Healthy lifestyles in pre-service teachers in Israel: the impact of academic institutions

PurposeThis study examines the impact of academic institutions on changes to students’ awareness and habits regarding a healthy lifestyle, specifically through nutrition and physical exercise, following the Covid-19 pandemic.Design and subjectsIn May 2020, quantitative online questionnaires were completed by 266 pre-service teachers (83.5% female), aged 19–63, who were studying at an academic institution in Israel.SettingThe questionnaire, which included health-related 15 items, as well as a number of demographic questions, was distributed via social media, academic mailing lists, and the researchers’ colleagues.MethodsThe respondents were asked to provide socio-demographic data and information regarding their health-related habits, such as smoking and exercising, at two timepoints: prior to the Covid-19 pandemic and during the first lockdown in Israel (March–May 2020).AnalysisStatistical analysis included paired t-tests, Wilcoxon and McNemar tests, Pearsons’s correlations, and hierarchical regressions.ResultsThe academic institution’s promoting of a healthy lifestyle, as perceived by students, was found to contribute to the explained variance (EPV) of their maintaining a healthy lifestyle, prior to and during the Covid-19 pandemic (R2 = 9.4%, p < .001and R2 = 2.4%, p = 0.009, respectively), beyond the respondents’ demographic characteristics. Moreover, correlations were found between the institution’s promoting of a healthy lifestyle at both timepoints. Respondents who perceived their institution as promoting a healthy lifestyle prior to the pandemic maintained healthier lifestyles than their peers; healthier lifestyles were also maintained by respondents who were unmarried, non-smokers, more educated, and watched less television. Finally, the institution’s promoting of a healthy lifestyle prior to the pandemic significantly contributed to the students’ maintaining a healthy lifestyle and healthy nutrition during the pandemic.ConclusionThe findings of this study highlight the impact of academic institutions on maintaining healthy lifestyles, even in times of crises and emergencies, thereby contributing to public health

A Supportive Role of Mesenchymal Stem Cells on Insulin-Producing Langerhans Islets with a Specific Emphasis on The Secretome

Type 1 Diabetes (T1D) is a chronic autoimmune disease characterized by a gradual destruction of insulin-producing β-cells in the endocrine pancreas due to innate and specific immune responses, leading to impaired glucose homeostasis. T1D patients usually require regular insulin injections after meals to maintain normal serum glucose levels. In severe cases, pancreas or Langerhans islet transplantation can assist in reaching a sufficient β-mass to normalize glucose homeostasis. The latter procedure is limited because of low donor availability, high islet loss, and immune rejection. There is still a need to develop new technologies to improve islet survival and implantation and to keep the islets functional. Mesenchymal stem cells (MSCs) are multipotent non-hematopoietic progenitor cells with high plasticity that can support human pancreatic islet function both in vitro and in vivo and islet co-transplantation with MSCs is more effective than islet transplantation alone in attenuating diabetes progression. The beneficial effect of MSCs on islet function is due to a combined effect on angiogenesis, suppression of immune responses, and secretion of growth factors essential for islet survival and function. In this review, various aspects of MSCs related to islet function and diabetes are described

sFasL—The Key to a Riddle: Immune Responses in Aging Lung and Disease

By dint of the aging population and further deepened with the Covid-19 pandemic, lung disease has turned out to be a major cause of worldwide morbidity and mortality. The condition is exacerbated when the immune system further attacks the healthy, rather than the diseased, tissue within the lung. Governed by unremittingly proliferating mesenchymal cells and increased collagen deposition, if inflammation persists, as frequently occurs in aging lungs, the tissue develops tumors and/or turns into scars (fibrosis), with limited regenerative capacity and organ failure. Fas ligand (FasL, a ligand of the Fas cell death receptor) is a key factor in the regulation of these processes. FasL is primarily found in two forms: full length (membrane, or mFasL) and cleaved (soluble, or sFasL). We and others found that T-cells expressing the mFasL retain autoimmune surveillance that controls mesenchymal, as well as tumor cell accumulation following an inflammatory response. However, mesenchymal cells from fibrotic lungs, tumor cells, or cells from immune-privileged sites, resist FasL+ T-cell-induced cell death. The mechanisms involved are a counterattack of immune cells by FasL, by releasing a soluble form of FasL that competes with the membrane version, and inhibits their cell death, promoting cell survival. This review focuses on understanding the previously unrecognized role of FasL, and in particular its soluble form, sFasL, in the serum of aged subjects, and its association with the evolution of lung disease, paving the way to new methods of diagnosis and treatment

Local dynamic changes in confined extracellular environments within organs

1. Herein we review past work that has studied the composition of luminal fluid in organs, with a focus on measures of calcium and pH in the exocrine glands. This luminal environment is 'external' to the mammalian body and is not subject to the usual mechanisms of homeostatic control. Instead, it is controlled by the behaviour of the cells that line the lumen. 2. We discuss the likely possibility that rapid and local changes in calcium and pH occur within microdomains in the lumen. Further, we present preliminary evidence, using live cell imaging of intact pancreatic fragments, that supports the idea that pH changes do occur. Our evidence indicates that exocytosis of secretory granules in pancreatic acinar cells leads to a loss of protons from the granule and a subsequent local acidification of the lumen. 3. These changes in luminal composition are placed in the context of diseases of the pancreas, such as cystic fibrosis and pancreatitis, both of which are known to result in perturbations of luminal fluid composition

Role of voltage-dependent calcium channels in stimulus–secretion coupling in rabbit carotid body chemoreceptor cells

We have defined Ca(2+) channel subtypes expressed in rabbit carotid body (CB) chemoreceptor cells and their participation in the stimulus-evoked catecholamine (CA) release. Ca(2+) currents (I(Ca)) activated at –30 mV, peaked at +10 mV and were fully blocked by 200 μm Cd(2+). L-type channels (sensitive to 2 μm nisoldipine) activated at –30 mV and carried 21 ± 2% of total I(Ca). Non-L-type channels activated at potentials positive to –10 mV and carried: N channels (sensitive to 1 μm ω-conotoxin-GVIA) 16 ± 1% of total I(Ca), P/Q channels (sensitive to 3 μm ω-conotoxin-MVIIC after nisoldipine plus GVIA) 23 ± 3% of total I(Ca) and R channels (resistant to all blockers combined) 40 ± 3% of total I(Ca). CA release induced by hypoxia, hypercapnic acidosis, dinitrophenol (DNP) and high K(+)(o) in the intact CB was inhibited by 79–98% by 200 μm Cd(2+). Hypoxia, hypercapnic acidosis and DNP, depolarized chemoreceptor cells and eventually generated repetitive action potential discharge. Nisoldipine plus MVIIC nearly abolished the release of CAs induced by hypoxia and hypercapnic acidosis and reduced by 74% that induced by DNP. All these secretory responses were insensitive to GVIA. 30 and 100 mm K(+)(o) brought resting membrane potential (E(m)) of chemoreceptor cells (–48.1 ± 1.2 mV) to –22.5 and +7.2 mV, respectively. Thirty millimolar K(+)(o)-evoked release was abolished by nisoldipine but that induced by 100 mm K(+)(o) was mediated by activation of L, N, and P/Q channels. Data show that tested stimuli depolarize rabbit CB chemoreceptor cells and elicit CA release through Ca(2+) entry via voltage-activated channels. Only L and P/Q channels are tightly coupled to the secretion of CA

EPAC signalling pathways are involved in low PO2 chemoreception in carotid body chemoreceptor cells

Chemoreceptor cells of the carotid bodies (CB) are activated by hypoxia and acidosis, responding with an increase in their rate of neurotransmitter release, which in turn increases the electrical activity in the carotid sinus nerve and evokes a homeostatic hyperventilation. Studies in isolated chemoreceptor cells have shown that moderate hypoxias (≈ 46 mmHg) produces smaller depolarisations and comparable Ca2+ transients but a much higher catecholamine (CA) release response in intact CBs than intense acidic/hypercapnic stimuli (20% CO2, pH 6.6). Similarly, intense hypoxia (≈ 20 mmHg) produces smaller depolarizations and Ca2+ transients in isolated chemoreceptor cells but a higher CA release response in intact CBs than a pure depolarizing stimulus (30–35 mm external K+). Studying the mechanisms responsible for these differences we have found the following. (1) Acidic hypercapnia inhibited ICa (∼60%; whole cell) and CA release (∼45%; intact CB) elicited by ionomycin and high K+. (2) Adenylate cyclase inhibition (SQ-22536; 80 μm) inhibited the hypoxic release response (>50%) and did not affect acidic/hypercapnic release, evidencing that the high gain of hypoxia to elicit neurotransmitter release is cAMP dependent. (3) The last effect was independent of PKA activation, as three kinase inhibitors (H-89, KT 5720 and Rp-cAMP; ≥ 10 × IC50) did not alter the hypoxic release response. (4) The Epac (exchange protein activated by cAMP) activator (8-pCPT-2′-O-Me-cAMP, 100 μm) reversed the effects of the cyclase inhibitor. (5) The Epac inhibitor brefeldin A (100 μm) inhibited (54%) hypoxic induced release. Our findings show for the first time that an Epac-mediated pathway mediates O2 sensing/transduction in chemoreceptor cells