1,041 research outputs found
Unsuspected Pulmonary Embolism in Observation Unit Patients
Objective: Many emergency department (ED) patients with cardiopulmonary symptoms such as chest pain or dyspnea are placed in observation units but do not undergo specific diagnostic testing for pulmonary embolism (PE). The role of observation units in the diagnosis of PE has not been studied. We hypothesized that there was a small but significant rate of unsuspected PE in our observation unit population.Methods: We performed a retrospective chart review at an urban academic hospital of all ED patients with an International Classification of Diseases, Ninth Revision diagnosis of PE between January 2005 and July 2006. The number of such patients assigned to observation at any point in their stay was recorded, in addition to events leading to diagnosis and subsequent in-hospital outcomes.Results: Thirteen of the 190 ED patients diagnosed with PE were placed in the observation unit. Six of these either had a known recent diagnosis of PE or had testing for PE initiated prior to placement in the observation unit. Two of the remaining seven patients with undiagnosed PE were placed in observation for undifferentiated chest pain, accounting for 0.09% of the 2190 patients under the chest pain protocol. Twelve of 13 PE patients (92%) were admitted with an average stay of 4.3 days. Of the 13 patients, five were ultimately determined after admission to not have PE, leaving a rate of confirmed PE in the observation unit population of 0.12% (8/6182), with five of eight being classified as unsuspected prior to assignment to observation (0.08% rate).Conclusion: We identified a small number of patients assigned to observation with unsuspected PE. The high rate of hospital admission and prolonged hospital stay suggests that patients with PE are inappropriate for observation status. Given the low incidence of unsuspected PE, there may be a need for a specific approach to screening for PE in observation unit patients.[WestJEM. 2009;10:130-134.
Th2/Th1 Cytokine Imbalance Is Associated With Higher COVID-19 Risk Mortality
A major component of COVID-19 severe respiratory syndrome is the patient’s immune response to the SARS-CoV-2 virus and the consequential multi-organ inflammatory response. Several studies suggested a potential role of CD4+ T cells in COVID-19 severe respiratory syndrome. We first hypothesized that there is a type 2 helper (Th2)/type 1 helper (Th1) imbalance in older age, male, asthma, smokers, and high ACE2 expression phenotype in the airway of non-infected patients. Next, we hypothesized that a Th2/Th1 imbalance may predict higher mortality in COVID-19 infected hospitalized patients with and without patient reported current asthma. We first analyzed publicly available gene expression from the sputum of 118 moderate-to-severe asthma patients and 21 healthy controls, and from nasal epithelium of 26 healthy current smokers and 21 healthy never smokers. Secondly, we profiled 288 new serum proteomics samples measured at admission from patients hospitalized within the Mount Sinai Health System with positive SARS-CoV-2 infection. We first computed Th1 and Th2 pathway enrichment scores by gene set variation analysis and then compared the differences in Th2 and Th1 pathway scores between patients that died compared to those that survived, by linear regression. The level of Th2/Th1 imbalance, as determined by the enrichment score, was associated with age, sex, and ACE2 expression in sputum, and with active smoking status in nasal epithelium (p \u3c 0.05). Th2/Th1 imbalance at hospital admission in sera of patients was not significantly associated with death from COVID-19 (p = 0.11), unless evaluated in the asthmatic strata (p = 0.01). Using a similar approach we also observed a higher Th17/Th1 cytokine imbalance in all deceased patients compared to those that survived (p \u3c 0.001), as well as in the asthmatic strata only (p \u3c 0.01). Th2/Th1 imbalance is higher in the sera of asthma patients at admission that do not survive COVID-19, suggesting that the Th2/Th1 interplay may affect patient outcomes in SARS-CoV2 infection. In addition, we report that Th17/Th1 imbalance is increased in all patients that die of COVID-19
Quasielastic 12C(e,e'p) Reaction at High Momentum Transfer
We measured the 12C(e,e'p) cross section as a function of missing energy in
parallel kinematics for (q,w) = (970 MeV/c, 330 MeV) and (990 MeV/c, 475 MeV).
At w=475 MeV, at the maximum of the quasielastic peak, there is a large
continuum (E_m > 50 MeV) cross section extending out to the deepest missing
energy measured, amounting to almost 50% of the measured cross section. The
ratio of data to DWIA calculation is 0.4 for both the p- and s-shells. At w=330
MeV, well below the maximum of the quasielastic peak, the continuum cross
section is much smaller and the ratio of data to DWIA calculation is 0.85 for
the p-shell and 1.0 for the s-shell. We infer that one or more mechanisms that
increase with transform some of the single-nucleon-knockout into
multinucleon knockout, decreasing the valence knockout cross section and
increasing the continuum cross section.Comment: 14 pages, 7 figures, Revtex (multicol, prc and aps styles), to appear
in Phys Rev
Direct Activation of STING in the Tumor Microenvironment Leads to Potent and Systemic Tumor Regression and Immunity
SummarySpontaneous tumor-initiated T cell priming is dependent on IFN-β production by tumor-resident dendritic cells. On the basis of recent observations indicating that IFN-β expression was dependent upon activation of the host STING pathway, we hypothesized that direct engagement of STING through intratumoral (IT) administration of specific agonists would result in effective anti-tumor therapy. After proof-of-principle studies using the mouse STING agonist DMXAA showed a potent therapeutic effect, we generated synthetic cyclic dinucleotide (CDN) derivatives that activated all human STING alleles as well as murine STING. IT injection of STING agonists induced profound regression of established tumors in mice and generated substantial systemic immune responses capable of rejecting distant metastases and providing long-lived immunologic memory. Synthetic CDNs have high translational potential as a cancer therapeutic
Disease Progression in Hemodynamically Stable Patients Presenting to the Emergency Department With Sepsis
Aggressive diagnosis and treatment of patients presenting to the emergency department (ED) with septic shock has been shown to reduce mortality. To enhance the ability to intervene in patients with lesser illness severity, a better understanding of the natural history of the early progression from simple infection to more severe illness is needed
Partial complementation of Sinorhizobium meliloti bacA mutant phenotypes by the Mycobacterium tuberculosis BacA protein
The Sinorhizobium meliloti BacA ABC transporter protein plays an important role in its nodulating symbiosis with the legume alfalfa (Medicago sativa). The Mycobacterium tuberculosis BacA homolog was found to be important for the maintenance of chronic murine infections, yet its in vivo function is unknown. In the legume plant as well as in the mammalian host, bacteria encounter host antimicrobial peptides (AMPs). We found that the M. tuberculosis BacA protein was able to partially complement the symbiotic defect of an S. meliloti BacA-deficient mutant on alfalfa plants and to protect this mutant in vitro from the antimicrobial activity of a synthetic legume peptide, NCR247, and a recombinant human \u3b2-defensin 2 (HBD2). This finding was also confirmed using an M. tuberculosis insertion mutant. Furthermore, M. tuberculosis BacA-mediated protection of the legume symbiont S. meliloti against legume defensins as well as HBD2 is dependent on its attached ATPase domain. In addition, we show that M. tuberculosis BacA mediates peptide uptake of the truncated bovine AMP, Bac71-16. This process required a functional ATPase domain. We therefore suggest that M. tuberculosis BacA is important for the transport of peptides across the cytoplasmic membrane and is part of a complete ABC transporter. Hence, BacA-mediated protection against host AMPs might be important for the maintenance of latent infections
Structure of the mirror nuclei Be and B in a microscopic cluster model
The structure of the mirror nuclei Be and B is studied in a
microscopic and three-cluster model
using a fully antisymmetrized 9-nucleon wave function. The two-nucleon
interaction includes central and spin-orbit components and the Coulomb
potential. The ground state of Be is obtained accurately with the
stochastic variational method, while several particle-unbound states of both
Be and B are investigated with the complex scaling method.The
calculation for Be supports the recent identification for the existence of
two broad states around 6.5 MeV, and predicts the and
states at about 4.5 MeV and 8 MeV, respectively. The
similarity of the calculated spectra of Be and B enables one to
identify unknown spins and parities of the B states. Available data on
electromagnetic moments and elastic electron scatterings are reproduced very
well. The enhancement of the 1 transition of the first excited state in
Be is well accounted for. The calculated density of Be is found to
reproduce the reaction cross section on a Carbon target. The analysis of the
beta decay of Li to Be clearly shows that the wave function of Be
must contain a small component that cannot be described by the simple model. This small component can be well accounted for by extending a
configuration space to include the distortion of the -particle to
and partitions.Comment: 24 page
Chronic psychosocial and financial burden accelerates 5-year telomere shortening: findings from the Coronary Artery Risk Development in Young Adults Study.
Leukocyte telomere length, a marker of immune system function, is sensitive to exposures such as psychosocial stressors and health-maintaining behaviors. Past research has determined that stress experienced in adulthood is associated with shorter telomere length, but is limited to mostly cross-sectional reports. We test whether repeated reports of chronic psychosocial and financial burden is associated with telomere length change over a 5-year period (years 15 and 20) from 969 participants in the Coronary Artery Risk Development in Young Adults (CARDIA) Study, a longitudinal, population-based cohort, ages 18-30 at time of recruitment in 1985. We further examine whether multisystem resiliency, comprised of social connections, health-maintaining behaviors, and psychological resources, mitigates the effects of repeated burden on telomere attrition over 5 years. Our results indicate that adults with high chronic burden do not show decreased telomere length over the 5-year period. However, these effects do vary by level of resiliency, as regression results revealed a significant interaction between chronic burden and multisystem resiliency. For individuals with high repeated chronic burden and low multisystem resiliency (1 SD below the mean), there was a significant 5-year shortening in telomere length, whereas no significant relationships between chronic burden and attrition were evident for those at moderate and higher levels of resiliency. These effects apply similarly across the three components of resiliency. Results imply that interventions should focus on establishing strong social connections, psychological resources, and health-maintaining behaviors when attempting to ameliorate stress-related decline in telomere length among at-risk individuals
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