Job stress matters: Understanding how job stress moderates the relationship between person-environment fit and innovative work behavior in the Thai food industry.

This study investigates the impact of person-environment fit and job stress on innovative work behavior within Thailand's food industry. Through a comprehensive survey conducted among supervisors in the food industry, validated scales were utilized to measure person-environment fit, job stress, and innovative work behavior while controlling demographic variables. Employing hierarchical regression analysis and moderation analysis, the study examines the direct and moderating effects of person-environment fit and job stress on innovative work behavior. Results reveal a significant positive relationship between person-environment fit and innovative work behavior, with job stress moderating this relationship. Notably, specific points of interaction between job stress levels and person-environment fit are identified, shedding light on nuanced dynamics within the food industry. This research introduces a novel approach by integrating the Job Demands-Resources Model with person-environment fit theory to explore how specific stressors unique to the food industry can influence innovation. The study also pioneers the use of industry-specific measures for assessing job stress and innovation, which were developed and validated within this context. This research contributes to both theoretical and practical knowledge by enhancing our understanding of innovation mechanisms in the food industry and providing actionable insights for fostering creativity and innovation among employees. The study's originality lies not only in its emphasis on the context of the food industry but also in its development of tailored theoretical and methodological approaches to address the sector's unique challenges and opportunities.

Real-world visual acuity outcomes for patients with naïve neovascular age-related macular degeneration treated with aflibercept, ranibizumab, or bevacizumab in the Republic of Korea.

BACKGROUND: To compare the visual outcomes of different anti-vascular endothelial growth factor (VEGF) drugs, including aflibercept, ranibizumab, and bevacizumab, in a real-world setting in Korea. METHODS: We collected data from patients who received monotherapy using one of these three anti-VEGF drugs as naïve treatment after being diagnosed with neovascular age-related macular degeneration. The number of injections and visual acuity (VA) outcomes of each cohort were obtained and pairwise comparisons were performed using propensity score matching. RESULTS: A total of 254 aflibercept, 238 ranibizumab, and 282 bevacizumab treatment-naïve eyes were included. The mean VA change at 3 years for all cohorts combined was -1.8 letters, and the mean number of injections was 9.4. In the direct comparison of the three drugs, the mean change in the VA letter score was +2.0 letters for aflibercept and -11.7 letters for bevacizumab (P < 0.001). The number of aflibercept injections was significantly higher than the number of bevacizumab injections (P = 0.002). The visual outcomes for aflibercept and ranibizumab were +4.7 letters and -1.9 letters, respectively, and comparable results were obtained (P = 0.13). The VA outcomes for ranibizumab and bevacizumab were also not significantly different (P = 0.09). The numbers of injections for aflibercept, ranibizumab, and bevacizumab were 10.8, 6.7, and 8.8, respectively. Significant differences were observed between the injection frequencies comparisons of aflibercept and ranibizumab and ranibizumab and bevacizumab (P < 0.001 and P = 0.002, respectively). CONCLUSIONS: In the Korean clinical medical environment, which included various confounding factors, especially socioeconomic ones, the aflibercept VA outcome was significantly better than that of bevacizumab, and aflibercept injections were the most numerous. These real-world data imply that the drug effect as well as the environment in which the drug can be sufficiently used affected patient final VA scores.

Helicobacter pylori VacA-induced mitochondrial damage in the gastric pit cells of the antrum and therapeutic rescue.

Exploring host cell specificity, pathogenicity, and molecular mechanisms of the vacuolating cytotoxin A (VacA), secreted by Helicobacter pylori (Hp) is crucial for developing novel treatment strategies. VacA affects subcellular events, particularly mitochondria, at a cell-type-specific level. However, the lack of reliable models that mimic VacA-induced subcellular damages and enable novel drug screening linked to the human stomach clinically limits our understanding of the mitochondrial networks in vivo. Here, human antrum gastric organoids (hAGOs) and tissue samples from Hp-infected patients were used to show the toxic effects of VacA-induced mitochondrial damage mainly in mucus-producing gastric pit cells by employing transcriptional, translational, and functional analyses. In VacA-intoxicated or Hp-infected hAGOs, robust mitochondrial fragmentation in gastric pit cells reduced ATP production during respiration, and loss of mucosal barrier integrity was first demonstrated experimentally. Using hAGOs, clinically relevant small molecules were screened for efficacy, and MLN8054, an Aurora kinase A inhibitor, reversed VacA-induced mitochondrial damage and loss of gastric epithelium integrity. MLN8054 was effective in VacA-treated and Hp-infected hAGOs and mice, highlighting hAGOs as a promising drug-screening model. These findings suggest that mitochondrial quality control may serve as a promising therapeutic target for Hp VacA-mediated toxicity and disease progression.

Hyperexcitability precedes CA3 hippocampal neurodegeneration in a dox-regulatable TDP-43 mouse model of ALS-FTD.

Neuronal hyperexcitability is a hallmark of amyotrophic lateral sclerosis (ALS) but its relationship with the TDP-43 aggregates that comprise the predominant pathology in over 90% of ALS cases remains unclear. Emerging evidence in tissue and slice culture models indicate that TDP-43 pathology induces neuronal hyperexcitability suggesting it may be responsible for the excitotoxicity long believed to be a major driver of ALS neuron death. Here, we characterized hyperexcitability and neurodegeneration in the hippocampus of doxycycline-regulatable rNLS8 mice (NEFH-tTA x tetO-hTDP-43ΔNLS), followed by treatment with AAV encoded DREADDs and anti-seizure medications to measure the effect on behavioral function and neurodegeneration. We found that approximately half of the CA3 neurons in the dorsal hippocampus are lost between 4 and 6 weeks after TDP-43ΔNLS induction. Neurodegeneration was preceded by selective hyperexcitability in the mossy fiber - CA3 circuit, leading us to hypothesize that glutamate excitotoxicity may be a significant contributor to neurodegeneration in this model. Interestingly, hippocampal injection of AAV encoded inhibitory DREADDs (hM4Di) and daily activation with CNO ligand rescued anxiety deficits on elevated zero maze (EZM) but did not reduce neurodegeneration. Therapeutic doses of the anti-seizure medications, valproic acid and levetiracetam, did not improve behavior or prevent neurodegeneration. These results highlight the complexity of TDP-43 - induced alterations to neuronal excitability and suggest that whereas targeting hyperexcitability can meliorate some behavioral deficits, it may not be sufficient to halt or slow neurodegeneration in TDP-43-related proteinopathies. Significance Statement: Cytoplasmic aggregates of TAR DNA Binding Protein 43 (TDP-43) are the predominant pathology in over 90% of Amyotrophic lateral sclerosis (ALS) and the majority of frontotemporal lobar degeneration (FTLD-TDP) cases. Understanding how TDP-43 pathology promotes neurodegeneration may lead to therapeutic strategies to slow disease progression in humans. Recent reports in mouse and cell culture models suggest loss-of-normal TDP-43 function may drive neuronal hyperexcitability, a key physiological hallmark of ALS and possible contributor to neurodegeneration. In this study, we identified region-specific hyperexcitability that precedes neurodegeneration in the inducible rNLS8 TDP-43 mouse model. Suppressing hyperexcitability with chemogenetics improved behavioral function but did not reduce hippocampal neuron loss. Anti-seizure medications had no beneficial effects suggesting directly targeting hyperexcitability may not be therapeutically effective.

Erratum: Correction of Figure in the Article "Viral, Immunologic, and Laboratory Parameters in Patients With and Without Post-Acute Sequelae of SARS-CoV-2 Infection (PASC)".

This corrects the article on p. e237 in vol. 39, PMID: 39252682.

HM-chromanone attenuates obesity and adipose tissue inflammation by downregulating SREBP-1c and NF-κb pathway in high-fat diet-fed mice.

Background: Obese adipose tissue produces various pro-inflammatory cytokines that are major contributors to adipose tissue inflammation.Objective: The present study aimed to determine the effects of HM-chromanone (HMC) against obesity and adipose tissue inflammation in high-fat diet-fed mice.Materials and methods: Twenty-four C57BL/6J male mice were divided into three groups: ND (normal diet), HFD (high-fat diet), and HFD + HMC. The ND group was fed a normal diet, whereas the HFD and HFD + HMC groups were fed a high-fat diet. After 10 weeks of feeding, the animals were orally administered the treatments daily for 9 weeks. The ND and HFD group received distilled water as treatment. The HFD+HMC group was treated with HM-chromaone (50 mg/kg).Results: HM-chromanone administration decreased body weight, fat mass, and adipocyte diameter. HM-chromanone also improved plasma lipid profiles, decreased leptin levels, and increased adiponectin levels. The inhibiting effect of HM-chromanone on SREBP-1c, PPARγ, C/EBPα, and FAS decreased adipogenesis, thereby alleviating lipid accumulation. Furthermore, HM-chromanone administration exhibited a reduction in macrophage infiltration and the expression of pro-inflammatory cytokines. HM-chromanone suppressed the phosphorylation of IκBα and NF-κB, leading to the inhibition of iNOS and COX2 expressions, resulting in decreased inflammation in adipose tissue.Discussion and conclusion: These results highlight the anti-obesity and anti-inflammatory properties of HM-chromanone, achieved through the downregulation of the SREBP-1c and NF-κB pathway in high-fat diet-fed mice.

Lactobacillus plantarum NCHBL-004 modulates high-fat diet-induced weight gain and enhances GLP-1 production for blood glucose regulation.

OBJECTIVES: This study investigated the therapeutic potential of Lactobacillus plantarum NCHBL-004 (NCHBL-004) in the treatment of obesity and associated metabolic disorders. METHODS: Mice were fed either a normal diet (ND) or a high-fat diet (HFD) with oral administration of NCHBL-004. After euthanasia, blood, liver and adipose tissue were collected. Furthermore, the microbiome and short-chain fatty acids (SCFAs) were analyzed from feces. RESULTS: Oral administration of live NCHBL-004 to mice fed a HFD resulted in notable reductions in weight gain, improvements in glucose metabolism, and maintenance of balanced lipid levels. A comparative analysis with other Lactobacillus strains highlighted the superior efficacy of NCHBL-004. Moreover, heat-killed NCHBL-004 demonstrated beneficial effects similar to those of live NCHBL-004. Additionally, administration of live NCHBL-004 induced glucagon-like peptide 1 (GLP-1) production and increased the levels of short-chain fatty acids (SCFAs), including acetate and propionate, in feces, positively influencing liver lipid metabolism and mitigating inflammation. Consistent with this, analysis of the gut microbiome following NCHBL-004 administration showed increases in SCFA-producing microbes with increased proportions of Lactobacillus spp. and a significant increase in the proportion of microbes capable of promoting GLP-1 secretion. CONCLUSIONS: These findings underscore the potential of both live and inactivated NCHBL-004 as potential therapeutic approaches to managing obesity and metabolic disorders, suggesting avenues for further investigation and clinical applications.

Combined copper isotope and elemental signatures in bivalves and sediments from the Korean coast: Applicability for monitoring anthropogenic contamination.

This study investigates the applicability of elemental and Cu isotope compositions in sediments and bivalves from the Korean coast to monitor anthropogenic Cu contamination. Sediments with high Cu (>64.4 mg/kg) and/or moderate enrichment levels (EFCu) exhibit homogenous δ65CuAE647 values (-0.12 to +0.16 ‰), suggesting similar anthropogenic Cu fingerprints along the Korean coast. Sediments with Cu concentrations near natural background levels (< 20.6 mg/kg) display large isotopic variability (Δ65Cumax-mim: ~0.8 ‰), encompassing those from sediments under anthropic influences. We hypothesize that Cu isotopic compositions of Korean geology are heterogeneous, therefore, natural end-members of source mixing models should be established locally at small scales. Cu concentrations in Oysters correlate with sediments, and their isotopic compositions are more suitable for monitoring Cu contamination, while mussel's regulatory mechanisms seem to affect source records. The current Cu isotope data will help to detect shifts attributable to anthropic contamination in future biomonitoring.

Corrigendum: 2023 Korean Society of Menopause - Osteoporosis Guidelines Part I.

This corrects the article on p. 1 in vol. 30, PMID: 38714490.

Serum Cholesterol Level Changes during Gonadotropin-Releasing Hormone-Agonist Therapy in Premenopausal Female Patients with Breast Cancer.

OBJECTIVES: To investigate the changes in cholesterol levels during medical ovarian suppression. METHODS: We reviewed the medical records and blood test results of 187 female patients with breast cancer who underwent gonadotropin-releasing hormone (GnRH)-agonist therapy for > 24 weeks at our hospital between 1 January 2018 and 31 December 2020. The study excluded patients in this cohort who had previously been diagnosed with dyslipidemia, diabetes, or had recently received lipid-lowering agents, resulting in a final sample size of 152 participants. The age at diagnosis and preoperative body mass index (BMI) were included as baseline demographics. A generalized additive mixed model was applied to analyze the relationship between the duration of GnRH-agonist treatment and changes in cholesterol levels. RESULTS: The study participants had a mean age of 42.5 ± 5.2 years and a mean preoperative BMI of 23.0 ± 3.6 kg/m²; the mean GnRH-agonist therapy duration was 19.3 months (range: 5.6-37.7 months); and the total cholesterol level before GnRH-agonist treatment was 171 mg/dL that was significantly higher at 181 mg/dL (P = 0.03) during the most recent measurement. The total cholesterol level was unaffected by the GnRH-agonist therapy until 19.3 months after which it significantly increased by 1.28 mg/dL per month (P = 0.011). There was no significant effect of age, preoperative BMI, or the glomerular filtration rate on the total cholesterol levels. CONCLUSIONS: Long-term GnRH agonist therapy for > 19 months can cause a significant increase in the serum cholesterol levels. To prevent complications, patients receiving the treatment should be informed and monitored for the possible progression of dyslipidemia.

Viral, Immunologic, and Laboratory Parameters in Patients With and Without Post-Acute Sequelae of SARS-CoV-2 Infection (PASC).

BACKGROUND: The pathophysiological mechanisms underlying the post-acute sequelae of severe acute respiratory syndrome coronavirus 2 infection (PASC) are not well understood. Our study aimed to investigate various aspects of theses mechanisms, including viral persistence, immunological responses, and laboratory parameters in patients with and without PASC. METHODS: We prospectively enrolled adults aged ≥ 18 years diagnosed with coronavirus disease 2019 (COVID-19) between August 2022 and July 2023. Blood samples were collected at three time-points: within one month of diagnosis (acute phase) and at 1 month, and 3 months post-diagnosis. Following a recent well-designed definition of PASC, PASC patients were defined as those with a questionnaire-based PASC score ≥ 12 persisting for at least 4 weeks after the initial COVID-19 diagnosis. RESULTS: Of 57 eligible COVID-19 patients, 29 (51%) had PASC, and 28 (49%) did not. The PASC group had significantly higher nucleocapsid protein (NP) antigenemia 3 months after COVID-19 diagnosis (P = 0.022). Furthermore, several cytokines, including IL-2, IL-17A, VEGF, RANTES, sCD40L, IP-10, I-TAC, and granzyme A, were markedly elevated in the PASC group 1 and/or 3 month(s) after COVID-19 diagnosis. In contrast, the median values of several serological markers, including thyroid markers, autoimmune indicators, and stress-related hormones, were within the normal range. CONCLUSION: Levels of NP antigen and of various cytokines involved in immune responses become significantly elevated over time after COVID-19 diagnosis in PASC patients compared to non-PASC patients. This suggests that PASC is associated with prolonged immune dysregulation resulting from heightened antigenic stimulation.

Camera-Based 3D Semantic Scene Completion With Sparse Guidance Network.

Semantic scene completion (SSC) aims to predict the semantic occupancy of each voxel in the entire 3D scene from limited observations, which is an emerging and critical task for autonomous driving. Recently, many studies have turned to camera-based SSC solutions due to the richer visual cues and cost-effectiveness of cameras. However, existing methods usually rely on sophisticated and heavy 3D models to process the lifted 3D features directly, which are not discriminative enough for clear segmentation boundaries. In this paper, we adopt the dense-sparse-dense design and propose a one-stage camera-based SSC framework, termed SGN, to propagate semantics from the semantic-aware seed voxels to the whole scene based on spatial geometry cues. Firstly, to exploit depth-aware context and dynamically select sparse seed voxels, we redesign the sparse voxel proposal network to process points generated by depth prediction directly with the coarse-to-fine paradigm. Furthermore, by designing hybrid guidance (sparse semantic and geometry guidance) and effective voxel aggregation for spatial geometry cues, we enhance the feature separation between different categories and expedite the convergence of semantic propagation. Finally, we devise the multi-scale semantic propagation module for flexible receptive fields while reducing the computation resources. Extensive experimental results on the SemanticKITTI and SSCBench-KITTI-360 datasets demonstrate the superiority of our SGN over existing state-of-the-art methods. And even our lightweight version SGN-L achieves notable scores of 14.80% mIoU and 45.45% IoU on SeamnticKITTI validation with only 12.5 M parameters and 7.16 G training memory. Code is available at https://github.com/Jieqianyu/SGN.

Influence of different types of dietary sugars on the intestinal mucosa and hepatic lipid metabolism in germ-free mice.

The excessive consumption of dietary sugar induces changes in gut microbiota, which is associated with obesity and metabolic dysregulation. This study investigated the effects of monosaccharide and fructooligosaccharide (FOS) intake on metabolic function and intestinal environment in germ-free (GF) mice lacking gut microbiota. GF mice were provided with a chow diet and administered a water solution containing 15 % glucose, fructose, or FOS for 4 weeks. Compared with FOS, glucose, and fructose induced increased hepatic lipid accumulation, increased adipocyte size in white adipose tissue, and upregulated hepatic lipogenic gene expression. FOS exhibited notably higher activation of hepatic AMP-activated protein kinase compared with those consuming glucose or fructose. Moreover, the number of goblet cells in the intestinal mucosa increased significantly with FOS consumption. Collectively, these findings indicate that while monosaccharides caused metabolic disorders in GF mice, FOS alleviated these disorders and increased the number of goblet cells in the intestinal mucosa. These results provide evidence for the occurrence of these effects independently of the gut microbiota.

Not on the right rung for me? How status inconsistency leads to avoidance of status-threatening ties in NCAA.

This study examines the impact of status inconsistency on status-threatening activities within NCAA Division I men's basketball teams. Specifically, we focus on a nested form of status that includes both individual and group-level elements. We argue that organizations dealing with status inconsistency stemming from such nested form face challenges in reducing status inconsistency. To maintain their deserved status, these status-inconsistent organizations tend to avoid activities that could further threaten their status, despite potential economic gains. An analysis of NCAA Division I men's basketball scheduling data from 2000 to 2019 provides robust support to our theoretical arguments. Our findings suggest that the status inconsistency between a team's status and its conference status diminished the likelihood of scheduling games with non-Division I teams, a behavior considered counter-normative in this context. This effect is most prominent among teams in "Mid Major" conferences, while teams with recent participation in the NCAA Tournament show a mitigated effect.

Association between maxillary incisor width and craniofacial measurements: A cone beam computed tomography study.

STATEMENT OF PROBLEM: Accurate prediction of maxillary central incisor width (CIW) is essential in prosthodontics for selecting appropriately sized denture teeth. While traditional methods exist, the digital era may offer more reliable techniques for anterior tooth selection. PURPOSE: The purpose of this study was to investigate the correlation between CIW and craniofacial measurements derived from cone beam computed tomography (CBCT) scans to identify predictors for CIW and examine possible sexual dimorphism. MATERIAL AND METHODS: A retrospective analysis was conducted on 80 three-dimensional skull models (40 men, 40 women; age range: 20 to 48 years) generated from segmented CBCT scans. Measurements included CIW, interpterygoid hamulus distance, bi-orbital width, interorbital distance, and piriform aperture width. Statistical analyses comprised independent t tests, bivariate correlations, and multiple linear regression (α=.05). RESULTS: Significant sexual dimorphism was observed in CIW, interpterygoid hamulus distance, and bi-orbital width (P<.05). CIW positively correlated with bi-orbital width (r=.75, P<.001) and piriform aperture width (r=.49, P<.001). Multiple regression analysis revealed bi-orbital width, and interorbital distance, along with sex, as significant predictors of CIW (R²=.59, P<.001). CONCLUSIONS: Bony bi-orbital width, interorbital distance, and sex can be used to estimate the maxillary CIW.

A Robust Method for Simultaneous Determination and Risk Assessment of Multiresidual Pesticides in Fishery Products.

In this study, we developed and validated a multiresidue analytical method for the simultaneous detection of 24 pesticides in fishery products. Using the EN15662 extraction method and C18 as the adsorbent for purification, the validation results complied with Codex guidelines, achieving recovery rates between 70% and 120% and relative standard deviation values (%RSD) within 20%, indicating excellent performance. The limit of detection ranged from 0.25 to 0.8 ng/kg, and the limit of quantification was between 3 and 10 ng/g, providing sufficient sensitivity to comply with future regulatory standards. The calibration curves for all 24 pesticides exhibited great linearity (R2 > 0.98), also satisfying the Codex requirements. The matrix effect was less than 30% for some pesticides-within ±20%-indicating minimal interference from impurities. An analysis of 300 fishery samples from nine regions across South Korea detected lufenuron at 10 ng/g in eels; however, the risk assessment was below 0.19%, posing no significant hazard to public health. This newly developed analytical method proved effective for the multi-analysis of pesticide residues in fishery products, offering rapid and reliable monitoring of the import and export safety of fishery products.

Herbal Formula Extract Ameliorates Anxiety and Cognitive Impairment via Regulation of the Reelin/Dab-1 Pathway in a Murine Model of Post-Traumatic Stress Disorder.

We investigated the effects of epigenetic modifications on post-traumatic stress disorder (PTSD) using a novel combination of herbal medicines from Panax ginseng, Astragalus membranaceus, Atractylodes macrocephala, and Glycyrrhiza uralensis. The herbal formula extract (HFE) (250 mg/kg) was administered orally once daily for 14 days to determine its effects on PTSD in mice by combining prolonged stress and foot shock. The open field and Y-maze tests determined the effect of HFE on PTSD-induced anxiety and cognition. Hippocampal neuronal plastic changes and molecular mechanism were verified. Treatment with HFE decreased anxiety-like behavior and enhanced cognition. Moreover, it reduced the number of PTSD-related hilar ectopic granule cells in the dentate gyrus (DG). PTSD mice showed reduced neuronal plasticity of doublecortin+ cells in the DG, which was restored by HFE treatment. HFE reversed PTSD-induced inhibition of the Reelin/Dab1 pathway, a critical signaling cascade involved in brain development, and regulated Reelin methylation. Furthermore, DNA methylation, methyl-CpG binding protein 2, and DNA methyltransferase 1, which were elevated in the hippocampus of PTSD mice, were restored following HFE treatment. HFE increased the expression of synaptic plasticity-related factors in the hippocampus of PTSD mice. Our findings suggest that HFE can facilitate PTSD treatment by alleviating behavioral abnormalities through the restoration of hippocampal dysfunction via regulation of the Reelin/Dab-1 pathway and DNA methylation in the hippocampus.

Polyubiquitinated PCNA triggers SLX4-mediated break-induced replication in alternative lengthening of telomeres (ALT) cancer cells.

Replication stresses are the major source of break-induced replication (BIR). Here, we show that in alternative lengthening of telomeres (ALT) cells, replication stress-induced polyubiquitinated proliferating cell nuclear antigen (PCNA) (polyUb-PCNA) triggers BIR at telomeres and the common fragile site (CFS). Consistently, depleting RAD18, a PCNA ubiquitinating enzyme, reduces the occurrence of ALT-associated promyelocytic leukemia (PML) bodies (APBs) and mitotic DNA synthesis at telomeres and CFS, both of which are mediated by BIR. In contrast, inhibiting ubiquitin-specific protease 1 (USP1), an Ub-PCNA deubiquitinating enzyme, results in an increase in the above phenotypes in a RAD18- and UBE2N (the PCNA polyubiquitinating enzyme)-dependent manner. Furthermore, deficiency of ATAD5, which facilitates USP1 activity and unloads PCNAs, augments recombination-associated phenotypes. Mechanistically, telomeric polyUb-PCNA accumulates SLX4, a nuclease scaffold, at telomeres through its ubiquitin-binding domain and increases telomere damage. Consistently, APB increase induced by Ub-PCNA depends on SLX4 and structure-specific endonucleases. Taken together, our results identified the polyUb-PCNA-SLX4 axis as a trigger for directing BIR.