Utilization of Single-Incision Laparoscopy in the Management of Ingested Magnets.

Background: A ban on neodymium magnets was lifted by the U.S. Consumer Product Safety Commission in 2016. Pediatric gastroenterologists and surgeons were increasingly tasked with removing these problematic objects. The purpose of this study was to assess the utility of single-incision laparoscopic surgery (SILS) in the management of ingested magnets. Patients and Methods: This is a single-center, retrospective assessment of surgical interventions for ingested magnets. International Classification of Disease, 10th revision codes were used to identify 349 patients ≤21 years of age evaluated for foreign body ingestion over a 4.5-year period. A medical record review helped isolate 29 (8.3%) magnet ingestions, 9 requiring surgical intervention. RedCap was used for analysis. Results: Of 9 surgical patients, 7 underwent SILS intervention by 1 surgeon. Another surgeon performed an open operation, whereas a third performed a multiport operation. Of the 7 SILS cases, 3 were completed without conversion to open. In one of these cases, bowel resection with primary anastomosis was performed. For SILS cases, average operating room time was 109 minutes (38-170 minutes), time to enteral feeds was 23 hours (0.28-79.2 hours), and hospital length of stay (LOS) was 3.8 days (1.96-6.68 days). Thirty-day readmission for SILS was 14.3%. No other complications were observed. Conclusions: SILS has been safely utilized for magnet retrieval. It offers an ability to identify the affected intestinal segment and an opportunity to intervene extracorporeally through an uncapped port. In addition, knowing where matted bowel is located can direct a limited incision during conversion to laparotomy. This may confer benefits of decreased pain, shortened time to enteral feeds, and decreased hospital LOS.

Institutional response to the 2022 iodinated contrast shortage: A narrative review.

INTRODUCTION: The iodinated contrast material (ICM) shortage of 2022 has affected healthcare systems worldwide, forcing institutions to adapt by implementing interventions to conserve ICM without compromising patient care. We aim to present the practices proven to be effective in reducing ICM consumption to improve resource allocation in trauma patients. METHODS: A literature search of PubMed, Google Scholar, and Cochrane was conducted. Studies investigating the utility of ICM in the management of trauma & emergency surgery patients, as well as institutional interventions that were implicated as a response to the ICM shortage of 2022 were included for review. RESULTS: Eight articles were selected and reviewed. The use of alternative, non-contrast-enhanced imaging modalities, particularly non-contrast-enhanced CT (NECT), was found to be effective in reducing ICM consumption. Other institutions have implemented strategies to reduce the ICM dose for each imaging study performed, including decreasing ICM dose itself as well as reducing tube voltage, which was shown to reduce ICM use by 50%. Waste minimization by splitting single-dose contrast vials into smaller aliquots utilized for multiple imaging studies has also been an effective method. Additionally, assembling a Radiology Command Center Team, responsible for monitoring ICM supplies while offering 24/7 consults regarding options for alternative imaging, has resulted in an overall reduction in contrast consumption of 50% in 7 days. CONCLUSION: In response to the ICM shortage of 2022, most healthcare institutions have found the use of alternative imaging modalities to be effective in reducing ICM consumption. Other effective measures include ICM dose reduction and ICM waste minimization.

Deletion of the herpes simplex virus 1 UL49 gene results in mRNA and protein translation defects that are complemented by secondary mutations in UL41.

Herpes simplex virus 1 (HSV-1) virions, like those of all herpesviruses, contain a protein layer termed the tegument localized between the capsid and the envelope. VP22, encoded by the U(L)49 gene, is one of the most abundant tegument proteins in HSV-1 virions. Studies with a U(L)49-null mutant showed that the absence of VP22 resulted in decreased protein synthesis at late times in infection. VP22 is known to form a tripartite complex with VP16 and vhs through direct interactions with VP16. Given that U(L)49-null mutants have been shown to acquire spontaneous secondary mutations in the U(L)41 gene, which encodes vhs, we hypothesized that VP22 and vhs may play antagonistic roles during HSV-1 infections. In the present study, we show that the protein synthesis defect observed in U(L)49-null virus infections was rescued by a secondary, compensatory frameshift mutation in U(L)41. A double mutant bearing a deletion of U(L)49 and a point mutation in vhs previously shown to specifically abrogate vhs's RNase activity also resulted in a rescue of protein synthesis. To determine whether the U(L)49(-) protein synthesis defect, and the rescue by secondary mutations in vhs, occurred at the mRNA and/or translational levels, quantitative reverse transcriptase PCR (qRT-PCR) and polysome analyses were performed. We found that the absence of VP22 caused a small decrease in mRNA levels as well as a defect in polysome assembly that was independent of mRNA abundance. Both defects were complemented by the secondary mutations in vhs, indicating functional interplay between VP22 and vhs in both accumulation and translation of viral mRNAs.

Deletion of UL21 causes a delay in the early stages of the herpes simplex virus 1 replication cycle.

The herpes simplex virus 1 (HSV-1) U(L)21 gene encodes a 62-kDa tegument protein with homologs in the alpha-, beta-, and gammaherpesvirus subfamilies. In the present study, we characterized a novel U(L)21-null virus and its genetic repair to determine whether this protein plays a role in early stages of the HSV-1 replication cycle. Single-step growth analyses, protein synthesis time courses, and mRNA quantifications indicated that the absence of U(L)21 results in a delay early in the HSV-1 replication cycle.