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Background Prostate cancer (PCa) is the most diagnosed cancer in Australian men, and the number of survivors is growing with advances in diagnosis and treatment. Work participation following PCa diagnosis and treatment becomes a significant aspect of quality of life and survivorship. Using a qualitative phenomenological approach, we explored the work-related experiences of PCa survivors in Australia. Methods Semi-structured telephone interviews were conducted with 16 men (6 salaried employees, 10 self-employed; 8 diagnosed ≥ 5 years) purposively sampled from a community setting. Interviews were inductively analysed. Results Five main themes emerged: motivations to work; treatment decisions and work; the effects of PCa and its treatment on ability to participate in work; being an employee versus being self-employed; and personal agency. PCa and its treatment side-effects were detrimental to men’s work capacity and ability, and could persist over an extended period. Most men expressed a strong desire to retain work or return to work. Discussions with healthcare professionals about work-related consequences were largely missing when treatment decisions were made. Self-employed men faced greater challenges than their salaried counterparts due to high financial burden and limited social and business support. Family, workplace and wider community support, and self-care, enhanced men’s work participation experiences. Conclusions PCa and its treatment substantially and persistently impacted men’s working lives, and their experiences were diverse and multifaceted. Self-employed and long-term PCa survivors face greater challenges and are at high risk of poor work outcomes. A systematic approach and involvement of stakeholders at all levels is required to support ongoing work participation.

BackgroundTranscutaneous carbon dioxide (TcCO2) monitoring is a non-invasive alternative to arterial blood sampling. The aim of this review was to determine the accuracy and precision of TcCO2 measurements.MethodsMedline and EMBASE (2000–2016) were searched for studies that reported on a measurement of PaCO2 that coincided with a measurement of TcCO2. Study selection and quality assessment (using the revised Quality Assessment of Diagnostic Accuracy Studies tool (QUADAS-2)) were performed independently. The Grading Quality of Evidence and Strength of Recommendation approach was used to summarise the strength of the body of evidence. Pooled estimates of the mean bias between TcCO2 and PaCO2 and limits of agreement with outer 95% CIs (termed population limits of agreement) were calculated.ResultsThe mean bias was −0.1 mm Hg and the population limits of agreement were −15 to 15 mm Hg for 7021 paired measurements taken from 2817 participants in 73 studies, which was outside of the clinically acceptable range (7.5 mm Hg). The lowest PaCO2 reported in the studies was 18 mm Hg and the highest was 103 mm Hg. The major sources of inconsistency were sensor location and temperature. The population limits of agreement were within the clinically acceptable range across 3974 paired measurements from 1786 participants in 44 studies that applied the sensor to the earlobe using the TOSCA and Sentec devices (−6 to 6 mm Hg).ConclusionThere are substantial differences between TcCO2 and PaCO2 depending on the context in which this technology is used. TcCO2 sensors should preferentially be applied to the earlobe and users should consider setting the temperature of the sensor higher than 42°C when monitoring at other sites.Systematic review registration numberPROSPERO; CRD42017057450.

Background In gut microbiome studies, the cultured gut microbial resource plays essential roles, such as helping to unravel gut microbial functions and host-microbe interactions. Although several major studies have been performed to elucidate the cultured human gut microbiota, up to 70% of the Unified Human Gastrointestinal Genome species have not been cultured to date. Large-scale gut microbial isolation and identification as well as availability to the public are imperative for gut microbial studies and further characterizing human gut microbial functions. Results In this study, we constructed a human Gut Microbial Biobank (hGMB; homepage: hgmb.nmdc.cn ) through the cultivation of 10,558 isolates from 31 sample mixtures of 239 fresh fecal samples from healthy Chinese volunteers, and deposited 1170 strains representing 400 different species in culture collections of the International Depository Authority for long-term preservation and public access worldwide. Following the rules of the International Code of Nomenclature of Prokaryotes, 102 new species were characterized and denominated, while 28 new genera and 3 new families were proposed. hGMB represented over 80% of the common and dominant human gut microbial genera and species characterized from global human gut 16S rRNA gene amplicon data ( n = 11,647) and cultured 24 “most-wanted” and “medium priority” taxa proposed by the Human Microbiome Project. We in total sequenced 115 genomes representing 102 novel taxa and 13 previously known species. Further in silico analysis revealed that the newly sequenced hGMB genomes represented 22 previously uncultured species in the Unified Human Gastrointestinal Genome (UHGG) and contributed 24 representatives of potentially “dark taxa” that had not been discovered by UHGG. The nonredundant gene catalogs generated from the hGMB genomes covered over 50% of the functionally known genes (KEGG orthologs) in the largest global human gut gene catalogs and approximately 10% of the “most wanted” functionally unknown proteins in the FUnkFams database. Conclusions A publicly accessible human Gut Microbial Biobank (hGMB) was established that contained 1170 strains and represents 400 human gut microbial species. hGMB expands the gut microbial resources and genomic repository by adding 102 novel species, 28 new genera, 3 new families, and 115 new genomes of human gut microbes. 6-6epGnHGpob5sGsfPZJHQ Video abstract

Conventional alloy design based on a single primary element has reached its limits in terms of performance optimization. An alloy design strategy with multi-principal elements has recently been uncovered to overcome this bottleneck. Multicomponent alloys, generally referred to as high-entropy alloys (HEAs), exhibit many promising properties, especially outstanding mechanical performance at cryogenic, ambient, and elevated temperatures. In this article, we focus on precipitation-hardened HEAs, which are potential candidates for next-generation structural materials, especially at high temperatures. The key issues involved include precipitation behaviors, phase stability, and phase control, all of which provide useful guidelines for further development of high-temperature materials with superior performance. In particular, we address the formation of cellular γ′ precipitates at grain boundaries, which is closely related to the embrittlement of HEAs at intermediate temperatures. Critical issues and design strategies in developing HEAs for high-temperature applications are also discussed.

Mice are widely used as experimental models for gut microbiome (GM) studies, yet the majority of mouse GM members remain uncharacterized. Here, we report the construction of a mouse gut microbial biobank (mGMB) that contains 126 species, represented by 244 strains that have been deposited in the China General Microorganism Culture Collection. We sequence and phenotypically characterize 77 potential new species and propose their nomenclatures. The mGMB includes 22 and 17 species that are significantly enriched in ob/ob and wild-type C57BL/6J mouse cecal samples, respectively. The genomes of the 126 species in the mGMB cover 52% of the metagenomic nonredundant gene catalog (sequence identity ≥ 60%) and represent 93–95% of the KEGG-Orthology-annotated functions of the sampled mouse GMs. The microbial and genome data assembled in the mGMB enlarges the taxonomic characterization of mouse GMs and represents a useful resource for studies of host-microbe interactions and of GM functions associated with host health and diseases. Here, the authors established and characterized the mouse gut microbial biobank (mGMB), which includes 244 strains and 126 species that enlarges previous mouse intestinal bacterial collections and represents a resource for studies using mouse models to investigate microbiome-associated health and disease.

The use of microbial inoculant is a promising strategy to improve plant health, but their efficiency often faces challenges due to difficulties in successful microbial colonization in soil environments. To this end, the application of biostimulation products derived from microbes is expected to resolve these barriers via direct interactions with plants or soil pathogens. However, their effectiveness and mechanisms for promoting plant growth and disease resistance remain elusive. In this study, we showed that root irrigation with the extracts of Streptomyces ahygroscopicus strain 769 (S769) solid fermentation products significantly reduced watermelon Fusarium wilt disease incidence by 30% and increased the plant biomass by 150% at a fruiting stage in a continuous cropping field. S769 treatment led to substantial changes in both bacterial and fungal community compositions, and induced a highly interconnected microbial association network in the rhizosphere. The root transcriptome analysis further suggested that S769 treatment significantly improved the expression of the MAPK signalling pathway, plant hormone signal transduction and plant–pathogen interactions, particular those genes related to PR‐1 and ethylene, as well as genes associated with auxin production and reception. Together, our study provides mechanistic and empirical evidences for the biostimulation products benefiting plant health through coordinating plant and rhizosphere microbiome interaction. The application of biostimulation products derived from microbes is a promising strategy for mitigating soil‐borne disease without the necessity of root colonization. Here, the author demonstrated that the extracts of Streptomyces ahygroscopicus strain 769 solid fermentation products were effective in reducing watermelon Fusarium wilt incidence. This was achieved through directly priming plant immune responses and indirectly cultivating a highly interconnected and mutually beneficial rhizosphere microbial community.

Background Flammulina filiformis (previously known as Asian F. velutipes ) is a popular commercial edible mushroom. Many bioactive compounds with medicinal effects, such as polysaccharides and sesquiterpenoids, have been isolated and identified from F. filiformis , but their biosynthesis and regulation at the molecular level remains unclear. In this study, we sequenced the genome of the wild strain F. filiformis Liu355, predicted its biosynthetic gene clusters (BGCs) and profiled the expression of these genes in wild and cultivar strains and in different developmental stages of the wild F. filiformis strain by a comparative transcriptomic analysis. Results We found that the genome of the F. filiformis was 35.01 Mb in length and harbored 10,396 gene models. Thirteen putative terpenoid gene clusters were predicted and 12 sesquiterpene synthase genes belonging to four different groups and two type I polyketide synthase gene clusters were identified in the F. filiformis genome. The number of genes related to terpenoid biosynthesis was higher in the wild strain (119 genes) than in the cultivar strain (81 genes). Most terpenoid biosynthesis genes were upregulated in the primordium and fruiting body of the wild strain, while the polyketide synthase genes were generally upregulated in the mycelium of the wild strain. Moreover, genes encoding UDP-glucose pyrophosphorylase and UDP-glucose dehydrogenase, which are involved in polysaccharide biosynthesis, had relatively high transcript levels both in the mycelium and fruiting body of the wild F. filiformis strain . Conclusions F. filiformis is enriched in a number of gene clusters involved in the biosynthesis of polysaccharides and terpenoid bioactive compounds and these genes usually display differential expression between wild and cultivar strains, even in different developmental stages. This study expands our knowledge of the biology of F. filiformis and provides valuable data for elucidating the regulation of secondary metabolites in this unique F. filiformis strain.

Tea is one of the most popular beverages across the world and is made exclusively from cultivars of Camellia sinensis. Many wild relatives of the genus Camellia that are closely related to C. sinensis are native to Southwest China. In this study, we first identified the distinct genetic divergence between C. sinensis and its wild relatives and provided a glimpse into the artificial selection of tea plants at a genome-wide level by analyzing 15,444 genomic SNPs that were identified from 18 cultivated and wild tea accessions using a high-throughput genome-wide restriction site-associated DNA sequencing (RAD-Seq) approach. Six distinct clusters were detected by phylogeny inferrence and principal component and genetic structural analyses, and these clusters corresponded to six Camellia species/varieties. Genetic divergence apparently indicated that C. taliensis var. bangwei is a semi-wild or transient landrace occupying a phylogenetic position between those wild and cultivated tea plants. Cultivated accessions exhibited greater heterozygosity than wild accessions, with the exception of C. taliensis var. bangwei. Thirteen genes with non-synonymous SNPs exhibited strong selective signals that were suggestive of putative artificial selective footprints for tea plants during domestication. The genome-wide SNPs provide a fundamental data resource for assessing genetic relationships, characterizing complex traits, comparing heterozygosity and analyzing putatitve artificial selection in tea plants.

Keratinocytes, the most important cell type constituting the epidermis, migrate to restore the epithelial barrier during wound healing and are a crucial step in wound healing. This study utilized bioinformatics analysis of comprehensive expression datasets of aberrantly expressed genes in wound healing to identify the abnormal expression of the critical transcription factor Fos-like antigen-1 (FOSL1), which is involved in various diseases. Currently, there is limited research on the role of FOSL1 in wound healing, and its molecular mechanisms remain unclear. This study explores the role and regulatory mechanisms of FOSL1 in the wound-healing process. A comprehensive expression dataset of abnormal genes in wound repair was constructed by bioinformatics analysis. Mouse trauma models and mouse wound splint models were constructed to verify the role of FOSL1 in vivo. Real-time quantitative polymerase chain reaction (qRT-PCR), immunoblot, immunofluorescence staining, and HE staining were used to confirm the analysis, and FOSL1 was used as the target in the wound healing process. At the cellular level, using 5ʹ-ethynyl-2ʹ-deoxyuridine (EdU) assay, Transwell assay, Migration assay, western blotting and immunofluorescence, FOSL1 promoted the molecular mechanism of wound repair by regulating the proliferation and migration of keratinocytes through IL-17 signaling pathway. Bioinformatics analysis revealed differential expression of FOSL1 during wound healing. In the mouse back wound model, qRT-PCR, western blotting (WB), and immunofluorescence staining showed significant upregulation of FOSL1 and IL-17 expression during wound tissue healing, indicating a close association between FOSL1 and mouse wound healing. In the mouse wound splinting model, subcutaneous injection of recombinant FOSL1 protein contributed to wound surface healing. Overexpression of FOSL1 in HaCaT cells promoted their proliferation and migration abilities. When IL-17 inhibitor was added to HaCaT cells, both FOSL1 overexpression and knockdown inhibited the proliferation and migration abilities of HaCaT cells. Thus, this study confirms that FOSL1 promotes keratinocyte proliferation and migration through the IL-17 signaling pathway, facilitating wound healing in epidermal wound repair. The results of this study indicate that FOSL1 plays a key role in epidermal wound healing, and elucidate a new molecular mechanism by which FOSL1 promotes keratinocyte proliferation and migration through IL-17 signaling pathway in epidermal wound repair, thereby promoting wound healing.

Background Targeting glucose uptake by glucose transporter (GLUT) inhibitors is a therapeutic opportunity, but efforts on GLUT inhibitors have not been successful in the clinic and the underlying mechanism remains unclear. We aim to identify the key metabolic changes responsible for cancer cell survival from glucose limitation and elucidate its mechanism. Methods The level of phosphorylated YAP was analyzed with Western blotting and Phos-tag immunoblotting. Glucose limitation-induced metabolic changes were analyzed using targeted metabolomics (600MRM). The anti-cancer role of metabolite was examined using colony formation assay and APC min/ + mice. Co-immunoprecipitation, LS-MS, qRT-PCR, and immunofluorescence were performed to explore the underlying mechanisms. Results We found that D-Ribose-5-phosphate (D5P), a product of the pentose phosphate pathway connecting glucose metabolism and nucleotide metabolism, functions as a metabolic checkpoint to activate YAP under glucose limitation to promote cancer cell survival. Mechanistically, in glucose-deprived cancer cells, D5P is decreased, which facilitates the interaction between MYH9 and LATS1, resulting in MYH9-mediated LATS1 aggregation, degradation, and further YAP activation. Interestingly, activated YAP further promotes purine nucleoside phosphorylase (PNP)-mediated breakdown of purine nucleoside to restore D5P in a feedback manner. Importantly, D5P synergistically enhances the tumor-suppressive effect of GLUT inhibitors and inhibits cancer progression in mice. Conclusions Our study identifies D5P as a metabolic checkpoint linking glucose limitation stress and YAP activation, indicating that D5P may be a potential anti-cancer metabolite by enhancing glucose limitation sensitivity.