Mycobacteriophages are viruses that infect mycobacterial hosts such as Mycobacterium smegmatis and Mycobacterium tuberculosis. All mycobacteriophages characterized to date are dsDNA tailed phages, and have either siphoviral or myoviral morphotypes. However, their genetic diversity is considerable, and although sixty-two genomes have been sequenced and comparatively analyzed, these likely represent only a small portion of the diversity of the mycobacteriophage population at large. Here we report the isolation, sequencing and comparative genomic analysis of 18 new mycobacteriophages isolated from geographically distinct locations within the United States. Although no clear correlation between location and genome type can be discerned, these genomes expand our knowledge of mycobacteriophage diversity and enhance our understanding of the roles of mobile elements in viral evolution. Expansion of the number of mycobacteriophages grouped within Cluster A provides insights into the basis of immune specificity in these temperate phages, and we also describe a novel example of apparent immunity theft. The isolation and genomic analysis of bacteriophages by freshman college students provides an example of an authentic research experience for novice scientists.

In this study, we explored whether topical application of antibodies targeting tumor necrosis factor‐α (TNF‐α) or interleukin‐6 (IL‐6) conjugated to hyaluronic acid (HA) could reduce the extension of necrosis by modulating inflammation locally in a partial‐thickness rat burn model. Partial‐thickness to deep partial‐thickness burn injuries present significant challenges in healing, as these burns often progress following the initial thermal insult, resulting in necrotic expansion and increased likelihood of secondary complications. Necrotic expansion is driven by a microenvironment with elevated levels of pro‐inflammatory mediators, and local neutralization of these using antibody conjugates could reduce burn progression. Trichrome‐stained tissue sections indicated the least necrotic tissue in (anti‐TNF‐α)‐HA‐treated sites, while (anti‐IL‐6)‐HA‐treated sites displayed similar outcomes to saline controls. This was confirmed by vimentin immunostaining, which demonstrated that HA treatment alone reduced burn progression by nearly 30%, but (anti‐TNF‐α)‐HA reduced it by approximately 70%. At all time points, (anti‐TNF‐α)‐HA‐treated sites showed reduced tissue levels of IL‐1β compared to controls, suggesting inhibition of a downstream mediator of inflammation. Decreased macrophage infiltration in (anti‐TNF‐α)‐HA‐treated sites compared to controls was elucidated by immunohistochemical staining of macrophages, suggesting a reduction in overall inflammation in all time points. These results suggest that local targeting of TNF‐α may be an effective strategy for preventing progression of partial‐thickness burns.

Nemaline myopathy is a rare inherited disorder characterized by weakness, hypotonia and depressed deep tendon reflexes. It is clinically and genetically heterogeneous, with the most severe phenotype presenting as perinatal akinesia, severe muscle weakness, feeding difficulties and respiratory failure, leading to early mortality. Pathogenic variants in twelve genes, encoding components of the sarcomere or factors related to myogenesis, have been reported in patients affected with the disorder. Here, we describe an early, lethal presentation of decreased fetal movements, hypotonia, muscle weakness, and neonatal respiratory failure requiring ventilator support in three siblings from a consanguineous family. All exhibited perinatal fractures, and thus, a skeletal dysplasia was considered as possibly contributing to the phenotype. However, whole exome sequencing revealed a homozygous, loss-of-function pathogenic variant in LMOD3, which has recently been associated with nemaline myopathy and, in a subset of patients, perinatal fractures. This case demonstrates the importance of considering congenital neuromuscular disorders in the differential diagnosis of perinatal fractures.

Catel-Manzke syndrome is a rare autosomal recessive disorder characterized by Pierre Robin sequence with hyperphalangy and clinodactyly of the index finger. Recently, homozygous or compound heterozygous pathogenic variants in TGDS have been discovered to cause Catel-Manzke syndrome. Here, we describe a 12-month-old male with molecularly confirmed Catel-Manzke syndrome who presented with Pierre Robin sequence (but without cleft palate) and hyperphalangy, and we compare his phenotype with the seven previously described patients with pathogenic variants in TGDS. Our patient is on the severe end of the phenotypic spectrum, presenting with respiratory complications and failure to thrive. Furthermore, our finding of a homozygous p.Ala100Ser pathogenic variant in our patient supports that it is a common mutation in Catel-Manzke syndrome.

Learning Objectives: After studying this article, the participant should be able to: 1. Describe surgical techniques associated with mastopexy and mastopexy augmentation. 2. Understand the evolution of mastopexy and augmentation mastopexy. 3. Address patient goals. 4. Achieve a favorable cosmetic outcome. Summary: The surgical techniques associated with mastopexy and mastopexy augmentation have continued to evolve. Traditional mastopexy techniques have included periareolar, circumvertical, and inverted-T patterns; however, adjuncts to these have included the use of various surgical mesh materials, implants, and fat grafting. This evidence-based article reviews how the techniques of mastopexy and augmentation mastopexy have evolved to best address patient goals and provide a favorable cosmetic outcome.