Abstract-Receptor-associated late transducer (RALT) is a feedback inhibitor of epidermal growth factor receptor signaling. RALT has been shown previously to be induced in the ischemic heart and to promote cardiomyocyte apoptosis in vitro. However, the role of RALT in cardiac hypertrophy remains unclear. We hypothesized that forced expression of RALT in the murine heart would protect the heart against cardiac hypertrophy in vivo. We investigated the effect of cardiac overexpression of rat RALT on cardiac hypertrophy induced by angiotensin II and isoproterenol in RALT transgenic mice and wild-type littermates. The extent of cardiac hypertrophy was assessed by 2D and M-mode echocardiography as well as by molecular and pathological analyses of cardiac samples. Constitutive expression of rat RALT in cardiac myocytes of murine heart attenuated both hypertrophic and inflammatory responses and preserved cardiac function. These beneficial effects were associated with the attenuation of the epidermal growth factor receptor-dependent cascade that was triggered by angiotensin II and isoproterenol stimulation. Additional evidence demonstrated that RALT expression blocked fibrosis in vivo and collagen synthesis in vitro. Therefore, cardiac overexpression of RALT improves cardiac function and inhibits maladaptive hypertrophy, inflammation, and fibrosis through attenuating epidermal growth factor receptor-dependent signaling. Key Words: RALT Ⅲ EGFR Ⅲ ERK1/2 Ⅲ cardiac hypertrophy Ⅲ heart failure Ⅲ fibrosis C ardiac hypertrophy is a response of the myocardium to increased workload, characterized by increased myocardial mass with extracellular matrix accumulation. 1,2 Although initially a beneficial adaptive response, prolonged hypertrophy may result in ventricular dilatation and heart failure. 3,4 One evolving concept is that the underlying signaling mechanism, rather than the presence of hypertrophy alone, may determine the functional outcome of cardiac hypertrophy. Thus, it is important to define and modulate the specific signaling mechanism activated by each hypertrophic stimulus and its effect on the cardiac phenotype.Epidermal growth factor receptor (EGFR) transactivation is an important step in the activation of downstream tyrosine kinases and serves as a scaffold for various signaling molecules in cardiac myocytes. 5 Inhibition of EGFR activation by its inhibitor AG1478 and the metalloproteinase inhibitor BB94 significantly attenuated cardiac hypertrophy in vitro and in vivo. 6,7 However, neither systemic effects of these interventions nor nonspecific effects of the chemical inhibitors can be excluded. Indeed, Kagiyama et al 8 showed that inhibition of EGFR by antisense oligonucleotides in mice caused a significant reduction of blood pressure, which could secondarily affect the extent of cardiac hypertrophy. These observations prompted us to investigate a molecular target that specifically blocks EGFR transactivation for inhibiting cardiac hypertrophy and heart failure. One such protein is receptor-associated late transduc...

Background Both midline catheters (MCs) and peripherally inserted central catheters (PICCs) can cause catheter‐related bloodstream infection (CRBSI), but the prevalence associated with each is not clear. Objective To compare the risk of CRBSI between MCs and PICCs with a meta‐analysis. Methods The Web of Science Core Collection, PubMed, Scopus, Embase, The Cochrane Library and ProQuest were searched. All studies comparing the risk of CRBSI between MCs and PICCs were included. Selected studies were assessed for methodological quality using the Downs and Black checklist. Two authors independently assessed the literature and extracted the data. A fixed effects model was used to generate estimates of CRBSI risk in patients with MCs versus PICCs. Publication bias was evaluated, and meta‐analyses were conducted with RevMan 5.3. Results A total of 167 studies were identified. Ten studies were collected, involving 33,322 patients. The prevalence of CRBSI with MCs and PICCs was 0.58% (40/6,900) and 0.48% (127/26,422), respectively. Meta‐analysis showed that the prevalence of CRBSI was not significantly different between MCs and PICCs (RR = 0.77, 95% CI: 0.50–1.17, p = .22). While the result showed that the prevalence of CRBSI with MCs was lower than that with PICCs (RR = 0.55, 95% CI: 0.33–0.92, p = .02) after poor‐quality studies were removed. The sensitivity analysis shows that the results from this meta‐analysis are fair in overall studies and non‐poor‐quality studies. All studies have no significant publication bias. Conclusions This study provides the first systematic assessment of the risk of CRBSI between MCs and PICCs and provides evidence for the selection of appropriate vascular access devices for intravenous infusion therapy in nursing. The prevalence of CRBSI was not significantly different between them.

Objective. To study the association between sleep duration and the incidence of type 2 diabetes mellitus (T2DM) and to provide a theoretical basis for the prevention of T2DM through a meta-analysis. Methods. PubMed, Web of Science, Scopus, Embase, Cochrane Library, ProQuest, CNKI, Wanfang, VIP, and SINOMED were searched from their inception until May 2020. All cohort studies on the relationship between sleep duration and T2DM in adults were included. According to the inclusion and exclusion criteria, two authors independently assessed the literature and extracted the data. Metaregression and publication bias were evaluated, and sensitivity and meta-analyses were conducted with RevMan 5.3. Results. A total of 17 studies were collected, involving 737002 adults. The incidence of T2DM was 4.73% in short sleep duration (SSD) ( t ≤ 6   h ), 4.39% in normal sleep duration (NSD) ( 6   h < t < 9   h ), and 4.99% in long sleep duration (LSD) ( t ≥ 9   h ). The meta-analysis demonstrated that SSD increased the risk of T2DM compared with NSD ( RR = 1.22 , 95% CI: 1.15-1.29, P < 0.001 ), LSD increased the risk of T2DM compared with NSD ( RR = 1.26 , 95% CI: 1.15-1.39, P < 0.001 ), and the risk of T2DM has no significant difference between SSD and LSD ( RR = 0.97 , 95% CI: 0.89-1.05, P = 0.41 ). The sensitivity of each study was robust and the publication bias was weak. Conclusion. SSD or LSD can increase the risk of T2DM.