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.

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).