Objective The c-Jun NH2-terminal kinases (JNK) are regulated by a wide variety of cellular stresses and have been implicated in apoptotic signaling. Macrophages express two JNK isoforms, JNK1 and JNK2, which may have different effects on cell survival and atherosclerosis. Approach and Results To dissect the impact of macrophage JNK1 and JNK2 on early atherosclerosis, Ldlr−/− mice were reconstituted with wild type (WT), Jnk1−/− and Jnk2−/− hematopoietic cells and fed a high-cholesterol diet. Jnk1−/−→Ldlr−/− mice have larger atherosclerotic lesions with more macrophages and fewer apoptotic cells than mice transplanted with WT or Jnk2−/− cells. Moreover, genetic ablation of JNK to a single allele (Jnk1+/−/Jnk2−/− or Jnk1−/−/Jnk2+/−) in marrow of Ldlr−/− recipients further increased atherosclerosis compared to Jnk1−/−→Ldlr−/− and WT→Ldlr−/− mice. In mouse macrophages, anisomycin-mediated JNK signaling antagonized Akt activity, and loss of Jnk1 gene obliterated this effect. Similarly, pharmacological inhibition of JNK1, but not JNK2, markedly reduced the antagonizing effect of JNK on Akt activity. Prolonged JNK signaling in the setting of ER stress gradually extinguished Akt and Bad activity in WT cells with markedly less effects in Jnk1−/− macrophages, which were also more resistant to apoptosis. Consequently, anisomycin increased and JNK1 inhibitors suppressed ER stress-mediated apoptosis in macrophages. We also found that genetic and pharmacologic inhibition of phosphatase and tensin homolog (PTEN) abolished the JNK-mediated effects on Akt activity, indicating that PTEN mediates crosstalk between these pathways. Conclusions Loss of Jnk1, but not Jnk2, in macrophages protects them from apoptosis increasing cell survival and this accelerates early atherosclerosis.

Purpose of Review As the prevalence of diabetes mellitus in the USA continues to rise, so does the popularity of diabetes management devices such as continuous glucose monitors (CGMs) and insulin pumps. The use of this technology has been shown to improve outpatient glycemic outcomes and quality of life and oftentimes may be continued in the hospital setting. Our aim is to review the current guidelines and available evidence on the continuation of insulin pumps and CGMs in the inpatient setting.Recent Findings Patients with diabetes are at higher risk for hospitalizations and complications due to hyper-or hypoglycemia, metabolic co-morbidities, or as seen recently, more severe illness from infections such as SARS-CoV-2. The maintenance of euglycemia is important to decrease both morbidity and mortality in the hospital setting. There is consensus among experts and medical societies that inpatient use of diabetes technology in carefully selected patients with proper institutional protocols is safe and can improve inpatient glycemic outcomes and reduce hypoglycemia. During the COVID-19 pandemic, CGMs played a vital role in managing hyperglycemia in some hospitalized patients. Summary Insulin pumps and CGMs have the potential to transform glycemic management in hospitalized patients. In order for institutions to safely and effectively incorporate these technologies on their inpatient units, hospital-based providers will need to be able to understand how to manage and utilize these devices in their practice in conjunction with diabetes experts.