Improving Environmental Health in Schools.

School environmental conditions have immediate and long-term effects on student health and learning. Relying on disconnected, inconsistent, voluntary, or unenforced environmental standards has not resulted in sufficient protection of students from toxic insults. Furthermore, the United States public school system was not prepared to navigate a potentially deadly infectious disease like COVID-19. Although Department of Education agencies have policies to establish clean and safe learning spaces, deficiencies are evident. This article highlights common environmental challenges in schools and opportunities for improvement. Voluntary adoption of rigorous environmental policies by grassroots efforts alone is unlikely to occur in all school systems. In the absence of a legally enforced requirement, the dedication of sufficient resources to update infrastructure and build the environmental health workforce capacity is equally unlikely to occur. Environmental health standards in schools should not be voluntary. Science-based standards should be comprehensive, and part of an actionable, integrated strategy that includes preventive measures and addresses environmental health issues sustainably. Establishing an Integrated Environmental Management approach for schools will require a coordinated capacity-building effort, community-based implementation efforts, and enforcement of minimal standards. Schools will need ongoing technical support and training for staff, faculty, and teachers sufficient to enable them to assume greater oversight and responsibility for environmental management of their schools. Ideally, a holistic approach will include all environmental health components, including IAQ, IPM, green cleaning, pesticide and chemical safety, food safety, fire prevention, building legacy pollutant management, and drinking water quality. Thus, creating a comprehensive management system with continuous monitoring and maintenance. Clinicians who care for children can serve as advocates for children's health beyond their clinic walls by advising parents and guardians to be aware of school conditions and management practices. Medical professionals have always been valued and influential members of communities and school boards. In these roles they can greatly assist in identifying and providing solutions to reduce environmental hazards in schools.

Energy expenditure and bone formation share a common sensitivity to AP-1 transcription in the hypothalamus.

The regulation of bone and fat homeostasis and its relationship to energy expenditure has recently been the focus of increased attention because of its potential relevance to osteoporosis, obesity, and diabetes. Although central effectors within the hypothalamus have been shown to contribute to the regulation of both energy balance and bone homeostasis, little is known of the underlying mechanisms, including the possible involvement of transcriptional factors within the hypothalamus. Transgenic mice overexpressing ΔFosB, a splice variant of the AP-1 transcription factor FosB with mixed agonist-antagonistic properties, have increased energy expenditure and bone mass. Because these mice express ΔFosB in bone, fat, and hypothalamus, we sought to determine 1) whether overexpression of ΔFosB within the hypothalamus was sufficient to regulate energy expenditure and whether it would also regulate bone mass, and 2) whether these effects were the result of antagonism to AP-1. Our results show that stereotactic injection of an adeno-associated virus vector to restrict overexpression of ΔFosB to the ventral hypothalamus of wild-type mice induced a profound increase in both energy expenditure and bone formation and bone mass. This effect was phenocopied, at an even stronger level, by overexpression of a dominant-negative DNJunD, a pure AP-1 antagonist. Taken together, these results suggest that downregulation of AP-1 activity in the hypothalamus profoundly increases energy expenditure and bone formation, leading to both a decrease in adipose mass and an increase in bone mass. These findings may have physiological implications because ΔFosB is expressed and regulated in the hypothalamus.

Role of cAMP response element-binding protein in the rat locus ceruleus: regulation of neuronal activity and opiate withdrawal behaviors.

The transcription factor cAMP response element-binding protein (CREB) is implicated in mediating the actions of chronic morphine in the locus ceruleus (LC), but direct evidence to support such a role is limited. Here, we investigated the influence of CREB on LC neuronal activity and opiate withdrawal behaviors by selectively manipulating CREB activity in the LC using viral vectors encoding genes for CREBGFP (wild-type CREB tagged with green fluorescent protein), caCREBGFP (a constitutively active CREB mutant), dnCREBGFP (a dominant-negative CREB mutant), or GFP alone as a control. Our results show that in vivo overexpression of CREBGFP in the LC significantly aggravated particular morphine withdrawal behaviors, whereas dnCREBGFP expression attenuated these behaviors. At the cellular level, CREBGFP expression in the LC in vivo and in vitro had no significant effect on neuronal firing at baseline but enhanced the excitatory effect of forskolin (an activator of adenylyl cyclase) on these neurons, which suggests that the cAMP signaling pathway in these neurons was sensitized after CREB expression. Moreover, in vitro studies showed that caCREBGFP-expressing LC neurons fired significantly faster and had a more depolarized resting membrane potential compared with GFP-expressing control cells. Conversely, LC neuronal activity was decreased by dnCREBGFP, and the neurons were hyperpolarized by this treatment. Together, these data provide direct evidence that CREB plays an important role in controlling the electrical excitability of LC neurons and that morphine-induced increases in CREB activity contribute to the behavioral and neural adaptations associated with opiate dependence and withdrawal.