Multi-morbidities are Not a Driving Factor for an Increase of COPD-Related 30-Day Readmission Risk

Background and Objective: Chronic obstructive pulmonary disease (COPD) is the third leading cause of death in the United States. COPD is expensive to treat, whereas the quality of care is difficult to evaluate due to the high prevalence of multi-morbidity among COPD patients. In the US, the Hospital Readmissions Reduction Program (HRRP) was initiated by the Centers for Medicare and Medicaid Services to penalize hospitals for excessive 30-day readmission rates for six diseases, including COPD. This study examines the difference in 30-day readmission risk between COPD patients with and without comorbidities.Methods: In this retrospective cohort study, we used Cox regression to estimate the hazard ratio of 30-day readmission rates for COPD patients who had no comorbidity and those who had one, two or three, or four or more comorbidities. We controlled for individual, hospital and geographic factors. Data came from three sources: Healthcare Cost and Utilization Project (HCUP) State Inpatient Databases (SID), Area Health Resources Files (AHRF) and the American Hospital Association’s (AHA’s) annual survey database for the year of 2013.Results: COPD patients with comorbidities were less likely to be readmitted within 30 days relative to patients without comorbidities (aHR from 0.84 to 0.87, p \u3c 0.05). In a stratified analysis, female patients with one comorbidity had a lower risk of 30-day readmission compared to female patients without comorbidity (aHR = 0.80, p \u3c 0.05). Patients with public insurance who had comorbidities were less likely to be readmitted within 30 days in comparison with those who had no comorbidity (aHR from 0.79 to 0.84, p \u3c 0.05).Conclusion: COPD patients with comorbidities had a lower risk of 30-day readmission compared with patients without comorbidity. Future research could use a different study design to identify the effectiveness of the HRRP

Research on dynamic characteristics of spiral basilar membrane after replacing artificial auditory ossicle based on the reconstructed human ear model

In this paper, PATRAN software was used to establish a complete 3D finite element model of human ears, and it was then combined with NASTRAN software to analyze frequency responses. This paper conducted a detailed analysis on the dynamic parameters including umbo and stapes displacements of normal human ears under sound pressures 90 dB and 105 dB. The numerically computational results were compared with experimental data. When the analyzed frequency was less than 1000 Hz, the computational result of numerical simulation was well consistent with the upper limit. When the analyzed frequency was more than 1000 Hz, the computational result of numerical simulation was well consistent with the lower limit. Therefore, the numerically computational model was reliable. In addition, based on the verified model, this paper studied vibration characteristics of spiral basilar membrane after replacing artificial auditory ossicle based on the whole hearing system, and found that vibration characteristics of spiral basilar membrane had an obvious change at low and high frequencies after replacing artificial auditory ossicle TORP. Using finite element method to analyze vibration characteristics of spiral basilar membrane can well predict the hearing recovery effect after replacing artificial auditory ossicle. Compared with normal ears, the vibration level of spiral basilar membrane after replacing artificial auditory ossicle has slowed down in 100 Hz-600 Hz, 2000 Hz-4000 Hz and 7000 Hz-10000 Hz, and has been strengthened in 600 Hz-2000 Hz and 4000 Hz-7000 Hz, which provided some help for the hearing recovery at the high-frequency band

Diquarks and the Semi-Leptonic Decay of Λb\Lambda_{b} in the Hybrid Scheme

In this work we use the heavy-quark-light-diquark picture to study the semileptonic decay $\Lambda_b \to \Lambda_c+l+\bar{\nu}_l$ in the so-called hybrid scheme. Namely, we apply the heavy quark effective theory (HQET) for larger $q^2$ (corresponding to small recoil), which is the invariant mass square of $l+\bar\nu$, whereas the perturbative QCD approach for smaller $q^2$ to calculate the form factors. The turning point where we require the form factors derived in the two approaches to be connected, is chosen near $\rho_{cut}=1.1$. It is noted that the kinematic parameter $\rho$ which is usually adopted in the perturbative QCD approach, is in fact exactly the same as the recoil factor $\omega=v\cdot v'$ used in HQET where $v$, $v'$ are the four velocities of $\Lambda_b$ and $\Lambda_c$ respectively. We find that the final result is not much sensitive to the choice, so that it is relatively reliable. Moreover, we apply a proper numerical program within a small range around $\rho_{cut}$ to make the connection sufficiently smooth and we parameterize the form factor by fitting the curve gained in the hybrid scheme. The expression and involved parameters can be compared with the ones gained by fitting the experimental data. In this scheme the end-point singularities do not appear at all. The calculated value is satisfactorily consistent with the data which is recently measured by the DELPHI collaboration within two standard deviations.Comment: 16 pages, including 4 figures, revtex

BOOST: A fast approach to detecting gene-gene interactions in genome-wide case-control studies

Gene-gene interactions have long been recognized to be fundamentally important to understand genetic causes of complex disease traits. At present, identifying gene-gene interactions from genome-wide case-control studies is computationally and methodologically challenging. In this paper, we introduce a simple but powerful method, named `BOolean Operation based Screening and Testing'(BOOST). To discover unknown gene-gene interactions that underlie complex diseases, BOOST allows examining all pairwise interactions in genome-wide case-control studies in a remarkably fast manner. We have carried out interaction analyses on seven data sets from the Wellcome Trust Case Control Consortium (WTCCC). Each analysis took less than 60 hours on a standard 3.0 GHz desktop with 4G memory running Windows XP system. The interaction patterns identified from the type 1 diabetes data set display significant difference from those identified from the rheumatoid arthritis data set, while both data sets share a very similar hit region in the WTCCC report. BOOST has also identified many undiscovered interactions between genes in the major histocompatibility complex (MHC) region in the type 1 diabetes data set. In the coming era of large-scale interaction mapping in genome-wide case-control studies, our method can serve as a computationally and statistically useful tool.Comment: Submitte

2-Anilino-4,6-dimethyl­pyrimidinium chloro­acetate

In the crystal structure of the title compound, C12H14N3 +·C2H2ClO2 −, the chloro­acetate anion is linked to the N-(4,6-dimethyl­pyrimidin-2-yl)aniline cation by N—H⋯O hydrogen bonding. Within the cation, the pyrimidine ring is twisted with respect to the phenyl ring by a dihedral angle of 7.59 (4)°