The next big earthquake may inflict a multi-hazard crisis - Insights from COVID-19, extreme weather and resilience in peripheral cities of Israel.

The occurrence of a natural disaster in an area already coping with an epidemic, constitutes a multi-hazard event. Such events are more likely than ever during the ongoing COVID-19 pandemic. In regions that seasonally experience extreme-weather disasters, such multi-hazard crises are imminent. People living along the Dead Sea Fault and in the Negev are used to harsh weather conditions and to the hardship of living in isolation. While self-reliance and community-support are often the norm in the daily life of residents in in peripheral communities, in an emergency they may be crucial for survival. Worldwide remote communities with limited response and medical infrastructure and resources may struggle to cope with the aftermath of an earthquake while potentially coping with a concurrent epidemic or extreme weather. In this work we focus on the effect of concurring disasters and seasonal stressors. In particular we discuss how various disasters would affect the Covid-19 infection rate, and we demonstrate that in Israel's periphery cities, heat-stress is a consistent and significant seasonal stressor that would hamper emergency and recovery operations. We also suggest that transient tourist population in these remote cities is expected to burden local emergency efforts and facilities. A seasonal over burden parameter is proposed to describe how seasonal tourism and weather conditions enhance the hardship and risk in a multi-hazard situation. A case study shows that high-resolution spatial analysis of risk and preparedness together with a temporal analysis of seasonal effects, may be used to detect specific neighborhoods with high or low resilience and capacity to cope with disasters. Our work demonstrates the need for spatial and temporal, multi-hazard analysis for improving local resilience and emergency plans in periphery cities and communities exposed to seasonal harsh weather.

Secretion of oxytocin in pregnant and parturient cows: corpus luteum may contribute to plasma oxytocin at term.

Plasma oxytocin (OT) concentrations were determined in 14 late-pregnant and parturient Angus-Hereford cows. Jugular and utero-ovarian veins were cannulated for simultaneous withdrawal of blood samples. Samples were collected at 10-min intervals for 6 h once weekly beginning 60-14 days before the date of expected delivery (group 1), or daily 3-7 days before the due date (group 2). In a third group, samples were collected at 15-min intervals every other day for 12 h beginning 1 wk before calving. Basal levels of OT were low, the overall mean for both veins was 0.46 +/- 0.03 microU/ml until a week before parturition, and then increased to 0.77 +/- 0.1 microU/ml (P < 0.02). Spurts of OT occurred intermittently on all days. Interpeak intervals averaged 71.0 +/- 10.7 min until Day -14, and from Day -14 to Day -1 the intervals were 44.0 +/- 5.3 min (P < 0.05). From Day -60 to Day -25 the amplitudes of OT peaks were low and similar in both veins (mean 1.37 +/- 0.1 microU/ml). From Day -14 to Day -1 the peak amplitudes were 3.6 +/- 0.4 microU/ml on average (P < 0.02). During the last 2 wk the utero-ovarian peak of OT was frequently higher than the peripheral peak. In addition, a number of spurts were observed in the utero-ovarian vein only (solo peaks). On the day of parturition during the first stage of labor, peak amplitudes had increased to 7.3 +/- 2.0 microU/ml, and the interpeak intervals had become shorter than before labor (mean 25.1 +/- 2.6 min). A large surge of OT initiated the expulsive stage of labor. Basal levels rose to 43.1 +/- 16 microU/ml and 38.7 +/- 12.6 microU/ml, and peak levels to 77.4 +/- 19.1 microU/ml and 91.6 +/- 21 microU/ml in the jugular and utero-ovarian veins, respectively. Interpeak intervals had decreased to 17.2 +/- 3.3 min (P < 0.05). Oxytocin levels remained high after delivery of the calf until the placenta was expelled. The posterior pituitary was the source of circulating OT during most of gestation and labor, but the solo peaks observed during late gestation in the utero-ovarian vein were probably of luteal origin or possibly of caruncular origin, because near term, both tissues express OT mRNA. Fetal posterior pituitary is another possible source for these peaks. Our conclusions are that during bovine pregnancy, low amplitude spurts of OT are secreted intermittently; near term, both the frequency and peak amplitude of the spurts increase; and during labor, a dramatic increase in plasma OT precedes the expulsion of the calf. The main source of OT is the posterior pituitary, but near term, a utero-ovarian source secretes additional OT into the systemic circulation.

Phorbol esters inhibit agonist-stimulated phosphoinositide hydrolysis in neuronal primary cultures.

The effects of phorbol esters on neurotransmitter-stimulated phosphoinositide (PI) hydrolysis in neurons in primary culture were investigated. Ten-day-old neuronal cultures were incubated with [3H]inositol for 2-3 days, exposed to phorbol esters, and the release of [3H]inositol phosphates was measured in the presence of 10 mM lithium. Pretreatment of the neuronal cultures with 1 microM phorbol myristate acetate (PMA) inhibited alpha 1, muscarinic, and glutamate receptor-mediated PI hydrolysis in a time-dependent manner with maximal inhibition observed after a 20-30 min preincubation. The active beta-phorbol didecanoate inhibited stimulated PI hydrolysis, but its stereo-isomer alpha-phorbol didecanoate was without effect at 1 microM. PMA was about 10 times more potent at inhibiting PI hydrolysis stimulated by norepinephrine and glutamate compared to carbachol. The order of potency of the various phorbol esters for inhibition of stimulated PI hydrolysis and the differences between active and inactive stereoisomers suggests that the activation of protein kinase C may mediate the inhibitory effects. Thus, stimulation of neuronal protein kinase C may represent a mechanism for the regulation of agonist-stimulated PI hydrolysis.

Variations in membrane sensitivity of brain region synaptosomes to the effects of ethanol in vitro and chronic in vivo treatment.

The effects of chronic ethanol treatment on the membrane order of synaptosomes from the cerebral cortex, striatum, cerebellum, brainstem, and hippocampus of rats were determined by measuring the fluorescence polarization of diphenylhexatriene (DPH) that had been incorporated into the synaptosomal membranes. Fischer-344 rats either were fed a nutritionally complete ethanol-containing liquid diet for 5 months or pair-fed with a diet that contained sucrose substituted isocalorically for ethanol. Polarization values for synaptosomes from all the brain regions studied were similar except for those from cerebral cortical synaptosomal membranes, which were significantly less ordered. Ethanol in vitro (30-500 mM) decreased the polarization values in synaptosomes from sucrose-control rats for all brain regions, although the sensitivity of cerebellar synaptosomes to the membrane disordering effects of ethanol in vitro was significantly greater that of synaptosomes from other brain regions. Chronic ethanol treatment did not alter baseline polarization for any brain region. Cerebellar and brainstem synaptosomes from the ethanol-fed rats were significantly less susceptible to the membrane disordering effects of ethanol in vitro compared to their sucrose controls, suggesting that chronic ethanol administration results in tolerance to ethanol's membrane effects. Striatal synaptosomes exhibited intermediate tolerance, whereas the sensitivities of cortical and hippocampal synaptosomes to membrane disordering by ethanol in vitro were not significantly affected by the chronic ethanol treatment. These results suggest that synaptosomal membranes have different membrane order requirements depending on the brain region from which they are prepared. Variations in brain regional neuronal membrane sensitivity to ethanol and differential tolerance development may contribute to some of the acute and chronic behavioral effects of ethanol.