In adult patients with acute appendicitis, the risk of developing advanced pathology and postoperative complications increases with time; therefore, delayed appendectomy is unsafe. As delays in seeking medical help are difficult to control, prompt appendectomy is mandatory. Because these conclusions are derived from retrospective data, a prospective study is required to confirm their validity.
A review of 561 cases of cecal volvulus that were published between 1959 and 1989 along with 7 new cases, was performed to characterize the clinical and laboratory profile and to evaluate the various surgical options in treating this life-threatening condition. The age and sex distribution of these patients have changed over the years and shifted toward older patients (mean, 53 years) and female predominance (female:male ratio, 1.4:1). The clinical presentation was usually of distal closed-loop small bowel obstruction. Forty-six percent of the plain abdominal radiographs were suspected for cecal volvulus, but only 17 percent were diagnostic. Barium enema had a high rate of accuracy (88 percent) and was associated with minimal complications. True volvulus was 6 times more common than bascule, and gangrenous cecum was found in 20 percent of cases. Detorsion alone and cecopexy had almost similar complications, mortality, and recurrence rates (15, 10, and 13 percent, respectively), whereas, resection, which was performed primarily for gangrenous cecum, had higher rates. However, the highest rates of complications (52 percent), mortality (22 percent), and recurrence (14 percent) were noticed after cecostomy. These data suggest that resection should be reserved for patients with necrotic cecum and that detorsion is sufficient for patients with viable cecum. Cecostomy should be abandoned.
Endotoxin-induced microvascular lung injury in mice is a commonly used experimental model of the acute respiratory distress syndrome (ARDS). The present paper aimed to characterize this popular model in a comprehensive and systematic fashion. Male C57bl/6 mice (n = 5) were administered an LD55 dose of E. coli endotoxin (15 mg/kg, i.p.), and lungs were harvested at several time points and evaluated for injury as well as for expression of a variety of inflammatory mediators. Endotoxin induced many features characteristic of acute microvascular lung injury. These included early (1-2 h) expression of inflammatory mediators (IL-1alpha, IL-1beta, IL-4, IL-6, IL-10, TNF-alpha, interferon-alpha, interferon gamma, and MCP-1) and leukocyte accumulation in lung tissue (lung myeloperoxidase activity 18.5 +/- 7.8 U/g tissue, P < 0.05), followed by pulmonary edema (lung water content index 17.4% +/- 2.5%, P < 0.05) and mortality. Histopathological evaluation of lung tissue was compatible with these findings. The characterization of this murine model of endotoxin-induced microvascular injury will facilitate its utilization in ARDS research.
SUMMARYAdenosine-to-inosine (A-to-I) RNA editing is a post-transcriptional modi®cation of pre-mRNA catalysed by an RNA-speci®c adenosine deaminase (ADAR). A-to-I RNA editing has been previously reported in the pre-mRNAs of brain glutamate and serotonin receptors and in lung tissue during in¯ammation. Here we report that systemic in¯ammation markedly induces inosinecontaining mRNA to approximately 5% of adenosine in total mRNA. Induction was the result of upregulation of A-to-I RNA editing as both dsRNA editing activity and ADAR1 expression were increased in the spleen, thymus and peripheral lymphocytes from endotoxin-treated mice. Upregulation of ADAR1 was con®rmed in vitro in T lymphocytes and macrophages stimulated with a variety of in¯ammatory mediators including tumour necrosis factor-a and interferon-g. A late induction of RNA editing was detected in concanavalin A-activated splenocytes stimulated with interleukin-2 in vitro. Taken together, these data suggest that a large number of inosine-containing mRNAs are produced during acute in¯ammation via up-regulation of ADAR1-mediated RNA editing. These events may affect the in¯ammatory and immune response through modulation of protein production.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.