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Objectives Burnout among health care workers is highly prevalent and has profound impact on quality of care. Hospital on‐duty schedules lead to long working hours and short sleeping hours; both are common factors associated with burnout. We examined the dose‐response relationship and the potential mediating role of sleeping hours on the association between working hours and burnout among health care workers. Methods We collected data on the burnout status, using the Mandarin version of the Copenhagen Burnout Inventory (subscales measure work‐related and personal burnouts), working hours, sleeping hours, and relevant measures for 2081 health care personnel who underwent a routine health examination in a medical center in Taiwan during 2016‐2017. Four subgroups were compared: physicians (n = 369), nurses (n = 973), technicians (n = 391), and administrators (n = 348). Results Average weekly working hours are associated with burnout scores in a non‐linear dose‐response manner. Compared with a work week of 40 hours, the odds ratio of work‐related burnout doubled when hours exceeded 60, tripled when hours exceeded 74, and quadrupled when hours exceeded 84. Physicians’ burnout is less susceptible to incremental increases in working hours, compared to the situations in other health care workers. The proportions eliminated by reducing sleeping hours were 25%‐73% for physicians and 7%‐29% for nurses respectively. Conclusions Our findings suggest that working hours are associated with burnout, and the association was partially mediated by sleeping hours.

In addition to the regulation of social and emotional behaviors, the hypothalamic neuropeptide oxytocin has been shown to stimulate neurogenesis in adult dentate gyrus; however, the mechanisms underlying the action of oxytocin are still unclear. Taking advantage of the conditional knockout mouse model, we show here that endogenous oxytocin signaling functions in a non-cell autonomous manner to regulate survival and maturation of newly generated dentate granule cells in adult mouse hippocampus via oxytocin receptors expressed in CA3 pyramidal neurons. Through bidirectional chemogenetic manipulations, we also uncover a significant role for CA3 pyramidal neuron activity in regulating adult neurogenesis in the dentate gyrus. Retrograde neuronal tracing combined with immunocytochemistry revealed that the oxytocin neurons in the paraventricular nucleus project directly to the CA3 region of the hippocampus. Our findings reveal a critical role for oxytocin signaling in adult neurogenesis. Oxytocin (OXT) has been implicated in adult neurogenesis. Here the authors show that CA3 pyramidal cells in the adult mouse hippocampus express OXT receptors and receive inputs from hypothalamic OXT neurons; activation of OXT signaling in CA3 pyramidal cells promotes the survival and maturation of newborn neurons in the dentate gyrus in a non-cell autonomous manner.

New products can evoke anticipatory emotions such as hope and anxiety. On the one hand, consumers might hope that innovative offerings will produce goal-congruent outcomes; on the other hand, they might also be anxious about possible outcomes that are goal-incongruent. The authors demonstrate the provocative and counterintuitive finding that strong anxiety about potentially goal-incongruent outcomes from a new product actually enhances (vs. weakens) consequential adoption intentions (Study 1) and actual adoption (Studies 2 and 3) when hope is also strong. The authors test action planning (a form of elaboration) and perceived control over outcomes as serial mediators to explain this effect. They find that the proposed mechanism holds even after they consider alternative explanations, including pain/gain inferences, confidence in achieving goal-congruent outcomes, global elaboration, affective forecasts, and motivated reasoning. Managerially, the findings suggest that when bringing a new product to market, new product adoption may be greatest when hope and anxiety are both strong. The findings also point to ways in which marketers might enhance hope and/or anxiety, and they suggest that the use of potentially anxiety-inducing tactics such as disclaimers in ads and on packages might not deter adoption when hope is also strong.

There is limited evidence that long-term exposure to ambient air pollution increases the risk of childhood autism spectrum disorder (ASD). The objective of the study was to investigate the associations between long-term exposure to air pollution and newly diagnostic ASD in Taiwan. We conducted a population-based cohort of 49,073 children age less than 3 years in 2000 that were retrieved from Taiwan National Insurance Research Database and followed up from 2000 through 2010. Inverse distance weighting method was used to form exposure parameter for ozone (O3), carbon monoxide (CO), nitrogen dioxide (NO2), sulfur dioxide (SO2), and particles with aerodynamic diameter less than 10 µm (PM10). Time-dependent Cox proportional hazards (PH) model was performed to evaluate the relationship between yearly average exposure air pollutants of preceding years and newly diagnostic ASD. The risk of newly diagnostic ASD increased according to increasing O3, CO, NO2, and SO2 levels. The effect estimate indicating an approximately 59% risk increase per 10 ppb increase in O3 level (95% CI 1.42–1.79), 37% risk increase per 100 ppb in CO (95% CI 1.31–1.44), 340% risk increase per 10 ppb increase in NO2 level (95% CI 3.31–5.85), and 17% risk increase per 1 ppb in SO2 level (95% CI 1.09–1.27) was stable with different combinations of air pollutants in the multi-pollutant models. Our results provide evident that children exposure to O3, CO, NO2, and SO2 in the preceding 1 year to 4 years may increase the risk of ASD diagnosis.

Positive fluid balance is a prognostic factor for mortality in patients with sepsis; however, the association between cumulated fluid balance (CFB) and sepsis-induced multi-organ dysfunction syndrome (MODS) has yet to be elucidated. In this study, we sought to determine whether CFB is correlated with MODS and mortality in cases of septic shock. The study retrospectively recruited patients with septic shock from the intensive care unit of a tertiary care hospital. Multiple organ dysfunction syndrome (MODS) was identified as sequential organ failure assessment (SOFA) score ≥ 2 in more than one organ system. The CFB is the sum of all daily intake and output. An independent t-test, single and multivariate logistic regression, the receiver operating characteristic (ROC) curves, and the Pearson correlation coefficient were used to determine whether a relationship exists between CFB and the development of MODS and mortality. Among the 104 patients enrolled in the study, 58 (55.8%) survived more than 28 days, and 73 (70.2%) developed MODS on day 3. The values of CFB in the first 24 hours and 72 hours after diagnosis of septic shock in patients with MODS were higher than these in patients without MODS (1086.6 ± 176.3 vs. 325.5 ± 205.7 ml, p = 0.013 and 2408 ± 361 vs. 873.1 ± 489 ml, p < 0.0001). In a multivariate logistic regression, the independent factors associated with the development of MODS on day 3 were APACHE II score at ICU admission (27.6 ± 7.6 in patients with MODS vs. 20.5 ± 6.4 in those without; O.R. 1.18; 95% C.1 I. 1.08-1.30; p < 0.001), disseminated intravascular coagulopathy (DIC) (n = 28; 38.4% vs. n = 2; 6.5%; O.R. 23.67; 95% C.I. 3.58-156.5; p = 0.001), and CFB in the first 72 hours (72-hr CFB) > median (1767.50ml) (n = 41; 56.2% vs. n = 11; 35.5%; O.R. 3.67; 95% C.I., 1.18-11.40; p = 0.024). Moreover, a multivariate logistic regression also identified neoplasm (n = 25; 54.3% vs. n = 17; 29.3%; O.R. 3.45; 95% C.I. 1.23-10.0; p = 0.019) and 72-hr CFB > median (n = 30; 65.2% vs. n = 21; 36.2%; O.R. 4.13; 95% C.I. 1.34-12.66; p = 0.013) as independent factors associated with 28-day mortality. 72-hr CFB values were strongly correlated with the SOFA score (r = 0.445, p < 0.0001). The area under the ROC curve revealed that 72-hr CFB has good discriminative power in associating the development of MODS (0.644, p = 0.002) and predicting subsequent 28-day mortality (0.704, p < 0.0001). 72-hr CFB appears to be correlated with the likelihood of developing MODS and mortality in patients with septic shock. Thus, it appears that 72-hr CFB could perhaps be used as an indicator for MODS and a predictor for mortality in those patients.

The Elongator complex catalyzes posttranscriptional tRNA modifications by attaching carboxy-methyl (cm 5 ) moieties to uridine bases located in the wobble position. The catalytic subunit Elp3 is highly conserved and harbors two individual subdomains, a radical S -adenosyl methionine (rSAM) and a lysine acetyltransferase (KAT) domain. The details of its modification reaction cycle and particularly the substrate specificity of its KAT domain remain elusive. Here, we present the co-crystal structure of bacterial Elp3 (DmcElp3) bound to an acetyl-CoA analog and compare it to the structure of a monomeric archaeal Elp3 from Methanocaldococcus infernus (MinElp3). Furthermore, we identify crucial active site residues, confirm the importance of the extended N-terminus for substrate recognition and uncover the specific induction of acetyl-CoA hydrolysis by different tRNA species. In summary, our results establish the clinically relevant Elongator subunit as a non-canonical acetyltransferase and genuine tRNA modification enzyme. Elp3 is the catalytic subunit of the eukaryotic Elongator complex that catalyzes posttranscriptional tRNA modifications. Here the authors present the crystal structures of an acetyl-CoA analog bound bacterial Elp3 and a monomeric archaeal Elp3 and show that Elp3 functions as a tRNA modification enzyme in all domains of life.

Reactive oxygen species (ROS) have been recognized as prevalent contributors to the development of inner retinal injuries including optic neuropathies such as glaucoma, non‐arteritic anterior ischemic optic neuropathy, traumatic optic neuropathy, and Leber hereditary optic neuropathy, among others. This underscores the pivotal significance of oxidative stress in the damage inflicted upon retinal tissue. To combat ROS‐related challenges, this study focuses on creating an injectable and tissue‐adhesive hydrogel with tailored antioxidant properties for retinal applications. GelCA, a gelatin‐modified hydrogel with photo‐crosslinkable and injectable properties, is developed. To enhance its antioxidant capabilities, curcumin‐loaded polydopamine nanoparticles (Cur@PDA NPs) are incorporated into the GelCA matrix, resulting in a multifunctional nanocomposite hydrogel referred to as Cur@PDA@GelCA. This hydrogel exhibits excellent biocompatibility in both in vitro and in vivo assessments, along with enhanced tissue adhesion facilitated by NPs in an in vivo model. Importantly, Cur@PDA@GelCA demonstrates the potential to mitigate oxidative stress when administered via intravitreal injection in retinal injury models such as the optic nerve crush model. These findings underscore its promise in advancing retinal tissue engineering and providing an innovative strategy for acute neuroprotection in the context of inner retinal injuries. This study addresses inner retinal injuries, emphasizing the role of reactive oxygen species (ROS). GelCA, a photo‐crosslinkable and injectable hydrogel synthesized by grafting cinnamic acid onto gelatin is developed. Incorporating curcumin‐loaded polydopamine nanoparticles results in Cur@PDA@GelCA, a multifunctional nanocomposite hydrogel. This innovative hydrogel demonstrates excellent biocompatibility, enhanced tissue adhesion, and the potential to mitigate oxidative stress in retinal injury models.

Euryhaline teleosts can survive in environments with different salinities. Cortisol is an important hormone for acclimation to seawater (SW) of euryhaline teleosts. Osmotic stress transcription factor 1 (OSTF1), also called the transforming growth factor-beta stimulated clone 22 domain 3 (tsc22d3), was first reported in tilapia as an acute response gene and protein under hyperosmotic stress, and it is regulated by cortisol. To date, most studies on OSTF1 have focused on freshwater inhabitants, such as tilapia, medaka, and catadromous eel. The expression of OSTF1 and the correlation between OSTF1 and cortisol in marine inhabitant euryhaline teleosts, to our knowledge, remain unclear. This study reveals the changes in the expression levels of branchial OSTF1, plasma cortisol levels, and their correlation in the marine inhabitant milkfish with ambient salinities. The two sequences of milkfish TSC22D3 transcripts were classified as OSTF1a and OSTF1b. Both genes were expressed universally in all detected organs and tissues but were the most abundant in the liver. Similar gene expression levels of ostf1a and ostf1b were found in SW- and fresh water (FW)-acclimated milkfish gills, an important osmoregulatory organ. Within 12 hours of being transferred from FW to SW, the gene expression level of ostf1b increased significantly (4 folds) within 12 h, whereas the expression level of ostf1a remained constant. Moreover, cortisol levels increased rapidly after being transferred to a hyperosmotic environment. After an intraperitoneal injection of cortisol, the gene expression levels of ostf1a and ostf1b were elevated. However, under hyperosmotic stress, ostf1a gene expression remained stable. Overall, the results revealed that ostf1b was the primary gene in milkfish responding to hypertonic stress, and cortisol concentration increased after the transfer of milkfish from FW to SW. Furthermore, cortisol injection increased the expression of ostf1a and ostf1b . As a result, factors other than cortisol may activate ostf1b in milkfish gills in response to an environmental salinity challenge.

Current harmonics in six-phase permanent magnet synchronous motors (PMSMs) arise from inherent asymmetries caused by manufacturing tolerances and nonlinear characteristics in the inverter output. Additionally, magnetic saturation and slight imbalances in the windings introduce flux linkage asymmetries, resulting in both fundamental current imbalance and low-order harmonics. Although these imbalances are minor and do not indicate fault conditions, they can cause uneven copper loss and eventually reduce the overall service life of the motor. This paper proposes a harmonic suppression strategy for mitigating imbalance current harmonics in non-ideal six-phase PMSMs. The method integrates back-electromotive force harmonic feedforward compensation (BEMF-HFC) with harmonic synchronous reference frame current control (HSRF-CC). An imbalance flux linkage harmonic model is developed in simulations to replicate the measured imbalance phase currents and to validate the effectiveness of the proposed strategy. The experimental setup is built using a microcontroller from Texas Instruments (TI), which generates six-phase complementary PWM signals for the power stage and receives feedback signals including phase currents, DC bus voltage, and rotor position. Rotor position is acquired through a 12-pole resolver and a 12-bit resolver-to-digital converter (RDC). The six-phase PMSM used in the tests is specified with 12 poles, a rated DC bus voltage of 600 V, a rated current of 200 Arms, and a rated rotor speed of 1200 rpm. Compared with conventional harmonic suppression strategies that do not target imbalance current harmonics, the proposed method achieves a better current balance and lower total harmonic distortion (THD). At 1200 rpm, the magnitude deviation of the fundamental, third, and fifth current harmonics is reduced from 8.61%, 2.88%, and 2.94% to 1.19%, 1.02%, and 0.5%, respectively.

Software-defined networking (SDN) is a new network architecture that provides programmable networks, more efficient network management, and centralized control than traditional networks. The TCP SYN flooding attack is one of the most aggressive network attacks that can seriously degrade network performance. This paper proposes detection and mitigation modules against SYN flooding attacks in SDN. We combine those modules, which have evolved from the cuckoo hashing method and innovative whitelist, to get better performance compared to current methods Our approach reduces the traffic through the switch and improves detection accuracy, also the required register size is reduced by half for the same accuracy.