Quasiparticle Nodal Plane in the Fulde-Ferrell-Larkin-Ovchinnikov State of FeSe.

The Fulde-Ferrell-Larkin-Ovchinnikov (FFLO) state, characterized by Cooper pairs condensed at finite momentum, has been a long-sought state that remains unresolved in many classes of fermionic systems, including superconductors and ultracold atoms. A fascinating aspect of the FFLO state is the emergence of periodic nodal planes in real space, but its observation is still lacking. Here we investigate the superconducting order parameter at high magnetic fields H applied perpendicular to the ab plane in a high-purity single crystal of FeSe. The heat capacity and magnetic torque provide thermodynamic evidence for a distinct superconducting phase at the low-temperature/high-field corner of the phase diagram. Despite the bulk superconductivity, spectroscopic-imaging scanning tunneling microscopy performed on the same crystal demonstrates that the order parameter vanishes at the surface upon entering the high-field phase. These results provide the first demonstration of a pinned planar node perpendicular to H, which is consistent with a putative FFLO state.

Scalable Majorana vortex modes in iron-based superconductors.

The iron-based superconductor FeTe x Se1-x is one of the material candidates hosting Majorana vortex modes residing in the vortex cores. It has been observed by recent scanning tunneling spectroscopy measurement that the fraction of vortex cores having zero-bias peaks decreases with increasing magnetic field on the surface of FeTe x Se1-x . The hybridization of two Majorana vortex modes cannot simply explain this phenomenon. We construct a three-dimensional tight-binding model simulating the physics of over a hundred Majorana vortex modes in FeTe x Se1-x . Our simulation shows that the Majorana hybridization and disordered vortex distribution can explain the decreasing fraction of the zero-bias peaks observed in the experiment; the statistics of the energy peaks off zero energy in our Majorana simulation are in agreement with the experiment. These agreements lead to an important indication of scalable Majorana vortex modes in FeTe x Se1-x . Thus, FeTe x Se1-x can be one promising platform having scalable Majorana qubits for quantum computing.

Zero-energy vortex bound state in the superconducting topological surface state of Fe(Se,Te).

Majorana quasiparticles in condensed matter are important for topological quantum computing1-3, but remain elusive. Vortex cores of topological superconductors may accommodate Majorana quasiparticles that appear as the Majorana bound state (MBS) at zero energy4,5. The iron-based superconductor Fe(Se,Te) possesses a superconducting topological surface state6-9 that was investigated by scanning tunnelling microscopy (STM) studies, which suggest such a zero-energy vortex bound state (ZVBS)10,11. Here we present ultrahigh energy-resolution spectroscopic imaging (SI)-STM to clarify the nature of the vortex bound states in Fe(Se,Te). We found the ZVBS at 0 ± 20 µeV, which constrained its MBS origin, and showed that some vortices host the ZVBS but others do not. We show that the fraction of vortices hosting the ZVBS decreases with increasing magnetic field and that local quenched disorders are not related to the ZVBS. Our observations elucidate the necessary conditions to realize the ZVBS, which paves the way towards controllable Majorana quasiparticles.

A scanning tunneling microscope for spectroscopic imaging below 90 mK in magnetic fields up to 17.5 T.

We describe the development and performance of an ultra-high vacuum scanning tunneling microscope working under combined extreme conditions of ultra-low temperatures and high magnetic fields. We combined a top-loading dilution refrigerator and a standard bucket dewar with a bottom-loading superconducting magnet to achieve 4.5 days operating time, which is long enough to perform various spectroscopic-imaging measurements. To bring the effective electron temperature closer to the mixing-chamber temperature, we paid particular attention to filtering out radio-frequency noise, as well as enhancing the thermal link between the microscope unit and the mixing chamber. We estimated the lowest effective electron temperature to be below 90 mK by measuring the superconducting-gap spectrum of aluminum. We confirmed the long-term stability of the spectroscopic-imaging measurement by visualizing superconducting vortices in the cuprate superconductor Bi2Sr2CaCu2O8+δ .

Author Correction: Full-gap superconductivity in spin-polarised surface states of topological semimetal ß-PdBi2.

The original version of this article contained an error in Fig. 3. The calculated patterns of quasiparticle interference in the figure were incorrect due to the wrong Wannier transformation in the calculation. This correction does not affect the discussion or the conclusion of the article.

Full-gap superconductivity in spin-polarised surface states of topological semimetal ß-PdBi2.

A bulk superconductor possessing a topological surface state at the Fermi level is a promising system to realise long-sought topological superconductivity. Although several candidate materials have been proposed, experimental demonstrations concurrently exploring spin textures and superconductivity at the surface have remained elusive. Here we perform spectroscopic-imaging scanning tunnelling microscopy on the centrosymmetric superconductor ß-PdBi2 that hosts a topological surface state. By combining first-principles electronic-structure calculations and quasiparticle interference experiments, we determine the spin textures at the surface, and show not only the topological surface state but also all other surface bands exhibit spin polarisations parallel to the surface. We find that the superconducting gap fully opens in all the spin-polarised surface states. This behaviour is consistent with a possible spin-triplet order parameter expected for such in-plane spin textures, but the observed superconducting gap amplitude is comparable to that of the bulk, suggesting that the spin-singlet component is predominant in ß-PdBi2.Although several materials have been proposed as topological superconductors, spin textures and superconductivity at the surface remain elusive. Here, Iwaya et al. determine the spin textures at the surface of a superconductor ß-PdBi2 and find the superconducting gap opening in all spin-polarised surface states.

Bipartite electronic superstructures in the vortex core of Bi2Sr2CaCu2O8+δ.

The central issue in the physics of cuprate superconductivity is the mutual relationship among superconductivity, pseudogap and broken-spatial-symmetry states. A magnetic field B suppresses superconductivity, providing an opportunity to investigate the competition among these states. Although various B-induced electronic superstructures have been reported, their energy, spatial and momentum-space structures are unclear. Here, we show using spectroscopic-imaging scanning tunnelling microscopy on Bi2Sr2CaCu2O8+δ that there are two distinct B-induced electronic superstructures, both being localized in the vortex core but appearing at different energies. In the low-energy range where the nodal Bogoliubov quasiparticles are well-defined, we observe the so-called vortex checkerboard that we identify as the B-enhanced quasiparticle interference pattern. By contrast, in the high-energy region where the pseudogap develops, the broken-spatial-symmetry patterns that pre-exist at B=0 T is locally enhanced in the vortex core. This evidences the competition between superconductivity and the broken-spatial-symmetry state that is associated with the pseudogap.

Top-down assessment of the Asian carbon budget since the mid 1990s.

Increasing atmospheric carbon dioxide (CO2) is the principal driver of anthropogenic climate change. Asia is an important region for the global carbon budget, with 4 of the world's 10 largest national emitters of CO2. Using an ensemble of seven atmospheric inverse systems, we estimated land biosphere fluxes (natural, land-use change and fires) based on atmospheric observations of CO2 concentration. The Asian land biosphere was a net sink of -0.46 (-0.70-0.24) PgC per year (median and range) for 1996-2012 and was mostly located in East Asia, while in South and Southeast Asia the land biosphere was close to carbon neutral. In East Asia, the annual CO2 sink increased between 1996-2001 and 2008-2012 by 0.56 (0.30-0.81) PgC, accounting for ∼35% of the increase in the global land biosphere sink. Uncertainty in the fossil fuel emissions contributes significantly (32%) to the uncertainty in land biosphere sink change.

Distribution of pituitary adenylate cyclase-activating polypeptide (PACAP) in the human testis and in testicular germ cell tumors.

Pituitary adenylate cyclase-activating peptide (PACAP) is a neuropeptide expressed in the central nervous system and peripheral organs. Previous studies revealed the role and distribution of PACAP in the rodent testis, however, its presence in the human testis and in testicular germ cell tumors is not known. We used RT-PCR and immunohistological observations to investigate whether human testicular tissue and testicular germ cell tumors contain PACAP. The mRNAs for PACAP and its receptors were detected in total RNA extracted from human testes. PACAP immunoreactivity was observed in spermatogonia and spermatids from normal testes. In contrast, diffuse PACAP immunopositivity was observed in seminoma tumor cells, while only faint immunoreactivity was observed in embryonal carcinoma cells. Our data suggest that PACAP may play a role in human spermatogenesis and in testicular germ cell tumor development.

Anti-aging effects of co-enzyme Q10 on periodontal tissues.

Oxidative stress is associated with age-related reactions. The anti-oxidative effects of a reduced form of co-enzyme Q10 (rCoQ10) suppress oxidative stress, which may contribute to the prevention of age-related inflammatory reactions. We examined the effects of topically applied rCoQ10 on periodontal inflammatory reactions in a rat aging model. Male Fischer 344 rats, 2 (n = 6) and 4 mos (n = 18) of age, were used. All of the two-month-old rats and 6 of the four-month-old rats were sacrificed and 12 remaining four-month-old rats received topically applied ointment with or without 1% rCoQ10 on the gingival surface until they reached 6 mos of age. The rats showed an age-dependent increase in circulating oxidative stress. RCoQ10 decreased oxidative DNA damage and tartrate-resistant acid-phosphatase-positive osteoclasts in the periodontal tissue at 6 mos of age as compared with the control. The same conditions lowered gene expression of caspase-1 and interleukin-1ß in the periodontal tissue. Furthermore, Nod-like receptor protein 3 inflammasomes were less activated in periodontal tissues from rCoQ10-treated rats as compared with the control rats. Our results suggest that rCoQ10 suppresses age-related inflammatory reactions and osteoclast differentiation by inhibiting oxidative stress.

Rapamycin causes upregulation of autophagy and impairs islets function both in vitro and in vivo.

Autophagy is a lysosomal degradation process of redundant or faulty cell components in normal cells. However, certain diseases are associated with dysfunctional autophagy. Rapamycin, a major immunosuppressant used in islet transplantation, is an inhibitor of mammalian target of rapamycin and is known to cause induction of autophagy. The objective of this study was to evaluate the in vitro and in vivo effects of rapamycin on pancreatic ß cells. Rapamycin induced upregulation of autophagy in both cultured isolated islets and pancreatic ß cells of green fluorescent protein-microtubule-associated protein 1 light chain 3 transgenic mice. Rapamycin reduced the viability of isolated ß cells and down-regulated their insulin function, both in vitro and in vivo. In addition, rapamycin increased the percentages of apoptotic ß cells and dead cells in both isolated and in vivo intact islets. Treatment with 3-methyladenine, an inhibitor of autophagy, abrogated the effects of rapamycin and restored ß-cell function in both in vitro experiments and animal experiments. We conclude that rapamycin-induced islet dysfunction is mediated through upregulation of autophagy, with associated downregulation of insulin production and apoptosis of ß cells. The results also showed that the use of an autophagy inhibitor abrogated these effects and promoted islet function and survival. The study findings suggest that targeting the autophagy pathway could be beneficial in promoting islet graft survival after transplantation.

IgG4-related inflammatory pseudotumor of the trigeminal nerve: another component of IgG4-related sclerosing disease?

IgG4-related IPTs have been reported in various sites and may form part of the spectrum of systemic IgG4-related sclerosing disease. Some pseudotumors are clinically and radiologically indistinguishable from malignant tumors. We present the first case of an IgG4-related IPT of the trigeminal nerve diagnosed histopathologically without involvement of any of the common sites. The trigeminal nerve pseudotumor may represent a component of IgG4-related sclerosing disease.

Blood rheology and the low-density lipoprotein cholesterol/high-density lipoprotein cholesterol ratio in dyslipidaemic and normolipidaemic subjects.

The association between blood rheology and the ratio of low-density lipoprotein cholesterol (LDL-C) to high-density lipoprotein cholesterol (HDL-C) was investigated in 142 dyslipidaemic and 253 normolipidaemic subjects. Blood rheology was examined by the microchannel method and fasting serum concentrations of LDL-C, triglyceride and HDL-C were measured. Passage time of whole blood correlated positively with LDL-C concentration, triglyceride concentration and LDL-C/HDL-C ratio, and negatively with HDL-C concentration. Passage time of whole blood was significantly higher in dyslipidaemic and normolipidaemic subjects with LDL-C/HDL-C ratio > 2.0 than in those with ratio < 1.5. Thus, dyslipidaemic subjects had impaired blood rheology, elevated LDL-C and triglyceride concentrations and elevated LDL-C/HDL-C ratio, and reduced HDL-C concentrations. Dyslipidaemic and normolipidaemic subjects with a more elevated LDL-C/HDL-C ratio had greater blood rheology impairment than those with a less elevated ratio. These data suggest that an elevated LDL-C/HDL-C ratio may be helpful in predicting impaired blood rheology.

Spin-related current suppression in a semiconductor quantum dot spin-diode structure.

We experimentally study the transport features of electrons in a spin-diode structure consisting of a single semiconductor quantum dot (QD) weakly coupled to one nonmagnetic and one ferromagnetic (FM) lead, in which the QD has an artificial atomic nature. A Coulomb stability diamond shows asymmetric features with respect to the polarity of the bias voltage. For the regime of two-electron tunneling, we find anomalous suppression of the current for both forward and reverse bias. We discuss possible mechanisms of the anomalous current suppression in terms of spin blockade via the QD-FM interface at the ground state of a two-electron QD.

Impaired blood rheology and elevated remnant-like lipoprotein particle cholesterol in hypercholesterolaemic subjects.

Blood rheology, fasting serum concentrations of remnant-like lipoprotein particle cholesterol (RLP-C) and concentrations of other lipids were compared in 23 hypercholesterolaemic and 69 normocholesterolaemic subjects, and the relationship between red blood cell (RBC) deformability and RLP-C concentrations were studied in a different set of six hypercholesterolaemic and six normocholesterolaemic subjects. Passage time of whole blood and concentrations of total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C) and RLP-C were significantly higher in hypercholesterolaemic than in normocholesterolaemic subjects. Passage time of whole blood correlated positively with TC, TG, LDL-C and RLP-C and negatively with high-density lipoprotein cholesterol. Furthermore, the passage time of 10% haematocrit-adjusted RBCs in phosphate-buffered saline, which reflects RBC deformability, correlated positively with the passage time of whole blood and RLP-C. Thus, hypercholesterolaemic subjects had impaired blood rheology and elevated RLP-C concentrations, which may be associated with the pathophysiology of atherosclerosis in hypercholesterolaemic subjects. Impaired RBC deformability may contribute to impaired blood rheology associated with elevated RLP-C in hypercholesterolaemic subjects.

Adenovirus-mediated gene expression of the human c-FLIP(L) gene protects pig islets against human CD8(+) cytotoxic T lymphocyte-mediated cytotoxicity.

Cell-mediated immunity, especially of human CD8+ cytotoxic T lymphocytes (CTLs) is believed to have an important role in the long-term survival of pig islet xenografts. Protection against human CD8+ CTL cytotoxicity may reduce the direct damage to pig islets and enable long-term xenograft survival in pig-to-human islet xenotransplantation. We have previously reported that c-FLIP(S/L) genes, which are potent inhibitors of death receptor-mediated proapoptotic signals through binding competition with caspase-8 for recruitment to the Fas-associated via death domain (FADD), markedly suppress human CD8+ CTL-mediated xenocytotoxicity. In addition, the cytoprotective effects of c-FLIP(L) seem to be significantly stronger than those of c-FLIP(S). Accordingly, in the present study, expression of c-FLIP(L) was induced in intact pig islets by adenoviral transduction. Consequently, the cytoprotective capacity of the transgene in pig islets was examined in in vitro and in vivo exposure to human CD8+ CTLs. Cells from untransduced islets or mock islets were sensitive to CD8+ CTL-mediated lysis (59.3% +/- 15.9% and 64.0% +/- 8.9% cytotoxicity, respectively). In contrast, cells from pig islets transduced with the c-FLIP(L) gene were markedly protected from lysis (30.5% +/- 3.5%). Furthermore, prolonged xenograft survival was elicited from pig islets transduced with this molecule as assessed using an islet transplant model using the rat kidney capsule. Thus, these data indicate that intact pig islets can be transduced to express c-FLIP(L) with adenovirus. Pig islets expressing c-FLIP(L) are significantly resistant to human CTL killing and further exhibit beneficial effects to prolong xenograft survival.

In vivo controlling of cellular response to pig islet xenografts by adenovirus-mediated expression of either membrane-bound human FasL or human decoy Fas.

The critical problem with clinical islet transplantation for patients with type 1 diabetes is the severe shortage of human donors. Pig islet xenotransplantation has the potential to provide a virtually unlimited source of donor pancreata. However, our previous studies demonstrated that cell-mediated rejection, especially human CD8(+) cytotoxic T lymphocyte (CTL)-mediated cytotoxicity, remains a major obstacle for long-term islet xenograft survival. Moreover, we have demonstrated that the overexpression of either membrane-bound human FasL (mFasL) or human decoy Fas antigen (decoy Fas) in pig islets not only prevented CTL xenocytotoxicity in vitro, but also prolonged histological survival of pig islet xenografts in vivo. Therefore, the aim of the present study was to determine whether adenoviral transfer of these genes into pig islets ex vivo prior to transplantation had a beneficial effect on posttransplantation glycemic control of diabetic recipients. Isolated pig islets were transfected with adenovirus vector carrying complementary DNA (cDNA) of either mFasL or decoy Fas. The transfected islets were transplanted under the kidney capsule of diabetic recipient rats. Rats transplanted with either mFasL- or decoy Fas-transfected pig islet grafts showed significantly suppressed blood glucose levels from 12 hours to 18 hours posttransplantation compared with control groups transplanted with empty vector-transfected pig islets. Unfortunately, blood glucose levels of these groups were increased, with no significant difference observed at 24 hours posttransplantation. However, transgenic expression of these molecules with clinically tolerable amount of immunosuppressants may be more effective to achieve islet xenograft survival in the future.

Rapamycin induces autophagy in islets: relevance in islet transplantation.

Islet transplantation can provide insulin independence in patients with type 1 diabetes mellitus. However, islet allograft recipients exhibit a gradual decline in insulin independence, and only 10% do not require insulin at 5 years. This decline may reflect drug toxicity to islet beta cells. Rapamycin, a central immunosuppressant in islet transplantation, is a mammalian target of rampamycin inhibitor that induces autophagy. The relative contributions of autophagy in transplanted islets are poorly understood. Therefore, in the present study we sought to evaluate the effects of rapamycin on islet beta cells. Rapamycin treatment of islets resulted in accumulation of membrane-bound light chain 3 (LC3-II) protein, an early marker of autophagy. In addition, rapamycin treatment of isolated islets elicited not only reduction of viability but also downregulation of in vitro potency. To further examine the occurrence of autophagy in rapamycin-treated islets, we used GFP (green fluorescent protein)-LC3 transgenic mice that express a fluorescent autophagosome marker. The GFP-LC3 signals were markedly increased in rapamycin treated islets compared with control islets. In addition, to show improvement by blockade of autophagic signaling, islets were treated with rapamycin in the presence of 3-methyladenine, which inhibits autophagy. Thereafter, both islet viability and islet potency were dramatically improved. The number of GFP-LC3 dots clearly increased after 3-MA treatment. Thus, rapamycin treatment of islets induces autophagy in vitro. This phenomenon may contribute to the progressive graft dysfunction of transplanted islets. Therapeutically targeting this novel signaling may yield significant benefits for long-term islet survival.

Intracellular and extracellular remodeling effectively prevents human CD8(+)cytotoxic T lymphocyte-mediated xenocytotoxicity by coexpression of membrane-bound human FasL and pig c-FLIP(L) in pig endothelial cells.

Human CD8(+) cytotoxic T lymphocyte (CTL)-mediated cytotoxicity, which participates in xenograft rejection, is mediated mainly by the Fas/FasL apoptotic pathway. We previously developed methods to inhibit human CTL xenocytotoxicity by extracellular remodeling using overexpression of membrane-bound human FasL on pig xenograft cells, and by intracellular blockade of death receptor-mediated apoptotic signals, such as the Fas/FasL pathway using the pig c-FLIP(L) molecule. To investigate the cooperative effects of both membrane-bound FasL and pig c-FLIP(L), we cotransfected both genes into pig endothelial cells (PEC). The double remodeling with these molecules effectively prevented CD8(+) CTL killing. Although double transfectants and single high transfectants of either membrane-bound FasL or c-FLIP(L) gene displayed similar inhibition of CTL cytotoxicity, the expression levels of these 2 molecules in double transfectants were almost half the expression levels of single transfectants. Furthermore, to show in vivo prolongation of xenograft survival, we transplanted PEC transfectants under the rat kidney capsule. Prolonged survival was displayed by PEC double transfectant xenografts whereas those from either parental PEC or MOCK (vehicle control) were completely rejected by day 5 posttransplantation. These data suggested that intracellular and extracellular remodeling by coexpression of membrane-bound FasL and pig c-FLIP(L) in xenograft cells may prevent an innate cellular response to xenografts. The gene compatibility of these molecules to generate transgenic pigs may be sufficient to create a window of opportunity to facilitate long-term xenograft survival.