Absolute pore size distributions from NMR

NMR measurements on core samples saturated with brine returns valuable information on the porous structure of the rock core. Monitoring a single fluid component in a relaxation experiment reflects the pore size distribution and thus the degree of sorting of the porous rock. The basic assumptions are that the mobility of the component confined in the porous rock is of such a value that a small fraction of the probing molecules experience the surfaces of the pores and that the surface relaxation strength is fairly independent of pore size. Then one may combine diffusion measurements at short observation times returning a value for the average surface to volume ratio with ordinary relaxation time measurements to obtain an absolute pore size distribution instead of the standard T2 distributions or T1-T2 correlated two dimensional distributions

11 beta-hydroxysteroid dehydrogenase type 1 regulates glucocorticoid-induced insulin resistance in skeletal muscle

OBJECTIVE: Glucocorticoid excess is characterized by increased adiposity, skeletal myopathy, and insulin resistance, but the precise molecular mechanisms are unknown. Within skeletal muscle, 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) converts cortisone (11-dehydrocorticosterone in rodents) to active cortisol (corticosterone in rodents). We aimed to determine the mechanisms underpinning glucocorticoid-induced insulin resistance in skeletal muscle and indentify how 11beta-HSD1 inhibitors improve insulin sensitivity. \ud RESEARCH DESIGN AND METHODS: Rodent and human cell cultures, whole-tissue explants, and animal models were used to determine the impact of glucocorticoids and selective 11beta-HSD1 inhibition upon insulin signaling and action. \ud RESULTS: Dexamethasone decreased insulin-stimulated glucose uptake, decreased IRS1 mRNA and protein expression, and increased inactivating pSer$^{307}$ insulin receptor substrate (IRS)-1. 11beta-HSD1 activity and expression were observed in human and rodent myotubes and muscle explants. Activity was predominantly oxo-reductase, generating active glucocorticoid. A1 (selective 11beta-HSD1 inhibitor) abolished enzyme activity and blocked the increase in pSer$^{307}$ IRS1 and reduction in total IRS1 protein after treatment with 11DHC but not corticosterone. In C57Bl6/J mice, the selective 11beta-HSD1 inhibitor, A2, decreased fasting blood glucose levels and improved insulin sensitivity. In KK mice treated with A2, skeletal muscle pSer$^{307}$ IRS1 decreased and pThr$^{308}$ Akt/PKB increased. In addition, A2 decreased both lipogenic and lipolytic gene expression.\ud CONCLUSIONS: Prereceptor facilitation of glucocorticoid action via 11beta-HSD1 increases pSer$^{307}$ IRS1 and may be crucial in mediating insulin resistance in skeletal muscle. Selective 11beta-HSD1 inhibition decreases pSer$^{307}$ IRS1, increases pThr$^{308}$ Akt/PKB, and decreases lipogenic and lipolytic gene expression that may represent an important mechanism underpinning their insulin-sensitizing action

Saturation Diving Alters Folate Status and Biomarkers of DNA Damage and Repair

Exposure to oxygen-rich environments can lead to oxidative damage, increased body iron stores, and changes in status of some vitamins, including folate. Assessing the type of oxidative damage in these environments and determining its relationships with changes in folate status are important for defining nutrient requirements and designing countermeasures to mitigate these effects. Responses of humans to oxidative stressors were examined in participants undergoing a saturation dive in an environment with increased partial pressure of oxygen, a NASA Extreme Environment Mission Operations mission. Six participants completed a 13-d saturation dive in a habitat 19 m below the ocean surface near Key Largo, FL. Fasting blood samples were collected before, twice during, and twice after the dive and analyzed for biochemical markers of iron status, oxidative damage, and vitamin status. Body iron stores and ferritin increased during the dive (P<0.001), with a concomitant decrease in RBC folate (P<0.001) and superoxide dismutase activity (P<0.001). Folate status was correlated with serum ferritin (Pearson r = −0.34, P<0.05). Peripheral blood mononuclear cell poly(ADP-ribose) increased during the dive and the increase was significant by the end of the dive (P<0.001); γ-H2AX did not change during the mission. Together, the data provide evidence that when body iron stores were elevated in a hyperoxic environment, a DNA damage repair response occurred in peripheral blood mononuclear cells, but double-stranded DNA damage did not. In addition, folate status decreases quickly in this environment, and this study provides evidence that folate requirements may be greater when body iron stores and DNA damage repair responses are elevated

Optimising sampling and analysis protocols in environmental DNA studies

Ecological surveys risk incurring false negative and false positive detections of the target species. With indirect survey methods, such as environmental DNA, such error can occur at two stages: sample collection and laboratory analysis. Here we analyse a large qPCR based eDNA data set using two occupancy models, one of which accounts for false positive error by Griffin et al. (2020), and a second that assumes no false positive error by Stratton et al. (2020). Additionally, we apply the Griffin et al. (2020) model to simulated data to determine optimal levels of replication at both sampling stages. The Stratton et al. (2020) model, which assumes no false positive results, consistently overestimated both overall and individual site occupancy compared to both the Griffin et al. (2020) model and to previous estimates of pond occupancy for the target species. The inclusion of replication at both stages of eDNA analysis (sample collection and in the laboratory) reduces both bias and credible interval width in estimates of both occupancy and detectability. Even the collection of >1 sample from a site can improve parameter estimates more than having a high number of replicates only within the laboratory analysis

The Smart City Active Mobile Phone Intervention (SCAMPI) study to promote physical activity through active transportation in healthy adults: a study protocol for a randomised controlled trial

Abstract Background The global pandemic of physical inactivity represents a considerable public health challenge. Active transportation (i.e., walking or cycling for transport) can contribute to greater total physical activity levels. Mobile phone-based programs can promote behaviour change, but no study has evaluated whether such a program can promote active transportation in adults. This study protocol presents the design and methodology of The Smart City Active Mobile Phone Intervention (SCAMPI), a randomised controlled trial to promote active transportation via a smartphone application (app) with the aim to increase physical activity. Methods/design A two-arm parallel randomised controlled trial will be conducted in Stockholm County, Sweden. Two hundred fifty adults aged 20–65 years will be randomised to either monitoring of active transport via the TRavelVU app (control), or to a 3-month evidence-based behaviour change program to promote active transport and monitoring of active travel via the TRavelVU Plus app (intervention). The primary outcome is moderate-to-vigorous intensity physical activity (MVPA in minutes/day) (ActiGraph wGT3x-BT) measured post intervention. Secondary outcomes include: time spent in active transportation measured via the TRavelVU app, perceptions about active transportation (the Transport and Physical Activity Questionnaire (TPAQ)) and health related quality of life (RAND-36). Assessments are conducted at baseline, after the completed intervention (after 3 months) and 6 months post randomisation. Discussion SCAMPI will determine the effectiveness of a smartphone app to promote active transportation and physical activity in an adult population. If effective, the app has potential to be a low-cost intervention that can be delivered at scale. Trial registration ClinicalTrials.gov NCT03086837; 22 March, 2017

Cross Adaptation - Heat and Cold Adaptation to Improve Physiological and Cellular Responses to Hypoxia

To prepare for extremes of heat, cold or low partial pressures of O2, humans can undertake a period of acclimation or acclimatization to induce environment specific adaptations e.g. heat acclimation (HA), cold acclimation (CA), or altitude training. Whilst these strategies are effective, they are not always feasible, due to logistical impracticalities. Cross adaptation is a term used to describe the phenomenon whereby alternative environmental interventions e.g. HA, or CA, may be a beneficial alternative to altitude interventions, providing physiological stress and inducing adaptations observable at altitude. HA can attenuate physiological strain at rest and during moderate intensity exercise at altitude via adaptations allied to improved oxygen delivery to metabolically active tissue, likely following increases in plasma volume and reductions in body temperature. CA appears to improve physiological responses to altitude by attenuating the autonomic response to altitude. While no cross acclimation-derived exercise performance/capacity data have been measured following CA, post-HA improvements in performance underpinned by aerobic metabolism, and therefore dependent on oxygen delivery at altitude, are likely. At a cellular level, heat shock protein responses to altitude are attenuated by prior HA suggesting that an attenuation of the cellular stress response and therefore a reduced disruption to homeostasis at altitude has occurred. This process is known as cross tolerance. The effects of CA on markers of cross tolerance is an area requiring further investigation. Because much of the evidence relating to cross adaptation to altitude has examined the benefits at moderate to high altitudes, future research examining responses at lower altitudes should be conducted given that these environments are more frequently visited by athletes and workers. Mechanistic work to identify the specific physiological and cellular pathways responsible for cross adaptation between heat and altitude, and between cold and altitude, is warranted, as is exploration of benefits across different populations and physical activity profiles