The mini-midline catheter is a new technology for catheter placement that opens up a new field of peripheral venous access devices(PVADs)and plays an important role in the intravenous treatment of patients with fragile vasculature and difficult intravenous access(DIVA).Mini-midline catheter is more economical and easier to puncture than midline catheter,longer retention time than short cannula,lower catheter-related complications,it is the preferred solution for venous vascular access device(VAD)in short-to medium-term infusion and has been widely used in intravenous infusion abroad.Domestic research and application of this technology are still in the exploratory stage,and the specifications,guidelines and expert consensus for mini midline catheters have not yet been released,and there is a lack of standardized operation procedures,indications,contraindications and other guidelines.More studies with higher quality and multi-center linkage cooperation need to be carried out to provide a theoretical and practical basis for the formulation of industry standards for mini midline catheters in line with clinical practice.The definition,attributes,innovation,indications,advantages and disadvantages of the mini midline catheter were reviewed,so as to provide reference for clinical application.

Post-acute pancreatitis diabetes is one of the most common distant complications of acute pancreatitis. However, its incidence has been underestimated for a long time, indicating that it has not been taken seriously by healthcare professionals in clinical practice. This article provides a review of the urgent need for healthcare professionals to focus on the current status, adverse outcomes, screening and management aspects of diabetes after acute pancreatitis, and aims to provide a reference for healthcare professionals in their relevant clinical work.

Sleep is essential for the maintenance of human normal functions.Nowadays,the occurrence of active sleep deprivation(ASD)or passive sleep depriva-tion(PSD)is becoming more and more common due to the inability of the body adapting to the rapid changes in the internal and external environment.SD is not only an action,a brief process or a result,but also a directly or indirectly sustained state,which is associated to sleep time,circadian rhythm or sleep quality.SD can lead to numerous adverse effects on the body,such as sleep-related acute and chronic diseases.Long-term SD increases the risk of neurological and cardiovascular dis-eases as well as immune system dysfunction.In addi-tion,SD may affect the reproductive health of the body,giving rise to a series of potential fertility problems.In recent years,the correlation research and mechanism between SD and the related diseases have become a focus of scholars' attention.Numerous lines of evidence suggest that pathological sleep,such as insomnia and sleep apnea syndrome,is associated with impaired repro-ductive function.Disruptions in the circadian rhythm can also lead to impaired hypothalamic-pituitary-gonadal(HPG)axis function and thereby interfere with the repro-ductive process.Our research team has demonstrated that SD significantly affects the fertility of male and female rats and has adverse effects on reproduction.By new generation sequencing(NGS)and RT-PCR verifica-tion,we have identified differently expressed genes that are involved in mediating the effect of SD on fertility.However,the mechanisms and biological macromolecules regulated by SD are worthy of being further explored.This paper provides a brief review of SD research and then focuses on the adverse impact of SD on fertility,conducting a literature review to sort out the ideas and pro-vide references for research in this field.

Endoplasmic reticulum stress(ERS)is closely related to the mechanisms of multiple diseases,and regulation of ERS has become a therapeutic target for several diseases.Previous studies by our group have demonstrated that ERS can be alleviated and neuronal cells can be protected by downregulating ERS-related proteins such as GRP78,caspase12 and caspase3.The research on ERS inhibitors has progressed rapidly in recent years,and they can be classified into various types such as molecular chaperones,small molecule compounds and natural products,such as 4-phenylbutyric acid(4-PBA),tauroursodeoxycholic acid(TUDCA)and tumor necrosis factor α-stimulating factor 6(TSG-6),etc.These inhibitors can regulate the ERS signaling pathway through different pathways,such as:silent information regulator 1(SIRT1)promotes the expression of anti-apop-totic proteins by inhibiting the PERK-eIF2α-ATF4-CHOP pathway,thus reducing apoptosis.In addition,SIRT1 deacetylates XBP-1,regulates the IRE1α-XBP1 signaling pathway,and inhibits the expressions of GRP78 and CHOP,thereby reducing the protein load of endoplasmic reticulum(ER)and alleviating ERS;PDE4 inhibitor regu-lates c-Jun-mediated apoptotic pathway,reduces the interaction between IRE1 and TRAF2,and attenuates the level of c-Jun phosphorylation,thereby restoring ER homeostasis.In addition,PDE4 inhibitor activates the antioxidant-acting Nrf-2 pathway,decreases the concen-tration of intracellular calcium ion and reduces the pro-duction of ROS;TSG-6 exerts anti-inflammatory effects by regulating the secretion of inflammatory factors through PERK-eIF-2α-NF-κB p65 and IRE1α-TRAF2-NF-κB p65 signaling pathways.In-depth exploration of the potential mechanism of action of ERS inhibitors is of great signifi-cance for finding ways to treat related diseases by regu-lating ERS.

OBJECTIVE To investigate the mecha-nism of endoplasmic reticulum stress in cerebral isch-emic stroke from a theoretical perspective based on net-work pharmacology.METHODS GeneCards and OMIM databases were used to screen out the related targets of cerebral ischemic stroke and endoplasmic reticulum stress.And Venny2.1.0 was used to draw Venn's diagram to get the intersecting genes between cerebral ischemic stroke and endoplasmic reticulum stress.String data-base was used to get the protein-protein interaction(PPI)diagram and cytoscape was used for visualization analy-sis.The key genes were screened out by cytohubba plug-in,and enrichment analysis was performed.RESULTS Network pharmacology showed that there were 3744 cerebral ischemic stroke-related targets and 8675 endo-plasmic reticulum stress-related targets.After screening,41 common targets were got.There were 37 nodes,390 edges in the PPI network,namely,there were 37 interact-ing proteins and 390 interacting relationships.The key genes identified by cytohubba plug-in were IL-6,ALB,INS,TNF,AKT1,CASP3,MAPK3,TP53,SIRT1 and VEGF.The biological process involves reaction to oxida-tive stress,the regulation of neuron death,and negative regulation of cell differentiation,etc.;cellular components were related to the membrane raft,smooth endoplasmic reticulum,endoplasmic reticulum lumen and other com-ponents;molecular function aspects were related to sig-naling receptor activator activity,chaperone binding and protease binding.Enrichment analysis of pathway revealed that the intersecting targets were involved in PI3K/Akt pathway and protein processing in endoplasmic reticulum,etc.CONCLUSION The endoplasmic reticu-lum stress in cerebral ischemic stroke is related to the bi-ological processes of reaction to oxidative stress,the reg-ulation of neuron death,and negative regulation of cell differentiation,the mechanism may be related to neuroin-flammation and apoptosis.

During cerebral ischemia-reperfusion injury(CIRI),endoplasmic reticulum stress(ERS)leads to the development and progression of a series of deleterious physiological responses such as oxidative stress,dis-turbed calcium ion homeostasis,inflammation,apoptosis and autophagy.The unfolded protein response(UPR)is the main pathway activated by ERS,which regulates the expression of related factors within the endoplasmic reticu-lum(ER)and reduces protein translation levels.Prolonged and intense ERS may lead to cell death.Excessive ERS induces apoptosis mediated by C/EBP homologous pro-tein(CHOP),caspase-12 and c-Jun N-terminal kinase(JNK),thereby exacerbating brain damage.The thresh-old for the transition from adaptive mechanisms to apop-totic mechanisms during ERS depends on multiple fac-tors,including the cell status and environment,signaling pathway activity status,cumulative cascade,and the dose and time of ERS inducers.Further research is needed to completely elucidate the mechanism of ERS.Although the factors associated with the PERK and ATF6 path-ways are less extensively studied,their regulators still exist.Deficiency of protein tyrosine phosphatase 1B(PTP1B)leads to increased phosphorylation of PERK-eIF2α,while regulation of the proteasome and regulation of the XBP1 target gene WFS1 may also affect ATF6 sta-bility.In addition,differences in the structure,gene expres-sion,and metabolism of different types of neurons,as well as in their internal environment,may lead to differ-ences in their response to and impact on ERS.Differenc-es in UPR signaling pathways occur in hippocampal neurons and medial thalamic cells,and Purkinje cells and pyramidal cells may be more sensitive to ERS than other types of neurons.Our group's previous study found that ERS induced apoptosis in neurons after the onset of CIRI by regulating proteins such as GRP78,CHOP and caspase-12,but the effects of UPR activation on different cells need to be further investigated.

Objective:To understand the status quo of the job preparedness among newly recruited nurses and analyze its influencing factors.Methods:Totally 355 newly recruited nurses who joined 5 Class Ⅲ Grade A hospitals nationwide between September 2021 and September 2022 were selected by convenience sampling and investigated by general information surveys, the Work Readiness Scale for Graduate Nurses and the Transition Shock of Newly Graduated Nurses Scale. Logistic regression was employed to analyze the influencing factors of the job preparedness among these newly recruited nurses.Results:A total of 355 questionnaires were distributed, and 350 valid responses were received, with a valid response rate of 98.6%. The overall score for the job preparedness of the newly recruited nurses was (271.05±49.97), with a standardized total score of (73.26±13.57). 208 individuals (59.4%) scored high (standardized total score ≥70), while 142 individuals (40.6%) scored low (standardized total score<70). Logistic regression analysis revealed that the department of employment, part-time job experience, harmonious relationships with classmates during schooling, and the level of transition shock were influencing factors for the job preparedness of the newly recruited nurses ( P<0.05) . Conclusions:The job preparedness of newly recruited nurses is influenced by various factors. Nursing educators and managers should adopt targeted educational and management strategies based on the nurses' different experiences, interpersonal relationships, department of employment, and level of transition shock to enhance their job preparedness.

Objective:To clarify peripheral Th17 level in SSc patients and its correlation with disease.Methods:Chinese databases CNKI, CBM, Wanfang and VIP, and English databases PubMed, EMBASE, Web of Science, Cochrane Library and Science Direct were searched to collect a case-control study on the content of Th17 cells in peripheral blood of patients with SSc. The papers published when the database was first developed in 25 February 2021. Meta-analysis was conducted using Stata 12.0 software, and I2 and Egger tests were used to evaluate the heterogeneity and publication bias between studies. Results:A total of 26 case-controls were included in the study, including 1 160 patients with SSc and 778 healthy controls. Overall, the percentage of Th17 cells in SSc patients was higher than in healthy controls [SMD(95% CI)=1.85 (1.33, 2.38), P<0.001], which was most significant in IL-17 +Th17 concentration [SMD(95% CI)=1.88 (1.28, 2.48), P<0.001]. As for disease activity, the proportion of Th17 cells in active SSc patients was much higher than those of patients in remission [SMD(95% CI)=1.92 (1.12, 2.71), P<0.001]. SSc patients had a reduced Th17 level after receiving DMARDs treatment [SMD(95% CI)=-0.74 (-1.05, -0.42), P=0.029]. Conclusion:The number of Th17 cells increase significantly in the peripheral blood of patients with SSc, and is related to disease activity. DMARDs can be used to treat this disease by downregulating Th17 levels.

Objective:To explore the characteristics of intestinal microbiota in patients with systemic lupus erythematosus (SLE), and further explore the relationship between microbiota and CD4 +T lymphocyte subsets and disease activity. Methods:Fecal samples were collected from 96 patients with SLE, and 96 sex- and age-matched healthy controls (HCs). The gut microbiota were investigated via 16s rRNA sequencing. Flow cytometry was used to detect peripheral CD4 +T lymphocyte subsets of Th1, Th2, Th17 and Treg cells. Indicators of disease activity such as erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), complement C3 and C4, Systemic lupus erythematosus disease activity index(SLEDAI) for each patient were recorded. Differential abundance analysis was carried out using the edgeR algorithm. The Wilcoxon rank-sum test was used to compare alpha diversity indices, bacterial abundances, and the F/B ratio between groups. R (version 4.0.1) was used for comparative statistics, and Pearson′s correlation analysis was used to assess the correlations between the relative abundances of bacterial genera and serum levels of ESR, CRP, C3 and C4 in the samples. Results:The alpha estimators of richness (ACE and Chao 1) were significantly reduced in SLE feces samples compared with those of HCs ( P<0.01). Bacterial diversity estimators, including the Shannon ( P<0.01) and Simpson′s ( P<0.01) indices, were also significantly lower in SLE. Significant differences in gut microbiota composition between SLE and HCs were found using the edgeR algorithm. Compared with HC, 24 species of bacteria were significantly different in SLE patients at the genus level ( P<0.05). Moreover, there was a significant positive correlation between CRP and Coprococcus ( r=0.30, P=0.014), C4 and Corynebacterium ( r=0.31, P=0.013) and Faecalibacterium( r=0.25, P=0.048), Hemoglobin and Morganella( r=0.41, P=0.001), as well as SLIDA and Corynebacterium( r=0.25, P=0.047). In terms of lymphocyte subsets, there was significant positive correlation between B cells, Treg cells and Eubacterium eligens group, as well as CD8 +T, CD4 +T, NK cells and Corynebacterium. In additional, Th1 was positively correlated with Shigella Escherichia coli ( r=0.52, P=0.008), and Th2 was positively correlated with Dielma ( r=0.51, P<0.001). Conclusion:The abundance and diversity of intestinal flora in SLE patients were significantly reduced, and the differentially expressed bacteria were closely related to the CD4 +T lymphocyte subsets and disease activity indicators of patients.

Objective:To identify differentially expressed genes (DEGs) associated with the progression of synovitis in RA by using bioinformatics analysis and explore the effects of DMARDs such as methotrexate, tocilizumab and rituximab on the DEGs in RA synovium.Methods:RA expression profile microarray data GSE7307、GSE12021、GSE55457、GSE55235、GSE77298、GSE89408 were acquired from the public gene chip database (GEO), including 113 synovial tissue samples from RA and 70 healthy controls (HC). At the same time, synovial expression microarrays GSE45867, GSE24742 and GSE97165 after DMARDs treatment were obtained. These data included 8 samples treated with methotrexate, 12 treated with tocilizumab, 12 treated with rituximab and 19 treated with combined tDMARDs. R software was used to screen DEGs and Venn plots using gene ontology function enrichment and Kyoto encyclopedia of genes and genomes pathway enrichment analysis. Hub genes were selected by STRING online analysis tool and Cytoscape software.Results:Compared with HC, 797 DEGs were up-regulated and 434 DEGs were down-regulated in the synovial tissue of RA. These DEGs were mainly enriched in T cell activation, immune response-activating cell surface receptor signaling pathway. Using Cytoscape and cytoHubba to obtain 5 sets of DEGs based on the STRING database model, the degree algorithm screened out 10 hub genes: LCK, SYK, PTPRC, HLA-DRA, LYN, NCAPG, TOP2A, JUN, CXCR4, CCNB1. Methotrexate treatment significantly up-regulated 20 DEGs and down-regulated 30 DEGs. Rituximab treatment up-regulated 100 DEGs and down-regulated 55 DEGs. Tocilizumab treatment up-regulated 91 DEGs and down-regulated 317 DEGs. These altered DEGs were enriched in regulating cell adhesion, leukocyte-cell adhesion, leukocyte transfer, and insulin-like growth factor receptor signaling pathways. It was worth noting that after treatment, a total of 306 high-expressing DEGs were down-regulated, and 36 low-expressing DEGs were up-regulated.Conclusion:LCK, insulin-like growth factor receptor signaling pathway, etc. are the responsible molecular mechanisms and key pivot genes for the occurrence and development of RA, and the treatment of DMARDs, which are closely related to the response of RA to the treatment of DMARDs.