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PurposeThis study investigates the neck/shoulder pain (NSP) and low back pain (LBP) among current high school students in Shanghai and explores the relationship between these pains and their possible influences, including digital products, physical activity, and psychological status.MethodsAn anonymous self-assessment was administered to 3,600 students across 30 high schools in Shanghai. This questionnaire examined the prevalence of NSP and LBP and the level of physical activity as well as the use of mobile phones, personal computers (PC) and tablet computers (Tablet). The CES-D (Center for Epidemiological Studies Depression) scale was also included in the survey. The survey data were analyzed using the chi-square test, univariate logistic analyses and a multivariate logistic regression model.ResultsThree thousand sixteen valid questionnaires were received including 1,460 (48.41%) from male respondents and 1,556 (51.59%) from female respondents. The high school students in this study showed NSP and LBP rates of 40.8% and 33.1%, respectively, and the prevalence of both influenced by the student’s grade, use of digital products, and mental status; these factors affected the rates of NSP and LBP to varying degrees. The multivariate logistic regression analysis revealed that Gender, grade, soreness after exercise, PC using habits, tablet use, sitting time after school and academic stress entered the final model of NSP, while the final model of LBP consisted of gender, grade, soreness after exercise, PC using habits, mobile phone use, sitting time after school, academic stress and CES-D score.ConclusionsHigh school students in Shanghai showed high prevalence of NSP and LBP that were closely related to multiple factors. Appropriate interventions should be implemented to reduce the occurrences of NSP and LBP.

Acute lung injury (ALI) is still a leading cause of morbidity and mortality in critically ill patients. Recently, our and other studies have found that hydrogen gas (H₂) treatment can ameliorate the lung injury induced by sepsis, ventilator, hyperoxia, and ischemia-reperfusion. However, the molecular mechanisms by which H₂ ameliorates lung injury remain unclear. In the current study, we investigated whether H₂ or hydrogen-rich saline (HS) could exert protective effects in a mouse model of ALI induced by intratracheal administration of lipopolysaccharide (LPS) via inhibiting the nuclear factor κB (NF-κB) signaling pathway-mediated inflammation and apoptosis. Two percent of H₂ was inhaled for 1 h beginning at 1 and 6 h after LPS administration, respectively. We found that LPS-challenged mice exhibited significant lung injury characterized by the deterioration of histopathology and histologic scores, wet-to-dry weight ratio, and oxygenation index (PaO₂/FIO₂), as well as total protein in the bronchoalveolar lavage fluid (BALF), which was attenuated by H₂ treatment. Hydrogen gas treatment inhibited LPS-induced pulmonary early and late NF-κB activation. Moreover, H₂ treatment dramatically prevented the LPS-induced pulmonary cell apoptosis in LPS-challenged mice, as reflected by the decrease in TUNEL (deoxynucleotidyl transferase dUTP nick end labeling) staining-positive cells and caspase 3 activity. Furthermore, H₂ treatment markedly attenuated LPS-induced lung neutrophil recruitment and inflammation, as evidenced by downregulation of lung myeloperoxidase activity, total cells, and polymorphonuclear neutrophils in BALF, as well as proinflammatory cytokines (tumor necrosis factor α, interleukin 1β, interleukin 6, and high-mobility group box 1) and chemokines (keratinocyte-derived chemokine, macrophage inflammatory protein [MIP] 1α, MIP-2, and monocyte chemoattractant protein 1) in BALF. In addition, i.p. injection of 10 mL/kg hydrogen-rich saline also significantly attenuated the LPS-induced ALI. Collectively, these results demonstrate that molecular hydrogen treatment ameliorates LPS-induced ALI through reducing lung inflammation and apoptosis, which may be associated with the decreased NF-κB activity. Hydrogen gas may be useful as a novel therapy to treat ALI. munosorbent assay; H₂-hydrogen gas; HMGB1-high-mobility group box 1; HS-hydrogen-rich saline; i.t.-intratracheal; KC-keratinocyte-derived chemokine; LPS-lipopolysaccharide; MCP-1-monocyte chemoattractant protein 1; MIP-1α-macrophage inflammatory protein 1α; MIP-2-macrophage inflammatory protein 2; MPO-myeloperoxidase; PBS-phosphate-buffered saline; PMNs-polymorphonuclear neutrophils; TUNEL-deoxynucleotidyl transferase dUTP nick end labeling; W/D-wet-to-dry.

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