Aims
A meta‐analysis was conducted of the prevalence rates of compassion satisfaction, compassion fatigue and burnout to identify the factors influencing these rates.
Background
The extents of ...compassion fatigue and burnout adversely affect nursing efficiency. However, the reported prevalence rates vary considerably.
Methods
Data were acquired from electronic databases. Random effects meta‐analyses were performed to obtain pooled estimates of the prevalence rates of compassion satisfaction, compassion fatigue and burnout and their respective instrumental scores. Meta‐regression analyses were performed to identify factors influencing these rates.
Results
Data from 21 studies were used for the meta‐analysis. The prevalence rates of compassion satisfaction, compassion fatigue and burnout were 47.55%, 52.55% and 51.98%, respectively. The possession of Bachelor's or Master's degrees by the nurses was significantly inversely associated with the percent prevalence of compassion fatigue (coefficient: −1.187) and burnout (coefficient: −0.810). The compassion fatigue score was also significantly inversely associated with nursing status as registered or licensed practical nurse (coefficient: −0.135).
Conclusion
In nursing, the prevalence rates of compassion fatigue and burnout are high. Better education and training may have a moderating effect on compassion fatigue and burnout and could improve the quality of life of nurses.
The high storage capacity versus high selectivity trade‐off barrier presents a daunting challenge to practical application as an acetylene (C2H2) adsorbent. A structure–performance relationship ...screening for sixty‐two high‐performance metal–organic framework adsorbents reveals that a moderate pore size distribution around 5.0–7.5 Å is critical to fulfill this task. A precise pore space partition approach was involved to partition 1D hexagonal channels of typical MIL‐88 architecture into finite segments with pore sizes varying from 4.5 Å (SNNU‐26) to 6.4 Å (SNNU‐27), 7.1 Å (SNNU‐28), and 8.1 Å (SNNU‐29). Coupled with bare tetrazole N sites (6 or 12 bare N sites within one cage) as high‐density H‐bonding acceptors for C2H2, the target MOFs offer a good combination of high C2H2/CO2 adsorption selectivity and high C2H2 uptake capacity in addition to good stability. The optimized SNNU‐27‐Fe material demonstrates a C2H2 uptake of 182.4 cm3 g−1 and an extraordinary C2H2/CO2 dynamic breakthrough time up to 91 min g−1 under ambient conditions.
Benchmark metal–organic framework (MOF) adsorbents for C2H2/CO2 separation are reported. The MOFs offer moderate pore size distributions, which are regulated by precise pore space partitions and coupled with a high‐density of hydrogen‐bonding acceptors.
Distinctive from their normal counterparts, cancer cells exhibit unique metabolic dependencies on glutamine to fuel anabolic processes. Specifically, pancreatic ductal adenocarcinoma (PDAC) cells ...rely on an unconventional metabolic pathway catalyzed by aspartate aminotransferase, malate dehydrogenase 1 (MDH1), and malic enzyme 1 to rewire glutamine metabolism and support nicotinamide adenine dinucleotide phosphate (NADPH) production. Here, we report that methylation on arginine 248 (R248) negatively regulates MDH1. Protein arginine methyltransferase 4 (PRMT4/CARM1) methylates and inhibits MDH1 by disrupting its dimerization. Knockdown of MDH1 represses mitochondria respiration and inhibits glutamine metabolism, which sensitizes PDAC cells to oxidative stress and suppresses cell proliferation. Meanwhile, re-expression of wild-type MDH1, but not its methylation-mimetic mutant, protects cells from oxidative injury and restores cell growth and clonogenic activity. Importantly, MDH1 is hypomethylated at R248 in clinical PDAC samples. Our study reveals that arginine methylation of MDH1 by CARM1 regulates cellular redox homeostasis and suppresses glutamine metabolism of pancreatic cancer.
Display omitted
•Arginine methylation at R248 negatively regulates MDH1 activity•PRMT4/CARM1 methylates MDH1 at R248 and inhibits its dimerization•MDH1 methylation suppresses glutamine metabolism of pancreatic cancer•R248 methylation of MDH1 is downregulated in clinical PDAC samples
Wang et al. show that arginine methylation at R248 of MDH1, which is catalyzed by PRMT4/CARM1, regulates glutamine metabolism and redox homeostasis of pancreatic cancer cells. MDH1 methylation is downregulated in human PDAC samples.
In order to discover pesticidal lead compounds with high activity and low toxicity, a series of novel benzamides substituted with pyrazole-linked 1,2,4-oxadiazole were designed via bioisosterism. The ...chemical structures of the target compounds were confirmed via 1H NMR, 13C NMR and HRMS analysis. The preliminary bioassay showed that most compounds exhibited good lethal activities against Mythimna separate, Helicoverpa armigera, Ostrinia nubilalis and Spodoptera frugiperda at 500 mg/L. Particularly in the case of Mythimna separate, compound 14q (70%) exhibited obvious insecticidal activity. In addition, compound 14h demonstrated good fungicidal activity against Pyricularia oryae with an inhibition rate of 77.8%, and compounds 14e, 14k, 14n and 14r also showed certain antifungal activities (55.6–66.7%). The zebrafish toxicity test showed that the LC50 of compound 14h was 14.01 mg/L, which indicated that it may be used as a potential leading compound for further structural optimization.
Besides the conventional carbon sources, acetyl-CoA has recently been shown to be generated from acetate in various types of cancers, where it promotes lipid synthesis and tumour growth. The ...underlying mechanism, however, remains largely unknown. We find that acetate induces a hyperacetylated state of histone H3 in hypoxic cells. Acetate predominately activates lipogenic genes ACACA and FASN expression by increasing H3K9, H3K27 and H3K56 acetylation levels at their promoter regions, thus enhancing de novo lipid synthesis, which combines with its function as the metabolic precursor for fatty acid synthesis. Acetyl-CoA synthetases (ACSS1, ACSS2) are involved in this acetate-mediated epigenetic regulation. More importantly, human hepatocellular carcinoma with high ACSS1/2 expression exhibit increased histone H3 acetylation and FASN expression. Taken together, this study demonstrates that acetate, in addition to its ability to induce fatty acid synthesis as an immediate metabolic precursor, also functions as an epigenetic metabolite to promote cancer cell survival under hypoxic stress.
Long noncoding RNAs (lncRNAs) play nonnegligible roles in the epigenetic regulation of cancer cells. This study aimed to identify a specific lncRNA that promotes the colorectal cancer (CRC) ...progression and could be a potential therapeutic target.
We screened highly expressed lncRNAs in human CRC samples compared with their matched adjacent normal tissues. The proteins that interact with LINRIS (Long Intergenic Noncoding RNA for IGF2BP2 Stability) were confirmed by RNA pull-down and RNA immunoprecipitation (RIP) assays. The proliferation and metabolic alteration of CRC cells with LINRIS inhibited were tested in vitro and in vivo.
LINRIS was upregulated in CRC tissues from patients with poor overall survival (OS), and LINRIS inhibition led to the impaired CRC cell line growth. Moreover, knockdown of LINRIS resulted in a decreased level of insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2), a newly found N
-methyladenosine (m
A) 'reader'. LINRIS blocked K139 ubiquitination of IGF2BP2, maintaining its stability. This process prevented the degradation of IGF2BP2 through the autophagy-lysosome pathway (ALP). Therefore, knockdown of LINRIS attenuated the downstream effects of IGF2BP2, especially MYC-mediated glycolysis in CRC cells. In addition, the transcription of LINRIS could be inhibited by GATA3 in CRC cells. In vivo experiments showed that the inhibition of LINRIS suppressed the proliferation of tumors in orthotopic models and in patient-derived xenograft (PDX) models.
LINRIS is an independent prognostic biomarker for CRC. The LINRIS-IGF2BP2-MYC axis promotes the progression of CRC and is a promising therapeutic target.
•Enzymatic hydrolysis disrupted the α-helices of tree peony seed protein.•Alcalase had the strong hydrolytic ability for tree peony seed protein.•Alcalase hydrolysate had well physicochemical ...properties.•Alcalase hydrolysate exhibited superior antioxidant ability to TPSP.
The physicochemical and antioxidant properties of tree peony seed protein (TPSP) hydrolysates by Alcalase, Neutrase, Papain, Protamex, and Flavourzyme were investigated in this study. The physicochemical properties were characterized by SDS-PAGE, particle size distribution, fourier transform infrared and fluorescence spectroscopy etc. The antioxidant activities were determined by DPPH radical, ABTS radical, Fe2+ chelating, and reducing power. The results showed five proteases produced hydrolysates with a significantly reduced average particle size, α-helices, and surface hydrophobicity compared to TPSP. Alcalase and Neutrase hydrolysis enhanced the nutritional value of the hydrolysates. Alcalase hydrolysates possessed the highest degree of hydrolysis (27.97%) and lowest molecular weight (<13 kDa) with average particle size (231.33 nm). Alcalase hydrolysate displayed the highest radical scavenging (DPPH IC50 = 0.18 mg/mL, ABTS IC50 = 1.57 mg/mL), Fe2+ chelating activity (IC50 = 0.99 mg/mL), and reducing power (0.594). These results provide the fundamentals for TPSP hydrolysates as antioxidants to be employed in food industry or pharmaceutical industry.
Pim‐3 is a member of the Provirus integrating site Moloney murine leukemia virus (Pim) family, which belongs to the Ca2+/calmodulin‐dependent protein kinase (CaMK) group and exhibits serine/threonine ...kinase activity. Similar to other members of the Pim family (i.e. Pim‐1 and Pim‐2), Pim‐3 can prevent apoptosis and promote cell survival and protein translation, thereby enhancing cell proliferation of normal and malignant cells. Pim‐3 is expressed in vital organs, such as the heart, lung, and brain. However, minimal phenotypic changes in Pim‐3‐deficient mice suggest that Pim‐3 may be physiologically dispensable. Pim‐3 expression is enhanced in several cancer tissues, particularly those of endoderm‐derived organs, including the liver, pancreas, colon, and stomach. The development of hepatocellular carcinoma is accelerated in mice expressing the Pim‐3 gene selectively in the liver only when these mice are treated with a hepatocarcinogen, indicating that Pim‐3 can act as a promoter but not as an initiator. Moreover, inhibition of Pim‐3 expression can retard in vitro cell proliferation of hepatocellular, pancreatic, and colon carcinoma cell lines by promoting cell apoptosis. Furthermore, a Pim‐3 kinase inhibitor has been reported to inhibit cell proliferation in an in vivo xenograft model using a human pancreatic cancer cell line without inducing any major adverse effects. Thus, Pim‐3 kinase may be a candidate molecule for the development of molecular targeting drugs against cancer. (Cancer Sci 2011; 102: 1437–1442)
Epidermal growth factor receptor (EGFR) is a tyrosine kinase receptor involved in homeostatic regulation of normal cells and carcinogenesis of epithelial malignancies. With rapid development of the ...precision medicine era, a series of new therapies targeting EGFR are underway. Four EGFR monoclonal antibody drugs (cetuximab, panitumumab, nimotuzumab, and necitumumab) are already on the market, and a dozen other EGFR monoclonal antibodies are in clinical trials. Here, we comprehensively review the newly identified biological properties and anti-tumor mechanisms of EGFR monoclonal antibodies. We summarize recently completed and ongoing clinical trials of the classic and new EGFR monoclonal antibodies. More importantly, according to our new standard, we re-classify the complex evolving tumor cell resistance mechanisms, including those involving exosomes, non-coding RNA and the tumor microenvironment, against EGFR monoclonal antibodies. Finally, we analyzed the limitations of EGFR monoclonal antibody therapy, and discussed the current strategies overcoming EGFR related drug resistance. This review will help us better understand the latest battles between EGFR monoclonal antibodies and resistant tumor cells, and the future directions to develop anti-tumor EGFR monoclonal antibodies with durable effects.
To develop new compounds with high activity, broad spectrum and low-toxicity, 17 benzamides substituted with quinoline-linked 1,2,4-oxadiazole were designed using the splicing principle of active ...substructures and were synthesized. The biological activities were evaluated against 10 fungi, indicating that some of the synthetic compounds showed excellent fungicidal activities. For example, at 50 mg/L, the inhibitory activity of 13p (3-Cl-4-Cl substituted, 86.1%) against Sclerotinia sclerotiorum was superior to that of quinoxyfen (77.8%), and the inhibitory activity of 13f (3-CF3 substituted, 77.8%) was comparable to that of quinoxyfen. The fungicidal activities of 13f and 13p to Sclerotinia sclerotiorum were better than that of quinoxyfen (14.19 mg/L), with EC50 of 6.67 mg/L and 5.17 mg/L, respectively. Furthermore, the acute toxicity of 13p was 19.42 mg/L, classifying it as a low-toxic compound.
PDF
