Using a Military-Civilian Partnership to Enhance Clinical Readiness and Sustainment for Air Force Critical Care Nurses.

BACKGROUND: Decreases in size, capability, clinical volumes, case mixes, and complex care opportunities in military treatment facilities contribute to the atrophy of clinical skills among medical professionals in these facilities. LOCAL PROBLEM: The COVID-19 pandemic resulted in a 39% decline in admissions to a military critical care unit. The decrease in patient census contributed to skill sustainment challenges. METHODS: To identify methods to combat skill atrophy, the CINAHL and PubMed databases were searched using the terms peacetime effect, military-civilian partnership, and skill sustainment. Active-duty critical care nurses stationed at a military treatment facility implemented a military-civilian partnership with a civilian medical facility for clinical skill sustainment. RESULTS: One year after implementation, 39 critical care nurses had completed 511 shifts, gaining clinical experiences seldom achieved at the military facility. A survey of these nurses demonstrated that 8 of 17 (47%) gained experience treating patients requiring intra-aortic balloon pumps or continuous renal replacement therapy, 6 of 17 (36%) gained experience with patients requiring a ventricular assist device, 12 of 17 (71%) acquired hands-on experience with intracranial pressure monitoring, and 14 of 17 (82%) reported vasoactive intravenous infusion manipulation. CONCLUSIONS: This article highlights the importance of evaluating clinical practice within the military health system, developing military-civilian partnerships, and removing military-civilian partnership barriers for nurses and other health care professionals. Failure to implement military-civilian partnerships may adversely affect the clinical competency of the military nurse force.

Social Determinant of Unconventional Resilience: Tactical Engagement in Medical-Martial Creativity.

Building on our strategic framework and operational model, we will discuss findings from our ethnographic study entitled, "The Impact of Catastrophic Injury Exposure on Resilience in Special Operations Surgical Teams (SOST)." Our goal is to establish that medical-martial creativity supports Special Operation Forces (SOF) medics' ability to fluidly modulate pressure amid real-time military medical decision-making in austere environments. We will use qualitative quotes to explore how SOST medics express medical-martial creativity in support of unconventional resilience. We continue to highlight tactical engagement by using bag sets as a metaphor for understanding the practical performance of this social determinant. To achieve our goals, we will: 1) define the social determinant of medical-martial creativity and provide a brief background on creativity; 2) thematize various ways in which medical-martial creativity is optimized or degraded; and 3) relate tactical engagement with medical-martial creativity to our metaphor of bag sets. We conclude by gesturing to how medical-martial creativity enables SOF medics' ingenuity, which allows them to freely maneuver complex real-time decision-making to support SOF mission success.

Impaired insulin-stimulated glucose transport in ATM-deficient mouse skeletal muscle.

There are reports that ataxia telangiectasia mutated (ATM) plays a role in insulin-stimulated Akt phosphorylation, although this is not the case in some cell types. Because Akt plays a key role in insulin signaling, which leads to glucose transport in skeletal muscle, the predominant tissue in insulin-stimulated glucose disposal, we examined whether insulin-stimulated Akt phosphorylation and (or) glucose transport would be decreased in skeletal muscle of mice lacking functional ATM, compared with muscle from wild-type mice. We found that in vitro insulin-stimulated Akt phosphorylation was normal in soleus muscle from mice with 1 nonfunctional allele of ATM (ATM+/-) and from mice with 2 nonfunctional alleles (ATM-/-). However, insulin did not stimulate glucose transport or the phosphorylation of AS160 in ATM-/- soleus. ATM protein level was markedly higher in wild-type extensor digitorum longus (EDL) than in wild-type soleus. In EDL from ATM-/- mice, insulin did not stimulate glucose transport. However, in contrast to findings for soleus, insulin-stimulated Akt phosphorylation was blunted in ATM-/- EDL, concomitant with a tendency for insulin-stimulated phosphatidylinositol 3-kinase activity to be decreased. Together, the findings suggest that ATM plays a role in insulin-stimulated glucose transport at the level of AS160 in muscle comprised of slow and fast oxidative-glycolytic fibers (soleus) and at the level of Akt in muscle containing fast glycolytic fibers (EDL).

Reduced endothelin converting enzyme-1 and endothelin-3 mRNA in the developing bowel of male mice may increase expressivity and penetrance of Hirschsprung disease-like distal intestinal aganglionosis.

Hirschsprung disease (distal intestinal aganglionosis, HSCR) is a multigenic disorder with incomplete penetrance, variable expressivity, and a strong male gender bias. Recent studies demonstrated that these genetic patterns arise because gene interactions determine whether enteric nervous system (ENS) precursors successfully proliferate and migrate into the distal bowel. We now demonstrate that male gender bias in the extent of distal intestinal aganglionosis occurs in mice with Ret dominant-negative mutations (RetDN) that mimic human HSCR. We hypothesized that male gender bias could result from reduced expression of a gene already known to be essential for ENS development. Using quantitative real-time polymerase chain reaction (PCR) we demonstrated reduced levels of endothelin converting enzyme-1 and endothelin-3 mRNA in the male mouse bowel at the time that ENS precursors migrate into the colon. Other HSCR-associated genes are expressed at comparable levels in male and female mice. Testosterone and Mullerian inhibiting substance had no deleterious effect on ENS precursor development, but adding EDN3 peptide to E11.5 male RetDN heterozygous mouse gut explants in organ culture significantly increased the rate of ENS precursor migration through the bowel.

Differential gene expression and functional analysis implicate novel mechanisms in enteric nervous system precursor migration and neuritogenesis.

Enteric nervous system (ENS) development requires complex interactions between migrating neural-crest-derived cells and the intestinal microenvironment. Although some molecules influencing ENS development are known, many aspects remain poorly understood. To identify additional molecules critical for ENS development, we used DNA microarray, quantitative real-time PCR and in situ hybridization to compare gene expression in E14 and P0 aganglionic or wild type mouse intestine. Eighty-three genes were identified with at least two-fold higher expression in wild type than aganglionic bowel. ENS expression was verified for 39 of 42 selected genes by in situ hybridization. Additionally, nine identified genes had higher levels in aganglionic bowel than in WT animals suggesting that intestinal innervation may influence gene expression in adjacent cells. Strikingly, many synaptic function genes were expressed at E14, a time when the ENS is not needed for survival. To test for developmental roles for these genes, we used pharmacologic inhibitors of Snap25 or vesicle-associated membrane protein (VAMP)/synaptobrevin and found reduced neural-crest-derived cell migration and decreased neurite extension from ENS precursors. These results provide an extensive set of ENS biomarkers, demonstrate a role for SNARE proteins in ENS development and highlight additional candidate genes that could modify Hirschsprung's disease penetrance.