozygotes reveals that the mouse floxed Pax6 tm1Ued allele produces abnormal eye phenotypes

Analysis of abnormal phenotypes produced by different types of mutations has been crucial for our understanding of gene function. Some floxed alleles that retain a neomycin-resistance selection cassette (neo cassette) are not equivalent to wild-type alleles and provide useful experimental resources. Pax6 is an important developmental gene and the aim of this study was to determine whether the floxed Pax6(tm1Ued) (Pax6(fl)) allele, which has a retained neo cassette, produced any abnormal eye phenotypes that would imply that it differs from the wild-type allele. Homozygous Pax6(fl/fl) and heterozygous Pax6(fl/+) mice had no overt qualitative eye abnormalities but morphometric analysis showed that Pax6(fl/fl) corneas tended be thicker and smaller in diameter. To aid identification of weak effects, we produced compound heterozygotes with the Pax6(Sey-Neu) (Pax6(−)) null allele. Pax6(fl/−) compound heterozygotes had more severe eye abnormalities than Pax6(+/−) heterozygotes, implying that Pax6(fl) differs from the wild-type Pax6(+) allele. Immunohistochemistry showed that the Pax6(fl/−) corneal epithelium was positive for keratin 19 and negative for keratin 12, indicating that it was abnormally differentiated. This Pax6(fl) allele provides a useful addition to the existing Pax6 allelic series and this study demonstrates the utility of using compound heterozygotes with null alleles to unmask cryptic effects of floxed alleles. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s11248-016-9962-4) contains supplementary material, which is available to authorized users

Multi-ancestry genome-wide association study of asthma exacerbations

Altres ajuts: European Regional Development Fund "ERDF A way of making Europe"; Allergopharma-EAACI award 2021; SysPharmPedia grant from the ERACoSysMed 1st Joint Transnational Call from the European Union under the Horizon 2020; Sandler Family Foundation; American Asthma Foundation; RWJF Amos Medical Faculty Development Program; National Heart, Lung, and Blood Institute of the National Institutes of Health (R01HL117004, R01HL128439, R01HL135156, X01HL134589, R01HL141992, R01HL141845); National Institute of Health and Environmental Health Sciences (R01ES015794, R21ES24844); National Institute on Minority Health and Health Disparities (NIMHD) (P60MD006902, R01MD010443, R56MD013312); National Institute of General Medical Sciences (NIGMS) (RL5GM118984); Tobacco-Related Disease Research Program (24RT-0025, 27IR-0030); National Human Genome Research Institute (NHGRI) (U01HG009080); GlaxoSmithKline and Utrecht Institute for Pharmaceutical Sciences; Slovenian Research Agency (P3-0067); SysPharmPediA grant, co-financed by the Ministry of Education, Science and Sport Slovenia (MIZS) (C3330-16-500106); NHS Research Scotland; Wellcome Trust Biomedical Resource (099177/Z/12/Z); Genotyping National Centre (CeGEN) CeGen-PRB3-ISCIII (AC15/00015); UK Medical Research Council and Wellcome (102215/2/13/2); University of Bristol; Swedish Heart-Lung Foundation, Swedish Research Council; Region Stockholm (ALF project and database maintenance); NHS Chair of Pharmacogenetics via the UK Department of Health; Innovative Medicines Initiative (IMI) (115010); European Federation of Pharmaceutical Industries and Associations (EFPIA); Spanish National Cancer Research Centre; Fundación Canaria Instituto de Investigación Sanitaria de Canarias (PIFIISC19/17); Erasmus Medical Center; Erasmus University Rotterdam; Netherlands Organization for the Health Research and Development (ZonMw); the Research Institute for Diseases in the Elderly (RIDE); Ministry of Education, Culture and Science; Ministry for Health, Welfare and Sports; European Commission (DG XII); Municipality of Rotterdam; German Federal Ministry of Education and Research (Bundesministerium für Bildung und Forschung, BMBF); U.S. National Institutes of Health (HL07966); European Social Fund "ESF Investing in your future"; Ministerio de Ciencia, Innovación y Universidades; Universidad de La Laguna (ULL); European Academy of Allergy and Clinical Immunology (EAACI); European Respiratory Society (ERS) (LTRF202101-00861); Ministry of Education, Science and Sport of the Republic of Slovenia (C3330-19-252012); Singapore Ministry of Education Academic Research Fund; Singapore Immunology Network (SIgN); National Medical Research Council (NMRC Singapore); Biomedical Research Council (BMRC Singapore); Agency for Science Technology and Research (A*STAR Singapore, N-154-000-038-001, R-154-000-191-112, R-154-000-404-112, R-154-000-553-112, R-154-000-565-112, R-154-000-630-112, R-154-000-A08-592, R-154-000-A27-597, R-154-000-A91-592, R-154-000-A95-592, R-154-000-B99-114, BMRC/01/1/21/18/077, BMRC/04/1/21/19/315, SIgN-06-006, SIgN-08-020, NMRC/1150/2008, H17/01/a0/008); Sime Darby Technology Centre; First Resources Ltd; Genting Plantation; Olam International; U.S. National Institutes of Health (HL138098).Background: Asthma exacerbations are a serious public health concern due to high healthcare resource utilization, work/school productivity loss, impact on quality of life, and risk of mortality. The genetic basis of asthma exacerbations has been studied in several populations, but no prior study has performed a multi-ancestry meta-analysis of genome-wide association studies (meta-GWAS) for this trait. We aimed to identify common genetic loci associated with asthma exacerbations across diverse populations and to assess their functional role in regulating DNA methylation and gene expression. Methods: A meta-GWAS of asthma exacerbations in 4989 Europeans, 2181 Hispanics/Latinos, 1250 Singaporean Chinese, and 972 African Americans analyzed 9.6 million genetic variants. Suggestively associated variants (p ≤ 5 × 10) were assessed for replication in 36,477 European and 1078 non-European asthma patients. Functional effects on DNA methylation were assessed in 595 Hispanic/Latino and African American asthma patients and in publicly available databases. The effect on gene expression was evaluated in silico. Results: One hundred and twenty-six independent variants were suggestively associated with asthma exacerbations in the discovery phase. Two variants independently replicated: rs12091010 located at vascular cell adhesion molecule-1/exostosin like glycosyltransferase-2 (VCAM1/EXTL2) (discovery: odds ratio (OR) = 0.82, p = 9.05 × 10 and replication: OR = 0.89, p = 5.35 × 10) and rs943126 from pantothenate kinase 1 (PANK1) (discovery: OR = 0.85, p = 3.10 × 10 and replication: OR = 0.89, p = 1.30 × 10). Both variants regulate gene expression of genes where they locate and DNA methylation levels of nearby genes in whole blood. Conclusions: This multi-ancestry study revealed novel suggestive regulatory loci for asthma exacerbations located in genomic regions participating in inflammation and host defense