Similarity of percolation thresholds on the hcp and fcc lattices

Extensive Monte-Carlo simulations were performed in order to determine the precise values of the critical thresholds for site ($p^{hcp}_{c,S} = 0.199 255 5 \pm 0.000 001 0$) and bond ($p^{hcp}_{c,B} = 0.120 164 0 \pm 0.000 001 0$) percolation on the hcp lattice to compare with previous precise measuremens on the fcc lattice. Also, exact enumeration of the hcp and fcc lattices was performed and yielded generating functions and series for the zeroth, first, and second moments of both lattices. When these series and the values of $p_c$ are compared to those for the fcc lattice, it is apparent that the site percolation thresholds are different; however, the bond percolation thresholds are equal within error bars, and the series only differ slightly in the higher order terms, suggesting the actual values are very close to each other, if not identical.Comment: 10 pages, 4 figures, submitted to J. Stat. Phy

Catholic Student Protest and Campus Change at Loyola University in New Orleans, 1964-1971

This study analyzes the development of the student protest movement at Loyola University New Orleans from1964 to 1971. It focuses on student protests against racial discrimination and the Vietnam War, student agitation for greater freedom on campus, and battles that Loyola\u27s faculty had with the university administration. This study argues that Loyola\u27s student protesters were acting as Catholics against situations they believed were immoral and unjust. In this sense, they were ahead of the Jesuit clergy at Loyola, who took action only after student protest on those issues. Indeed, student protest filled a void of moral leadership that the Jesuit administration at Loyola failed to provide. Moreover, in the areas of student participation in university governance, changes in curriculum and university restrictions, and student rights and freedoms, the student protesters joined with Catholic commentators who advocated for major changes at the country\u27s Catholic universities

Micro Evidence on the Adjustment of Sticky-Price Goods: It's How Often, not How Much

We use a unique panel data set to analyze price setting in restaurants in Switzerland 1977-93, for items known to have sticky prices. The macroeconomic environment during this time period allows us to examine how firms adjust prices at low (0%) and fairly high (7%) inflation. Our results indicate that firms strongly react to inflation in the timing of their price adjustment: hazard of price changes is increasing with time and becomes steeper at higher inflation rates. However, we find little evidence that the amount by which they change the price responds to the inflation rate.sticky prices; inflation; nominal inertia

Effective potential for SU(2) Polyakov loops and Wilson loop eigenvalues

We simulate SU(2) gauge theory at temperatures ranging from slightly below $T_c$ to roughly $2T_c$ for two different values of the gauge coupling. Using a histogram method, we extract the effective potential for the Polyakov loop and for the phases of the eigenvalues of the thermal Wilson loop, in both the fundamental and adjoint representations. We show that the classical potential of the fundamental loop can be parametrized within a simple model which includes a Vandermonde potential and terms linear and quadratic in the Polyakov loop. We discuss how parametrizations for the other cases can be obtained from this model.Comment: 16 pages, 39 figure

Unraveling disease mechanisms of different lung pathologies with single-cell RNA sequencing

The respiratory system is composed of different tissues with their respective cell types that together work in concert to perform air conductance and gas exchange. With the advent of single-cell RNA-sequencing (scRNA-seq), it is now possible to comprehensively interrogate the function of each individual cell in homeostatic and diseased states. In this dissertation, various roles of epithelial, mesenchymal, and immune cell types of the respiratory system in idiopathic pulmonary fibrosis (IPF) and corona virus disease 2019 (COVID-19) were investigated with scRNA-seq. IPF is a chronic interstitial lung disease characterized by the progressive scarring of the lung parenchyma. Previous studies that surveyed the cellular landscape of IPF lungs utilized explant lungs that reflect end-stage fibrosis. To uncover disease mechanisms of airway cell types in early-stage fibrosis, air-liquid interface (ALI) cultures of primary cells taken from newly diagnosed IPF patients were used. This identified proinflammatory epithelial cells, profibrotic basal cells, and primed fibroblasts as early-stage drivers of IPF. Treatment with antifibrotic compounds nintedanib, pirfenidone, and saracatinib fail to completely ameliorate the identified signatures. With the emergence of the COVID-19 pandemic and its extensive public health burden, it was imperative to understand the molecular mechanisms of viral entry and disease pathology to identify potential risk factors and therapeutic targets. In the early stages of the pandemic, viral entry factors ACE2, TMPRSS2, and FURIN were found to be expressed by a transient secretory cell type (differentiating from secretory to ciliated cell) of the airway mucosa and by alveolar type 2 cells of the alveolar epithelium. With further investigation of severe COVID-19, the early-stage of COVID-19 infection characterized itself with a hyperactivated immune response mediated by proinflammatory macrophages. On the other hand, late-stage COVID-19, especially those with acute respiratory distress syndrome (ARDS), was characterized by an accumulation of profibrotic macrophages and activated myofibroblasts that drove pulmonary scarring and fibrosis. Although IPF and COVID-19 are different diseases by their own right, they share a commonality in aberrant wound healing responses. Both diseases are characterized by tissue inflammation that is followed by a profibrotic phase. Unlike in IPF where the tissue remodeling is progressive and chronic, COVID-19 ARDS-associated fibrosis undergoes a resolution phase. Future studies comparing the cellular and transcriptional landscape of both conditions in early and late stages of disease will uncover pathogenic mechanisms and therapeutic targets of lung fibrosis. The application of high-resolution transcriptomic profiling techniques such as scRNA-seq permits the interrogation of individual cell types and their direct contribution to the development of diseases. Moreover, it allows the comparison and transfer of identified pathomechanisms across different pulmonary diseases and, in doing so, provides deeper and generalizable insights. As this field continues to evolve, it will undoubtedly continue to provide a deeper understanding of respiratory diseases.Das respiratorische System setzt sich aus verschiedenen Geweben und ihren zugrundeliegenden Zelltypen zusammen, die gemeinsam Luftaufnahme und Gasaustausch gewährleisten. Mit dem Aufkommen der Einzelzell-RNA-Sequenzierung (scRNA-seq) ist es nun möglich, die Funktion jeder einzelnen Zelle in homöostatischen und kranken Zuständen umfassend zu untersuchen. In dieser Dissertation wurden verschiedene Rollen von Epithel-, Mesenchymal- und Immunzelltypen des Atmungssystems bei idiopathischer Lungenfibrose (IPF) und der Coronavirus-Krankheit-2019 (COVID-19) mit scRNA-seq untersucht. IPF ist eine chronische interstitielle Lungenerkrankung, die durch eine fortschreitende Vernarbung des Lungenparenchyms gekennzeichnet ist. Frühere Studien, die die Zellkomposition von IPF-Lungen untersuchten, verwendeten Lungenexplantate, die das Endstadium der Fibrose widerspiegeln. Um Krankheitsmechanismen von Atemwegszelltypen im Frühstadium der Fibrose aufzudecken, wurden Air-Liquid-Interface (ALI)-Kulturen von primären Zellen verwendet, die frisch diagnostizierten IPF-Patienten entnommen wurden. Dabei wurden proinflammatorische Epithelzellen, profibrotische Basalzellen und aktivierte Fibroblasten als treibende Kräfte im Frühstadium der IPF identifiziert. Die Behandlung mit den antifibrotischen Wirkstoffen Nintedanib, Pirfenidon und Saracatinib führte nicht zu einer vollständigen Verbesserung der identifizierten Signaturen. Mit dem Beginn der COVID-19-Pandemie und ihrer großen Belastung für die öffentliche Gesundheit war es unerlässlich, die molekularen Mechanismen des Viruseintritts und der Krankheitspathologie zu verstehen, um potenzielle Risikofaktoren und therapeutische Ansätze zu identifizieren. In den frühen Stadien der Pandemie wurde festgestellt, dass die viralen Eintrittsfaktoren ACE2, TMPRSS2 und FURIN von einem vorübergehenden sekretorischen Zelltyp (der sich von sekretorischen zu ziliierten Zellen differenziert) der Atemwegsschleimhaut und von Typ-2 -Pneumozyten des Alveolarepithels exprimiert werden. Bei der weiteren Untersuchung von schweren COVID-19 Verläufen zeigte sich, dass das Frühstadium der COVID-19-Infektion durch eine hyperaktivierte Immunantwort charakterisiert ist, die durch proinflammatorische Makrophagen vermittelt wird. Andererseits war das Spätstadium der COVID-19-Infektion, insbesondere bei Patienten mit akutem Atemnotsyndrom (ARDS), durch eine Anhäufung von profibrotischen Makrophagen und aktivierten Myofibroblasten gekennzeichnet, die die pulmonale Narbenbildung und Fibrose vorantrieben. Obwohl es sich bei IPF und COVID-19 um unterschiedliche Krankheiten handelt, ähneln sie sich in ihrer gestörten Wundheilung. Beide Krankheiten sindS durch eine Gewebeentzündung gekennzeichnet, auf die eine profibrotische Phase folgt. Im Gegensatz zur IPF, bei der die Gewebeveränderung fortschreitend und chronisch ist, durchläuft die COVID-19 ARDS-assoziierte Fibrose eine Reparationsphase. Zukünftige Studien, die die zelluläre und transkriptionelle Landschaft beider Erkrankungen in frühen und späten Stadien vergleichen, werden pathogene Mechanismen und therapeutische Ansätze der Lungenfibrose aufdecken können. Die Anwendung hochauflösender transkriptomischer Sequenzierung wie scRNA-seq ermöglicht die Untersuchung einzelner Zelltypen und ihren Beitrag zur Entstehung von Krankheiten. Darüber hinaus ermöglicht sie den Vergleich und die Übertragbarkeit identifizierter Pathomechanismen über verschiedene Lungenkrankheiten hinweg und liefert so tiefere und generalisierbare Erkenntnisse. Da sich dieses Feld stetig weiter entwickelt, wird es zweifellos auch weiterhin zu einem tieferen Verständnis von Atemwegserkrankungen beitragen

Modeling the growth of fingerprints improves matching for adolescents

We study the effect of growth on the fingerprints of adolescents, based on which we suggest a simple method to adjust for growth when trying to recover a juvenile's fingerprint in a database years later. Based on longitudinal data sets in juveniles' criminal records, we show that growth essentially leads to an isotropic rescaling, so that we can use the strong correlation between growth in stature and limbs to model the growth of fingerprints proportional to stature growth as documented in growth charts. The proposed rescaling leads to a 72% reduction of the distances between corresponding minutiae for the data set analyzed. These findings were corroborated by several verification tests. In an identification test on a database containing 3.25 million right index fingers at the Federal Criminal Police Office of Germany, the identification error rate of 20.8% was reduced to 2.1% by rescaling. The presented method is of striking simplicity and can easily be integrated into existing automated fingerprint identification systems