Optimizing the Electrocardiogram and Pressure Monitoring

journal articleBiomedical Informatic

Exit rates of accountable care organizations that serve high proportions of beneficiaries of racial and ethnic minority groups

Importance: The Medicare Shared Savings Program provides financial incentives for accountable care organizations (ACOs) to reduce costs of care. The structure of the shared savings program may not adequately adjust for challenges associated with caring for patients with high medical complexity and social needs, a population disproportionately made up of racial and ethnic minority groups. If so, ACOs serving racial and ethnic minority groups may be more likely to exit the program, raising concerns about the equitable distribution of potential benefits from health care delivery reform efforts. Objective: To evaluate whether ACOs with a high proportion of beneficaries of racial and ethnic minority groups are more likely to exit the Medicare Shared Savings Program and identify characteristics associated with this disparity. Design, Setting, and Participants: This retrospective observational cohort study used secondary data on Medicare Shared Savings Program ACOs from January 2012 through December 2018. Bivariate and multivariate cross-sectional regression analyses were used to understand whether ACO racial and ethnic composition was associated with program exit, and how ACOs with a high proportion of beneficaries of racial and ethnic minority groups differed in characteristics associated with program exit. Exposures: Racial and ethnic composition of an ACO\u27s beneficiaries. Main Outcomes and Measures: Shared savings program exit before 2018. Results: The study included 589 Medicare Shared Savings Program ACOs. The ACOs in the highest quartile of proportion of beneficaries of racial and ethnic minority groups were designated high-proportion ACOs (145 [25%]), and those in the lowest 3 quartiles were designated low-proportion ACOs (444 [75%]). In unadjusted analysis, a 10-percentage point increase in the proportion of beneficiaries of racial and ethnic minority groups was associated with a 1.12-fold increase in the odds of an ACO exit (95% CI, 1.00-1.25; P = .04). In adjusted analysis, there were significant associations among high-proportion ACOs between characteristics such as patient comorbidities, disability, and clinician composition and a higher likelihood of exit. Conclusions and Relevance: The study results suggest that ACOs that served a higher proportion of beneficaries of racial and ethnic minority groups were more likely to exit the Medicare Shared Savings Program, partially because of serving patients with greater disease severity and complexity. These findings raise concerns about how current payment reform efforts may differentially affect racial and ethnic minority groups

Antenatal risk factors for peanut allergy in children

<p>Abstract</p> <p>Background</p> <p>Prenatal factors may contribute to the development of peanut allergy. We evaluated the risk of childhood peanut allergy in association with pregnancy exposure to Rh immune globulin, folic acid and ingestion of peanut-containing foods.</p> <p>Methods</p> <p>We conducted a web-based case-control survey using the Anaphylaxis Canada Registry, a pre-existing database of persons with a history of anaphylaxis. A total of 1300 case children with reported peanut allergy were compared to 113 control children with shellfish allergy. All were evaluated for maternal exposure in pregnancy to Rh immune globulin and folic acid tablet supplements, as well as maternal avoidance of dietary peanut intake in pregnancy.</p> <p>Results</p> <p>Receipt of Rh immune globulin in pregnancy was not associated with a higher risk of peanut allergy (odds ratio [OR] 0.86, 95% confidence interval [CI] 0.51 to 1.45), nor was initiation of folic acid tablet supplements before or after conception (OR 0.53, 95% CI 0.19 to 1.48). Complete avoidance of peanut-containing products in pregnancy was associated with a non-significantly lower risk of peanut allergy (OR 0.53, 95% CI 0.27 to 1.03).</p> <p>Conclusion</p> <p>The risk of childhood peanut allergy was not modified by the following common maternal exposures in pregnancy: Rh immune globulin, folic acid or peanut-containing foods.</p> <p>Clinical implications</p> <p>Rh immune globulin, folic acid supplement use and peanut avoidance in pregnancy have yet to be proven to modulate the risk of childhood anaphylaxis to peanuts.</p> <p>Capsule Summary</p> <p>Identification of prenatal factors that contribute to peanut allergy might allow for prevention of this life-threatening condition. This article explores the role of three such factors.</p

Prospectus, April 18, 1984

CHORAL UNION DEMANDING AND REWARDING; News Digest; Is your child part of the identi-child program?; Budding playwrights get chance to have work produced; PC Happenings: Parkland wins Automotive Contest, German Club annual Springfest, EMT workshop offered, Petitions available for Stu-Go, Stu-Go lacks quorum; Here Comes the Easter Bunny (or the Easter Hare?); Faces We Make; Former Prospectus entertainment writer: Alender services held; Strange things at the library; Only Food Service Management course in area: Sutton leads Food Service Management program; Criminal justice program well rounded; Running may increase protein need; Easter means Easter egg time; Second Wind hosts race; Did You Know...; Classifieds; Creative Corner...Especially for you!!: Recollections, She\u27s More than a Nurse, You are a corn-fed steak..., Memories..., A fire burns, AKTING??????????????..., Sometimes in their heed to tact..., Clouds, Disturb Not the Dead, Follow the Wind, I don\u27t know why I bother..., Innoncent Eyes, Please tell me what it is you want..., Running scared from yourself and tripped, babe..., Time Bomb, Don\u27t go away--Linger on..., Class, Raggedy Ann lay in the back of an old station wagon..., Too Late, To God; Ice Capades comes to town: Skaters say it\u27s hard work but well worth it; few surprises during Hollywood\u27s biggest night; \u27Queen\u27 film at Assembly Hall; Director shines in film; \u27Go-Go\u27s\u27 are back on track; \u27Weird Al\u27 hits big time; Fan Club to host film; Parkland College 1984 baseball roster; Cobra men lose two; 1984 Parkland Outdoor Track Bests; Sports Digest; Women lose twin bill; Prospectus survey resultshttps://spark.parkland.edu/prospectus_1984/1024/thumbnail.jp

Two Polo-like kinase 4 binding domains in Asterless perform distinct roles in regulating kinase stability

Plk4 (Polo-like kinase 4) and its binding partner Asterless (Asl) are essential, conserved centriole assembly factors that induce centriole amplification when overexpressed. Previous studies found that Asl acts as a scaffolding protein; its N terminus binds Plk4’s tandem Polo box cassette (PB1-PB2) and targets Plk4 to centrioles to initiate centriole duplication. However, how Asl overexpression drives centriole amplification is unknown. In this paper, we investigated the Asl–Plk4 interaction in Drosophila melanogaster cells. Surprisingly, the N-terminal region of Asl is not required for centriole duplication, but a previously unidentified Plk4-binding domain in the C terminus is required. Mechanistic analyses of the different Asl regions revealed that they act uniquely during the cell cycle: the Asl N terminus promotes Plk4 homodimerization and autophosphorylation during interphase, whereas the Asl C terminus stabilizes Plk4 during mitosis. Therefore, Asl affects Plk4 in multiple ways to regulate centriole duplication. Asl not only targets Plk4 to centrioles but also modulates Plk4 stability and activity, explaining the ability of overexpressed Asl to drive centriole amplification

The Biometric Assemblage: Surveillance, Experimentation, Profit, and the Measuring of Refugee Bodies

Biometric technologies are routinely used in the response to refugee crises with the United Nations High Commissioner for Refugees (UNHCR) aiming to have all refugee data from across the world in a central population registry by the end of 2019. The article analyses biometrics, AI and blockchain as part of a technological assemblage, which I term the biometric assemblage. The article identifies five intersecting logics which explain wider transformations within the humanitarian sector and in turn shape the biometric assemblage. The acceleration of the rate of biometric registrations in the humanitarian sector between 2002 and 2019 reveals serious concerns regarding bias, data safeguards, data-sharing practices with states and commercial companies, experimentation with untested technologies among vulnerable people, and, finally, ethics. Technological convergence amplifies risks associated with each constituent technology of the biometric assemblage. The paper finally argues that the biometric assemblage accentuates asymmetries between refugees and humanitarian agencies and ultimately entrenches inequalities in a global context

Enhanced Discrimination of Malignant from Benign Pancreatic Disease by Measuring the CA 19-9 Antigen on Specific Protein Carriers

The CA 19-9 assay detects a carbohydrate antigen on multiple protein carriers, some of which may be preferential carriers of the antigen in cancer. We tested the hypothesis that the measurement of the CA 19-9 antigen on individual proteins could improve performance over the standard CA 19-9 assay. We used antibody arrays to measure the levels of the CA 19-9 antigen on multiple proteins in serum or plasma samples from patients with pancreatic adenocarcinoma or pancreatitis. Sample sets from three different institutions were examined, comprising 531 individual samples. The measurement of the CA 19-9 antigen on any individual protein did not improve upon the performance of the standard CA 19-9 assay (82% sensitivity at 75% specificity for early-stage cancer), owing to diversity among patients in their CA 19-9 protein carriers. However, a subset of cancer patients with no elevation in the standard CA 19-9 assay showed elevations of the CA 19-9 antigen specifically on the proteins MUC5AC or MUC16 in all sample sets. By combining measurements of the standard CA 19-9 assay with detection of CA 19-9 on MUC5AC and MUC16, the sensitivity of cancer detection was improved relative to CA 19-9 alone in each sample set, achieving 67–80% sensitivity at 98% specificity. This finding demonstrates the value of measuring glycans on specific proteins for improving biomarker performance. Diagnostic tests with improved sensitivity for detecting pancreatic cancer could have important applications for improving the treatment and management of patients suffering from this disease

A Toll-Like Receptor 2 Pathway Regulates the Ppargc1a/b Metabolic Co-Activators in Mice with Staphylococcal aureus Sepsis

Activation of the host antibacterial defenses by the toll-like receptors (TLR) also selectively activates energy-sensing and metabolic pathways, but the mechanisms are poorly understood. This includes the metabolic and mitochondrial biogenesis master co-activators, Ppargc1a (PGC-1α) and Ppargc1b (PGC-1β) in Staphylococcus aureus (S. aureus) sepsis. The expression of these genes in the liver is markedly attenuated inTLR2−/− mice and markedly accentuated in TLR4−/− mice compared with wild type (WT) mice. We sought to explain this difference by using specific TLR-pathway knockout mice to test the hypothesis that these co-activator genes are directly regulated through TLR2 signaling. By comparing their responses to S. aureus with WT mice, we found that MyD88-deficient and MAL-deficient mice expressed hepatic Ppargc1a and Ppargc1b normally, but that neither gene was activated in TRAM-deficient mice. Ppargc1a/b activation did not require NF-kβ, but did require an interferon response factor (IRF), because neither gene was activated in IRF-3/7 double-knockout mice in sepsis, but both were activated normally in Unc93b1-deficient (3d) mice. Nuclear IRF-7 levels in TLR2−/− and TLR4−/− mice decreased and increased respectively post-inoculation and IRF-7 DNA-binding at the Ppargc1a promoter was demonstrated by chromatin immunoprecipitation. Also, a TLR2-TLR4-TRAM native hepatic protein complex was detected by immunoprecipitation within 6 h of S. aureus inoculation that could support MyD88-independent signaling to Ppargc1a/b. Overall, these findings disclose a novel MyD88-independent pathway in S. aureus sepsis that links TLR2 and TLR4 signaling in innate immunity to Ppargc1a/b gene regulation in a critical metabolic organ, the liver, by means of TRAM, TRIF, and IRF-7

Antimetastatic gene expression profiles mediated by retinoic acid receptor beta 2 in MDA-MB-435 breast cancer cells

BACKGROUND: The retinoic acid receptor beta 2 (RARβ2) gene modulates proliferation and survival of cultured human breast cancer cells. Previously we showed that ectopic expression of RARβ2 in a mouse xenograft model prevented metastasis, even in the absence of the ligand, all-trans retinoic acid. We investigated both cultured cells and xenograft tumors in order to delineate the gene expression profiles responsible for an antimetastatic phenotype. METHODS: RNA from MDA-MB-435 human breast cancer cells transduced with RARβ2 or empty retroviral vector (LXSN) was analyzed using Agilent Human 1A Oligo microarrays. The one hundred probes with the greatest differential intensity (p < 0.004, jointly) were determined by selecting the top median log ratios from eight-paired microarrays. Validation of differences in expression was done using Northern blot analysis and quantitative RT-PCR (qRT-PCR). We determined expression of selected genes in xenograft tumors. RESULTS: RARβ2 cells exhibit gene profiles with overrepresentation of genes from Xq28 (p = 2 × 10(-8)), a cytogenetic region that contains a large portion of the cancer/testis antigen gene family. Other functions or factors impacted by the presence of exogenous RARβ2 include mediators of the immune response and transcriptional regulatory mechanisms. Thirteen of fifteen (87%) of the genes evaluated in xenograft tumors were consistent with differences we found in the cell cultures (p = 0.007). CONCLUSION: Antimetastatic RARβ2 signalling, direct or indirect, results in an elevation of expression for genes such as tumor-cell antigens (CTAG1 and CTAG2), those involved in innate immune response (e.g., RIG-I/DDX58), and tumor suppressor functions (e.g., TYRP1). Genes whose expression is diminished by RARβ2 signalling include cell adhesion functions (e.g, CD164) nutritional or metabolic processes (e.g., FABP6), and the transcription factor, JUN