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In this issue of Christian Bioethics, we invite chaplains and theologians to examine the role of the hospital chaplain in the contemporary institutional setting of the hospital. The simplicity of the chaplain's role is often taken for granted; yet, this role is actually multivalent, with duties and loyalties pulling from many different sides. Chaplains are people of faith, ordained and/or endorsed ministers, and pastoral care professionals; they are at once beholden to God, to their own faith expression, and to their sense of vocation, to the hospital, and to the patient. With various loyalties and responsibilities in mind, we must ask the question, "To whom is the chaplain beholden?" The responses in this issue critically and constructively examine this question, providing theological resources that call chaplaincy away from the dominant modes of medicine. Whether through a primary loyalty to their calling, to God, to Divine presence, or to the spiritual formation of the patient, the authors in this special issue aim to help chaplains find theological resources to faithfully withstand the tensions they face in modern medical institutions. [ABSTRACT FROM AUTHOR]

In 2013, the United States Supreme Court legalized DNA collection of all felony arrestees upon arrest through its decision in Maryland v. King. Since then, the State of Ohio has broadened the use of arrestee DNA by subjecting it to familial DNA searches. Ohio's practice of conducting familial DNA searches of arrestee DNA violates the Fourth Amendment because arrestees have a reasonable expectation of privacy in the information that is extracted from a familial DNA search and it fails both the totality of the circumstances and the special needs tests. Further, these tests go against the intention of the Supreme Court when it legalized arrestee DNA collection as it specifically precluded the use of arrestee DNA collection in its Maryland v. King decision. [ABSTRACT FROM AUTHOR]

Prader–Willi Syndrome (PWS) is a human genetic condition that affects up to 1 in 10,000 live births. Affected infants present with hypotonia and developmental delay. Hyperphagia and increasing body weight follow unless drastic calorie restriction is initiated. Recently, our laboratory showed that one of the genes in the deleted locus causative for PWS, Snord116, maintains increased expression of hypothalamic Nhlh2, a basic helix–loop–helix transcription factor. We have previously also shown that obese mice with a deletion of Nhlh2 respond to a conjugated linoleic acid (CLA) diet with weight and fat loss. In this study, we investigated whether mice with a paternal deletion of Snord116 (Snord116m+/p−) would respond similarly. We found that while Snord116m+/p− mice and mice with a deletion of both Snord116 alleles were not significantly obese on a high-fat diet, they did lose body weight and fat on a high-fat/CLA diet, suggesting that the genotype did not interfere with CLA actions. There were no changes in food intake or metabolic rate, and only moderate differences in exercise performance. RNA-seq and microbiome analyses identified hypothalamic mRNAs, and differentially populated gut bacteria, that support future mechanistic analyses. CLA may be useful as a food additive to reduce obesity in humans with PWS. [ABSTRACT FROM AUTHOR]

Prader-Willi Syndrome (PWS) is a human genetic condition that affects up to 1 in 10,000 live births. Affected infants present with hypotonia and developmental delay. Hyperphagia and increasing body weight follow unless drastic calorie restriction is initiated. Recently, our laboratory showed that one of the genes in the deleted locus causative for PWS, Snord116 , maintains increased expression of hypothalamic Nhlh2 , a basic helix-loop-helix transcription factor. We have previously also shown that obese mice with a deletion of Nhlh2 respond to a conjugated linoleic acid (CLA) diet with weight and fat loss. In this study, we investigated whether mice with a paternal deletion of Snord116 ( Snord116 m+/p- ) would respond similarly. We found that while Snord116 m+/p- mice and mice with a deletion of both Snord116 alleles were not significantly obese on a high-fat diet, they did lose body weight and fat on a high-fat/CLA diet, suggesting that the genotype did not interfere with CLA actions. There were no changes in food intake or metabolic rate, and only moderate differences in exercise performance. RNA-seq and microbiome analyses identified hypothalamic mRNAs, and differentially populated gut bacteria, that support future mechanistic analyses. CLA may be useful as a food additive to reduce obesity in humans with PWS.

During September 3-November 16, 2020, daily confirmed cases of coronavirus disease 2019 (COVID-19) reported to the Wisconsin Department of Health Services (WDHS) increased at a rate of 24% per week, from a 7-day average of 674 (August 28-September 3) to 6,426 (November 10-16) (1). The growth rate during this interval was the highest to date in Wisconsin and among the highest in the United States during that time (1). To characterize potential sources of this increase, the investigation examined reported outbreaks in Wisconsin that occurred during March 4-November 16, 2020, with respect to their setting and number of associated COVID-19 cases., Competing Interests: All authors have completed and submitted the International Committee of Medical Journal Editors form for disclosure of potential conflicts of interest. No potential conflicts of interest were disclosed.