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Objective: Evaluation of the effect of endothelin type A (ETA) receptor blockade on the course of volume-overload heart failure in rats with angiotensin II-dependent hypertension. Methods: Ren-2 renin transgenic rats (TGR) were used as a model of hypertension. Heart failure was induced by creating an aorto-caval fistula (ACF). Selective ETA receptor blockade was achieved by atrasentan. For comparison, other rat groups received trandolapril, an angiotensinconverting enzyme inhibitor (ACEi). Animals first underwent ACF creation and 2 weeks later the treatment with atrasentan or trandolapril, alone or combined, was applied; the follow-up period was 20 weeks. Results: Eighteen days after creating ACF, untreated TGR began to die, and none was alive by day 79. Both atrasentan and trandolapril treatment improved the survival rate, ultimately to 56% (18 of 31 animals) and 69% (22 of 32 animals), respectively. Combined ACEi and ETA receptor blockade improved the final survival rate to 52% (17 of 33 animals). The effects of the three treatment regimens on the survival rate did not significantly differ. All three treatment regimens suppressed the development of cardiac hypertrophy and lung congestion, decreased left ventricle (LV) end-diastolic volume and LV end-diastolic pressure, and improved LV systolic contractility in ACF TGR as compared with their untreated counterparts. Conclusion: The treatment with ETA receptor antagonist delays the onset of decompensation of volume-overload heart failure and improves the survival rate in hypertensive TGR with ACF-induced heart failure. However, the addition of ETA receptor blockade did not enhance the beneficial effects beyond those obtained with standard treatment with ACEi alone. Keywords: endothelin system, hypertension, Ren-2 renin transgenic rat, renin–angiotensin system, volume-overload heart failure Abbreviations: ACE, angiotensin-converting enzyme; ACF, aorto-caval fistula; ACEi, angiotensin-converting enzyme inhibitor; ANG II, angiotensin II; ANG 1–7, angiotensin-(1–7); (þdP/dt)max, maximum rates of pressure rise; (dP/dt)max, maximum rates of pressure fall; ESPVR, end-systolic pressure–volume relationship; ETA, endothelin type A; ET-1, endothelin 1; HanSD, Hannover Sprague- Dawley rats; LV, left ventricle; LVEDP, left ventricle enddiastolic pressure; LVEDV, left ventricle end-diastolic volume; PRSW, preload recruitable stroke work; RAAS, renin–angiotensin–aldosterone system; RV, right ventricle; SNS, sympathetic nervous system; TGR, Ren-2 renin transgenic rats; TPR, total peripheral resistance

The lattice mismatch between interesting 2D materials and commonly available 3D substrates is one of the obstacles in the epitaxial growth of monolithic 2D/3D heterostructures, but a number of 2D materials have not yet been considered for epitaxy. Here we present the first molecular beam epitaxy growth of NiTe$_{2}$ 2D transition metal dichalcogenide. Importantly, the growth is realized on a nearly lattice matched GaAs(111)B substrate. Structural properties of the grown layers are investigated by electron diffraction, X-ray diffraction, and scanning tunnelling microscopy. Surface coverage and atomic scale order is evidenced by images obtained with atomic force, scanning electron, and transmission electron microscopy. Basic transport properties were measured confirming that NiTe$_{2}$ layers are metallic, with the Hall concentration of $10^{20}$cm$^{-3}$ to $10^{23}$cm$^{-3}$, depending on the growth conditions.

The intrarenal dopamine system has been thoroughly investigated at all levels, especially its role in salt-dependent and other forms of hypertension. However, the evidence regarding dopamine's tonic influence on renal tubular transport of sodium remains equivocal. We reinvestigated its tonic influence on sodium excretion and systemic and renal haemodynamics. Early effects of dopamine D1 receptor blockade using 90-min Schering 23390 (SCH) infusion were examined in anaesthetized rats on 7 days' high salt diet (HS), early uninephrectomized rats on 14 days' HS diet, drinking 1% saline (HS/UNX), and in spontaneously hypertensive rats (SHR). In the HS group (baseline BP ~133 mm Hg) renal intracortical SCH promptly decreased sodium, water and total solute excretion (UNa V, V, Uosm V), with significant difference from the solvent-infused group. BP and renal artery blood flow (RBF, Transonic probe) did not change. In HS/UNX model (baseline BP ~150 mm Hg), characterized by hypertrophy of the remaining kidney, the excretion parameters only tended to decrease whereas SCH induced an ~20% fall in RBF. In SHR (BP ~180 mm Hg), UNa V and V tended to increase in solvent-infused rats; this increasing tendency was abolished by SCH infusion. During experiments the renal vascular resistance increased significantly in SCH- and solvent-infused SHR. Despite some contradictory findings regarding the genuine tonic control of renal excretion by intrarenal dopamine, our results clearly support such role in rats on HS diet and in SHR, the model resembling human essential hypertension. The observations strengthen the experimental basis and the rationale for targeting the intrarenal dopamine system in attempts to combat arterial hypertension.

Background: The coincidence of congestive heart failure (CHF) and chronic kidney disease (CKD) results in poor survival rate. The aim of the study was to examine if renal denervation (RDN) would improve the survival rate in CHF induced by creation of aorto-caval fistula (ACF).Methods: Fawn-hooded hypertensive rats (FHH), a genetic model of spontaneous hypertension associated with CKD development, were used. Fawn-hooded low-pressure rats (FHL), without CKD, served as controls. RDN was performed 4 weeks after creation of ACF and the follow-up period was 10 weeks.Results: We found that intact (non-denervated) ACF FHH exhibited survival rate of 58.8% (20 out of 34 rats), significantly lower than in intact ACF FHL (81.3%, 26/32 rats). In intact ACF FHL albuminuria remained stable throughout the study, whereas in ACF FHH it increased significantly, up to a level 40-fold higher than the basal values. ACF FHL did not show increases in renal glomerular and tubulointerstitial injury as compared with FHL, while ACF FHH exhibited marked increases in kidney injury as compared with FHH. RDN did not improve the survival rate in either ACF FHL or ACF FHH and did not alter the course of albuminuria in ACF FHL. RDN attenuated the albuminuria, but did not reduce the kidney injury in ACF FHH.Conclusions: Our present results support the notion that even modest CKD increases CHF-related mortality. RDN did not attenuate CHF-dependent mortality in ACF FHH, it delayed the progressive rise in albuminuria, but it did not reduce the degree of kidney injury.

Earlier evidence from studies of rat hypertension models undermines the widespread view that the rate of renal medullary blood flow (MBF) is critical in control of arterial pressure (MAP). Here, we examined the role of MBF in rats that were normotensive, with modest short-lasting pressure elevation, or with overt established hypertension. The groups studied were anaesthetised Sprague-Dawley rats: (1) normotensive, (2) with acute i.v. norepinephrine-induced MAP elevation, and (3) with hypertension induced by unilateral nephrectomy followed by administration of deoxycorticosterone-acetate (DOCA) and 1% NaCl drinking fluid for 3 weeks. MBF was measured (laser-Doppler probe) and selectively increased using 4-h renal medullary infusion of bradykinin. MAP, renal excretion parameters and post-experiment medullary tissue osmolality and sodium concentration were determined. In the three experimental groups, baseline MAP was 117, 151 and 171 mmHg, respectively. Intramedullary bradykinin increased MBF by 45%, 65% and 70%, respectively, but this was not associated with a change in MAP. In normotensive rats a significant decrease in medullary tissue sodium was seen. The intramedullary bradykinin specifically increased renal excretion of water, sodium and total solutes in norepinephrine-treated rats but not in the two other groups. As previously shown in models of rat hypertension, in the normotensive rats and those with acute mild pressure elevation (resembling labile borderline human hypertension), 4-h renal medullary hyperperfusion failed to decrease MAP. Nor did it decrease in DOCA-salt model mimicking low-renin human hypertension. Evidently, within the 4-h observation, medullary perfusion was not a critical determinant of MAP in normotensive and hypertensive rats.

In the context of the ongoing debate on the mechanism of blood pressure (BP) regulation and pathophysiology of arterial hypertension ("renocentric" vs "neural" concepts), attention is focused on the putative regulatory role of changes in renal medullary blood flow (MBF). Experimental evidence is analysed with regard to the question whether an elevation of BP and renal perfusion pressure (RPP) is likely to increase MBF due to its impaired autoregulation. It is concluded that such increases have been clearly documented only in rats with extracellular fluid volume expansion. A possible translation of this finding to BP regulation in health and hypertension in humans may only be a matter of speculation. Within the "renocentric" theory, the key event leading to restoration of initial BP level is pressure natriuresis. Its relation to elevation of renal interstitial hydrostatic pressure and to the phenomenon of "wash-out" of renal medullary solutes by increasing MBF is discussed. We also assessed the validity of data supporting the putative mechanism of short-term restoration of elevated BP owing to the release of a vasodilator lipid (medullipin) by the medulla. The structure of the proposed medullary lipid is still undefined, and there is no sound evidence on its mediatory role in lowering elevated BP level. In conclusion, MBF change can hardly be regarded as a crucial event in the regulation of BP: it can be involved in the control of sodium excretion and BP only in some circumstances, although its contributory role cannot be excluded.

Current data indicate that heart failure (HF) is associated with inflammation and microvascular dysfunction and remodeling. These mechanisms could be involved in HF development and progression, especially in HF with preserved ejection fraction (HFpEF). We aimed to compare structural changes in retinal arterioles and carotid arteries between HF patients and patients without heart failure. This preliminary, retrospective, case-control study included 28 participants (14 patients with HFpEF and 14 age- and sex-matched healthy controls). Carotid intima-media thickness to lumen ratio (cIMTLR) was assessed using B-mode ultrasonography. Retinal arterioles wall- to-lumen ratio (rWLR) was assessed by adaptive optics camera rtx1. The HF patients had higher IMTLR (Δmedian [HFpEF–control group] 0.07, p = 0.01) and eWLR (Δmedian 0.03, p = 0.001) in comparison to patients without HF. In the whole study group, rWLR correlated significantly with IMTLR (r = 0.739, p = 0.001). Prevalence of arterial hypertension was similar in both groups, however, patients with HF had a significantly lower office, central and 24-h ambulatory blood pressure (systolic Δmedian −21 to −18 mmHg; diastolic Δmedian −23 to −10 mmHg). Our data suggests gradual and simultaneous progression of vascular remodeling in both retinal arterioles and carotid arteries in HFpEF patients. This process could be a marker of HF development. Significantly lower blood pressure values in HF group may indicate that vascular remodeling could be independent of BP control. Nevertheless, further and larger prospective studies allowing to reduce the impact of confounding and address temporality are warranted.

Pulsed current-induced magnetization reversal is investigated in the layer of (Ga,Mn)(Bi,As) dilute ferromagnetic semiconductor (DFS) epitaxially grown under tensile misfit strain causing perpendicular magnetic anisotropy in the layer. The magnetization reversal, recorded through measurements of the anomalous Hall effect, appearing under assistance of a static magnetic field parallel to the current, is interpreted in terms of the spin-orbit torque mechanism. Our results demonstrate that an addition of a small fraction of heavy Bi atoms, substituting As atoms in the prototype DFS (Ga,Mn)As and increasing the strength of spin-orbit coupling in the DFS valence band, significantly enhances the efficiency of current-induced magnetization reversal thus reducing considerably the threshold current density necessary for the reversal. Our findings are of technological importance for applications to spin-orbit torque-driven nonvolatile memory and logic elements., Comment: 8 pages, 5 figures

Association of congestive heart failure (CHF) and chronic kidney disease (CKD) worsens the patient's prognosis and results in poor survival rate. The aim of this study was to examine if addition of endothelin type A (ETCKD was induced by 5/6 renal mass reduction (5/6 NX) and CHF was elicited by volume overload achieved by creation of aorto-caval fistula (ACF). The follow-up was 24 weeks after the first intervention (5/6 NX). The treatment regimens were initiated 6 weeks after 5/6 NX and 2 weeks after ACF creation.The final survival in untreated group was 15%. The treatment with ETOur results show that treatment with ET

The purpose of this review was to discuss the role of sodium and inflammation in the pathophysiology of hypertension and the observed different hemodynamic effects of drugs. The Pathway-2 study revealed that similar reductions in vascular resistance after spironolactone and doxazosin resulted in opposite effects on sodium balance, water retention, and hemodynamic parameters. These and other clinical findings were bridged to recent experimental and physiological data. Tissue sodium accumulation in salt-sensitive individuals due to endothelial glycocalyx dysfunction causes macrophage infiltration, vascular inflammation, and local changes in angiotensin-2 and aldosterone concentrations. This inflammatory cascade leads to factor XII-related coagulation disorders with neutrophil extracellular trap formation (NETosis). This model of sodium-induced microcirculation impairment was used to explain the differences in central hemodynamic parameters after spironolactone or doxazosin treatment in resistant hypertension. Hypertension treatment by induced sodium removal or reduced sodium intake should reduce endothelial glycocalyx dysfunction, inflammation, NETosis, and coagulation disorders, leading to improved vascular health and cardiac diastolic function.

Thin layers of transition metal dichalcogenides have been intensively studied over the last few years due to their novel physical phenomena and potential applications. One of the biggest problems in laboratory handling and moving on to application-ready devices lies in the high sensitivity of their physicochemical properties to ambient conditions. We demonstrate that novel, in situ capping with an ultra-thin, aluminum film efficiently protects thin MoTe2 layers stabilizing their electronic transport properties after exposure to ambient conditions. The experiments have been performed on bilayers of 2H-MoTe2 grown by molecular beam epitaxy on large area GaAs(111)B substrates. The crystal structure, surface morphology and thickness of the deposited MoTe2 layers have been precisely controlled in situ with a reflection high energy electron diffraction system. As evidenced by high resolution transmission electron microscopy, MoTe2 films exhibit perfect arrangement in the 2H phase and the epitaxial relation to the GaAs(111)B substrates. After the growth, the samples were in situ capped with a thin (3 nm) film of aluminum, which oxidizes after exposure to ambient conditions. This oxide serves as a protective layer to the underlying MoTe2. Resistivity measurements of the MoTe2 layers with and without the cap, exposed to low vacuum, nitrogen and air, revealed a huge difference in their stability. The significant rise of resistance is observed for the unprotected sample while the resistance of the protected one is constant. Wide range temperature resistivity studies showed that charge transport in MoTe2 is realized by hopping with an anomalous hopping exponent of x ≃ 0.66, reported also previously for ultra-thin, metallic layers.

We found previously that intravenous kynurenic acid (KYNA), a native broad spectrum glutamate antagonist, increases renal blood flow and induces natriuresis in anesthetized spontaneously hypertensive rats (SHR). Since such changes may affect systemic circulation and can potentially find therapeutic application, in this study we examined long term influence of orally administered KYNA on systemic and renal hemodynamics and renal excretion in conscious SHR. KYNA was administered in drinking water at a dose of 25 mg/kg/day for 3 weeks. Heart rate (HR), systolic (SBP), and mean arterial pressure (MAP) were measured through telemetry. The records were taken at the beginning of the study (control, day 0), and then on day 7, 14, and 21 of treatment. Diuresis (V), total solute excretion (UosmV), and sodium excretion (UNaV) were determined on days 0, 7, and 14. KYNA consistently decreased HR, from 319 ± 8 to 291 ± 5, 299 ± 9 and 284 ± 6 beats/min on day 7, 14, and 21, respectively, (− 9, − 6, and − 11%; p

We found recently that in Ren-2 transgenic hypertensive rats (TGR) addition of soluble epoxide hydrolase inhibitor (sEHi) to treatment with angiotensin-converting enzyme inhibitor (ACEi), surprisingly, increased the mortality due to heart failure (HF) induced by creation of the aorto-caval fistula (ACF). Since TGR exhibit sex-related differences in mortality, we examined here if such differentiation exists also in the response to the treatment with ACEi (trandolapril), alone or combined with sEHi [cis-4-[4-(3-adamantan-1-yl-ureido)cyclohexyloxy]benzoic acid, (c-AUCB)]. ACEi improved survival in males to 74 % (vs. 0 %) and in females to 65 % (vs. 32 %). ACEi and sEHi combined also improved the survival in male ACF TGR, however, it was significantly less (38 %) than after ACEi alone. In contrast, in females the combined treatment significantly improved the final survival rate (84 %). There were no significant sex-linked differences in survival rate in untreated or treated normotensive Hannover Sprague-Dawley rats. In conclusion, in HF patients with co-existing hypertension and RAS hyperactivity, the sex may co-determine the rate of HF progression, and can influence the effectiveness of the therapeutic measures applied. Therefore, in the relevant pre-clinical studies the sex-linked differences should be seriously considered. Our data indicate that TGR might be an optimal model for such studies.

The aim of the present study was to perform kidney messenger ribonucleic acid (mRNA) analysis in normotensive, Hannover Sprague–Dawley (HanSD) rats and hypertensive, Ren-2 renin transgenic rats (TGR) after doxorubicin-induced heart failure (HF) with specific focus on genes that are implicated in the pathophysiology of HF-associated cardiorenal syndrome. We found that in both strains renin and angiotensin-converting enzyme mRNA expressions were upregulated indicating that the vasoconstrictor axis of the renin–angiotensin system was activated. We found that pre-proendothelin-1, endothelin-converting enzyme type 1 and endothelin type A receptor mRNA expressions were upregulated in HanSD rats, but not in TGR, suggesting the activation of endothelin system in HanSD rats, but not in TGR. We found that mRNA expression of cytochrome P-450 subfamily 2C23 was downregulated in TGR and not in HanSD rats, suggesting the deficiency in the intrarenal cytochrome P450-dependent pathway of arachidonic acid metabolism in TGR. These results should be the basis for future studies evaluating the pathophysiology of cardiorenal syndrome secondary to chemotherapy-induced HF in order to potentially develop new therapeutic approaches.

We investigated the role of the interaction between hypertension and the renin-angiotensin system in the pathophysiology of myocardial ischemia/reperfusion injury. We hypothesized that in the early phase of angiotensin II (ANG II)-dependent hypertension with developed left ventricular hypertrophy, cardioprotective mechanism(s) are fully activated. The experiments were performed in transgenic rats with inducible hypertension, noninduced rats served as controls. The early phase of ANG II-dependent hypertension was induced by five-days (5 days) dietary indole-3-carbinol administration. Cardiac hypertrophy, ANG II and ANG 1–7 levels, protein expression of their receptors and enzymes were determined. Separate groups were subjected to acute myocardial ischemia/reperfusion injury, and infarct size and ventricular arrhythmias were assessed. Induced rats developed marked cardiac hypertrophy accompanied by elevated ANG levels. Ischemia/reperfusion mortality was significantly higher in induced than noninduced rats (52.1 and 25%, respectively). The blockade of AT1 receptors with losartan significantly increased survival rate in both groups. Myocardial infarct size was significantly reduced after 5 days induction (by 11%), without changes after losartan treatment. In conclusion, we confirmed improved cardiac tolerance to ischemia/reperfusion injury in hypertensive cardiohypertrophied rats and found that activation of AT1 receptors by locally produced ANG II in the heart was not the mechanism underlying infarct size reduction.

Purpose of Review To analyze the impact of sodium retention states on the course of COVID-19 and propose possible interventions to curb disease progression. Recent Findings Numerous data confirm a positive association of non-communicable diseases, aging, and other sodium-retaining states, including iatrogenic ones, with more severe sometimes fatal clinical course of COVID-19. Reasons for this effect could include increased angiotensin signaling via the AT1R receptor. The endothelial glycocalyx also plays an important role in infection, leading to a vicious cycle of inflammation and tissue sodium retention when damaged. RAS inhibitors may help restore glycocalyx function and prevent severe organ damage. Anticoagulants, especially heparin, may also have therapeutic applications due to antithrombotic, anti-inflammatory, glycocalyx-repairing, and antialdosteronic properties. The ambiguous influence of some diuretics on sodium balance was also discussed. Summary Abnormal sodium storage and increased angiotensin-converting enzyme activity are related to the severity of COVID-19. Inducing sodium removal and reducing intake might improve outcomes.

Background: Chymase generates angiotensin II (ANG II) independently of angiotensin-converting enzyme in tissues and it contributes to vascular remodeling and development of hypertension, however the exact mechanism of its action is unclear. Methods: Hence, the effects of chymase inhibition were examined in anesthetized spontaneously hypertensive rats (SHR) in two stages of the disease development, ie. pre-hypertensive (SHR7) and with established hypertension (SHR16). Chymostatin, a commercial chymase inhibitor, was infused intravenously alone or in subsequent groups co-infused with captopril. Results: Mean blood pressure (MBP), total renal blood flow (RBF) and ANG II content (plasma and tissues) were measured. In SHR16 chymase blockade significantly decreased MBP (−6%) and plasma (−38%), kidney (−71%) and heart (−52%) ANG II levels. In SHR7 chymostatin did not influence MBP or RBF, but significantly decreased heart ANG II level. Conclusion: Jointly, functional studies and ANG II determinations support the evidence that in SHR chymase can raise plasma ANG II and contribute to blood pressure elevation. We propose that addition of chymase blockade to ACE inhibition could be a promising approach in the treatment of hypertensive patients resistant to therapy with ACE-inhibitors alone.

Thin layers of transition metal dichalcogenides have been intensively studied over the last few years due to their novel physical phenomena and potential applications. One of the biggest problems in laboratory handling and moving on to application-ready devices lies in the high sensitivity of their physicochemical properties to ambient conditions. We demonstrate that novel, in situ capping with an ultra-thin, aluminum film efficiently protects thin MoTe2 layers stabilizing their electronic transport properties after exposure to ambient conditions. The experiments have been performed on bilayers of 2H-MoTe2 grown by molecular beam epitaxy on large area GaAs(111)B substrates. The crystal structure, surface morphology and thickness of the deposited MoTe2 layers have been precisely controlled in situ with a reflection high energy electron diffraction system. As evidenced by high resolution transmission electron microscopy, MoTe2 films exhibit perfect arrangement in the 2H phase and the epitaxial relation to the GaAs(111)B substrates. After the growth, the samples were in situ capped with a thin (3 nm) film of aluminum, which oxidizes after exposure to ambient conditions. This oxide serves as a protective layer to the underlying MoTe2. Resistivity measurements of the MoTe2 layers with and without the cap, exposed to low vacuum, nitrogen and air, revealed a huge difference in their stability. The significant rise of resistance is observed for the unprotected sample while the resistance of the protected one is constant. Wide range temperature resistivity studies showed that charge transport in MoTe2 is realized by hopping with an anomalous hopping exponent of x ≃ 0.66, reported also previously for ultra-thin, metallic layers.

OBJECTIVES The global morbidity and mortality related to hypertension and associated disorders increases continuously and novel therapeutic strategies are still in high demand. Increasing evidence suggests the important role in blood pressure regulation of cytochrome P-450-dependent metabolites of arachidonic acid. Epoxyeicosatrienoic acids (EETs) induce vasodilation and natriuresis, and have renoprotective and anti-inflammatory properties. 20-HETE is an arachidonic acid metabolite with both prohypertensive and antihypertensive activities. To explore the pathophysiological role of arachidonic acid metabolites in more detail, we examined the antihypertensive efficiency of EET-A, a stable analog of 14,15-EET, and of AAA, a novel antagonist of the 20-HETE receptors. METHODS Male spontaneously hypertensive rats (SHR) were treated for 5 weeks with EET-A, AAA or the combination; age-matched untreated SHR and normotensive Wistar-Kyoto rats served as controls. EET-A and AAA were administered in drinking water at 10 mg/kg/day each. SBP was measured by telemetry and urine, blood, and tissue samples were collected for relevant analyses. RESULTS EET-A or AAA given alone had no significant effect on SHR blood pressure. In contrast, combined treatment with AAA and EET-A was significantly antihypertensive, causing a decrease in SBP from 180 ± 3 to 160 ± 5 mmHg (P

Objective: We evaluated the hypothesis that the development of renal dysfunction and congestive heart failure (CHF) caused by volume overload in rats with angiotensin II (ANG II)-dependent hypertension is associated with altered renal vascular responsiveness to ANG II and to epoxyeicosatrienoic acids (EETs). Methods: Ren-2 transgenic rats (TGRs) were used as a model of ANG II-dependent hypertension. CHF was induced by volume overload achieved by the creation of the aorto-caval fistula (ACF). Renal blood flow (RBF) responses were determined to renal arterial administration of ANG II, native 11,12-EET, an analog of 14,15-EETs (EET-A), norepinephrine (NE), acetylcholine (Ach) and bradykinin (Bk) in healthy (i.e., sham-operated) TGR and ACF TGR (5 weeks after ACF creation). Results: Selective intrarenal administration of neither vasoactive drug altered mean arterial pressure in any group. Administration of ANG II caused greater decreases in RBF in ACF TGR than in sham-operated TGR, whereas after administration of NE the respective decreases were comparable in the 2 groups. Administration of Ach and Bk elicited significantly higher RBF increases in ACF TGR as compared with sham-operated TGR. In contrast, administration of 11,12-EET and EET-A caused significantly smaller RBF increases in ACF TGR than in sham-operated TGR. Conclusion: The findings show that 5 weeks after creation of ACF, the TGR exhibit exaggerated renal vasoconstrictor responses to ANG II and reduced renal vasodilatory responses to EETs, suggesting that both these alterations might play an important role in the development of renal dysfunction in this model of CHF.

The adenosine (Ado) system may participate in regulation of kidney function in diabetes mellitus (DM), therefore we explored its role and interrelation with NO in the control of renal circulation and excretion in normoglycemic (NG) and streptozotocin-diabetic (DM) rats. Effects of theophylline (Theo), a non-selective Ado receptor antagonist, were examined in anaesthetized NG or in streptozotocin induced diabetic (DM) rats, untreated or after blockade of NO synthesis with l-NAME. We measured arterial blood pressure (MABP), whole kidney blood flow and renal regional flows: cortical and outer- and inner-medullary (IMBF), determined as laser-Doppler fluxes. Renal excretion of water, total solutes and sodium and in situ renal tissue NO signal (selective electrodes) were also determined. Theo experiments disclosed minor baseline vasoconstrictor and vasodilator tone in the kidney of NG and DM rats, respectively. NO blockade increased baseline MABP and decreased renal haemodynamics, similarly in NG and DM rats, indicating comparable vasodilator influence of NO in the two groups. Unexpectedly, in all rats with intact NO synthesis, Ado receptor blockade increased kidney tissue NO. In NO-deficient NG and DM rats, Ado receptor blockade induced comparable renal vasodilatation, suggesting similar vasoconstrictor influence of the Ado system. However, DM rats showed an unexplained association of decreased MABP and IMBF and increased NO signal. Higher baseline renal excretion in DM rats indicated inhibition of renal tubular reabsorption due to the prevalence of natriuretic A2 over antinatriuretic A1 receptors. In conclusion, the experiments provided new insights in functional interrelation of adenosine and NO in normoglycaemia and streptozotocin-diabetes.

We critically discuss various experimental methods to determine Curie temperature T C of (Ga,Mn)As thin layers or other conducting magnetic materials by means of electric charge transport measurements. They all base on the influence of sample magnetization on the magnetoresistivity tensor ρ and are an alternative to the method based upon an analysis of the temperature derivative of the sample resistance (Novak et al., 2008). These methods can be applied even when standard SQUID magnetometers are difficult or impossible to use – for example for extremely small samples or in the case of experiments performed at very specific physical conditions, e.g. at high hydrostatic pressure inside the clamp cell. We show that the use of the so called Arrott plot prepared with the use of high magnetic field isotherms ρ xx ( H 0 ) , ρ xy ( H 0 ) ( H 0 – external magnetic field) may lead to substantial (of the order of 10 K) divergence of the obtained T C values depending on the assumptions which are necessary to make in this case and depending on the direction of a magnetic anisotropy easy axis. We also propose a number of ways how to obtain, basing on low magnetic field isotherms ρ xx ( H 0 ) , ρ xy ( H 0 ) , clear and characteristic features which are closely related to the ferromagnetic–paramagnetic phase transition.

• The Ga 1-x Mn x As/InGaAs layer exhibits a strong sensitivity to the magnetic field and temperature.

Background/Aims: Reduction of renal blood flow (RBF) is commonly thought to be a causative factor of renal dysfunction in congestive heart failure (CHF), but the exact mechanism of the renal hypoperfusion is not clear. Apart from the activation of neurohormonal systems controlling intrarenal vascular tone, the cause might be altered reactivity of the renal vasculature to endogenous vasoactive agents. Methods: To evaluate the role of this mechanism, we assessed by an ultrasonic transient-time flow probe maximum RBF responses to renal artery infusion of angiotensin II (ANG II), norepinephrine (NE) and acetylcholine (Ach) in healthy male rats and animals with compensated and decompensated CHF. CHF was induced by volume overload achieved by the creation of the aorto-caval fistula (ACF) in Hannover Sprague-Dawley rats. Results: Maximum responses in RBF to ANG II were similar in rats studied five weeks (compensated phase) and 20 weeks (decompensated phase) after ACF creation when compared to sham-operated rats. On the other hand, NE elicited larger maximum decreases in RBF in rats with CHF (five and 20 weeks post-ACF) than in sham-operated controls. We observed greater maximum vasodilatory responses to Ach only in rats with a compensated stage of CHF (five weeks post-ACF). Conclusion: Greater renal vasoconstrictor responsiveness to ANG II or reduced renal vasodilatation in response to Ach do not play a decisive role in the development of renal dysfunction in ACF rats with compensated and decompensated CHF. On the other hand, exaggerated renal vascular responsiveness to NE may be here a contributing causative factor, active in either CHF phase.

Endothelin 1 (ET-1) seems essential in salt-dependent hypertension, and activation of ETA receptors causes renal vasoconstriction. However, the response in the renal medulla and the role of tissue NO availability has never been adequately explored in vivo. We examined effects of ETA and ETB receptor blockade (atrasentan and BQ788) on blood pressure (MAP), medullary blood flow (MBF) and medullary tissue NO. Effects of systemic and intramedullary blocker application were compared in anesthetized normotensive ET-1-pretreated Sprague-Dawley rats (S-D), in salt-dependent hypertension (HS/UNX) and in spontaneously hypertensive rats (SHR). Total renal blood flow (RBF) was measured using a Transonic renal artery probe, MBF as laser-Doppler flux, and tissue NO signal using selective electrodes. In normotensive rats ET-1 significantly increased MAP, decreased RBF (-20%) and renal medullary NO. In HS/UNX rats atrasentan decreased MAP and increased medullary NO, earlier and more profoundly with intravenous infusion. In SHR atrasentan decreased MAP, more effectively with intravenous infusion; the increase in tissue NO (∼10%) was similar with both routes; however, only intramedullary atrasentan increased MBF. No consistent responses to BQ788 were seen. We confirmed dominant role of ETA receptors in regulation of blood pressure and renal hemodynamics in normotensive and hypertensive rats and provided novel evidence for the role of ETA in control of intrarenal NO bioavailability in salt-dependent and spontaneous hypertension. Under conditions of activation of the endothelin system ETB stimulation preserved medullary perfusion.

The core-multishell wurtzite structure (In, Ga) As-(Ga, Al) As-(Ga, Mn) As semiconductor nanowires have been successfully grown on GaAs(111) B substrates using MBE technique. The nanowires cores we ...

The purpose of this review was to discuss the role of sodium and inflammation in the pathophysiology of hypertension and the observed different hemodynamic effects of drugs. The Pathway-2 study revealed that similar reductions in vascular resistance after spironolactone and doxazosin resulted in opposite effects on sodium balance, water retention, and hemodynamic parameters. These and other clinical findings were bridged to recent experimental and physiological data. Tissue sodium accumulation in salt-sensitive individuals due to endothelial glycocalyx dysfunction causes macrophage infiltration, vascular inflammation, and local changes in angiotensin-2 and aldosterone concentrations. This inflammatory cascade leads to factor XII-related coagulation disorders with neutrophil extracellular trap formation (NETosis). This model of sodium-induced microcirculation impairment was used to explain the differences in central hemodynamic parameters after spironolactone or doxazosin treatment in resistant hypertension. Hypertension treatment by induced sodium removal or reduced sodium intake should reduce endothelial glycocalyx dysfunction, inflammation, NETosis, and coagulation disorders, leading to improved vascular health and cardiac diastolic function.

Introduction In search for new therapeutic measures of congestive heart failure (CHF) attention focused on the role of epoxyeicosatrienoic acids (EETs), cytochrome P450-dependent epoxygenase pathway metabolites of arachidonic acid, with antihypertensive and organ-protective actions. The EETs are rapidly broken-down by soluble epoxide hydrolase (sEH). Blocking sEH and increasing tissue EETs bioavailability had antihypertensive and cardio- and renoprotective effects. The studies of the biological mechanisms underlying the sex-related differences in the CHF and in the responses to new pharmacological measures are missing. The rat model in which CHF is induced by volume overload by creation of the aorto-caval fistula (ACF) is recommended for preclinical studies by American Heart Association. It has been noticed that the hypertensive rat transgenic for the mouse Ren-2 renin gene (TGR) presents a unique angiotensin II-dependent model of hypertension. We found that male ACF TGR displayed tissue deficiency of EETs, and increasing intrarenal EETs levels by pharmacological blockade of sEH attenuated the progression of CHF in male ACF TGR. However, we did not examine if this effect occurs also in female ACF TGR. Purpose The aim was to establish if sex-related differences, if present, are demonstrable with standard treatment with ACEi alone and with the combined treatment with ACEi and sEHi. Methods Male and female TGR rats were randomly assigned either to ACF procedure or to sham-operation. One week after the procedure rats were divided into the 8 experimental groups (sham-operated male TGR + placebo, ACF male TGR + placebo, ACF male TGR + ACEi, ACF male TGR + ACEi + sEHi, sham-operated female TGR + placebo, ACF female TGR + placebo, ACF female TGR + ACEi, ACF female TGR + ACEi + sEHi). C-AUCB was used as an sEHi and trandolapril as ACEi, both in drinking water in doses previously tested. The follow-up period was 50 weeks and the primary end-point was death from any cause. Results All sham-operated male and female TGR survived until the end of experiment. All untreated male ACF TGR animals died by week 20. In contrast, untreated female ACF survived in the rate of 32%. The treatment with ACEi improved survival rate similary in male as well as female ACF TGR (74% and 65%). The combined treatment with ACEi and sEHi worsened the survival in male ACF TGR as compared with ACF TGR + ACEi (38%). In contrast, the combined treatment with ACEi and sEHi in female ACF TGR significantly improved the course and the final survival rate (84%) as compared with female ACF TGR + ACEi alone. Picture 1 Conclusions The study suggests that in CHF individuals in whom hypertension and increased RAS activity run in parallel, the patients' sex is the co-determinant of CHF progression. In particular it can influence the effectiveness of the therapeutic measures applied to slow it down. Therefore, in pre- and clinical studies the sex-related differences should be seriously considered. Acknowledgement/Funding Ministry of Health of the Czech Republic grant no. 17- 28220A; Grant Agency of Charles University, project number 32218

An important complication of the prolonged left ventricle assist device support in patients with heart failure is unloading-induced cardiac atrophy which proved resistant to various treatments. Heterotopic heart transplantation (HTx) is the usual experimental model to study this process. We showed previously that implantation of the newly designed intraventricular spring expander can attenuate the atrophy when examined after HTx in the failing heart (derived from animals with established heart failure). The present study aimed to examine if enhanced isovolumic loading achieved by implantation of the expander would attenuate cardiac post-HTx atrophy also in the healthy heart. Cardiac atrophy was assessed as the ratio of the transplanted-to-native heart weight (HW) and its degree was determined on days 7, 14, 21 and 28 after HTx. The transplantation resulted in 32±3, 46±2, 48±3 and 46±3 % HW loss when measured at the four time points; implantation of the expander had no significant effect on these decreases. We conclude that enhanced isovolumic loading achieved by intraventricular implantation of the expander does not attenuate the development of cardiac atrophy after HTx in the healthy heart. This indicates that such an approach does not represent a useful therapeutic measure to attenuate the development of unloading-induced cardiac atrophy.

Background/Aims: We found recently that the aortocaval fistula (ACF)-induced heart failure (HF) results in higher mortality in female than in male rats. Possibly, the development of renal dysfunction in the females, unlike in males, is associated with altered renal vascular responsiveness to angiotensin II (ANG II). Methods: Five or 20 weeks after ACF creation (compensated and decompensated HF, respectively), we assessed renal blood flow (RBF) responses to intrarenal administration of ANG II, norepinephrine (NE), and acetylcholine (Ach) in female ACF and sham-operated rats. Results: In ACF females, ANG II decreased RBF more than in healthy animals, unlike with earlier published data in male ACF rats that responded similarly. Also, NE decreased RBF more in female ACF rats, whereas Ach increased RBF to the same extent in female ACF and sham-operated rats. RBF responses to intravenous administration of NE and Ach were almost identical in female and male ACF rats. Conclusion: Female ACF rats studied at the onset of HF decompensation reveal, in contrast to male rats, enhanced renal vascular responsiveness to both NE and ANG II. When associated with the demonstrated increased intrarenal ANG II and NE concentrations, such hyperresponsiveness might promote the development of renal dysfunction and accelerate HF decompensation.

This study evaluates the effects of chronic treatment with EET-A, an orally active epoxyeicosatrienoic acid (EETs) analog, on the course of aorto-caval fistula (ACF)-induced heart failure (HF) in Ren-2 transgenic rats (TGR), a model characterized by hypertension and augmented activity of the renin-angiotensin system (RAS). The results were compared with standard pharmacological blockade of the RAS using angiotensin-converting enzyme inhibitor (ACEi). The rationale for employing EET-A as a new treatment approach is based on our findings that apart from increased RAS activity, untreated ACF TGR also shows kidney and left ventricle (LV) tissue deficiency of EETs. Untreated ACF TGR began to die 17 days after creating ACF and were all dead by day 84. The treatment with EET-A alone or ACEi alone improved the survival rate: in 156 days after ACF creation, it was 45.5% and 59.4%, respectively. The combined treatment with EET-A and ACEi appeared to improve the final survival to 71%, however, the difference from either single treatment regimen did not reach significance. Nevertheless, our findings support the notion that targeting the cytochrome P-450-dependent epoxygenase pathway of arachidonic acid metabolism should be considered for the treatment of HF.

We have thoroughly investigated the planar Hall effect (PHE) in the epitaxial layers of the quaternary compound (Ga,Mn)(Bi,As). The addition of a small amount of heavy Bi atoms to the prototype dilute ferromagnetic semiconductor (Ga,Mn)As enhances significantly the spin–orbit coupling strength in its valence band, which essentially modifies certain magnetoelectric properties of the material. Our investigations demonstrate that an addition of just 1% Bi atomic fraction, substituting As atoms in the (Ga,Mn)As crystal lattice, causes an increase in the PHE magnitude by a factor of 2.5. Moreover, Bi incorporation into the layers strongly enhances their coercive fields and uniaxial magneto-crystalline anisotropy between the in-plane ⟨110⟩ crystallographic directions in the layers grown under a compressive misfit strain. The displayed two-state behaviour of the PHE resistivity at zero magnetic field, which may be tuned by the control of applied field orientation, could be useful for application in spintronic devices, such as nonvolatile memory elements.

Background: Early addition of endothelin (ET) type A (ETA) receptor blockade to complex renin–angiotensin system (RAS) blockade has previously been shown to provide better renoprotection against pr...

(Ga,Mn)As in wurtzite crystal structure, is coherently grown by molecular beam epitaxy on the {1100} side facets of wurtizte (Ga,In)As nanowires and further encapsulated by (Ga,Al)As and low temperature GaAs. For the first time a true long-range ferromagnetic magnetic order is observed in non-planar (Ga,Mn)As, which is attributed to a more effective hole confinement in the shell containing Mn by a proper selection/choice of both the core and outer shell materials., 13 pages, 7 figures

Background Malignant hypertension is a life-threatening condition, and its pathophysiology is still poorly understood. The present study was designed to evaluate the role of interaction of the renin-angiotensin system with 20-hydroxyeicosatetraenoic acid (20-HETE), a product of cytochrome P450 (CYP)–dependent ω-hydroxylase pathway, in the pathophysiology of angiotensin II (ANG II)–dependent malignant hypertension in Cyp1a1-Ren-2 transgenic rats. Methods Malignant hypertension was induced by 12 days׳ dietary administration of 0.3 % indole-3-carbinol (I3C), a natural xenobiotic that activates a mouse renin gene. We hypothesized that chronic administration of fenofibrate, 190mg/kg body weight, a lipid-lowering drug, should increase renal production of 20-HETE, a tubular transport inhibitor; an expected increase in sodium excretion would oppose the development of ANG II–dependent malignant hypertension. Blood pressure was monitored by radiotelemetry, and at the end of the experiment rats were prepared for renal functional studies to evaluate in vivo the pressure-natriuresis relationship in response to stepwise reductions in renal arterial pressure (RAP). Results In I3C-induced rats, the treatment with fenofibrate significantly attenuated hypertension and improved the slope of the pressure-natriuresis relationship. Although fenofibrate treatment increased kidney gene and protein expression of CYP4A1, a major isoform responsible for 20-HETE formation, it did not increase renal 20-HETE concentration. On the contrary, fenofibrate treatment significantly suppressed renin gene expression, plasma renin activity and plasma and kidney ANG II levels. Conclusions Fenofibrate treatment significantly attenuated the course of malignant hypertension in I3C-induced CYP1a1-Ren-2 transgenic rats, and the mechanism responsible for antihypertensive action was fenofibrate-induced suppression of renin-angiotensin system activity.

Magnetic and magneto-transport properties of thin layers of the (Ga,Mn)(Bi,As) quaternary dilute magnetic semiconductor grown by the low-temperature molecular-beam epitaxy technique on GaAs substrates have been investigated. Ferromagnetic Curie temperature and magneto-crystalline anisotropy of the layers have been examined by using magneto-optical Kerr effect magnetometry and low-temperature magneto-transport measurements. Postgrowth annealing treatment has been shown to enhance the hole concentration and Curie temperature in the layers. Significant increase in the magnitude of magnetotransport effects caused by incorporation of a small amount of Bi into the (Ga,Mn)As layers revealed in the planar Hall effect (PHE) measurements, is interpreted as a result of enhanced spin-orbit coupling in the (Ga,Mn)(Bi,As) layers. Two-state behaviour of the planar Hall resistance at zero magnetic field provides its usefulness for applications in nonvolatile memory devices., Comment: 10 pages, 3 figures, to be published in the Proceedings of ICSM-2016 conference

Activation of opioid receptors can alter cardiovascular function, an action possibly mediated by nitric oxide (NO). In this study we examined the effects of ([d-Ala(2)]-Endomorphin 2, TAPP), a synthetic opioid μ-receptor agonist, on blood pressure (MABP), tissue NO bioavailability and renal hemodynamics and excretion.In acute experiments with anesthetized normotensive male Sprague-Dawley rats TAPP was given as a short iv infusion at a dose of 1.2 or 12mg/kg and then MABP, renal medullary NO signal (polarographic electrode), total renal blood flow (RBF, renal artery Transonic probe), renal regional perfusion (laser-Doppler fluxes) and renal excretion were simultaneously measured over 2h.After 1.2mg/kg dose MABP decreased progressively from 121±7 to 114±9mmHg (-6%, p0.05) while kidney tissue NO signal increased from 29.1±2.7 to 31.7±3.1nA (6%, p0.04). Both effects were prevented by Naloxone methiodide, a peripheral opioid receptor inhibitor. RBF and renal regional perfusion were not altered by either dose of TAPP; renal sodium excretion changes were highly variable and were not affected by Naloxone pretreatment.Briefly, we found that in anesthetized normotensive rats stimulation of peripheral opioid receptors with TAPP caused a prolonged decrease in arterial pressure, a change that was associated and probably causally related to an increase in tissue NO. The data suggest that synthetic opioids that do not penetrate the blood-brain barrier and are potentially non-addictive could be considered for antihypertensive therapy.

Background Small renal arteries have a significant role in the regulation of renal hemodynamics and blood pressure (BP). To study potential changes in the regulation of vascular function in hypertension, we examined renal vasodilatory responses of small arteries from nonclipped kidneys of the 2-kidney, 1-clip Goldblatt hypertensive rats to native epoxyeicosatrienoic acids (EETs) that are believed to be involved in the regulation of renal vascular function and BP. A total of 2 newly synthesized EET analogues were also examined. Materials and Methods Renal interlobular arteries isolated from the nonclipped kidneys on day 28 after clipping were preconstricted with phenylephrine, pressurized and the effects of a 14,15-EET analogue, native 14,15‐EET and 11,12‐ether-EET‐8ZE, an analogue of 11,12-EET, on the vascular diameter were determined and compared to the responses of arteries from the kidneys of sham-operated rats. Results In the arteries from nonclipped kidneys isolated in the maintenance phase of Goldblatt hypertension, the maximal vasodilatory response to 14,15-EET analogue was 30.1 ± 2.8% versus 49.8 ± 7.2% in sham-operated rats; the respective values for 11,12-ther-EET-8ZE were 31.4 ± 6.4% versus 80.4 ± 6%, and for native EETs they were 41.7 ± 6.6% versus 62.8 ± 4.4% ( P ≤ 0.05 for each difference). Conclusions We propose that reduced vasodilatory action and decreased intrarenal bioavailability of EETs combined with intrarenal angiotensin II levels that are inappropriately high for hypertensive rats underlie functional derangements of the nonclipped kidneys of 2-kidney, 1-clip Goldblatt hypertensive rats. These derangements could play an important role in pathophysiology of sustained BP elevation observed in this animal model of human renovascular hypertension.

Doxorubicin&rsquo, s (DOX) cardiotoxicity contributes to the development of chemotherapy-induced heart failure (HF) and new treatment strategies are in high demand. The aim of the present study was to characterize a DOX-induced model of HF in Ren-2 transgenic rats (TGR), those characterized by hypertension and hyperactivity of the renin-angiotensin-aldosterone system, and to compare the results with normotensive transgene-negative, Hannover Sprague-Dawley (HanSD) rats. DOX was administered for two weeks in a cumulative dose of 15 mg/kg. In HanSD rats DOX administration resulted in the development of an early phase of HF with the dominant symptom of bilateral cardiac atrophy demonstrable two weeks after the last DOX injection. In TGR, DOX caused substantial impairment of systolic function already at the end of the treatment, with further progression observed throughout the experiment. Additionally, two weeks after the termination of DOX treatment, TGR exhibited signs of HF characteristic for the transition stage between the compensated and decompensated phases of HF. In conclusion, we suggest that DOX-induced HF in TGR is a suitable model to study the pathophysiological aspects of chemotherapy-induced HF and to evaluate novel therapeutic strategies to combat this form of HF, which are urgently needed.

Structural analysis of epitaxial layers of the (Ga,Mn)(Bi,As) quaternary dilute magnetic semiconductor (DMS), together with investigations of their magnetotransport properties, has been thoroughly performed. The obtained results are compared with those for the reference (Ga,Mn)As layers, grown under similar conditions, with the aim to reveal an impact of Bi incorporation on the properties of this DMS material. Incorporation of Bi into GaAs strongly enhances the spin-orbit coupling strength in this semiconductor, and the same has been expected for the (Ga,Mn)(Bi,As) alloy. In turn, importantly for specific spintronic applications, strong spin-orbit coupling in ferromagnetic systems opens a possibility of directly controlling the direction of magnetization by the electric current. Our investigations, performed with high-resolution X-ray diffractometry and transmission electron microscopy, demonstrate that the (Ga,Mn)(Bi,As) layers of high structural quality and smooth interfaces can be grown by means of the low-temperature molecular-beam epitaxy method, despite a large difference between the sizes of Bi and As atoms. Depending on the applied buffer layer, the DMS layers can be grown under either compressive or tensile misfit strain, which influences their magnetic properties. It is shown that even small 1% Bi content in the layers strongly affects their magnetoelectric properties, such as the coercive field and anisotropic magnetoresistance.

An association between congestive heart failure (CHF) and chronic kidney disease (CKD) results in extremely poor patient survival rates. Previous studies have shown that increasing kidney epoxyeicosatrienoic acids (EETs) by blocking soluble epoxide hydrolase (sEH), an enzyme responsible for EETs degradation, improves the survival rate in CHF induced by aorto-caval fistula (ACF) and attenuates CKD progression. This prompted us to examine if sEH inhibitor treatment would improve the outcome if both experimental conditions are combined. Fawn-hooded hypertensive (FHH) rats, a genetic model showing early CKD development was employed, and CHF was induced by ACF. Treatment with an sEH inhibitor was initiated 4 weeks after ACF creation, in FHH and in fawn-hooded low-pressure (FHL) rats, a control strain without renal damage. The follow-up period was 20 weeks. We found that ACF FHH rats exhibited substantially lower survival rates (all the animals died by week 14) as compared with the 64% survival rate observed in ACF FHL rats. The former group showed pronounced albuminuria (almost 30-fold higher than in FHL) and reduced intrarenal EET concentrations. The sEH inhibitor treatment improved survival rate and distinctly reduced increases in albuminuria in ACF FHH and in ACF FHL rats, however, all the beneficial actions were more pronounced in the hypertensive strain. These data indicate that pharmacological blockade of sEH could be a novel therapeutic approach for the treatment of CHF, particularly under conditions when it is associated with CKD.

Nearly 30% increase of the ferromagnetic phase transition temperature has been achieved in strained MnAs nanocrystals embedded in a wurtzite GaAs matrix. Wurtzite GaAs exerts tensile stress on hexagonal MnAs nanocrystals, preventing a hexagonal to orthorhombic structural phase transition, which in the bulk MnAs is combined with the magnetic one. This effect results in a remarkable shift of the magneto-structural phase transition temperature from 313 K in the bulk MnAs to above 400 K in the tensely strained MnAs nanocrystals. This finding is corroborated by the state of the art transmission electron microscopy, sensitive magnetometry and the first-principles calculations. The effect relies in defining a nanotube geometry of molecular beam epitaxy grown core-multishell wurtzite (Ga,In)As/(Ga,Al)As/(Ga,Mn)As/GaAs nanowires where the MnAs nanocrystals are formed during the thermal-treatment-induced phase separation of wurtzite (Ga,Mn)As into the GaAs:MnAs granular system. Such a unique combination of two types of hexagonal lattices provides possibility of attaining quasi-hydrostatic tensile strain in MnAs (impossible otherwise), leading to the substantial ferromagnetic phase transition temperature increase in this compound., Comment: 31 pages, 13 figures

SnTe topological crystalline insulator nanowires have been grown by molecular beam epitaxy on graphene/SiC substrates. The nanowires have cubic rock-salt structure, they grow along [001] crystallographic direction and have four sidewalls consisting of {100} crystal planes known to host metallic surface states with Dirac dispersion. Thorough high resolution transmission electron microscopy investigations show that the nanowires grow on graphene in the van der Walls epitaxy mode induced when the catalyzing Au nanoparticle mixes with Sn delivered from SnTe flux, providing liquid Au-Sn alloy. The nanowires are totally free from structural defects, but their {001} sidewalls are prone to oxidation, which points out on necessity of depositing protective capping in view of exploiting the magneto-electric transport phenomena involving charge carriers occupying topologically protected states., Comment: 7 pages, 8 figures