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Appropriate and effective home hazard reduction teaching reduces home injuries in children. The improved awareness of caregivers in child safety, and child supervision emphasizes the importance of this program.
To determine the effectiveness of an educational intervention on the knowledge of adolescents on prevention of unintentional injuries and first aid.
The study used one group pre-post intervention design, without external controls. A two-stage (at schools and classes) cluster sampling was used to enroll 1944 high school students in Ujjain district. The intervention consisted of educational intervention using lectures presented through Power Point presentations, pictures, and videos. Sixty sessions each wherein a questionnaire to assess knowledge of participants was administered before and after the educational intervention. The outcome was a change in knowledge score.
The study included 1944 school students [1105 (57%) boys] with mean (SD) age of 15.9 (1.3) years. The analysis of variance revealed the difference between the sum total of pre- and post-intervention scores was statistically significant (P <0.001), with a large effect size of 3.7. Younger students outperformed older students, boys outperformed girls, students of urban schools outperformed their rural counterparts, students of public schools outperformed those of private schools and students of Hindi medium schools outperformed students of English medium schools.
This school-based educational intervention significantly increased the knowledge of students on the prevention of unintentional injuries and first aid.
This school-based educational intervention significantly increased the knowledge of students on the prevention of unintentional injuries and first aid.
Children 0-14 years constitute about 31.4% of Indian population, among whom the magnitude and risk factors of childhood injuries have not been adequately studied.
To study the prevalence of and assess the factors associated with unintentional injuries among children aged 6 month - 18 years in various regions.
This multi-centric, cross-sectional, community-based study was conducted at 11 sites across India. States included were Gujarat, Karnataka, Madhya Pradesh, Punjab, Sikkim, Tamil Nadu, Uttarakhand, and West Bengal between March, 2018 and September, 2020. A total of 2341 urban and rural households from each site were selected based on probability proportionate to size. The World Health Organization (WHO) child injury questionnaire adapted to the Indian settings was used after validation. Information on injuries was collected for previous 12 months. Definitions for types (road traffic accidents, falls, burns, poisoning, drowning, animal-related injuries) and severity of injuries was adapted from the W of the study provide inputs for developing a comprehensive child injury prevention policy in the country. Child safe school with age-appropriate measures, a safe home environment, and road safety measures for children should be a three-pronged approach in minimizing the number and the severity of child injuries both in urban and rural areas.Recent reports indicate that patients with hepatocholangiocarcinoma (CHOL) have a higher morbidity and mortality rate for coronavirus disease (COVID-19). Anti-CHOL/COVID-19 medicines are inexistent. Vitamin A (VA) refers to a potent nutrient with anti-cytotoxic and anti-inflammatory actions. Therefore, this study aimed to determine the potential functions and molecular mechanisms of VA as a potential treatment for patients with both CHOL and COVID-19 (CHOL/COVID-19). The transcriptome data of CHOL patients were obtained from the Cancer Genome Analysis database. Furthermore, the network pharmacology approach and bioinformatics analysis were used to identify and reveal the molecular functions, therapeutic biotargets, and signaling of VA against CHOL/COVID-19. First, clinical findings identified the medical characteristics of CHOL patients with COVID-19, such as susceptibility gene, prognosis, recurrence, and survival rate. Anti-viral and anti-inflammatory pathways, and immunopotentiation were found as potential targets of VA against CHOL/COVID-19. These findings illustrated that VA may contribute to the clinical management of CHOL/COVID-19 achieved by induction of cell repair, suppression of oxidative stress and inflammatory reaction, and amelioration of immunity. Nine vital therapeutic targets (BRD2, NOS2, GPT, MAPK1, CXCR3, ICAM1, CDK4, CAT, and TMPRSS13) of VA against CHOL/COVID-19 were identified. selleck products For the first time, the potential pharmacological biotargets, function, and mechanism of action of VA in CHOL/COVID-19 were elucidated.Traumatic brain injury (TBI) is a highly lethal event with a poor prognosis. Recovering residual neuronal function in the intermediate stage of TBI is important for treatment; however, neuroinflammation and neuronal apoptosis impede residual neuronal repair processes. Considering that hyperglycemia influences inflammatory processes and neuronal survival, we examined the effects of high glucose on neuroinflammation and neuronal death during the intermediate phase of TBI. Rat models of type 2 diabetes mellitus and/or TBI were developed and behaviorally assessed. Neurological function and cognitive abilities were impaired in TBI rats and worsened by type 2 diabetes mellitus. Histopathological staining and analyses of serum and hippocampal mRNA and protein levels indicated that neuroinflammation and apoptosis were induced in TBI rats and exacerbated by hyperglycemia. Hyperglycemia inhibited hippocampal mitogen-activated protein kinase kinase 5 (MEK5) phosphorylation in TBI rats. In vitro assays were used to assess inflammatory factor expression, apoptotic protein levels and neuronal survival after MEK5 activation in TBI- and/or high-glucose-treated neurons. MEK5/extracellular signal-regulated kinase 5 (ERK5) pathway activation reduced the inflammation, cleaved caspase-3 expression, Bax/Bcl-2 ratio and apoptosis of TBI neurons, even under high-glucose conditions. Thus, high glucose exacerbated neuroinflammation and apoptosis in the intermediate stage post-TBI by inhibiting the MEK5/ERK5 pathway.
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