The dilemma of valuing geodiversity: geoconservation versus geotourism.

Geodiversity and geosystem services are confronting global threats. However, the majority of conservation strategies tend to overlook the geological component within ecosystems. The existing literature centres on biodiversity, ecosystem services and their economic valuation. In this paper, we conduct a systematic literature review to identify the gap in the assessment of geological diversity, pinpointing areas where scientific contributions are needed to safeguard geological resources. Our findings reveal a concentration of studies assessing geodiversity in European and Asian countries. While the majority of the reviewed papers emphasizes the recreational features and associated values of geological resources, promoting geotourism and recognizing its potential for economic growth, there is a significant oversight concerning the impact of tourism on geological resources. Existing assessments predominantly focus on visitors' perceptions and preferences, sidelining the inhabitants' perspective and their crucial roles in the conservation of geodiversity. This article is part of the Theo Murphy meeting issue 'Geodiversity for science and society'.

Linking geodiversity and geosystem services to human well-being for the sustainable utilization of the subsurface and the urban environment.

Because the functions of the subsurface are hidden from view, its important role in society is often ignored or taken for granted. The subsurface is, however, an essential part of the global ecosystem with important contributions to human well-being. Geodiversity is an important characteristic in this respect. Material supply is the more obvious role of the subsurface with projections of a doubling of global material use in 2060 as compared to 2017. Moreover, creating underground spaces and infrastructure are gaining importance in the urban environment. The main reason for the inadequate protection of geodiversity is the lack of a comprehensive and integrative framework. Linking socio-economic activities to biophysical system characteristics of the subsurface is facilitated by the geosystem services approach. Sustainable urban development strategies require including geodiversity in decision-making on human well-being and setting conditions for land use change. Spatial plans and decisions on the use of natural endowments should look at processes over much longer timeframes. In this paper, we explore the links between human well-being and the subsurface with an emphasis on the role of geodiversity. We set out a methodological framework and describe possible long term three-dimensional land use planning consequences for sustainable utilization of the subsurface. This article is part of the Theo Murphy meeting issue 'Geodiversity for science and society'.

Tumor necrosis factor-alpha induces hepatic insulin resistance in obese Zucker (fa/fa) rats via interaction of leukocyte antigen-related tyrosine phosphatase with focal adhesion kinase.

The molecular mechanism whereby tumor necrosis factor-alpha (TNF-alpha) induces insulin resistance in obesity is not well understood. Previously, we have shown that inhibition of TNF-alpha improved hepatic insulin sensitivity in obese Zucker rats without altering the tyrosine phosphorylation of liver insulin receptors (IRs), which indicates that the TNF-alpha and insulin-signaling cascades interact distally to the IR. To assess the effects of TNF-alpha on signaling molecules downstream from the IR, we analyzed the tyrosine phosphorylation patterns of liver homogenate proteins from TNF-alpha-neutralized fa/fa rats and showed that focal adhesion kinase (FAK) was consistently hyperphosphorylated (4.5-fold). Moreover, intravenous insulin increased hepatic FAK phosphorylation in a time-dependent manner in Sprague-Dawley rats, which suggests that TNF-alpha may induce hepatic insulin resistance by preventing FAK phosphorylation in response to insulin treatment. To explore the cellular mechanism whereby TNF-alpha regulates phosphorylation of FAK in the liver, we measured c-Src kinase activity and the abundance of 3 major protein tyrosine phosphatases (PTPs) (PTP-1B, leukocyte antigen-related tyrosine phosphatase [LAR], and src homology 2 domain-containing protein-tyrosine phosphatase [SHPTP-2]) in liver homogenates from obese Zucker rats after TNF-alpha blockade. Hepatic c-Src kinase activity was unaltered, but LAR protein was reduced by 75%. In addition, TNF-alpha blockade reduced hepatic PTP activity toward tyrosine phosphorylated FAK by 70%, and this was accounted for by immunodepletion of LAR. Incubation of HepG2 cells with TNF-alpha increased LAR protein levels in a dose-dependent manner. Additionally, pretreatment with TNF-alpha abolished insulin-stimulated tyrosine phosphorylation of FAK in HepG2 cells but had no effect on IR tyrosine phosphorylation or expression. These data suggest that TNF-alpha promotes LAR expression and thus prevents insulin-mediated tyrosine phosphorylation of FAK. This probably represents the interface between TNF-alpha and insulin signaling in the liver.

An in vivo model for elucidation of the mechanism of tumor necrosis factor-alpha (TNF-alpha)-induced insulin resistance: evidence for differential regulation of insulin signaling by TNF-alpha.

Tumor necrosis factor-alpha (TNF-alpha) has been shown to induce insulin resistance in cultured cells as well as in animal models. The aim of this study was to map the in vivo mechanism whereby TNF-alpha contributes to the pathogenesis of impaired insulin signaling, using obese and lean Zucker rats in which TNF-alpha activity was inhibited through adenovirus-mediated gene transfer. We employed a replication-incompetent adenovirus-5 (Ad5) vector to endogenously express a TNF inhibitor (TNFi) gene, which encodes a chimeric protein consisting of the extracellular domain of the human 55-kDa TNF receptor joined to a mouse IgG heavy chain. Control animals consisted of rats infected with the same titer of adenovirus carrying the lac-z complementary DNA, encoding for beta-galactosidase. There was a significant reduction in plasma insulin and free fatty acid levels in TNFi obese rats 2 days following Ad5 administration. The peripheral insulin sensitivity index was 50% greater, whereas hepatic glucose output was completely suppressed during hyperinsulinemic glucose clamps in TNFi obese animals, with no differences observed between the two lean groups. The improvement in peripheral and hepatic sensitivity to insulin seen in the obese animals was independent of insulin receptor (IR) number and insulin binding affinity for IR. However, TNF-alpha neutralization led to a 2.5-fold increase in tyrosine phosphorylation of IR in skeletal muscle, whereas this was unchanged in liver. There was also a 4-fold increase in particulate protein tyrosine phosphatase activity of skeletal muscle in TNFi obese animals vs. beta-galactosidase controls, whereas protein tyrosine phosphatase activity in liver was unchanged. These results suggest that TNF-alpha is a mediator of insulin resistance in obesity and may modulate IR signaling in skeletal muscle and liver through different pathways. TNF-alpha may affect insulin action in the liver either at sites distal to the IR or indirectly, possibly because of increased provision of gluconeogenic substrates or altered counterregulation. In addition, the Ad5-mediated gene delivery system employed here provides an in vivo model that is efficient and economical for exploring mechanisms involved in TNF-alpha-induced insulin resistance in various genetic models of obesity-linked diabetes.

New evidence on the relationship between substance use and adolescent sexual behavior.

Policymakers and the public have a clear interest in encouraging teens to delay becoming sexually active or, if they are sexually active, to use birth control. Many researchers have argued that reducing substance use among teens will accomplish both of these goals, yet work in this area has failed to control for unobservables that are potentially correlated with substance use and sexual behavior. Using a variety of estimation techniques and data from National Longitudinal Study of Adolescent Health, we estimate the effects of marijuana and alcohol use on two outcomes: the probability of being sexually active, and the probability of having sex without contraception. Our results highlight the importance of controlling for unobservables and indicate that the link between substance use and sexual behavior is much weaker than previously suggested.