Moving across Borders: The Work Life Experiences of Czech Cross-border Workers during the COVID-19 Pandemic.

The experiences of cross-border workers (CBWs) and the difficulties they face during the ongoing COVID-19 pandemic have been neglected in previous research. CBWs experience various stressors under normal circumstances, where they are often subjected to unequal working conditions and forced to transition between two different societies. The measures that were introduced in response to the COVID-19 pandemic, including the implementation of physical borders, further worsened the situation for these individuals.

Specialized and shared functions of diguanylate cyclases and phosphodiesterases in Streptomyces development.

The second messenger bis-3,5-cyclic di-guanosine monophosphate (c-di-GMP) determines when Streptomyces initiate sporulation. c-di-GMP signals are integrated into the genetic differentiation network by the regulator BldD and the sigma factor σ . However, functions of the development-specific diguanylate cyclases (DGCs) CdgB and CdgC, and the c-di-GMP phosphodiesterases (PDEs) RmdA and RmdB, are poorly understood.

Probiotic administration attenuates myocardial hypertrophy and heart failure after myocardial infarction in the rat.

Background: Probiotics are extensively used to promote gastrointestinal health, and emerging evidence suggests that their beneficial properties can extend beyond the local environment of the gut. Here, we determined whether oral probiotic administration can alter the progression of postinfarction heart failure.

Methods And Results: Rats were subjected to 6 weeks of sustained coronary artery occlusion and administered the probiotic Lactobacillus rhamnosus GR-1 or placebo in the drinking water ad libitum.

The obesity-related peptide leptin sensitizes cardiac mitochondria to calcium-induced permeability transition pore opening and apoptosis.

The obesity-related 16 kDa peptide leptin is synthesized primarily in white adipocytes although its production has been reported in other tissues including the heart. There is emerging evidence that leptin may contribute to cardiac pathology especially that related to myocardial remodelling and heart failure. In view of the importance of mitochondria to these processes, the goal of the present study is to determine the effect of leptin on mitochondria permeability transition pore opening and the potential consequence in terms of development of apoptosis.

Identification of a potent sodium hydrogen exchanger isoform 1 (NHE1) inhibitor with a suitable profile for chronic dosing and demonstrated cardioprotective effects in a preclinical model of myocardial infarction in the rat.

Sodium-hydrogen exchanger isoform 1 (NHE1) is a ubiquitously expressed transmembrane ion channel responsible for intracellular pH regulation. During myocardial ischemia, low pH activates NHE1 and causes increased intracellular calcium levels and aberrant cellular processes, leading to myocardial stunning, arrhythmias, and ultimately cell damage and death. The role of NHE1 in cardiac injury has prompted interest in the development of NHE1 inhibitors for the treatment of heart failure.

Plantar fascia-specific stretching versus radial shock-wave therapy as initial treatment of plantar fasciopathy.

Background: Whether plantar fascia-specific stretching or shock-wave therapy is effective as an initial treatment for proximal plantar fasciopathy remains unclear. The aim of this study was to test the null hypothesis of no difference in the effectiveness of these two forms of treatment for patients who had unilateral plantar fasciopathy for a maximum duration of six weeks and which had not been treated previously.

Methods: One hundred and two patients with acute plantar fasciopathy were randomly assigned to perform an eight-week plantar fascia-specific stretching program (Group I, n = 54) or to receive repetitive low-energy radial shock-wave therapy without local anesthesia, administered weekly for three weeks (Group II, n = 48).

Ginseng inhibits cardiomyocyte hypertrophy and heart failure via NHE-1 inhibition and attenuation of calcineurin activation.

Background: Ginseng is a medicinal plant used widely in Asia that has gained popularity in the West during the past decade. Increasing evidence suggests a therapeutic role for ginseng in the cardiovascular system. The pharmacological properties of ginseng are mainly attributed to ginsenosides, the principal bioactive constituents in ginseng.

Sodium-hydrogen exchange inhibition attenuates glycoside-induced hypertrophy in rat ventricular myocytes.

Aims: Cardiac glycosides induce cardiomyocyte hypertrophy via yet to be defined mechanisms. These hypertrophic effects are likely related to changes in intracellular signalling secondary to Na(+)-K(+) ATPase (NKA) inhibition which would produce elevations in intracellular sodium concentrations. Sodium-hydrogen exchanger isoform 1 (NHE-1) also contributes to intracellular sodium regulation.

Exercise training improves myocardial tolerance to ischemia in male but not in female rats.

Acute exercise increases myocardial tolerance to ischemia-reperfusion (I-R) injury in male but not in female rat hearts, possibly due to a decreased heat shock protein 70 (Hsp70) response in the female hearts. This study examined whether repetitive exercise training would increase Hsp70 and myocardial tolerance to I-R injury in female rat hearts. Adaptations in myocardial manganese superoxide dismutase (MnSOD) and endothelial nitric oxide synthase (eNOS) were also assessed.

Inhibition of phenylephrine-induced cardiomyocyte hypertrophy by activation of multiple adenosine receptor subtypes.

Plasma adenosine levels are elevated in cardiovascular disease including hypertension and heart failure, and the nucleoside has been proposed to serve as an endogenous antimyocardial remodeling factor. We studied the modulation of phenylephrine-induced hypertrophy by adenosine receptor activation in isolated neonatal cultured ventricular myocytes. Phenylephrine (10 muM) increased cell size by 35% and significantly increased expression of atrial natriuretic peptide.

Effective protection by NHE-1 inhibition in ischemic and reperfused heart under preconditioning blockade.

We compared the protective effects of ischemic preconditioning (IPC) and the Na(+)/H(+) exchanger-1 (NHE-1) inhibitor cariporide in isolated rat hearts subjected to global ischemia (45 or 90 min) and 30-min reperfusion and determined the protective effects of cariporide under IPC blockade with the mitochondrial ATP-sensitive K(+) channel blocker 5-hydroxydecanoate (5-HD). With 45-min ischemia, both IPC and cariporide equally increased maximum recovery of left ventricular developed pressure twofold (P < 0.05), although recovery was significantly greater with cariporide for the first 15 min of reperfusion.

Redox signaling of cardiac HSF1 DNA binding.

Experiments involving chemical induction of the heat shock response in simple biological systems have generated the hypothesis that protein denaturation and consequential binding of heat shock transcription factor 1 (HSF1) to proximal heat shock elements (HSEs) on heat shock protein (hsp) genes are the result of oxidation and/or depletion of intracellular thiols. The purpose of the present investigation was to determine the role of redox signaling of HSF1 in the intact animal in response to physiological and pharmacological perturbations. Heat shock and exercise induced HSF1-HSE DNA binding in the rat myocardium (P < 0.

Exercise improves postischemic cardiac function in males but not females: consequences of a novel sex-specific heat shock protein 70 response.

Exercise is a physiological inducer of the cardioprotective heat shock protein, Hsp70. The putative biological events involved in signaling this response exhibit sexual dimorphism. Thus, it was hypothesized that exercise-mediated induction of Hsp70 would demonstrate sex specificity.

Dehydroascorbic acid uptake by coronary artery smooth muscle: effect of intracellular acidification.

Dehydroascorbic acid (DHAA) enters cells via Na(+)-independent glucose transporters (GLUT) and is converted to ascorbate. However, we found that Na(+) removal inhibited [(14)C]DHAA uptake by smooth-muscle cells cultured from pig coronary artery. The uptake was examined for 2-12 min at 10-200 microM DHAA in either the presence of 134 mM Na(+) or in its absence (N-methyl D-glucamine, choline or sucrose replaced Na(+)).

Attenuation of compensatory right ventricular hypertrophy and heart failure following monocrotaline-induced pulmonary vascular injury by the Na+-H+ exchange inhibitor cariporide.

Pulmonary hypertension results in compensatory right ventricular (RV) hypertrophy. We studied the role of the Na+-H+ exchange (NHE) in the latter process by determining the effect of the NHE-1 inhibitor cariporide after monocrotaline-induced pulmonary artery injury. Sprague-Dawley rats received a control or cariporide diet for 7 days, at which time they were administered either monocrotaline (60 mg/kg) or its vehicle.

Na(+)/H(+) exchange inhibition reduces hypertrophy and heart failure after myocardial infarction in rats.

We investigated the effect of sodium/hydrogen exchange inhibition (NHE-1) on hypertrophy and heart failure after coronary artery ligation (CAL) in the rat. Animals were subjected to occlusion (or sham) of the left main coronary artery and immediately administered a control diet or one consisting of the NHE-1 inhibitor cariporide for 13-15 wk. Hearts were separated by small [30% of LV) infarcts.

Orally administered NHE1 inhibitor cariporide reduces acute responses to coronary occlusion and reperfusion.

Na+/H+ exchange (NHE) mediates myocardial ischemic and reperfusion injury. We examined the effects of dietary administration of the potent and selective NHE1 inhibitor cariporide on acute responses to coronary artery ligation and reperfusion in the anesthetized rat. Male Sprague-Dawley rats received control rat chow or an identical diet containing 3 parts per million of cariporide for 1 wk before 225 min of occlusion of the left main coronary artery or 45 min of occlusion followed by 180 min of reperfusion.

Na(+)-H+ exchange inhibition protects against mechanical, ultrastructural, and biochemical impairment induced by low concentrations of lysophosphatidylcholine in isolated rat hearts.

Lysophophatidylcholine (LysoPC) accumulates rapidly in the ischemic myocardium and is an important mediator of ischemia-induced cell injury. Na(+)-H+ exchange (NHE) inhibition has been demonstrated to protect the ischemic and reperfused myocardium. We determined whether NHE inhibition can also modulate cardiotoxicity produced by LysoPC (3 and 5 mumol/L) in isolated rat hearts.

Modulation of endothelin-1 effects on rat hearts and cardiomyocytes by nitric oxide and 8-bromo cyclic GMP.

Endothelin-1 (ET-1) has been demonstrated to produce numerous cardiac effects and increased production of the peptide has been shown in cardiac disease states. Although the cardiac effects of ET-1 have been examined extensively on its own, few studies have reported potential cross-talk between ET-1 with other endothelium-derived factors. We examined whether nitric oxide (NO) can modulate the effects of ET-1 on isolated rat hearts or ventricular myocytes.

Coronary arteriovenous fistula as a cause for reversible thallium-201 perfusion defect.

Exercise 201Tl SPECT imaging has become routinely accepted and utilized as a major screening test for atherosclerotic coronary artery disease. In appropriate clinical situations, an abnormal 201Tl study usually will require a subsequent coronary angiogram to confirm the presence of an abnormality and to define its pathologic anatomy. Although most reversible thallium defects will prove to be secondary to significant coronary artery atherosclerosis, congenital coronary or cardiac anomalies can occasionally be responsible, and it is useful to be aware of these, particularly in the evaluation of relatively young symptomatic patients.

Calcium dependent positive inotropic effects of low phorbol ester concentrations in isolated rat hearts.

Objective: The aim was to examine the cardiac effects of phorbol esters over a wide concentration range and to determine if the effects are related to Ca2+ availability.

Methods: Studies were carried out using isolated rat hearts exposed for 60 min either to phorbol 12-myristate 13-acetate (PMA, 10(-11) to 10(-6) M) or phorbol 12,13-dibutyrate (PDBu, 10(-12) to 10(-7) M) in the presence of either 1.25 or 2.

Comparative effects of Na+/H+ exchange inhibitors against cardiac injury produced by ischemia/reperfusion, hypoxia/reoxygenation, and the calcium paradox.

To examine the role of Na+/H+ exchange in cardiac injury, we compared the effect of amiloride (174 microM) with the markedly more specific and potent inhibitor 5-(N,N-hexamethylene) amiloride (HMA, 1 microM) against cardiac injury produced by reperfusion, reoxygenation, and the calcium paradox. Reperfusion after 15-min ischemia resulted in a 55 +/- 4% recovery in contractility, whereas in the presence of amiloride or HMA, recovery was increased to 82 +/- 5.8 and 72 +/- 7.

[Diagnosis of Perthes disease using magnetic resonance tomography].

Lateral displacement of the femoral head and slight flattening are typical radiological signs of early Legg-Calvé-Perthes disease. There is the value of magnetic resonance imaging (MRI) in demonstrating the congruity of the acetabular and femoral articular surfaces, the cartilage, the femoral head containment, intracapsular joint effusion, and hypertrophy synovium without using any ionizing radiation. Loss of containment because of lateralisation seems to be the result of medial hypertrophy of the femoral head cartilage.

Mucosal iron in the control of iron absorption in a rat intestinal transplant model.

Isogeneic intestinal transplantation of iron-loaded and iron-deficient intestine into iron-deficient rats was performed in 20 Lewis rats to isolate the effect of intestinal mucosal iron on iron absorption. Rats were iron loaded with three weekly IM injections of 50 mg of iron dextran and were rendered iron deficient with an iron-deficient diet for 3 weeks. Iron status was assessed by hepatic and gut mucosal iron determination.