Purpose
There is no review on the effect of work-related stressors on mental health of young workers. We systematically reviewed epidemiological evidence on this relationship.
Methods
The review ...searched eight databases: Embase, PubMed, Web of Science, Cinahl, Cochrane Library, Informit, PsycINFO, and Scopus from their respective start dates until May 2017. Studies that have examined a mental health outcome in relation to a work-related stressor as exposure in young workers were included. The review was reported based on the PRISMA statement.
Results
Three cross-sectional studies and six longitudinal cohort studies were included. Cross-sectional evidence showed that adverse work conditions including working overtime, job boredom, low skill variety, low autonomy, high job insecurity, and lack of reward were associated with poor mental health of young workers. Longitudinal evidence showed that high job demands, low job control, effort-reward imbalance, and low work support (men only) were associated with poor mental health. There was evidence on the contemporaneous relationship between two or more adverse work conditions and poor mental health.
Conclusions
Although more research (particularly high-quality longitudinal studies) is warranted in this area, our review indicates that work-related stressors have a negative impact on the mental health of young workers. The current review suggests that workplace interventions and policy are required to improve the quality of work for young workers.
Since the mid-1980s, our understanding of nutrient limitation of oceanic primary production has radically changed. Mesoscale iron addition experiments (FeAXs) have unequivocally shown that iron ...supply limits production in one-third of the world ocean, where surface macronutrient concentrations are perennially high. The findings of these 12 FeAXs also reveal that iron supply exerts controls on the dynamics of plankton blooms, which in turn affect the biogeochemical cycles of carbon, nitrogen, silicon, and sulfur and ultimately influence the Earth climate system. However, extrapolation of the key results of FeAXs to regional and seasonal scales in some cases is limited because of differing modes of iron supply in FeAXs and in the modern and paleo-oceans. New research directions include quantification of the coupling of oceanic iron and carbon biogeochemistry.
Spermatogenesis is a complex and dynamic cellular differentiation process critical to male reproduction and sustained by spermatogonial stem cells (SSCs). Although patterns of gene expression have ...been described for aggregates of certain spermatogenic cell types, the full continuum of gene expression patterns underlying ongoing spermatogenesis in steady state was previously unclear. Here, we catalog single-cell transcriptomes for >62,000 individual spermatogenic cells from immature (postnatal day 6) and adult male mice and adult men. This allowed us to resolve SSC and progenitor spermatogonia, elucidate the full range of gene expression changes during male meiosis and spermiogenesis, and derive unique gene expression signatures for multiple mouse and human spermatogenic cell types and/or subtypes. These transcriptome datasets provide an information-rich resource for studies of SSCs, male meiosis, testicular cancer, male infertility, or contraceptive development, as well as a gene expression roadmap to be emulated in efforts to achieve spermatogenesis in vitro.
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•Single-cell transcriptomes of >62,000 spermatogenic cells from mice and humans•Human SSC fate regulation pathways match those of functionally defined mouse SSCs•The hepatic stellate cell activation pathway is associated with SSC fate•Unique 3-gene identifiers distinguish 11 spermatogenic cell types in mice and humans
Hermann et al. present single-cell transcriptomes from >62,000 individual spermatogenic cells from immature and adult male mice and adult men. Their analysis facilitates resolution of SSCs and progenitor spermatogonia, elucidates the full range of gene expression changes during male meiosis and spermiogenesis, and derives unique gene expression signatures for eleven mouse and human spermatogenic cell types.
Background
Polypharmacy, frailty and malnutrition are known predictors of adverse outcomes in dialysis patients. Little has reported about their interaction and composite prognostic values. We aimed ...to describe the interaction between polypharmacy, frailty, nutrition, hospitalization, and survival in peritoneal dialysis patients.
Methods
In this prospective cohort study, we recruited 573 peritoneal dialysis patients. Drug burden was measured by medication number and daily pill load. Frailty and nutrition were assessed by the validated Frailty Score (FQ) and Subjective Global Assessment (SGA) respectively. All patients were followed for two years. Primary outcome was all-cause mortality. Secondary outcomes were fall and fracture episodes, hospitalization, change in FQ and SGA.
Results
At baseline, each patient took 7.5 ± 2.6 medications with 15.5 ± 8.5 tablets per day. Medication number, but not daily pill load predicted baseline FQ (p = 0.004) and SGA (p = 0.03). Over 2 years, there were 69 fall and 1,606 hospitalization episodes. In addition, 148 (25.8%) patients died, while FQ and SGA changed by 0.73 ± 4.23 and −0.07 ± 1.06 respectively in survivors. Medication number (hospitalization: p = 0.02, survival: p = 0.005), FQ (hospitalization: p < 0.001; survival: p = 0.01) predicted hospitalization and survival. Medication number also predicted fall episodes (p = 0.02) and frailty progression (p = 0.002). Daily pill load did not predict any of these outcomes.
Conclusions
Drug burden is high in peritoneal dialysis patients, and it carries important prognostic implication. Medication number but not pill load significantly predicted onset and progression of frailty, malnutrition, fall, hospitalization, and mortality.
Abstract
Despite advancements in human pluripotent stem cells (hPSCs) differentiation protocols to generate appropriate neuronal progenitors suitable for transplantation in Parkinson’s disease, ...resultant grafts contain low proportions of dopamine neurons. Added to this is the tumorigenic risk associated with the potential presence of incompletely patterned, proliferative cells within grafts. Here, we utilised a hPSC line carrying a FailSafe
TM
suicide gene (thymidine kinase linked to cyclinD1) to selectively ablate proliferative cells in order to improve safety and purity of neural transplantation in a Parkinsonian model. The engineered FailSafe
TM
hPSCs demonstrated robust ventral midbrain specification in vitro, capable of forming neural grafts upon transplantation. Activation of the suicide gene within weeks after transplantation, by ganciclovir administration, resulted in significantly smaller grafts without affecting the total yield of dopamine neurons, their capacity to innervate the host brain or reverse motor deficits at six months in a rat Parkinsonian model. Within ganciclovir-treated grafts, other neuronal, glial and non-neural populations (including proliferative cells), were significantly reduced—cell types that may pose adverse or unknown influences on graft and host function. These findings demonstrate the capacity of a suicide gene-based system to improve both the standardisation and safety of hPSC-derived grafts in a rat model of Parkinsonism.
Autophagy is an important cellular process that controls cells in a normal homeostatic state by recycling nutrients to maintain cellular energy levels for cell survival via the turnover of proteins ...and damaged organelles. However, persistent activation of autophagy can lead to excessive depletion of cellular organelles and essential proteins, leading to caspase-independent autophagic cell death. As such, inducing cell death through this autophagic mechanism could be an alternative approach to the treatment of cancers. Recently, we have identified a novel autophagic inducer, saikosaponin-d (Ssd), from a medicinal plant that induces autophagy in various types of cancer cells through the formation of autophagosomes as measured by GFP-LC3 puncta formation. By computational virtual docking analysis, biochemical assays and advanced live-cell imaging techniques, Ssd was shown to increase cytosolic calcium level via direct inhibition of sarcoplasmic/endoplasmic reticulum Ca(2+) ATPase pump, leading to autophagy induction through the activation of the Ca(2+)/calmodulin-dependent kinase kinase-AMP-activated protein kinase-mammalian target of rapamycin pathway. In addition, Ssd treatment causes the disruption of calcium homeostasis, which induces endoplasmic reticulum stress as well as the unfolded protein responses pathway. Ssd also proved to be a potent cytotoxic agent in apoptosis-defective or apoptosis-resistant mouse embryonic fibroblast cells, which either lack caspases 3, 7 or 8 or had the Bax-Bak double knockout. These results provide a detailed understanding of the mechanism of action of Ssd, as a novel autophagic inducer, which has the potential of being developed into an anti-cancer agent for targeting apoptosis-resistant cancer cells.
Suicide by road vehicle collision in Australia is under-explored with mixed findings. We aimed to address this research gap by examining time trends, different types of vehicle collision, and ...individual characteristics related to vehicle-collision suicide.
We retrospectively analyzed deaths by suicide between 1st January 2001 and 31st December 2017 in Australia, using coronial records from the National Coronial Information System. The travel mode used and collision counterpart were retrieved from records of death by vehicle-collision suicide using all available information. We conducted negative binomial regression analysis to examine annual changes in suicide rate by vehicle collision on a public road (N = 640) and other methods of suicide (N = 41,890), and logistic regression analysis to examine individual characteristics associated with the likelihood of dying by suicide via road vehicle collision.
Overall, the national suicide rate involving road vehicle collision significantly increased, while the rate by other methods significantly decreased. Drivers accounted for 61% of suicide events by vehicle collision, of which 72% were single-vehicle collisions (commonly involving a tree). For multiple-vehicle collision suicide events, 82% involved collision with a truck. Pedestrians accounted for more than one-third of suicide events, of which 58% involved collision with a truck and 23% involved collision with a car/van. Individuals who were male (odds ratio 1.15; 95% CI 0.88-1.50), aged <25 years old (odds ratio 5.27; 95% CI 3.05-9.10), non-Indigenous (odds ratio 3.36; 95% CI 1.71-6.62), and born overseas (odds ratio 1.40; 95% CI 1.10-1.79) were more likely to die by vehicle-collision suicide than by other methods of suicide.
This study provides a better understanding of road vehicle collision suicide in Australia and informs future research directions on topic. Our findings can be used to inform suicide prevention initiatives to reduce vehicle-collision suicide deaths.
Abstract Background The Ki67-LI is a valid surrogate for biologic behavior of neuroendocrine tumors (NETs), with higher levels associated with aggressive behavior. The World Health Organization (WHO) ...classifies NETs according to Ki67-LI (G1: <3%; G2 : 3–20%; G3: >20%). Little is known about the evolution of NETs histologic characteristics over the disease course. We sought to evaluate variations in Ki67-LI throughout NETs disease course. Methods We retrospectively reviewed the Sunnybrook Odette Cancer Center NET database for patients with multiple pathology specimens. Primary outcome was the WHO NET class based on Ki67-LI for each specimen. We assessed change in WHO class between specimens. Results Forty-three patients were retrieved, of which 39 had specimens from the primary tumor and a metastatic focus, and 4 had specimens from multiple metastatic foci. Sixteen (37.0%) were identified with Ki67-LI falling in different WHO classes on distinct biopsies. For 12 (75.0%) of those 16 patients, Ki67-LI showed enough variability for WHO class to be upstaged: 5 (31%) from G1 to G2, 2 (13%) from G2 to G3, and 5 (31%) from G1 to G3. Conclusion When multiple pathology specimens were available, Ki67-LI varied throughout NETs disease course, with a majority of cases upgraded to a higher WHO class. If confirmed, this finding may have implications in how neuroendocrine tumors are monitored and treated. Further research is warranted to confirm these findings, understand better the underlying mechanisms of Ki67 variability, and define its relationship to prognosis.
We present the discovery of a slowly evolving, extragalactic radio transient, FIRST J141918.9+394036, identified by comparing a catalog of radio sources in nearby galaxies against new observations ...from the Very Large Array Sky Survey. Analysis of other archival data shows that FIRST J141918.9+394036 faded by a factor of ∼50 over 23 years, from a flux of ∼26 mJy at 1.4 GHz in 1993 to an upper limit of 0.4 mJy at 3 GHz in 2017. FIRST J141918.9+394036 is likely associated with the small star-forming galaxy SDSS J141918.81+394035.8 at a redshift z = 0.01957 (d = 87 Mpc), which implies a peak luminosity L 3 × 1038 erg s−1. If interpreted as an isotropic synchrotron blast wave, the source requires an explosion of kinetic energy ∼1051 erg some time prior to our first detection in late 1993. This explosion is most likely associated with a long gamma-ray burst (GRB), but the radio source could also be interpreted as the nebula of a newly born magnetar. The radio discovery of either of these phenomena would be unprecedented. Joint consideration of the event light curve, host galaxy, lack of a counterpart GRB, and volumetric rate suggests that FIRST J141918.9+394036 is the afterglow of an off-axis ("orphan") long GRB. The long time baseline of this event offers the best available constraint in afterglow evolution as the bulk of shock-accelerated electrons become non-relativistic. The proximity, age, and precise localization of FIRST J141918.9+394036 make it a key object for understanding the aftermath of rare classes of stellar explosion.
Aim To determine the relationship of birth weight to later glucose and insulin metabolism.
Methods Systematic review of the published literature. Data sources were Medline and Embase. Included ...studies were papers reporting the relationship of birth weight with a measure of glucose or insulin metabolism after 1 year of age, including the prevalence of Type 2 diabetes mellitus (DM). Three reviewers ed information from each paper according to specified criteria.
Results Forty‐eight papers fulfilled the criteria for inclusion, mostly of adults in developed countries. Most studies reported an inverse relationship between birth weight and fasting plasma glucose concentrations (15 of 25 papers), fasting plasma insulin concentrations (20 of 26), plasma glucose concentrations 2 h after a glucose load (20 of 25), the prevalence of Type 2 DM (13 of 16), measures of insulin resistance (17 of 22), and measures of insulin secretion (16 of 24). The predominance of these inverse relationships and the demonstration in a minority of studies of other directions of the relationships could not generally be explained by differences between studies in the sex, age, or current size of the subjects. However, the relationship of birth weight with insulin secretion was inconsistent in studies of adults.
Conclusions The published literature shows that, generally, people who were light at birth have an adverse profile of later glucose and insulin metabolism. This is related to higher insulin resistance, but the relationship to insulin secretion in adults is less clear.
Diabet. Med. 20, 339–348 (2003)
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