What influences newly graduated registered nurses' intention to leave the nursing profession? An integrative review.

BACKGROUND: Newly graduated registered nurses leaving the nursing profession in the early stages of their career have enormous financial and time implications for nursing organizations and affect the quality of nursing care. OBJECTIVE: To identify the factors influencing newly graduated registered nurses' intention to leave the nursing profession over the past 10 years. METHODS: The framework developed by Whittemore and Knafl was used to conduct this integrative review. An electronic search was conducted for English articles to identify research studies published between 2011-2022 using the following databases of PubMed, MEDLINE, CINAHL, PsycINFO, and Scopus. Eligible publications were critically reviewed and scored using the Critical Appraisal Skills Program Checklist and the Center for Evidence-Based Management appraisal. RESULTS: Twenty-one studies were analyzed. The main factors affecting newly graduated registered nurses' intention to leave the nursing profession included demographic factors (age, educational level, year of experience, professional title, employment status, health status, shift, hospital location and size), supervisor and peer support, challenges in the workplace, cognitive and affective response to work, work environment (collegial nurse-physician relations, insufficient staffing level, person-work environment fit), gender stereotypes, autonomous motivation, role models, and resilience. CONCLUSIONS: The factors affecting newly graduated registered nurses' intention to leave the nursing profession are multifaceted and should receive continuous attention from nurse managers. The findings provide more comprehensive for nurse administrators to develop intervention strategies to mitigate newly graduated registered nurses' turnover intention.

Global, regional, and national epidemiology of migraine and tension-type headache in youths and young adults aged 15-39 years from 1990 to 2019: findings from the global burden of disease study 2019.

BACKGROUND: In recent years, headache disorders have garnered significant attention as a pressing global health issue. This concern is especially pronounced in low- to middle-income countries and exhibits a notable increase in prevalence among adolescents and young adults. Such a surge in these disorders has invariably diminished the quality of life for affected individuals. Despite its global impact, comprehensive studies exploring the ramifications of headache disorders in the younger population remain scant. Our study endeavored to quantify the global prevalence of headache disorders in individuals between the ages of 15 and 39, over a three-decade span from 1990 to 2019. METHODS: Our study, conducted from 1990 to 2019, evaluated the impact of headache disorders, specifically migraines and tension-type headaches (TTH), in 204 different countries and territories. This comprehensive assessment included a detailed analysis of incidence rates, prevalence, and disability-adjusted life-years (DALYs) across various demographics such as age, gender, year, geographical location, and Socio-demographic Index (SDI). RESULTS: In 2019, there were an estimated 581,761,847.2 migraine cases globally (95% UI: 488,309,998.1 to 696,291,713.7), marking a 16% increase from 1990. Concurrently, TTH cases numbered at 964,808,567.1 (95% UI: 809,582,531.8 to 1,155,235,337.2), reflecting a 37% rise since 1990. South Asia reported the highest migraine prevalence with 154,490,169.8 cases (95% UI: 130,296,054.6 to 182,464,065.6). High SDI regions exhibited the most substantial migraine prevalence rates both in 1990 (22,429 per 100,000 population) and 2019 (22,606 per 100,000 population). Among the five SDI classifications, the middle SDI region recorded the highest tally of TTH cases in both 1990 (210,136,691.6 cases) and 2019 (287,577,250 cases). Over the past 30 years, East Asia experienced the most pronounced surge in the number of migraine cases. On the whole, there was a discernible positive correlation between the disease burden of migraine and TTH and the SDI. CONCLUSION: Migraine and TTH represent formidable challenges in global health. The intensity of their impact exhibits marked disparities across nations and is distinctly elevated among women, individuals within the 30-39 age bracket, and populations characterized by a high SDI. The results of our research emphasize the imperative of assimilating migraine and TTH management into contemporary healthcare paradigms. Such strategic integration holds the potential to amplify public cognizance regarding pertinent risk factors and the spectrum of therapeutic interventions at hand.

Association between dietary theobromine with depression: a population-based study.

OBJECTIVE: The purpose of this study is to investigate the possible link between dietary theobromine intake and symptoms of depression. MATERIALS AND METHODS: These results are based on the responses of 3637 people who took part in the National Health and Nutrition Examination Survey in 2017-2018. Participants' daily theobromine intake was determined using a 24-h food questionnaire from the 2017-2018 cycle. Presence of depression was defined as a score of 5 or above on the Patient Health Questionnaire. Association between theobromine intake and depression was examined using a multivariate logistic regression adjusting for several relevant sociodemographic, lifestyle and health-related factors. RESULTS: A total of 6903 participants were included in the study. The results of multivariate logistic regression showed a correlation between depressive symptoms and theobromine intake (OR:1.17, 95%CI:1.02-1.34). CONCLUSIONS: Our cross-sectional population based study suggests that increased theobromine intake is associated with increased risk for depression. Nevertheless, more investigations are needed to confirm our findings.

The association of healthy eating index with periodontitis in National Health and Nutrition Examination Study 2011-2012.

Aim: Periodontitis is a chronic inflammatory disorder caused by periodontopathic bacteria that causes inflammation of the supporting tissues around teeth. Previous studies have found that daily dietary nutritional intake can influence the development of periodontal disease. However, research on the Healthy Eating Index's involvement in periodontitis is limited. The purpose of this study was to look at the link between the Healthy Eating Index and periodontitis. Methods and design: We examined data from the National Health and Nutrition Examination Study (NHANES), a nationally representative survey that was performed in 2-year cycles from 2011 to 2012. As part of our investigation, we used multivariate logistic regression models to investigate the independent relationship between the Healthy Eating Index and periodontitis. We used odds ratios (OR) with 95% confidence intervals to assess the significance of the connection (95% CI). Results: Individuals with a lower total healthy eating index were more likely to have periodontitis. A higher healthy diet index was associated with a lower prevalence of periodontitis (OR = 0.69; 95%CI: 0.49-0.97), according to adjusted multivariate regression models. The restricted cubic spline (RCS) analysis revealed that the non-linear relationship between HEI-2015 and periodontitis was statistically significant and that high HEI-2015 reduced periodontitis prevalence. Conclusion: The study's findings revealed that dietary structure was linked to the prevalence of periodontitis. Patients with a higher Healthy Eating Index were less likely to have periodontitis. There is a need for future prospective longitudinal studies to confirm causality.

Non-negative matrix factorization model-based construction for molecular clustering and prognostic assessment of head and neck squamous carcinoma.

Purpose: We aimed at exploring the efficacy of non-negative matrix factorization (NMF) model-based clustering for prognostic assessment of head and neck squamous carcinoma (HNSCC). Methods: The transcriptome microarray data of HNSCC samples were downloaded from The Cancer Genome Atlas (TCGA) and the Shanghai Ninth People's Hospital. R software packages were used to establish NMF clustering, from which relevant prognostic models were developed. Results: Based on NMF, samples were allocated into 2 subgroups. Predictive models were constructed using differentially expressed genes between the two subgroups. The high-risk group was associated with poor prognostic outcomes. Moreover, multi-factor Cox regression analysis revealed that the predictive model was an independent prognostic predictor. Conclusion: The NMF-based prognostic model has the potential for prognostic assessment of HNSCC.

Clinical Implications of Necroptosis Genes Expression for Cancer Immunity and Prognosis: A Pan-Cancer Analysis.

Background: Necroptosis, a form of programmed cell death, is increasingly being investigated for its controversial role in tumorigenesis and progression. Necroptosis suppresses tumor formation and tumor development by killing tumor cells; however, the necrotic cells also promote tumor formation and tumor development via the immunosuppressive effect of necroptosis and inflammatory response caused by cytokine release. Thus, the exact mechanism of necroptosis in pan-cancer remains unknown. Methods: The data of 11,057 cancer samples were downloaded from the TCGA database, along with clinical information, tumor mutation burden, and microsatellite instability information of the corresponding patients. We used the TCGA data in a pan-cancer analysis to identify differences in mRNA level as well as single nucleotide variants, copy number variants, methylation profiles, and genomic signatures of miRNA-mRNA interactions. Two drug datasets (from GDSC, CTRP) were used to evaluate drug sensitivity and resistance against necroptosis genes. Results: Necroptosis genes were aberrantly expressed in various cancers. The frequency of necroptosis gene mutations was highest in lung squamous cell carcinoma. Furthermore, the correlation between necroptosis gene expression in the tumor microenvironment and immune cell infiltration varied for different cancers. High necroptosis gene expression was found to correlate with NK, Tfh, Th1, CD8_T, and DC cells. These can therefore be used as biomarkers to predict prognosis. By matching gene targets with drugs, we identified potential candidate drugs. Conclusion: Our study showed the genomic alterations and clinical features of necroptosis genes in 33 cancers. This may help clarify the link between necroptosis and tumorigenesis. Our findings may also provide new approaches for the clinical treatment of cancer.

OAS3 is a Co-Immune Biomarker Associated With Tumour Microenvironment, Disease Staging, Prognosis, and Treatment Response in Multiple Cancer Types.

2',5'-oligoadenylate synthase (OAS) is a class of enzymes induced by interferons and mainly encoded by the OAS1, OAS2, and OAS3 genes, which activate the potential RNA enzymes to degrade viral mRNA, inhibit viral protein synthesis and promote apoptosis in virus-infected cells. OAS3 is associated with breast cancer prognosis. However, the expression and prognosis of OAS3 and tumour-infiltrating lymphocytes in pan-cancer remain unknown. In the present study, we have systematically investigated and confirmed the role of OAS3 in tumour immune infiltration, immune escape, tumour progression, response to treatment, and prognosis of different cancer types using various bioinformatics methods. The findings suggest that OAS3 is aberrantly expressed in almost all TCGA cancer types and subtypes and is associated with tumour staging, metastasis, and prognostic deterioration in different tumours. In addition, OAS3 expression is associated with the prognosis and chemotherapeutic outcomes of various cancers. In terms of immune-infiltrating levels, OAS3 expression is positively associated with the infiltration of immunosuppressive cells. These findings suggest that OAS3 is correlated with prognosis and immune-infiltrating levels.

Exploring the Effects of Magnesium Deficiency on the Quality Constituents of Hydroponic-Cultivated Tea (Camellia sinensis L.) Leaves.

Magnesium (Mg) plays important roles in photosynthesis, sucrose partitioning, and biomass allocation in plants. However, the specific mechanisms of tea plant response to Mg deficiency remain unclear. In this study, we investigated the effects of Mg deficiency on the quality constituents of tea leaves. Our results showed that the short-term (7 days) Mg deficiency partially elevated the concentrations of polyphenols, free amino acids, and caffeine but decreased the contents of chlorophyll and Mg. However, long-term (30 days) Mg-deficient tea displayed decreased contents of these constituents. Particularly, Mg deficiency increased the index of catechins' bitter taste and the ratio of total polyphenols to total free amino acids. Moreover, the transcription of key genes involved in the biosynthesis of flavonoid, caffeine, and theanine was differentially affected by Mg deficiency. Additionally, short-term Mg deficiency induced global transcriptome change in tea leaves, in which a total of 2522 differentially expressed genes were identified involved in secondary metabolism, amino acid metabolism, and chlorophyll metabolism. These results may help to elucidate why short-term Mg deficiency partially improves the quality constituents of tea, while long-term Mg-deficient tea may taste more bitter, more astringent, and less umami.

A Pyroptosis-Related Gene Signature for Predicting Survival in Glioblastoma.

BACKGROUND: In this study, a prognostic model based on pyroptosis-related genes was established to predict overall survival (OS) in patients with glioblastoma (GBM). METHODS: The gene expression data and clinical information of GBM patients were obtained from The Cancer Genome Atlas (TCGA), and bioinformatics analysis of differentially expressed genes was performed. LASSO Cox regression model was used to construct a three-pyroptosis-related gene signature, and validation was performed using an experimental cohort. RESULTS: A total of three pyroptosis-related genes (CASP4, CASP9, and NOD2) were used to construct a survival prognostic model, and experimental validation was performed using an experimental cohort. Receiver operating characteristic (ROC) analysis was performed, and the area under the ROC curves (AUC) was 0.921, 0.840, and 0.905 at 1, 3, and 5 years, respectively. Functional analysis revealed that T-cell activation, regulation of T-cell activation, leukocyte cell-cell adhesion, and positive regulation of cell adhesion among other immune-related functions were enriched, and immune-related processes were different between the two risk groups. CONCLUSION: In this study, a novel prognostic model based on three pyroptosis-related genes is constructed and used to predict the prognosis of GBM patients. The model can accurately and conveniently predict the 1-, 3-, and 5-year OS of GBM patients.

A Novel Model Based on Necroptosis-Related Genes for Predicting Prognosis of Patients With Prostate Adenocarcinoma.

Background: Necroptosis is a newly recognized form of cell death. Here, we applied bioinformatics tools to identify necroptosis-related genes using a dataset from The Cancer Genome Atlas (TCGA) database, then constructed a model for prognosis of patients with prostate cancer. Methods: RNA sequence (RNA-seq) data and clinical information for Prostate adenocarcinoma (PRAD) patients were obtained from the TCGA portal (http://tcga-data.nci.nih.gov/tcga/). We performed comprehensive bioinformatics analyses to identify hub genes as potential prognostic biomarkers in PRAD u followed by establishment and validation of a prognostic model. Next, we assessed the overall prediction performance of the model using receiver operating characteristic (ROC) curves and the area under curve (AUC) of the ROC. Results: A total of 5 necroptosis-related genes, namely ALOX15, BCL2, IFNA1, PYGL and TLR3, were used to construct a survival prognostic model. The model exhibited excellent performance in the TCGA cohort and validation group and had good prediction accuracy in screening out high-risk prostate cancer patients. Conclusion: We successfully identified necroptosis-related genes and constructed a prognostic model that can accurately predict 1- 3-and 5-years overall survival (OS) rates of PRAD patients. Our riskscore model has provided novel strategy for the prediction of PRAD patients' prognosis.

[Effects of UHRF1 on Estrogen Receptor and Proliferation, Invasion and Migration of BCPAP Cells in Thyroid Papillary Carcinoma].

OBJECTIVE: To investigate the effects of ubiquitin-like PDH and ring finger domain 1 (UHRF1) on the expression ratio of estrogen receptor (ER) α/ERß, and to explore the experimental mechanism of UHRF1 affecting the proliferation, invasion and migration of BCPAP cells in papillary thyroid carcinoma. METHODS: The protein and mRNA expressions of UHRF1, ERα and ERß in normal thyroid Nthy-ori3-1 cells and thyroid papillary carcinoma BCPAP cells were detected by Western blot and qRT-PCR. BCPAP cells were treated with Scrambled siRNA and UHRF1 siRNA, respectively. The expressions of ER α and ER ß mRNAs were detected by qRT-PCR. MTT and Transwell were used to determine the proliferation, invasion and migration in each group of BCPAP cells. RESULTS: Compared with Nthy-ori3-1 cells, the expressions of UHRF1 and ERα proteins and mRNAs in BCPAP cells were significantly up-regulated ( P<0.05), while the expressions of ERß protein and mRNA were significantly down-regulated ( P<0.05). Compared with the control group and Scrambled siRNA group, the expression of ER α mRNA in BCPAP cells transfected with UHRF1 siRNA was significantly decreased ( P<0.05), while the expression of ER ß mRNA was significantly increased ( P<0.05). The proliferation, invasion and migration of BCPAP cells transfected with UHRF1 siRNA were significantly decreased ( P<0.05). CONCLUSION: UHRF1 upregulates ERα/ERß expression ratio and promotes proliferation, invasion and migration of BCPAP cells in papillary thyroid carcinoma.

LincRNA-Gm4419 knockdown ameliorates NF-κB/NLRP3 inflammasome-mediated inflammation in diabetic nephropathy.

Diabetic nephropathy (DN) as the primary cause of end-stage kidney disease is a common complication of diabetes. Recent researches have shown the activation of nuclear factor kappa light-chain enhancer of activated B cells (NF-κB) and NACHT, LRR and PYD domain-containing protein 3 (NLRP3) inflammasome are associated with inflammation in the progression of DN, but the exact mechanism is unclear. Long noncoding RNAs (lncRNAs) have roles in the development of many diseases including DN. However, the relationship between lncRNAs and inflammation in DN remains largely unknown. Our previous study has revealed that 14 lncRNAs are abnormally expressed in DN by RNA sequencing and real-time quantitative PCR (qRT-PCR) in the renal tissues of db/db DN mice. In this study, these lncRNAs were verified their expressions by qRT-PCR in mesangial cells (MCs) cultured under high- and low-glucose conditions. Twelve lncRNAs displayed the same expressional tendencies in both renal tissues and MCs. In particular, long intergenic noncoding RNA (lincRNA)-Gm4419 was the only one associating with NF-κB among these 12 lncRNAs by bioinformatics methods. Moreover, Gm4419 knockdown could obviously inhibit the expressions of pro-inflammatory cytokines and renal fibrosis biomarkers, and reduce cell proliferation in MCs under high-glucose condition, whereas overexpression of Gm4419 could increase the inflammation, fibrosis and cell proliferation in MCs under low-glucose condition. Interestingly, our results showed that Gm4419 could activate the NF-κB pathway by directly interacting with p50, the subunit of NF-κB. In addition, we found that p50 could interact with NLRP3 inflammasome in MCs. In conclusion, our findings suggest lincRNA-Gm4419 may participate in the inflammation, fibrosis and proliferation in MCs under high-glucose condition through NF-κB/NLRP3 inflammasome signaling pathway, and may provide new insights into the regulation of Gm4419 during the progression of DN.

Curcumin pretreatment and post-treatment both improve the antioxidative ability of neurons with oxygen-glucose deprivation.

Recent studies have shown that induced expression of endogenous antioxidative enzymes thr-ough activation of the antioxidant response element/nuclear factor erythroid 2-related factor 2 (Nrf2) pathway may be a neuroprotective strategy. In this study, rat cerebral cortical neurons cultured in vitro were pretreated with 10 µM curcumin or post-treated with 5 µM curcumin, respectively before or after being subjected to oxygen-glucose deprivation and reoxygenation for 24 hours. Both pretreatment and post-treatment resulted in a significant decrease of cell injury as indicated by propidium iodide/Hoechst 33258 staining, a prominent increase of Nrf2 protein expression as indicated by western blot analysis, and a remarkable increase of protein expression and enzyme activity in whole cell lysates of thioredoxin before ischemia, after ischemia, and after reoxygenation. In addition, post-treatment with curcumin inhibited early DNA/RNA oxidation as indicated by immunocytochemistry and increased nuclear Nrf2 protein by inducing nuclear accumulation of Nrf2. These findings suggest that curcumin activates the expression of thioredoxin, an antioxidant protein in the Nrf2 pathway, and protects neurons from death caused by oxygen-glucose deprivation in an in vitro model of ischemia/reperfusion. We speculate that pharmacologic stimulation of antioxidant gene expression may be a promising approach to neuroprotection after cerebral ischemia.

[Establishment of a lung cancer A549 cell line stable over-expressing integrin linked kinase protein and its biological activity].

AIM: To establish a lung cancer A549 cell line stable over-expressing human integrin linked kinase (ILK) and study the effect of over-expression of ILK on biological activity of A549 cells. METHODS: Human ILK gene was amplified by RT-PCR, then cloned into pEGFP-C1 vector to construct pEGFP-ILK. After confirmed by restriction analysis and sequencing, the recombinant plasmid was transfected into A549 cells mediated with liposome, then G418-resistant clones of A549 cells (A549/pEGFP-ILK) as experimental group were obtained, and paralleled with the vector control (A549/pEGFP-C1) and A549 cell control. The expression and localization of EGFP-ILK fusion protein in A549 cells was observed by fluorescence microscopy. RT-PCR and Western blot were performed to detect the level of ILK mRNA and ILK protein of each group cells respectively. The cell proliferation was tested by methylthiazolyl tetrazolium (MTT) assay, and the cell apoptosis was measured by flow cytometry, and the morphologic changes of cells were observed by HE staining. RESULTS: Both restriction analysis and sequencing proved that the pEGFP-ILK plasmid was constructed correctly. The distribution of fluorescence of stable transfected A549 cells indicated that the product of ILK gene was mainly located in cytoplasm. Compared with A549/pEGFP-C1 group and A549 group, the level of ILK mRNA and ILK protein of A549/pEGFP-ILK cells were significantly increased, which over-expression ratio was 218.18% and 245.45% respectively (P<0.05). The proliferation ability of the A549 cells over-expressing ILK was increased significantly (P<0.05). However, the apoptosis of A549/pEGFP-ILK cell was inhibited significantly by over-expression of ILK (P<0.05). After HE staining, the increased mitosis were observed only in A549/pEGFP-ILK group cells. CONCLUSION: The lung cancer cell line stable over-expressing ILK protein was constructed successfully, and ILK over-expression could promote cell proliferation, inhibit cell apoptosis and increase mitosis.