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Träfflista för sökning "WFRF:(Bajaj J. S.) "

Search: WFRF:(Bajaj J. S.)

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  • 2021
  • swepub:Mat__t
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  • Adamo, Angela, et al. (author)
  • Star cluster formation in the most extreme environments: Insights from the HiPEEC survey
  • 2020
  • In: Monthly Notices of the Royal Astronomical Society. - : Oxford University Press (OUP). - 0035-8711 .- 1365-2966. ; 499:3, s. 3267-3294
  • Journal article (peer-reviewed)abstract
    • We present the Hubble imaging Probe of Extreme Environments and Clusters (HiPEEC) survey. We fit HST NUV to NIR broad-band and H α fluxes to derive star cluster ages, masses, and extinctions and determine the star formation rate (SFR) of six merging galaxies. These systems are excellent laboratories to trace cluster formation under extreme gas physical conditions, rare in the local Universe, but typical for star-forming galaxies at cosmic noon. We detect clusters with ages of 1-500 Myr and masses that exceed 107 M☉. The recent cluster formation history and their distribution within the host galaxies suggest that systems such as NGC 34, NGC 1614, and NGC 4194 are close to their final coalescing phase, while NGC 3256, NGC 3690, and NGC 6052 are at an earlier/intermediate stage. A Bayesian analysis of the cluster mass function in the age interval 1-100 Myr provides strong evidence in four of the six galaxies that an exponentially truncated power law better describes the observed mass distributions. For two galaxies, the fits are inconclusive due to low number statistics. We determine power-law slopes β ∼ −1.5 to −2.0 and truncation masses, Mc, between 106 and a few times 107 M☉, among the highest values reported in the literature. Advanced mergers have higher Mc than early/intermediate merger stage galaxies, suggesting rapid changes in the dense gas conditions during the merger. We compare the total stellar mass in clusters to the SFR of the galaxy, finding that these systems are among the most efficient environments to form star clusters in the local Universe.
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7.
  • Bhatia, V., et al. (author)
  • Beta-blocker Use and 30-day All-cause Readmission in Medicare Beneficiaries with Systolic Heart Failure
  • 2015
  • In: American Journal of Medicine. - : Elsevier BV. - 0002-9343. ; 128:7, s. 715-721
  • Journal article (peer-reviewed)abstract
    • BACKGROUND: Beta-blockers improve outcomes in patients with systolic heart failure. However, it is unknown whether their initial negative inotropic effect may increase 30-day all-cause readmission, a target outcome for Medicare cost reduction and financial penalty for hospitals under the Affordable Care Act. METHODS: Of the 3067 Medicare beneficiaries discharged alive from 106 Alabama hospitals (1998-2001) with a primary discharge diagnosis of heart failure and ejection fraction <45%, 2202 were not previously on beta-blocker therapy, of which 383 received new discharge prescriptions for beta-blockers. Propensity scores for beta-blocker use, estimated for each of the 2202 patients, were used to assemble a matched cohort of 380 pairs of patients receiving and not receiving beta-blockers who were balanced on 36 baseline characteristics (mean age 73 years, mean ejection fraction 27%, 45% women, 33% African American). RESULTS: Beta-blocker use was not associated with 30-day all-cause readmission (hazard ratio [HR] 0.87; 95% confidence interval [CI], 0.64-1.18) or heart failure readmission (HR 0.95; 95% CI, 0.57-1.58), but was significantly associated with lower 30-day all-cause mortality (HR 0.29; 95% CI, 0.12-0.73). During 4-year postdischarge, those in the beta-blocker group had lower mortality (HR 0.81; 95% CI, 0.67-0.98) and combined outcome of all-cause mortality or all-cause readmission (HR 0.87; 95% CI, 0.74-0.97), but not with all-cause readmission (HR 0.89; 95% CI, 0.76-1.04). CONCLUSIONS: Among hospitalized older patients with systolic heart failure, discharge prescription of beta-blockers was associated with lower 30-day all-cause mortality and 4-year combined death or readmission outcomes without higher 30-day readmission. Published by Elsevier Inc.
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8.
  • Harms, H. J., et al. (author)
  • Cardiopulmonary transit time : A novel PET imaging biomarker of in vivo physiology for risk stratification of heart transplant recipients
  • 2022
  • In: Journal of Nuclear Cardiology. - : Springer Nature. - 1071-3581 .- 1532-6551. ; 29, s. 1234-1244
  • Journal article (peer-reviewed)abstract
    • Background: Myocardial blood flow (MBF) can be quantified using dynamic PET studies. These studies also inherently contain tomographic images of early bolus displacement, which can provide cardiopulmonary transit times (CPTT) as measure of cardiopulmonary physiology. The aim of this study was to assess the incremental prognostic value of CPTT in heart transplant (OHT) recipients.Methods: 94 patients (age 56 +/- 16 years, 78% male) undergoing dynamic N-13-ammonia stress/rest studies were included, of which 68 underwent right-heart catherization. A recently validated cardiac allograft vasculopathy (CAV) score based on PET measures of regional perfusion, peak MBF and left-ventricular (LV) ejection fraction (LVEF) was used to identify patients with no, mild or moderate-severe CAV. Time-activity curves of the LV and right ventricular (RV) cavities were obtained and used to calculate the difference between the LV and RV bolus midpoint times, which represents the CPTT and is expressed in heartbeats. Patients were followed for a median of 2.5 years for the occurrence of major adverse cardiac events (MACE), including cardiovascular death, hospitalization for heart failure or acute coronary syndrome, or re-transplantation.Results: CPTT was significantly correlated with cardiac filling pressures (r = .434, P = .0002 and r = .439, P = .0002 for right atrial and pulmonary wedge pressure), cardiac output (r = - .315, P = .01) and LVEF (r = - .513, P < .0001). CPTT was prolonged in patients with MACE (19.4 +/- 6.0 vs 14.5 +/- 3.0 heartbeats, P < .001, N = 15) with CPTT >= 17.75 beats showing optimal discriminatory value in ROC analysis. CPTT >= 17.75 heartbeats was associated with a 10.1-fold increased risk (P < .001) of MACE and a 7.3-fold increased risk (P < .001) after adjusting for PET-CAV, age, sex and time since transplant.Conclusion: Measurements of cardiopulmonary transit time provide incremental risk stratification in OHT recipients and enhance the value of multiparametric dynamic PET imaging, particularly in identifying high-risk patients.
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9.
  • Shi, Z. J., et al. (author)
  • Chorioamnionitis in the Development of Cerebral Palsy: A Meta-analysis and Systematic Review
  • 2017
  • In: Pediatrics. - : American Academy of Pediatrics (AAP). - 0031-4005 .- 1098-4275. ; 139:6
  • Research review (peer-reviewed)abstract
    • CONTEXT: Chorioamnionitis (CA) has often been linked etiologically to cerebral palsy (CP). OBJECTIVES: To differentiate association from risk of CA in the development of CP. DATA SOURCES: PubMed, Cochrane Library, Embase, and bibliographies of original studies were searched by using the keywords (chorioamnionitis) AND ((cerebral palsy) OR brain). STUDY SELECTION: Included studies had to have: (1) controls, (2) criteria for diagnoses, and (3) neurologic follow-up. Studies were categorized based on: (1) finding incidence of CP in a CA population, or risk of CP; and (2) incidence of CA in CP or association with CP. DATA EXTRACTION: Two reviewers independently verified study inclusion and extracted data. RESULTS: Seventeen studies (125 256 CA patients and 5 994 722 controls) reported CP in CA. There was significantly increased CP inpreterm histologic chorioamnionitis (HCA; risk ratio [RR] = 1.34, P < .01), but not in clinical CA (CCA). Twenty-two studies (2513 CP patients and 8135 controls) reported CA in CP. There was increased CCA (RR = 1.43, P < .01), but no increase in IICA in preterm CP. Increased IICA was found (RR = 4.26, P < .05), as well as CCA in term/near-term CP (RR = 3.06, P < .01). CONCLUSIONS: The evidence for a causal or associative role of CA in CP is weak. Preterm HCA may be a risk factor for CP, whereas CCA is not. An association with term and preterm CP was found for CCA, but only with term CP for HCA.
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10.
  • Jacobsen, M.C., et al. (author)
  • A critical role for ATF2 transcription factor in the regulation of E-selectin expression in response to non-endotoxin components of Neisseria meningitidis
  • 2016
  • In: Cellular Microbiology. - : Wiley-Blackwell. - 1462-5814 .- 1462-5822. ; 18:1, s. 66-79
  • Journal article (peer-reviewed)abstract
    • Vascular injury is a serious complication of sepsis due to the gram-negative bacterium Neisseria meningitidis. One of the critical early steps in initiating this injury is via the interaction of leucocytes, particularly neutrophils, with adhesion molecules expressed on inflamed endothelium. We have previously demonstrated that both lipopolysaccharide (LPS) and non-LPS components of meningococci can induce very high levels of expression of the vascular endothelial cell adhesion molecule E-selectin, which is critical for early tethering and capture of neutrophils onto endothelium under flow. Using an LPS-deficient strain of meningococcus, we showed that very high levels of expression can be induced in primary endothelial cells, even in the context of weak activation of the major host signal transduction factor [nuclear factor-κB (NF-κB)]. In this study, we show that the particular propensity for N.meningitidis to induce high levels of expression is regulated at a transcriptional level, and demonstrate a significant role for phosphorylation of the ATF2 transcription factor, likely via mitogen-activated protein (MAP) kinases, on the activity of the E-selectin promoter. Furthermore, inhibition of E-selectin expression in response to the lpxA- strain by a p38 inhibitor indicates a significant role of a p38-dependent MAPK signalling pathway in ATF2 activation. Collectively, these data highlight the role that LPS and other bacterial components have in modulating endothelial function and their involvement in the pathogenesis of meningococcal sepsis. Better understanding of these multiple mechanisms induced by complex stimuli such as bacteria, and the specific inflammatory pathways they activate, may lead to improved, focused interventions in both meningococcal and potentially bacterial sepsis more generally.
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