Construct and clinical verification of a nurse-led rapid response systems and activation criteria.

BACKGROUND: Effective team leadership and good activation criteria can effectively initiate rapid response system (RRS) to reduce hospital mortality and improve quality of life. The first reaction time of nurses plays an important role in the rescue process. To construct a nurse-led (nurse-led RRS) and activation criteria and then to conduct a pragmatic evaluation of the nurse-led RRS. METHODS: We used literature review and the Delphi method to construct a nurse-led RRS and activation criteria based on the theory of "rapid response system planning." Then, we conducted a quasi-experimental study to verify the nurse-led RRS. The control group patients were admitted from August to October 2020 and performed traditional rescue procedures. The intervention group patients were admitted from August to October 2021 and implemented nurse-led RRS. The primary outcome was success rate of rescue. SETTING: Emergency department, Gansu Province, China. RESULTS: The nurse-led RRS and activation criteria include 4 level 1 indicators, 14 level 2 indicators, and 88 level 3 indicators. There were 203 patients who met the inclusion criteria to verify the nurse-led RRS. The results showed that success rate of rescue in intervention group (86.55%) was significantly higher than that in control group (66.5%), the rate of cardiac arrest in intervention group (33.61%) was significantly lower than that in control group (72.62%), the effective rescue time of intervention group (46.98 ± 12.01 min) was shorter than that of control group (58.67 ± 13.73 min), and the difference was statistically significant (P < 0.05). The rate of unplanned ICU admissions in intervention group (42.85%) was lower than that in control group (44.04%), but the difference was not statistically significant (P > 0.05). CONCLUSIONS: The nurse-led RRS and activation criteria can improve the success rate of rescue, reduce the rate of cardiac arrest, shorten the effective time of rescue, effectively improve the rescue efficiency of patients.

Alpha/beta interferon receptor deficiency in mice significantly enhances susceptibility of the animals to pseudorabies virus infection.

Pseudorabies virus, one of the neurotropic viruses, can infect numerous mammals. In particular, pseudorabies virus infection of swine occurs worldwide, and is a major threat to swine industry. However, the mechanism underlying the interaction between pseudorabies virus and host innate immune system is not fully understood. Here, we investigated the involvement of interferon α/ß (IFN-α/ß) receptor (IFNAR) in the pathogenesis of pseudorabies virus in a mouse model. The results showed that IFNAR-deficient (IFNAR-/-) mice were highly susceptible to the virus infection, as evidenced by markedly reduced survival rate of infected animals and increased viral replication. The expression of IFN-α/ß and relevant interferon-stimulated genes in IFNAR-/- mice was significantly lower than that in wild-type (WT) littermates after the viral infection. Moreover, in response to the virus challenge, IFNAR-/- mice displayed elevated levels of inflammatory cytokines including interleukin 6 (IL-6) and IL-1ß, and IFNAR-/- cells showed increased phosphorylation of STAT3. Collectively, these data reveal that the IFNAR-/- mice are more sensitive to pseudorabies virus infection than WT animals, and excessive IL-6/STAT3 response in IFNAR-/- mice may contribute to the pathogenesis. Our findings suggest that type I IFNs/IFNAR-dependent homeostatic control of the innate immunity is required for host defense against pseudorabies virus infection.

Human T-cell lymphotropic virus type 1 and its oncogenesis.

Human T-cell lymphotropic virus type 1 (HTLV-1) is the etiologic agent of adult T-cell leukemia/lymphoma (ATL), a rapidly progressing clonal malignancy of CD4+ T lymphocytes. Exploring the host-HTLV-1 interactions and the molecular mechanisms underlying HTLV-1-mediated tumorigenesis is critical for developing efficient therapies against the viral infection and associated leukemia/lymphoma. It has been demonstrated to date that several HTLV-1 proteins play key roles in the cellular transformation and immortalization of infected T lymphocytes. Of note, the HTLV-1 oncoprotein Tax inhibits the innate IFN response through interaction with MAVS, STING and RIP1, causing the suppression of TBK1-mediated phosphorylation of IRF3/IRF7. The HTLV-1 protein HBZ disrupts genomic integrity and inhibits apoptosis and autophagy of the target cells. Furthermore, it is revealed that HBZ enhances the proliferation of ATL cells and facilitates evasion of the infected cells from immunosurveillance. These studies provide insights into the molecular mechanisms by which HTLV-1 mediates the formation of cancer as well as useful strategies for the development of new therapeutic interventions against ATL. In this article, we review the recent advances in the understanding of the pathogenesis, the underlying mechanisms, clinical diagnosis and treatment of the disease caused by HTLV-1 infection. In addition, we discuss the future direction for targeting HTLV-1-associated cancers and strategies against HTLV-1.

Involvement of Host Non-Coding RNAs in the Pathogenesis of the Influenza Virus.

Non-coding RNAs (ncRNAs) are a new type of regulators that play important roles in various cellular processes, including cell growth, differentiation, survival, and apoptosis. ncRNAs, including small non-coding RNAs (e.g., microRNAs, small interfering RNAs) and long non-coding RNAs (lncRNAs), are pervasively transcribed in human and mammalian cells. Recently, it has been recognized that these ncRNAs are critically implicated in the virus-host interaction as key regulators of transcription or post-transcription during viral infection. Influenza A virus (IAV) is still a major threat to human health. Hundreds of ncRNAs are differentially expressed in response to infection with IAV, such as infection by pandemic H1N1 and highly pathogenic avian strains. There is increasing evidence demonstrating functional involvement of these regulatory microRNAs, vault RNAs (vtRNAs) and lncRNAs in pathogenesis of influenza virus, including a variety of host immune responses. For example, it has been shown that ncRNAs regulate activation of pattern recognition receptor (PRR)-associated signaling and transcription factors (nuclear factor κ-light-chain-enhancer of activated B cells, NF-κB), as well as production of interferons (IFNs) and cytokines, and expression of critical IFN-stimulated genes (ISGs). The vital functions of IAV-regulated ncRNAs either to against defend viral invasion or to promote progeny viron production are summarized in this review. In addition, we also highlight the potentials of ncRNAs as therapeutic targets and diagnostic biomarkers.