Unequal Implementation: The Impact of Government Anti-Plague Policies on the London Poor in 1665

1665 would be the year of London’s deadliest outbreak of plague which would shortly thereafter be known as the Great Plague. The Great Plague has been a fairly well researched occurrence of plague in Europe. In part because of the massive scope of destruction and its great impact on the quality of life of Londoners, the epidemic is useful for researching the response of the government to the plague. Records clearly indicate, and contemporary writers acknowledge that the poor were the primary victims of the plague. There are many argued reasons such as their poor living conditions, diet, and less access to proper hygiene, but this paper will focus specifically on the impact of government public health policies on the poor. This paper will argue that the government’s health policies not only failed to help the sick but in fact harmed the poor while at the same time these policies did little harm to the wealthy and in some ways gave privileges to them. Along with the official health policy, this paper will address inconsistencies in the application of public health policies and particularly the tool of quarantine

Motivators for Convalescent Plasma Donors during the COVID-19 Pandemic

This study will seek to explore the motivators for convalescent plasma donors during the COVID-19 pandemic. In 2020, the global pandemic caused by SARS-CoV-2 increased donations of transfusion products, particularly convalescent plasma from COVID-19 survivors that is used to provide passive antibody immunity to those infected. Convalescent plasma therapy has been identified as one of the only therapies for COVID-19 beyond supportive care. Much of the current research focuses on the current motivators of whole blood and plasma donations, commonly citing altruistic motivations, knowing someone who has previously donated, and social media influence as common motivators for donations. It is important to explore not only what motivates COVID-19 survivors to initially donate plasma, but also the motivations of repeat donors. By gaining a greater understanding of what these motivators are, we may be able to convert these convalescent plasma donors to regular blood donors.https://scholarworks.uvm.edu/comphp_gallery/1308/thumbnail.jp

Novel candidate genes influencing natural variation in potato tuber cold sweetening identified by comparative proteomics and association mapping

BACKGROUND: Higher plants evolved various strategies to adapt to chilling conditions. Among other transcriptional and metabolic responses to cold temperatures plants accumulate a range of solutes including sugars. The accumulation of the reducing sugars glucose and fructose in mature potato tubers during exposure to cold temperatures is referred to as cold induced sweetening (CIS). The molecular basis of CIS in potato tubers is of interest not only in basic research on plant adaptation to environmental stress but also in applied research, since high amounts of reducing sugars affect negatively the quality of processed food products such as potato chips. CIS-tolerance varies considerably among potato cultivars. Our objective was to identify by an unbiased approach genes and cellular processes influencing natural variation of tuber sugar content before and during cold storage in potato cultivars used in breeding programs. We compared by two-dimensional polyacrylamide gel electrophoresis the tuber proteomes of cultivars highly diverse for CIS. DNA polymorphisms in genomic sequences encoding differentially expressed proteins were tested for association with tuber starch content, starch yield and processing quality. RESULTS: Pronounced natural variation of CIS was detected in tubers of a population of 40 tetraploid potato cultivars. Significant differences in protein expression were detected between CIS-tolerant and CIS-sensitive cultivars before the onset as well as during cold storage. Identifiable differential proteins corresponded to protease inhibitors, patatins, heat shock proteins, lipoxygenase, phospholipase A1 and leucine aminopeptidase (Lap). Association mapping based on single nucleotide polymorphisms supported a role of Lap in the natural variation of the quantitative traits tuber starch and sugar content. CONCLUSIONS: The combination of comparative proteomics and association genetics led to the discovery of novel candidate genes for influencing the natural variation of quantitative traits in potato tubers. One such gene was a leucine aminopeptidase not considered so far to play a role in starch sugar interconversion. Novel SNP’s diagnostic for increased tuber starch content, starch yield and chip quality were identified, which are useful for selecting improved potato processing cultivars

The Xpc gene markedly affects cell survival in mouse bone marrow

The XPC protein (encoded by the xeroderma pigmentosum Xpc gene) is a key DNA damage recognition factor that is required for global genomic nucleotide excision repair (G-NER). In contrast to transcription-coupled nucleotide excision repair (TC-NER), XPC and G-NER have been reported to contribute only modestly to cell survival after DNA damage. Previous studies were conducted using fibroblasts of human or mouse origin. Since the advent of Xpc−/− mice, no study has focused on the bone marrow of these mice. We used carboplatin to induce DNA damage in Xpc−/− and strain-matched wild-type mice. Using several independent methods, Xpc−/− bone marrow was ∼10-fold more sensitive to carboplatin than the wild type. Importantly, 12/20 Xpc−/− mice died while 0/20 wild-type mice died. We conclude that G-NER, and XPC specifically, can contribute substantially to cell survival. The data are important in the context of cancer chemotherapy, where Xpc gene status and G-NER may be determinants of response to DNA-damaging agents including carboplatin. Additionally, altered cell cycles and altered DNA damage signalling may contribute to the cell survival end point

Imaging Lung Disease in Systemic Sclerosis

Interstitial lung disease and pulmonary hypertension (PH) are the most common cardiopulmonary findings in patients with systemic sclerosis (SSc). About two thirds of patients suffering from SSc develop scleroderma interstitial lung disease. PH is present in about 20% of SSc patients and is typically associated with severe lung disease, although it may be an isolated manifestation of SSc. High-resolution CT scanning is a key method for evaluating chest involvement. There are four roles of imaging in scleroderma interstitial lung disease: 1) detection of lung involvement, 2) identification of patients likely to respond to treatment, 3) assessment of treatment efficacy, and 4) exclusion of other significant diseases to include PH and cardiac and esophageal abnormalities

The non-octarepeat copper binding site of the prion protein is a key regulator of prion conversion

The conversion of the prion protein (PrP(C)) into prions plays a key role in transmissible spongiform encephalopathies. Despite the importance for pathogenesis, the mechanism of prion formation has escaped detailed characterization due to the insoluble nature of prions. PrP(C) interacts with copper through octarepeat and non-octarepeat binding sites. Copper coordination to the non-octarepeat region has garnered interest due to the possibility that this interaction may impact prion conversion. We used X-ray absorption spectroscopy to study copper coordination at pH 5.5 and 7.0 in human PrP(C) constructs, either wild-type (WT) or carrying pathological mutations. We show that mutations and pH cause modifications of copper coordination in the non-octarepeat region. In the WT at pH 5.5, copper is anchored to His96 and His111, while at pH 7 it is coordinated by His111. Pathological point mutations alter the copper coordination at acidic conditions where the metal is anchored to His111. By using in vitro approaches, cell-based and computational techniques, we propose a model whereby PrP(C) coordinating copper with one His in the non-octarepeat region converts to prions at acidic condition. Thus, the non-octarepeat region may act as the long-sought-after prion switch, critical for disease onset and propagation