Notch signaling pathway is evolutionarily conserved in mammals, which plays an important role in cell development and differentiation. In recent years, increasing evidence has shown that aberrant activation of Notch is associated with tumor process. Aberrant activation of Notch signaling pathway has been found in many different solid tumors can induce cell proliferation, metastasis and epithelial-mesenchymal transition. Notch receptor and its ligand are both single transmembrane protein, and Notch is activated when it binds to the Notch ligand of neighbor cells. The signal transduction of Notch signaling pathway is only between cells that are in contact with each other, which is independent of second messengers. Thus, Notch needs to cross talk with other signaling pathways, including PI3K/AKT, NF-κB, integrin and miRNAs, to precisely regulate cell fate. In this review, we summarize the roles of Notch signaling pathway in tumor metastasis and its regulatory mechanisms and discuss the current treatment strategies targeting Notch signal pathway.

The structure of human transmembrane pro-TNF-alpha was studied both in intact cell systems and in an in vitro translation system. In intact cell systems (LPS-induced THP-1 and TNF cDNA-transfected COS-7), a trimer of pro-TNF was detected after chemical cross-linking based on its molecular weight in Western blotting analysis. The trimer was shown to be a TNF-specific protein and could be partially cleaved to 26-kDa pro-TNF monomers by cleaving the cross-linkers. The trimeric structure was assembled intracellularly, because it could be detected in both the in vitro microsomal translation system and in THP-1 cells coincident with the appearance of pro-TNF in the cell lysate, prior to secretion of mature TNF. To further analyze the relationship between the trimeric structure and the biological activity of pro-TNF, we characterized several noncleavable pro-TNF deletion mutants. We observed a correlation between expression of TNF cytotoxicity in a juxtacrine fashion and detection of trimer. Thus, human pro-TNF-alpha, like the secreted mature TNF-alpha, has trimeric structure which is assembled intracellularly before transport to the cell surface and is apparently required for mediating its biologic activity.

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The function of the NAD(P)H oxidases (NOXs) family member NOX4 is to generate reactive oxygen species (ROS), however, the molecular function of NOX4 has not been fully studied and waiting to be clarified. To elucidate the function of endogenous Nox4 in human thyroid carcinomas, papillomatosis thyroid cancer cells were used to study the cell growth by knocking down the expression of NOX4 and knocking out its functional partner p22phox/CYBA. As a result, the increasement of mitochondrial ROS(mROS) was abolished due to both knockdown of NOX4 and p22phox knockout in hypoxia, which destabilized HIF1α decreasing glycolysis and retarded cell growth. These data suggests that Nox4 is potent oncotarget due to its role in regulating glycolysis through mROS-HIF1α pathway, thereby mediating proliferation in thyroid carcinomas.

2,5-Furandicarboxylic acid (FDCA) serves as a monomer in various polyesters and is often obtained through the oxidation of 5hydroxymethylfurfural. The solubility data of FDCA are of great value for the reaction process analysis and separation technology. The experimental solubility of FDCA in eight pure solvents (water, methanol, acetonitrile, acetic acid, ethyl acetate, methyl isobutyl ketone (MIBK), 1butanol, and isobutanol) and two binary solvent systems (water + acetonitrile and water + acetic acid) in the temperature range of 313.15− 363.15 K was determined. In pure solvents and binary mixtures, the solubility of FDCA increased with the increasing temperature. The order from largest to smallest solubility in pure solvents was as follows: methanol, 1-butanol, isobutanol, acetic acid, water, MIBK, ethyl acetate, and acetonitrile. The mole fraction of FDCA in binary mixtures increased first and then decreased with the increasing mole fraction of water. The solubility data were correlated with the UNIQUAC model, NRTL model, and WILSON model.

Compassion fatigue has emerged as a detrimental consequence of experiencing work-related stress among psychiatric nurses, and affected the job performance, emotional and physical health of psychiatric nurses. However, researches on Chinese psychiatric nurses’ compassion fatigue are dearth. This cross-sectional study aimed to investigate the prevalence and factors of compassion fatigue among Chinese psychiatric nurses. All participants completed the demographic questionnaire and the Chinese version of Professional Quality of Life Scale (ProQOL-CN). One-way ANOVA, t -tests, Levene test and multiple linear regression analysis were conducted to evaluate factors associated with compassion fatigue. A total of 352 psychiatric nurses in 9 psychiatric hospitals from the Chengdu, Wuhan, and Hefei were surveyed. The mean scores of compassion satisfaction, burnout and secondary traumatic stress were 32.59 ± 7.124, 26.92 ± 6.003 and 25.97 ± 5.365, respectively. Four variables of job satisfaction, exercise, had children, and age range from 36 to 50 years explained 30.7% of the variance in compassion satisfaction. Job satisfaction, sleeping quality, and marital status accounted for 40.4% variables in burnout. Furthermore, job satisfaction, average sleeping quality, and years of nursing experience remained significantly associated with secondary trauma stress, explaining 10.9% of the variance. Compassion satisfaction, burnout and secondary traumatic stress among Chinese psychiatric nurses were at the level of moderate. The higher job satisfaction, healthy lifestyle (high sleep quality and regular exercise), and family support (children, stable and harmonious marital status) positively influenced compassion satisfaction and negatively associated with burnout or secondary traumatic stress.

Background Compassion fatigue is described as the phenomenon of exhaustion and dysfunction in healthcare workers resulting from prolonged exposure to work‐related stress and compassion stress. Oncology nurses are at high risk for compassion fatigue. Aims Our study aims to estimate the levels, prevalence and related factors of compassion fatigue dimension in oncology nurses. Design Systematic review and meta‐analysis. Method Ten electronic databases were conducted in the systematic review and meta‐analysis. Time frame of the searches is from inception up to 31 January 2020. The research team independently conducted study selection, quality assessments, data extractions and analysis of all included studies. The means, standard deviations and prevalence of three dimensions of compassion fatigue were pooled using random‐effects meta‐analysis. The PRISMA guideline was used to report the systematic review and meta‐analysis. PROSPERO registration number: CRD42020205521. Results The systematic review included 21 studies, involving 6533 oncology nurses across 6 different countries. In our studies, the pooled mean scores of compassion satisfaction (CS), burnout (BO) and secondary traumatic stress (STS) were 35.47 (95% CI: 33.54–37.41), 24.94 (95% CI: 23.47–26.41) and 24.48 (95% CI: 23.36–25.60), respectively; the pooled prevalence of “low” rates of CS, “high” rates of BO and STS were 20% (CI 13%–28%), 22% (CI 18%–26%) and 22% (CI 17%–28%), respectively; furthermore, geographical regions (Asia) significantly affect the prevalence of compassion fatigue among oncology nurses. The compassion fatigue variables considered were demographic (age, marital status, education background, health condition and gender), work‐related (job satisfaction, income satisfaction, years of working experience, professional title, position and work environment) and other variables (social support, coping strategy, self‐compassion, professional cognition and psychological training). Conclusion Oncology nurses were at “moderate” level of compassion satisfaction, burnout and secondary traumatic stress, and 22% of oncology nurses suffered from “high” risk of compassion fatigue. Hospital administrators should develop interventions to address compassion fatigue phenomenon, and enhance the mental health of oncology nurses and nursing care results. Relevance to clinical practice Oncology unit warrants special attention, and oncology nurses are at high risk for compassion fatigue. However, the reported prevalence rates and oncology nurses with different characteristics vary considerably. The review provides a preliminary framework for nursing administrators to develop interventions to address compassion fatigue phenomenon, and enhance the psychological health of oncology nurses.

Several studies have indicated that only one cleavage site (Ala-1/Val+1) is involved in the release of mature TNF from human pro-TNF, whereas others have suggested that the linking sequence (residues -20 to -1) may be important. We previously demonstrated that a pro-TNF deletion mutant, delta -20- -1, was able to form a trimeric structure and mediate TNF cytotoxicity in a juxtacrine fashion without releasing mature TNF. We constructed seven mutants with smaller deletions within this region. Three 15-residue deletion mutants, delta -20- -6, delta -15- -1 and delta -20- -16, -10- -1, were noncleavable, although able to form a trimer and to mediate cytotoxicity through cell-to-cell contact. Three five- or ten-residue deletion mutants, delta -20- -16, delta -10- -1, and delta -5-, -1, behaved like the wild-type TNF; all formed a trimer and released mature TNF. These results suggested that in pro-TNF (1) the number of residues between the base of the trimer and the plasma membrane determines accessibility of the cleavage site to the pro-TNF processing enzyme(s) since small deletions did not block cleavage whereas large ones did regardless of the presence of the native cleavage site (-1/+1), (2) the native cleavage site is not sufficient for releasing mature TNF because mutant delta -20- -6, in which the native cleavage site was intact, was noncleavable, and (3) alternative cleavage site(s) may exist since mutants delta -10- -1 and delta -5- -1, which lack the native cleavage site, were cleavable.