In December 2019, the 2019 novel coronavirus disease (COVID‐19) caused by Severe Acute Respiratory Syndrome Coronavirus‐2 (SARS‐CoV‐2) first emerged in Wuhan, China. This has now spread worldwide and was declared a pandemic by March 2020. Initially, the pediatric population was described as low risk for severe COVID‐19. However, reports have emerged recently of cases of COVID‐19 in children with a systemic inflammatory disease, with features that overlap with Kawasaki Disease (KD). We describe the first 15 cases with multi‐system inflammatory syndrome in children (MIS‐C), temporally related to COVID‐19, who presented for care to a tertiary pediatric referral center in New York City. We discuss the disproportionate burden of disease among Hispanic/Latino and black/African‐American ancestry, the distinct cytokine signature across the disease spectrum (IL‐1/IL‐6), and the potential role and pathogenesis of SARS‐CoV‐2 in this new clinical entity. This article is protected by copyright. All rights reserved.

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Studies over the past 35 years in the nonobese diabetic (NOD) mouse have shown that a number of agents can prevent or even reverse type 1 diabetes mellitus (T1DM); however, these successes have not been replicated in human clinical trials. Although some of these interventions have delayed disease onset or progression in subsets of participants, none have resulted in a complete cure. Even in the most robust responders, the treatments do not permanently preserve insulin secretion or stimulate the proliferation of β cells, as has been observed in mice. The shortfalls of translating NOD mouse studies into the clinic questions the value of using this model in preclinical studies. In this Perspectives, we suggest how immunological and genetic differences between NOD mice and humans might contribute to the differential outcomes and suggest ways in which the mouse model might be modified or applied as a tool to develop treatments and improve understanding of clinical trial outcomes.

A retrospective investigation of skin and soft tissue infections caused by community-associated methicillin-resistant Staphylococcus aureus (MRSA) strains among inmates in a Wisconsin correctional facility suggested a shift in MRSA genotype. Case timeline indicated a displacement of USA400 clone by USA300 clone. The USA300 index case was associated with an infected new tattoo.

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The receptor for advanced glycation endproducts (RAGE) is expressed in T cells after activation with antigen and is constitutively expressed in T cells from patients at-risk for and with type 1 diabetes mellitus (T1D). RAGE expression was associated with an activated T cell phenotype, leading us to examine whether RAGE is involved in T cell signaling. In primary CD4+ and CD8+ T cells from patients with T1D or healthy control subjects, RAGE-cells showed reduced phosphorylation of Erk. To study T cell receptor signaling in RAGE+ or-T cells, we compared signaling in RAGE+/+ Jurkat cells, Jurkat cells with RAGE eliminated by CRISPR/Cas9, or silenced with siRNA. In RAGE KO Jurkat cells, there was reduced phosphorylation of Zap70, Erk and MEK, but not Lck or CD3ξ. RAGE KO cells produced less IL-2 when activated with anti-CD3 +/-anti-CD28. Stimulation with PMA restored signaling and (with ionomycin) IL-2 production. Silencing RAGE with siRNA also decreased signaling. Our studies show that RAGE expression in human T cells is associated with an activated signaling cascade. These findings suggest a link between inflammatory products that are found in patients with diabetes, other autoimmune diseases, and inflammation that may enhance T cell reactivity.

Conflicts of interest: D. Bogunovic has given lectures for Genentech, Inc, owns stock in Lab11 Therapeutics, LLC, and acknowledges support from the National Institutes of Health (grant nos. AI127372 and AI148963) as well as the March of Dimes. C. Cunningham-Rundles has received consulting fees from CSL Behring, Momenta, Atara, Pharming, and UBC; served on boards for CSL Behring and Takeda Pharmaceutical Company Limited; serves on the Scientific Advisory Board of the Immune Deficiency Foundation; and received support from the National Institutes of Health (grant nos. AI 101093, AI-086037, and AI-48693) and the David S. Gottesman Immunology Chair.

Mini‐implants are titanium alloy rods implanted in the bone of the hard palate to help secure dental prostheses like dentures, fixed crowns, and bridge installations. Recent research suggests presurgical determination of bone density quality provides increased mini‐implant surgical success rates. In replication of these methods, we evaluated 19 tomographic scans of crania using Osirix 8.5 imaging software. Bone density was recorded at 90 separate coordinates using Hounsfield units, measured at three millimeter intervals (mediolaterally and anteroposteriorly starting at the incisive foramen.) The data was then analyzed for age differences and average bone density throughout different regions of the hard palate including intra‐ and interobserver analysis. Sex differences were closely investigated in this study because prior research has indicated that women may have a higher palatal bone density than men.Support or Funding InformationStudent Summer Scholars Grant, Office of Undergraduate Research, Grand Valley State University