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This study is constructed of life course profiles of the educational trajectories of a cohort of rural girls from a village in the mountains of western China during critical educational reform years. Observational date were collected annually from 2000-2022. Findings show that even in remote mountainous region of China, village girls attained surprisingly advanced educational levels. Specifically, 76 percent of the participants had attained education beyond the compulsory level; 92 percent progressed to senior secondary school, and their graduation rate was 94 percent. The entrance rates to tertiary institutions rose to 100 percent of graduates. Notably, a substantial proportion of the participants, constituting 29 percent, persisted in tertiary education, with a notable 17 percent gaining admission to academic tertiary institutions. The case study conducted in Sha'anxi, situated in one of the most remote mountainous regions, illustrates a profound transition in schooling dynamics from rural to urban contexts. This comprehensive transformation prompts a reasonable inference that similar patterns of schooling migration are likely observable in less remote rural areas across China. Consequently, there arises a compelling argument for the integration of educational provisions in migrant "urban villages" and "peri-urban rural developments" into the municipal school systems, ensuring equitable allocation of resources to these under-resourced areas. Especially in light of China's significant aging population skewness, the integration of urban migrant educational provisions becomes even more imperative. [ABSTRACT FROM AUTHOR]

Dysregulation of macroautophagy/autophagy contributes to the delay of wound healing in diabetic skin. N6-methyladenosine (m6A) RNA modification is known to play a critical role in regulating autophagy. In this study, it was found that SQSTM1/p62 (sequestosome 1), an autophagy receptor, was significantly downregulated in two human keratinocyte cells lines with short-term high-glucose treatment, as well as in the epidermis of diabetic patients and a db/db mouse model with long-term hyperglycemia. Knockdown of SQSTM1 led to the impairment of autophagic flux, which was consistent with the results of high-glucose treatment in keratinocytes. Moreover, the m6A reader protein YTHDC1 (YTH domain containing 1), which interacted with SQSTM1 mRNA, was downregulated in keratinocytes under both the acute and chronic effects of hyperglycemia. Knockdown of YTHDC1 affected biological functions of keratinocytes, which included increased apoptosis rates and impaired wound-healing capacity. In addition, knockdown of endogenous YTHDC1 resulted in a blockade of autophagic flux in keratinocytes, while overexpression of YTHDC1 rescued the blockade of autophagic flux induced by high glucose. In vivo, knockdown of endogenous Ythdc1 or Sqstm1 inhibited autophagy in the epidermis and delayed wound healing. Interestingly, we found that a decrease of YTHDC1 drove SQSTM1 mRNA degradation in the nucleus. Furthermore, the results revealed that YTHDC1 interacted and cooperated with ELAVL1/HuR (ELAV like RNA binding protein 1) in modulating the expression of SQSTM1. Collectively, this study uncovered a previously unrecognized function for YTHDC1 in modulating autophagy via regulating the stability of SQSTM1 nuclear mRNA in diabetic keratinocytes. Abbreviations: ACTB: actin beta; AGEs: glycation end products; AL: autolysosome; AP: autophagosome; ATG: autophagy related; AKT: AKT serine/threonine kinase; ANOVA: analysis of variance; BECN1: beclin 1; Co-IP: co-immunoprecipitation; DEGs: differentially expressed genes; DM: diabetes mellitus; ELAVL1: ELAV like RNA binding protein 1; FTO: FTO alpha-ketoglutarate dependent dioxygenase; G: glucose; HaCaT: human keratinocyte; GO: Gene Ontology; GSEA: Gene Set Enrichment Analysis; HE: hematoxylin-eosin; IHC: immunohistochemical; IRS: immunoreactive score; KEAP1: kelch like ECH associated protein 1; KEGG: Kyoto Encyclopedia of Genes and Genomes; m6A: N6-methyladenosine; M: mannitol; MANOVA: multivariate analysis of variance; MAP1LC3: microtubule associated protein 1 light chain 3; MAP1LC3B: microtubule associated protein 1 light chain 3 beta; MeRIP: methylated RNA immunoprecipitation; METTL3: methyltransferase 3, N6-adenosine-methytransferase complex catalytic subunit; MTOR: mechanistic target of rapamycin kinase; MTORC1: mechanistic target of rapamycin complex 1; NBR1: NBR1 autophagy cargo receptor; NFE2L2: nuclear factor, erythroid 2 like 2; NG: normal glucose; NHEK: normal human epithelial keratinocyte; OE: overexpressing; p-: phospho-; PI: propidium iodide; PPIN: Protein-Protein Interaction Network; RBPs: RNA binding proteins; RIP: RNA immunoprecipitation; RNA-seq: RNA-sequence; RNU6–1: RNA, U6 small nuclear 1; ROS: reactive oxygen species; siRNAs: small interfering RNAs; SQSTM1: sequestosome 1; SRSF: serine and arginine rich splicing factor; T2DM: type 2 diabetes mellitus; TEM: transmission electron microscopy; TUBB: tubulin beta class I; WT: wild-type; YTHDC1: YTH domain containing 1. [ABSTRACT FROM AUTHOR]

Objective: To evaluate the hearing loss risk in different sectors and subunits in the mining industry and to identify associated occupations, in an attempt to locate gaps between hearing conservation efforts and hearing loss risks.Design: Descriptive statistics and frequency tables were generated by commodity types, subunit operations, and/or occupations. Temporal trends of the incidences of hearing loss were reported by commodity types.Study Sample: The MSHA Accident/Injury/Illness and MSHA Address/Employment databases from 2000 to 2014 were used.Results: Incidence rate of OHL was reported highest in the coal sector compared to other commodity types. Those members of the workforce that entered the mining industry after the year 2000 accounted for 6.5% and 19.0% of the total hearing loss records for coal and non-coal, respectively. High-risk occupations found in all three commodity sectors (coal; stone, sand, and gravel; and metal/non-metal) were electrician/helper/wireman, mechanic/repairman/helper, bulldozer/tractor operator, and truck driver.Conclusion: Hearing loss risks were not uniform across mining sectors, subunit operations, and occupations. In addition to the continuous efforts of implementing engineering controls to reduce machinery sound level exposure for operators, a multi-level approach may benefit those occupations with a more dynamic exposure profile – e.g., labour/utilityman/bullgang, electrician/helper/wireman, and mechanic/repairman/helper. [ABSTRACT FROM AUTHOR]

A new noise regulation for the mining industry became effective in 2000, providing a consistent regulatory requirement for both coal and non-coal mining divisions. The new rule required mines to implement hearing conservation programs, including a system of continuous noise monitoring, provision of hearing protection devices, audiometric testing, hearing loss training, and record keeping. The goal of this study was to assess hearing conservation program compliance, and excessive noise exposure and hearing loss risks for both coal and non-coal mining divisions through evaluating MSHA citations. We analyzed 13,446 MSHA citations from 2000-2014 pertinent to 30 CFR Part 62. Descriptive statistics were generated and comparisons were made among mines of different commodities. In addition, one-way ANOVA on ranks was conducted to estimate the correlation between excess risks and establishment size. Results showed that 25.6% of coal mines and 14.7% of non-coal mines were cited at least once during this period of time. Larger numbers of noncompliance were seen in stone, sand, and gravel mines (SSG). Results also suggested inadequate efforts in both audiometric testing and minimizing risk after excessive noise exposure. Finally, establishment size of mine was correlated with the increasing risk of noncompliance. We anticipate that this study can guide resource allocation for preventing noise-induced hearing loss, and help improve risk management in mining. [ABSTRACT FROM AUTHOR]

Objective: To analyse over 700,000 cross-sectional measurements from the Mine Safety and Health Administration (MHSA) and develop statistical models to predict noise exposure for a worker.Design: Descriptive statistics were used to summarise the data. Two linear regression models were used to predict noise exposure based on MSHA-permissible exposure limit (PEL) and action level (AL), respectively. Twofold cross validation was used to compare the exposure estimates from the models to actual measurement. The mean difference andt-statistic was calculated for each job title to determine whether the model predictions were significantly different from the actual data.Study sample: Measurements were acquired from MSHA through a Freedom of Information Act request.Results: From 1979 to 2014, noise exposure has decreased. Measurements taken before the implementation of MSHA’s revised noise regulation in 2000 were on average 4.5 dBA higher than after the law was implemented. Both models produced exposure predictions that were less than 1 dBA different than the holdout data.Conclusion: Overall noise levels in mines have been decreasing. However, this decrease has not been uniform across all mining sectors. The exposure predictions from the model will be useful to help predict hearing loss in workers in the mining industry. [ABSTRACT FROM PUBLISHER]

Suppressor of Hairless [Su(H)] is a DNA-binding protein of the Notch-signaling pathway, which is important for developmental processes and has been implicated in behavior plasticity. It acts as a transcriptional activator in the Notch pathway, but also as a repressor in the absence of Notch signaling. Our previous work has shown that Notch signaling contributes to long-term memory formation in the Drosophila adult brain. In the present report, we show that Su(H) null heterozygous mutants perform normally for learning, early memory, and anesthesia-resistant memory, whereas long-term memory is impaired. Interestingly, we find overexpressing wild- type Su(H) also causes long-term memory defect in Drosophila. Significantly, induction of a heat-shock inducible Su(H)+ transgene before training can fully rescue the memory defect of Su(H) mutants, thereby demonstrating an acute role for Su(H) in behavioral plasticity. We show that Su(H) is widely expressed in the adult brain. Transgenic expression of wild-type Su(H) in the Mushroom Bodies is sufficient to rescue the memory defect of Su(H) mutants. Our data clearly demonstrate that transcriptional activity of Su(H) in Notch signaling in the mushroom bodies is critical for the formation of long-term memory. [ABSTRACT FROM AUTHOR]

Abstract\nSIGNIFICANCE STATEMENTKeratinocyte and fibroblast dysfunctions contribute to delayed healing of diabetic wounds. Small extracellular vesicles (sEV) are key mediators of intercellular communication and are involved in the pathogenesis of several diseases. Recent findings suggest that sEV derived from high-glucose-treated keratinocyte (HaCaT-HG-sEV) can transport LINC01435 to inhibit tube formation and migration of HUVECs, thereby delaying wound healing. This study aimed to elucidate sEV-related communication mechanisms between keratinocytes and fibroblasts during diabetic wound healing. HaCaT-HG-sEV treatment and LINC01435 overexpression significantly decreased fibroblast collagen level and migration ability but significantly increased fibroblast autophagy. However, treatment with an autophagy inhibitor suppressed LINC01435 overexpression-induced decrease in collagen levels in fibroblasts. In diabetic mice, HaCaT-HG-sEV treatment decreased collagen levels and increased the expression of the autophagy-related proteins Beclin-1 and LC3 at the wound site, thereby delaying wound healing. Conclusively, LINC01435 in keratinocyte-derived sEV activates fibroblast autophagy and reduces fibroblast collagen synthesis, leading to impaired diabetic wound healing.Diabetic foot ulcers are a serious complication of diabetes and can lead to amputation and death. Therefore, it is crucial to comprehensively elucidate the mechanisms of delayed diabetic wound healing, with emphasis on the role of keratinocyte-derived small extracellular vesicles. In vivo and in vitro experiments showed that keratinocyte-derived small extracellular vesicles suppressed diabetic wound healing, which is partly attributed to the effects of their content (LINC01435) in fibroblasts. This study suggests that LINC01435 could be targeted to regulate diabetic wound healing. [ABSTRACT FROM AUTHOR]