A Prescription for Health Care

Too many people do not have access to the health care that they need and deserve. However, no one should have to suffer through and illness because they do not earn enough money to be able to buy health care. it is our responsibility to make sure that our entire community, regardless of their income, has access to these essential human services that our medical community is capable of providing. With the spiraling costs and constant development of advanced technology in health care, along with the existence of the third-party payment system, our country has created the most costly health care system in the world. Arguably, we have the best quality care money can buy, but too many people can\u27t afford to enjoy its benefits. Many proposals have been formulated to resolve the growing inequities and outrageous costs of American health care. some aspect of our current system has to give way to developing a more fair delivery strategy. Quality and easy access suffer as a result of creating a more efficient system, and vice versa. Although whatever measures we employ to offer our uninsured neighbors the security of health care, we will inevitably pay. Health care for all will not come without a cost. Although, as I have estimated, it is reasonable for us to assume we can afford the expanded coverage. I have speculated that the most effective way to deliver universal health care coverage would be to mandate that all employers offer health insurance to their workers and to expand Medicaid for the unemployed. In this way, we would be able to ensure that no one will suffer with an illness because of their inability to afford health care access

Analysis of wall mass transfer in a turbulent pipe flow combining extended POD and FIK identity

We combine extended proper orthogonal decomposition (EPOD) together with the Fukagata-Iwamoto-Kasagi (FIK) identity to quantify the role of individual coherent structures on the wall mass transfer in a turbulent pipe flow. Direct numerical simulation at a Reynolds number of 5300 (based on bulk velocity) is performed with the passive scalar released at the pipe inlet. The proper orthogonal decomposition (POD) eigenvalues show that the scalar field can be described by a more compact set of modes compared to the velocity field, and that these modes are skewed towards higher azimuthal wave numbers. POD modes for the scalar and EPOD modes for the velocity are visualized in the cross-stream plane to infer the capacity of each mode to transport scalar to and from the wall. A form of the FIK identity is derived for the wall mass transfer coefficient (Sherwood number, Sh) and employed to separate the contributions of the mean and fluctuating velocity and scalar fields. The FIK decomposition shows that the turbulent velocity/scalar correlations account for up to 65.8% of the total Sh. The contribution of each POD and EPOD mode to the Sh number is also computed; it is found that, using azimuthal wave numbers m=1–15 and POD modes n=1–10, it is possible to reconstruct 49% of the turbulent component of Sh, with the velocity modes containing only 31% of the turbulent kinetic energy. Quadrant analysis shows that these modes are related to ejection and sweep events near the wall, with the ejection events dominating

Resource allocation in the Covid-19 health crisis:are Covid-19 preventive measures consistent with the Rule of Rescue?

Abstract The Covid-19 pandemic has led to a health crisis of a scale unprecedented in post-war Europe. In response, a large amount of healthcare resources have been redirected to Covid-19 preventive measures, for instance population-wide vaccination campaigns, large-scale SARS-CoV-2 testing, and the large-scale distribution of protective equipment (e.g., N95 respirators) to high-risk groups and hospitals and nursing homes. Despite the importance of these measures in epidemiological and economic terms, health economists and medical ethicists have been relatively silent about the ethical rationales underlying the large-scale allocation of healthcare resources to these measures. The present paper seeks to encourage this debate by demonstrating how the resource allocation to Covid-19 preventive measures can be understood through the paradigm of the Rule of Rescue, without claiming that the Rule of Rescue is the sole rationale of resource allocation in the Covid-19 pandemic

Opposite effects of the rotational and translational energy on the rates of ion-molecule reactions near 0 K0\,\text{K}: the D2++NH3\text{D}_2^++\text{NH}_3 and D2++ND3\text{D}_2^++\text{ND}_3 reactions

The ion-molecule reactions $\text{D}_2^++\text{NH}_3$ and $\text{D}_2^++\text{ND}_3$ are studied at low collision energies ($E_{\text{coll}}$ from zero to $\sim k_\textrm{B}\cdot 50\,\text{K}$), with the $\text{D}_2^+$ ions in the ground rovibrational state and for different rotational temperatures of the ammonia molecules, using the Rydberg-Stark merged-beam approach. Two different rotational temperatures ($\sim\,15\,\text{K}$ and $\sim\,40\,\text{K}$), measured by (2+1) resonance-enhanced multiphoton-ionization spectroscopy, are obtained by using a seeded supersonic expansion in He and a pure ammonia expansion, respectively. The experimental data reveal a strong enhancement of the rate coefficients at the lowest collision energies caused by the charge-dipole interaction. Calculations based on a rotationally adiabatic capture model accurately reproduce the observed kinetic-energy dependence of the rate coefficients. The rate coefficients increase with increasing rotational temperature of the ammonia molecules, which contradicts the expectation that rotational excitation should average the dipoles out. Moreover, these reactions exhibit a pronounced inverse kinetic isotope effect. The difference is caused by nuclear-spin-statistical factors, and the smaller rotational constants and tunneling splittings in $\text{ND}_3$.Comment: 14 pages, 8 figure

Die Rolle von Macrophage Migration Inhibitory Factor (MIF) bei der malignen Transformation

Um die Funktion von MIF als Tautomerase auf genetischer Basis zu analysieren, untersuchten wir die MIFpg Maus, welche durch Punktmutation von Prolin1 zu Glycin einen Komplettverlust der enzymatischen Aktivität von MIF aufweist. Der Phänotyp der MIF-Defizienz in Fibroblasten besteht in verstärkter Kontaktinhibition, einem Defekt bei der malignen Transformation. Um die These über MIF als Enzym zu testen, untersuchten wir Fibroblasten von P1G-mutanten Mäusen. Laut unseren in vivo Analysen besitzen mutierte MIFpg-MEFs keine enzymatische Aktivität mehr. Die MIFpg-Maus, welche ein Mutation des Prolin1 aufweist, jener Aminosäure, welche als katalytische Basis der Isomeraseaktivität gilt, zeigte, dass MIFpg-Fibroblasten zwar einen Verlust der enzymatischen Aktivität als Isomerase, jedoch keine Defekte in der Ras-vermittelten Transformation aufwiesen. Daraus folgernd beruht die biologische Aktivität von MIF nicht auf dessen Isomeraseaktivität. Die p53-/- Mäuse entwickelten früh Tumore, meist Lymphome und Osteosarkome, mit einer daraus resultierenden frühen Letalität der adulten Maus. Die meisten Effekte von MIF scheinen durch p53 vermittelt zu werden, denn in Mäusen, welche sowohl für MIF als auch für p53 defizient sind, verschwindet der in MIFko-Mäusen beobachtete Phänotyp der verzögerten Tumorentstehung. Auch der in unseren Experimenten fehlende Unterschied in der Überlebenszeit von DKO im Vergleich zu p53-/- MIFflox/flox Mäusen, unterstützt die Annahme, dass die meisten Effekte von MIF in der Tumorgenese in vivo über p53 stattfinden. Unsere Ergebnisse lassen darauf schließen, dass die tumorregulierende Aktivität von MIF im Wesentlichen über Regulation der p53-Aktivität durch MIF auf dem C57Bl/6 Hintergrund erklärt ist. Zudem zeigen wir, dass diese Aktivität nicht durch die enzymatische Aktivität von MIF als Tautomerase erklärt ist

Estimation of the stage-wise costs of breast cancer in Germany using a modeling approach

Breast cancer (BC) is a heterogeneous disease representing a substantial economic burden. In order to develop policies that successfully decrease this burden, the factors affecting costs need to be fully understood. Evidence suggests that early-stage BC has a lower cost than a late stage BC. We aim to provide conservative estimates of BC's stage-wise medical costs from German healthcare and the payer's perspective. To this end, we conducted a literature review of articles evaluating stage-wise costs of BC in Germany through PubMed, Web of Science, and Econ Lit databases supplemented by Google Scholar. We developed a decision tree model to estimate BC-related medical costs in Germany using available treatment and cost information. The review generated seven studies; none estimated the stage-wise costs of BC. The studies were classified into two groups: case scenarios (five studies) and two studies based on administrative data. The first sickness funds data study (Gruber et al., 2012) used information from the year 1999 to approach BC attributable cost; their results suggest a range between €3,929 and €11,787 depending on age. The second study (Kreis, Plöthner et al., 2020) used 2011–2014 data and suggested an initial phase incremental cost of €21,499, an intermediate phase cost of €2,620, and a terminal phase cost of €34,513 per incident case. Our decision tree model-based BC stage-wise cost estimates were €21,523 for stage I, €25,679 for stage II, €30,156 for stage III, and €42,086 for stage IV. Alternatively, the modeled cost estimates are €20,284 for the initial phase of care, €851 for the intermediate phase of care, and €34,963 for the terminal phase of care. Our estimates for phases of care are consistent with recent German estimates provided by Kreis et al. Furthermore, the data collected by sickness funds are collected primarily for reimbursement purposes, where the German ICD-10 classification system defines a cancer diagnosis. As a result, claims data lack the clinical information necessary to understand stage-wise BC costs. Our model-based estimates fill the gap and inform future economic evaluations of BC interventions

Experimental Evaluation of Kolmogorov’s -5/3 and 2/3 Power Laws in the Developing Turbulent Round Jet

The current work investigates the validity of two cornerstone results of the Kolmogorov K41 theory of turbulence in terms of the typical power law representations viz. the -5/3 law for turbulence spectra and the 2/3 law for second order structure functions. The developing region of the jet has been chosen since it is an equilibrium flow once fully developed (but not necessarily in the development phase), it becomes fully developed over lengths that are practical on a laboratory scale and it is a high-intensity flow with accessibly resolvable scales in time and space. The developing region of the jet is thus the perfect testbed for these investigations, which can herein be accurately mapped using our in-house laser Doppler anemometry (LDA) system. The high turbulence intensity and high shear flow is challenging from a measurement technical perspective, which is perhaps why this flow is so underexplored. This software-driven LDA system was developed specifically to optimize measurement of high shear and high turbulence intensities accurately in challenging flows such as the turbulent round jet in air. The jet was investigated experimentally both in the developing (non-equilibrium) and in the developed regions (equilibrium). Velocity static moments at each point are first presented to show the time averaged flow behavior while the spatial energy spectra and second order structure functions are computed to evaluate the power laws postulated by Kolmogorov. Measurements from both the developed and from the developing parts of the jet are presented to show validity of the measurement technique and unveil the actual spectral shapes in the developing non-equilibrium region, respectively