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Objective: To examine the development and challenges of public health nursing education in China during the period of the Republic of China (1912‐1949). Methods: This study utilized a historical research design that combined a social framework and a policy framework to explore the early history of public health nursing education in China. Historical data were collected from periodicals, newspapers, archives, books and other sources. Results: Public health was integrated into the nursing school curriculum for the first time during the period of the Republic of China, and health facilities and nursing schools conducted early explorations of public health nurse training. However, public health nursing education faced difficulties in terms of the curriculum, personnel training, and the localization of education. Conclusions: The achievements and difficulties associated with public health nursing education in China during the period of the Republic of China provide a historical reference for the integration of public health into current basic nursing education and the compatibility between the training of public health nurses and practical needs. Comparative studies of early public health nursing education across countries are expected to offer a better understanding of current public health nursing education. [ABSTRACT FROM AUTHOR]

This study was to investigate the prevalence and severity of children's dental fluorosis (DF) in Shandong and identified the potential risk factors for DF. A total of 87 villages in Shandong were investigated to calculate the prevalence of DF and Community Fluorosis Index (CFI) in 2018–2019. Six hundred and seventy children were enrolled to identify the potential risk factors using univariate and multivariate logistic regressions. Goodman–Kruskal Gamma was used to explore the factors related to the severity of DF. In 87 villages, 1249 of 8700 (14.36%) children still have DF. The prevalence of DF in most villages was below 40% in 2018–2019. Water fluorine concentration when selected for the study and urinary fluorine concentration were related to the risk of DF (P < 0.001). Some eating habits, like lower frequency of eating fresh vegetables, eggs, and beans, were associated with the risk of DF (P < 0.001). The high water fluorine concentration, and lower frequency of eating fresh vegetables, eggs, and beans were also related to the severity of DF (P < 0.001). DF in children in Shandong province is still a common endemic disease. This study tries to provide a useful guide for the prevention and control of DF. [ABSTRACT FROM AUTHOR]

Acrylonitrile(AN) is a neurotoxin both in animals and humans, but its effects on acetylcholinesterase (AChE) activity remain controversial. This study aimed to determine the dose-response effects of AN on AChE activity and the modulatory role of ethanol pretreatment. A total of 144 Kunming mice were randomly divided into 18 groups: nine groups received 5% ethanol in their drinking water, and the remaining nine groups received regular tap water. One week later, both the ethanol and tap water only groups were given an intraperitoneal injection of AN at the following doses: 0 (control), 0.156, 0.3125, 0.625, 1.25, 2.5, 5, 10 or 20 mg AN/kg body weight. AChE activity was determined on whole blood and brain 24 h later. Blood AChE activity was higher in AN-injected mice than in controls at all doses. AChE activity in blood increased in a dose-dependent manner, peaking at 0.156 mg/kg, after which a gradual decrease ensued, displaying a β-typed dose-response relationship. In contrast, brain AChE activity, following a single AN injection, was consistently lower than in control mice, and continued to fall up to a dose of 0.313 mg/kg, and thereafter increased gradually with higher doses. Mice receiving a 20 mg/kg dose of AN exhibited AChE brain activity indistinguishable from that of control mice, demonstrating a typical U-typed dose-response relationship. The activity of AChE in the blood and brain of the AN + ethanol-treated groups displayed a shift to the right, and the magnitude of the decrease in AChE activity induced by AN was attenuated relative to the AN-only group. These results suggest that AN affects AChE activity in both mouse blood and brain in a hormetic manner. Pretreatment with ethanol modifies the effect of AN on AChE, indicating that parent AN has a more prominent role than its metabolites in modulating enzyme activity.

Background: As a ubiquitous environmental pollutant, methylmercury (MeHg) induces toxic effects in the nervous system, one of its main targets. However, the exact mechanisms of its neurotoxicity have not been fully elucidated. Hypoxia-inducible factor-1[alpha] (HIF-1[alpha]), a transcription factor, plays a crucial role in adaptive and cytoprotective responses in cells and is involved in cell survival, proliferation, apoptosis, inflammation, angiogenesis, glucose metabolism, erythropoiesis, and other physiological activities. Objectives: The aim of this study was to explore the role of HIF-1[alpha] in response to acute MeHg exposure in rat brain and primary cultured astrocytes to improve understanding of the mechanisms of MeHg-induced neurotoxicity and the development of effective neuroprotective strategies. Methods: Primary rat astrocytes were treated with MeHg (0-10 [micro]M) for 0.5 h. Cell proliferation and cytotoxicity were assessed with a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl diphenyltetrazolium bromide (MTT) assay and a lactate dehydrogenase (LDH) release assay, respectively. Reactive oxygen species (ROS) levels were analyzed to assess the level of oxidative stress using 2',7'-dichlorofluorescin diacetate (DCFH-DA) fluorescence. HIF-1[alpha], and its downstream proteins, glucose transporter 1 (GLUT-1), erythropoietin (EPO), and vascular endothelial growth factor A (VEGF-A) were analyzed by means of Western blotting. Real-time PCR was used to detect the expression of HIF-1[alpha] mRNA. Pretreatment with protein synthesis inhibitor (CHX), proteasome inhibitor (MG132), or proline hydroxylase inhibitor (DHB) were applied to explore the possible mechanisms of HIF-1[alpha] inhibition by MeHg. To investigate the role of HIF-1[alpha] in MeHg-induced neurotoxicity, cobalt chloride (Co[Cl.sub.2]), 2-methoxyestradiol (2-MeOE2), small interfering RNA (siRNA) transfection and adenovirus overexpression were used. Pretreatment with N-acetyl-L- cysteine (NAC) and vitamin E (Trolox) were used to investigate the putative role of oxidative stress in MeHg-induced alterations in HIF-1[alpha] levels. The expression of HIF-1[alpha] and related downstream proteins was detected in adult rat brain exposed to MeHg (0-10 mg/kg) for 0.5 h in vivo. Results: MeHg caused lower cell proliferation and higher cytotoxicity in primary rat astrocytes in a time- and concentration-dependent manner. In comparison with the control cells, exposure to 10 [micro]M MeHg for 0.5 h significantly inhibited the expression of astrocytic HIF-1[alpha], and the downstream genes GLUT-1, EPO, and VEGF-A (p < 0.05), in the absence of a significant decrease in HIF-1[alpha] mRNA levels. When protein synthesis was inhibited by CHX, MeHg promoted the degradation rate of HIF-1[alpha]. MG132 and DHB significantly blocked the MeHg-induced decrease in HIF-1[alpha] expression (p < 0.05). Overexpression of HIF-1[alpha] significantly attenuated the decline in MeHg-induced cell proliferation, whereas the inhibition of HIF-1[alpha] significantly increased the decline in cell proliferation (p < 0.05). NAC and Trolox, two established antioxidants, reversed the MeHg-induced decline in HIF-1[alpha] protein levels and the decrease in cell proliferation (p < 0.05). MeHg suppressed the expression of HIF- 1[alpha] and related downstream target proteins in adult rat brain. Discussion: MeHg induced a significant reduction in HIF-1[alpha] protein by activating proline hydroxylase (PHD) and the ubiquitin proteasome system (UPS) in primary rat astrocytes. Additionally, ROS scavenging by antioxidants played a neuroprotective role via increasing HIF-1[alpha] expression in response to MeHg toxicity. Moreover, we established that up-regulation of HIF-1[alpha] might serve to mitigate the acute toxicity of MeHg in astrocytes, affording a novel therapeutic target for future exploration. https://doi.org/10.1289/EHP5139, Introduction Methylmercury (MeHg) is a global environmental contaminant targeting the central nervous system (CNS) (Farina and Aschner 2017; Santos et al. 2016). Consumption of MeHg-containing fish products (Canuel et al. [...]