Discovery of mesoscopic nematicity wave in iron-based superconductors.

Nematicity is ubiquitous in the electronic phases of iron-based superconductors. The order parameter that characterizes the nematic phase has been investigated in momentum space, but its real-space arrangement remains largely unexplored. We use linear dichroism (LD) in a low-temperature laser­photoemission electron microscope to map out the nematic order parameter of nonmagentic FeSe and antiferromagnetic BaFe2(As0.87P0.13)2. In contrast to structural domains, which have atomic-scale domain walls, the LD patterns in both materials show peculiar sinusoidal waves of electronic nematicity with wavelengths more than 1000 times as long as the unit cell. Our findings put strong constraints on the theoretical investigation of electronic nematicity.

Pressure-induced reconstitution of Fermi surfaces and spin fluctuations in S-substituted FeSe.

FeSe is a unique high-[Formula: see text] iron-based superconductor in which nematicity, superconductivity, and magnetism are entangled with each other in the P-T phase diagram. We performed [Formula: see text]Se-nuclear magnetic resonance measurements under pressures of up to 3.9 GPa on 12% S-substituted FeSe, in which the complex overlap between the nematicity and magnetism are resolved. A pressure-induced Lifshitz transition was observed at 1.0 GPa as an anomaly of the density of states and as double superconducting (SC) domes accompanied by different types of antiferromagnetic (AF) fluctuations. The low-[Formula: see text] SC dome below 1 GPa is accompanied by strong AF fluctuations, whereas the high-[Formula: see text] SC dome develops above 1 GPa, where AF fluctuations are fairly weak. These results suggest the importance of the [Formula: see text] orbital and its intra-orbital coupling for the high-[Formula: see text] superconductivity.

High-T_{c} Superconductivity in FeSe at High Pressure: Dominant Hole Carriers and Enhanced Spin Fluctuations.

The importance of electron-hole interband interactions is widely acknowledged for iron-pnictide superconductors with high transition temperatures (T_{c}). However, the absence of hole pockets near the Fermi level of the iron-selenide (FeSe) derived high-T_{c} superconductors raises a fundamental question of whether iron pnictides and chalcogenides have different pairing mechanisms. Here, we study the properties of electronic structure in the high-T_{c} phase induced by pressure in bulk FeSe from magnetotransport measurements and first-principles calculations. With increasing pressure, the low-T_{c} superconducting phase transforms into the high-T_{c} phase, where we find the normal-state Hall resistivity changes sign from negative to positive, demonstrating dominant hole carriers in contrast to other FeSe-derived high-T_{c} systems. Moreover, the Hall coefficient is enlarged and the magnetoresistance exhibits anomalous scaling behaviors, evidencing strongly enhanced interband spin fluctuations in the high-T_{c} phase. These results in FeSe highlight similarities with high-T_{c} phases of iron pnictides, constituting a step toward a unified understanding of iron-based superconductivity.

Anisotropy of the superconducting gap in the iron-based superconductor BaFe2(As(1-x)P(x))2.

We report peculiar momentum-dependent anisotropy in the superconducting gap observed by angle-resolved photoemission spectroscopy in BaFe2(As(1-x)P(x))2 (x = 0.30, Tc = 30 K). Strongly anisotropic gap has been found only in the electron Fermi surface while the gap on the entire hole Fermi surfaces are nearly isotropic. These results are inconsistent with horizontal nodes but are consistent with modified s ± gap with nodal loops. We have shown that the complicated gap modulation can be theoretically reproduced by considering both spin and orbital fluctuations.

Detection of antiferromagnetic ordering in heavily doped LaFeAsO(1-x)H(x) pnictide superconductors using nuclear-magnetic-resonance techniques.

We studied double superconducting (SC) domes in LaFeAsO(1-x)H(x) by using 75As and 1H nuclear-magnetic-resonance techniques and unexpectedly discovered that a new antiferromagnetic (AF) phase follows the double SC domes on further H doping, forming a symmetric alignment of AF and SC phases in the electronic phase diagram. We demonstrated that the new AF ordering originates from the nesting between electron pockets, unlike the nesting between electron and hole pockets, as seen in the majority of undoped pnictides. The new AF ordering is derived from the features common to high-Tc pnictides; however, it has not been reported so far for other high-Tc pnictides because of their poor electron doping capability.

Tuning the dimensionality of the heavy fermion compound CeIn3.

Condensed-matter systems that are both low-dimensional and strongly interacting often exhibit unusual electronic properties. Strongly correlated electrons with greatly enhanced effective mass are present in heavy fermion compounds, whose electronic structure is essentially three-dimensional. We realized experimentally a two-dimensional heavy fermion system, adjusting the dimensionality in a controllable fashion. Artificial superlattices of the antiferromagnetic heavy fermion compound CeIn3 and the conventional metal LaIn3 were grown epitaxially. By reducing the thickness of the CeIn3 layers, the magnetic order was suppressed and the effective electron mass was further enhanced. Heavy fermions confined to two dimensions display striking deviations from the standard Fermi liquid low-temperature electronic properties, and these are associated with the dimensional tuning of quantum criticality.

Giant orbital Hall effect in transition metals: origin of large spin and anomalous Hall effects.

In transition metals and their compounds, the orbital degrees of freedom gives rise to an orbital current, in addition to the ordinary spin and charge currents. We reveal that considerably large spin and anomalous Hall effects observed in transition metals originate from an orbital Hall effect (OHE). To elucidate the origin of these novel Hall effects, a simple periodic s-d hybridization model is proposed as a generic model. The giant positive OHE originates from the orbital Aharonov-Bohm phase factor, and induces spin Hall conductivity that is proportional to the spin-orbit polarization at the Fermi level, which is positive (negative) in metals with more than (less than) half filling.

Intrinsic spin Hall Effect in the s-wave superconducting state: analysis of the Rashba model.

A general expression for spin Hall conductivity (SHC) in the s-wave superconducting state at finite temperatures is derived. Based on the expression, we study SHC in a two-dimensional electron gas model in the presence of Rashba spin-orbit interaction (SOI). SHC is zero in the normal state, whereas it takes a large negative value as soon as the superconductivity occurs, due to the change in the quasiparticle contributions. Since this remarkable behavior is independent of the strength of the SOI, it will be widely observed in thin films of superconductors with surface-induced Rashba SOI, or in various noncentrosymmetric superconductors.

Giant intrinsic spin and orbital hall effects in Sr2MO4 (M=Ru, Rh, Mo).

We investigate the intrinsic spin Hall conductivity (SHC) and the d-orbital Hall conductivity (OHC) in metallic d-electron systems, by focusing on the t2g-orbital tight-binding model for Sr2MO4 (M=Ru, Rh, Mo). The conductivities obtained are one or 2 orders of magnitude larger than predicted values for p-type semiconductors with approximately 5% hole doping. The origin of these giant Hall effects is the "effective Aharonov-Bohm phase" that is induced by the d-atomic angular momentum in connection with the spin-orbit interaction and the interorbital hopping integrals. The huge SHC and OHC generated by this mechanism are expected to be ubiquitous in multiorbital transition metal compounds, which opens the possibility of realizing spintronics as well as "orbitronics" devices.

Universality in heavy fermion systems with general degeneracy.

We discuss the relation between the T2 coefficient of electrical resistivity A and the T-linear specific-heat coefficient gamma for heavy-fermion systems with general N, where N is the degeneracy of quasiparticles. A set of experimental data reveals that the Kadowaki-Woods relation, A/gamma2=1 x 10(-5) muOmega cm(K mol/mJ)2, collapses remarkably for large-N systems, although this relation has been regarded to be commonly applicable to the Fermi liquids. Instead, based on the Fermi-liquid theory we propose a new relation, A /gamma2=1 x 10(-5) with A =A/1/2N(N-1) and gamma =gamma/1/2N(N-1). This new relation exhibits an excellent agreement with the data for the whole range of degenerate heavy fermions.

Sex differences in urethral pressure response to electrical stimulation of the hypogastric nerves in rats.

PURPOSE: This experiment was performed to study the pharmacology of transmitters mediating the response, and the characteristics of the hypogastric nerve (HGN) of female rats, because electrical stimulation of the HGN was found to unexpectedly reduce urethral pressure in female rats. MATERIALS AND METHODS: Male and female Wistar rats (weighing about 250 gm.), 10 weeks and 6 months old, respectively, were used under anesthesia. Fluid was infused from the bladder neck into the urethral lumen at a constant rate (0.5 ml./10 minutes), and infusion pressure signals were measured. Bilateral HGNs were electrically stimulated at 5 and 10 Hz for 30 s. RESULTS: Electrical stimulation of the HGN reduced urethral infusion pressure in about 80% of the female rats, and the introduction of N(omega)-nitro-L-arginine methylester (L-NAME, 30 mg./rat, i.v.) elevated the urethral pressure response from a reduced state. Prazosin (0.1 mg./kg., i.v.) and hexamethonium (10 mg./kg., i.v.), which inhibited elevation of urethral pressure in male rats, also reversed and inhibited the elevation of urethral pressure in the female rats treated with L-NAME. CONCLUSION: The HGN in female rats contained nerve endings that released nitric oxide (NO) and norepinephrine (NE). NO released during HGN stimulation inhibited the release of (NE) and reduced urethral infusion pressure in female rats. Nerves with synapses in the pelvic ganglia released NE in both male and female rats, but nerves that released NO did not have synapses in the ganglia. Only NE was released from the HGN nerve endings in male rats.

Effects of adrenergic alpha2-receptor agonists on urinary bladder contraction in conscious rats.

We investigated the effects of the adrenergic alpha2-receptor agonists clonidine, oxymetazoline and tizanidine on bladder contractions induced by infusing fluid into the bladders of conscious male rats. I.v. clonidine and oxymetazoline (both 0.01 to 0.1 mg/kg) caused bladder hyperactivity, expressed by shortening of the intercontraction interval. Tizanidine (0.1 mg/kg, i.v.) caused slight shortening of the intercontraction interval. The rank order of potency was clonidine = oxymetazoline >> tizanidine. Intrathecal (i.t.) injection of 10 microg clonidine and oxymetazoline, and intracerebroventricular (i.c.v) injection at 15 microg, produced almost the same pattern of bladder hyperactivity as that observed after i.v. injection of these drugs (0.03 mg/kg, i.v.). For all three administration routes of clonidine and oxymetazoline, i.v. idazoxan (0.3 mg/kg) exerted an inhibitory effect on the bladder hyperactivity induced by these drugs, except i.c.v injection of oxymetazoline. I.t. phenylephrine (30 microg) did not change the intercontraction interval. Although i.c.v. phenylephrine (15 microg) shortened the intercontraction interval, the potency was weaker than those of i.c.v. clonidine and oxymetazoline (15 microg). These results suggest that clonidine and oxymetazoline cause bladder hyperactivity by acting at adrenergic alpha2 receptors in the micturition centers of the lumbosacral and supraspinal regions.

Effects of nifedipine on bladder overactivity in rats with cerebral infarction.

PURPOSE: Our objective was to evaluate the effect of the calcium (Ca2+) channel blocking agent nifedipine on bladder overactivity induced by middle cerebral artery (MCA) occlusion and determine its site of action. MATERIALS AND METHODS: Seven days after implantation of a bladder catheter, a cannula for intracerebroventricular and intrathecal administration was implanted and the left MCA was occluded with 4-0 monofilament nylon thread in male SD rats. Twenty-four hours after the induction of cerebral ischemia, saline was infused into the bladder at a constant rate (200 microL/min.) and cystometrogram was measured in conscious state. Nifedipine was administered intracerebroventricularly (5 microL) or intrathecally (20 microL) at graded doses (0.15 ng.-0.15 microg., 0.15 microg. -1.5 microg., respectively). RESULTS: Bladder capacity in conscious rats was significantly reduced after the left MCA occlusion. Intracerebroventricular administration of nifedipine significantly increased bladder capacity in cerebral infarcted rats but not in sham operated rats. Furthermore there was no significant difference in bladder capacity between before and after intrathecal administration of nifedipine in cerebral infarcted rats. CONCLUSION: These results show that Ca2+ channel blocking agents can operate especially on the supraspinal central nervous system rather than on the spinal system in rats with neurogenic bladder overactivity following cerebral infarction.

Effect of K+ channel openers, KRN2391 and Ki1769, and nitroglycerin on the urinary tract of rats in vivo.

The effects of KRN2391 (N-cyano-N'-(nitroxyethyl)-3-pyridine carboximidamide methane-sulfonate), which possesses ATP-sensitive potassium (K+) channel opening (KCO) activity and nitrate activity; Ki1769 (N-cyano-N'-(phenylethyl)-3-pyridinecarboximidamide methanesulfonate), which possesses only KCO activity; and nitroglycerin (NG) were determined on the motility of the ureter, urinary bladder and urethra of rats. Bladder contraction was induced by infusion of fluid into the bladder of conscious rats and recorded on a cystometrogram. KRN2391 and Ki1769 (both 0.3 mg/kg, i.v.) prolonged the micturition interval immediately after the injection, but NG (5 mg/kg, i.v.) did not. Peristaltic movement of the ureter, recorded in anesthetized rats, was inhibited by i.v. injection of KRN2391 and Ki1769 (both 0.03 mg/kg). However, when NG, NaNO2, N-nitro L-arginine methylester and methylene blue were applied directly to the ureter, no change in movement of the ureter was detected. KRN2391 (0.03 mg/kg, i.v.) and Ki1769 (0.3 mg/kg, i.v.) reduced the resistance to fluid infusion through the urethral lumen in anesthetized rats, whereas NG (0.5 mg/kg, i.v.) only reduced this resistance transiently. These results indicate that KCO activity had an inhibitory effect on the motility of the ureter, bladder and urethra. On the other hand, nitrate activity had an inhibitory effect on urethral tonus, corresponding to that induced by KCO activity.

Inhibitory effects of tetrandrine and related synthetic compounds on angiogenesis in streptozotocin-diabetic rodents.

Structure-activity relationships of tetrandrine, isolated from a Kampo medicine, Stephania tetrandrae S. MOORE (root), and related synthetic compounds, were investigated in in vitro fetal bovine serum (FBS)-stimulated angiogenesis of cultured choroids in streptozotocin-diabetic Wistar rats, and air-pouch granuloma angiogenesis in vivo in diabetic mice. Tetrandrine, KS-1-1 (6,7-dimethoxy-1-[[4-[5-(6,7-dimethoxy-2-methyl-1,2,3,4-tetrahydroiso quinolinyl)methyl-2-methoxy]phenoxy]benzyl]-2-methyl-1,2,3,4-tetrahyd roisoquinoline), and KS-1-4 (6,7-dimethoxy-1-[[4-[4-(6,7-dimethoxy-2-methyl-1,2,3,4-tetrahydroiso quinolinyl)methyl]phenoxy]benzyl]-2-methyl-1,2,3,4-tetrahydroisoquino line), potently inhibited choroidal angiogenesis and air-pouch granuloma angiogenesis in the diabetic state. Their inhibitory effects on diabetic choroids were greater than those on normal choroids. Among these compounds, KS-1-4 inhibited only diabetic angiogenesis. These compounds significantly inhibited FBS-stimulated tube formation in vascular endothelial cells from normal rats. Tetrandrine and KS-1-4, but not KS-1-1, inhibited vascular endothelial growth factor- and platelet-derived growth factor-BB-stimulated angiogenesis in normal choroids. The bis[tetrahydroisoquinoline] moiety, connected by oxy-bis[phenylenemethylene] and 2,2'-dimethyl groups in tetrandrine, contributes to the inhibition of diabetic choroidal angiogenesis. KS-1-4 may be a candidate for anti-choroidopathy and retinopathy drugs in the diabetic state.

A quantitative assay for angiogenesis of cultured choroidal tissues in streptozotocin-diabetic Wistar and spontaneously diabetic GK rats.

Angiogenesis of cultured choroids was quantitatively assayed in spontaneously diabetic GK and a bolus-treated streptozotocin (STZ)-diabetic Wistar rats. The number and total length of microvessels budded from cultured choroidal explants were measured to use as angiogenic indices. Both indices in 10-week-old Wistar rats were increased in parallel by 5% fetal bovine serum (FBS) from days 2 to 7 in culture. These indices in STZ-rats (10 weeks of age) were increased by 5% FBS to a greater extent than those in age-matched normal rats. These enhanced actions of FBS were concentration-dependent. The explants of 16-week-old GK rats also increased these indices to a greater extent than those of age-matched Wistar rats. Aging to 18 weeks of age also increased choroidal angiogenesis in the normal rats. In conclusion, the assay model of choroidal angiogenesis was established by determining the number and length of microvessels in cultured choroidal explants. The diabetic states of STZ-Wistar and GK rats enhanced FBS-induced choroidal angiogenesis. This assay model is useful for determining angiogenic activity of growth factors and effective drugs in diabetic choroidopathy and retinopathy.

Urinary bladder response to hypogastric nerve stimulation after bilateral resection of the pelvic nerve or spinal cord injury in rats.

BACKGROUND: We examined the mechanism of urinary bladder motility return after bladder areflexia induced by interruption of the sacral parasympathetic outflow to the urinary bladder following damage to the sacral cord or pelvic nerves in the rat. METHODS: The L6 and S1 nerve bundles were resected near the vertebrae, and bilateral pelvic nerve resections (PNR) performed. Spinal cord injury (SCI) was performed by means of a legion generator at the T12 vertebra. Thirty days after PNR and SCI, cystometrograms were recorded under anesthesia. RESULTS: In all rats subjected to PNR or SCI, overflow incontinence continued, yet some rats subjected to SCI recovered within 2 weeks after the operation. Cystometrograms showed that repetitive bladder contractions appeared in rats subjected to SCI irrespective of hypogastric nerve (HGN) innervation, while bladder contractions did not appear in rats subjected to PNR. Electrical stimulation of the HGN induced higher bladder pressure elevation in rats who underwent PNR than in rats subjected to SCI. CONCLUSIONS: These results suggest that the generation of repetitive bladder contractions induced by bladder distention after bladder areflexia requires the presence of intact pelvic nerves that transmit sacral cord-originating excitatory information to the bladder. However, the HGN system and functioning pelvic nerve ganglia are not involved in this process. Also, the connection from the preganglionic HGN to the postganglionic parasympathetic nerves in the pelvic plexus did not form after PNR.

Effects of levcromakalim on ureteral peristaltic function and cystometrogram in rats.

We studied the effect of levcromakalim on the function of the urinary tract in rats. Using anesthetized rats, ureteral peristaltic movement of only the ureter region or the ureter with the kidney was induced by fluid infusion into the ureter lumen. Levcromakalim (0.03 and 0.3 mg/kg, i.v.) exerted a stronger inhibitory effect on the peristaltic movement of the ureter region distant from the pelvis than on that near the pelvis, and the inhibitory effect of levcromakalim (0.03 mg/kg, i.v.) was not antagonized by glibenclamide (0.1 mg/kg, i.v. or 10 mg/kg, i.p.). Topical application of levcromakalim (injection volume, 0.1 ml; 10(-4) or 10(-3) M), which was injected via a vessel near the ureter inhibited ureteral peristaltic movement and the inhibitory effect levcromakalim (10(-4) M), was not antagonized by glibenclamide (10(-3) M) injected via the same route. Levcromakalim (0.3 mg/kg, i.v.) did not interrupt micturition in anesthetized and conscious rats. In conscious rats, the micturition interval was prolonged; and in anesthetized rats, the peak pressure during micturition was reduced. After injection of levcromakalim (0.3 mg/kg, i.v.), vesicoureteral reflux did not occur. In the movements of the ureter, urinary bladder and urethra, levcromakalim exerted the strongest inhibitory effect on the ureteral peristalsis.