Doping and critical-temperature dependence of the energy gaps in Ba(Fe_{1-x}Co_x)_2As_2 thin films

The dependence of the superconducting gaps in epitaxial Ba(Fe_{1-x}Co_{x})_2As_2 thin films on the nominal doping x (0.04 \leq x \leq 0.15) was studied by means of point-contact Andreev-reflection spectroscopy. The normalized conductance curves were well fitted by using the 2D Blonder-Tinkham-Klapwijk model with two nodeless, isotropic gaps -- although the possible presence of gap anisotropies cannot be completely excluded. The amplitudes of the two gaps \Delta_{S} and \Delta_{L} show similar monotonic trends as a function of the local critical temperature T_{c}^{A} (measured in the same point contacts) from 25 K down to 8 K. The dependence of the gaps on x is well correlated to the trend of the critical temperature, i.e. to the shape of the superconducting region in the phase diagram. When analyzed within a simple three-band Eliashberg model, this trend turns out to be compatible with a mechanism of superconducting coupling mediated by spin fluctuations, whose characteristic energy scales with T_{c} according to the empirical law \Omega_{0}= 4.65*k_{B}*T_{c}, and with a total electron-boson coupling strength \lambda_{tot}= 2.22 for x \leq 0.10 (i.e. up to optimal doping) that slightly decreases to \lambda_{tot}= 1.82 in the overdoped samples (x = 0.15).Comment: 8 pages, 5 color figure

Resistivity in Co-doped Ba-122: comparison of thin films and single crystals

The temperature dependence of the resistivity of epitaxial Ba(Fe_(1-x)Co_x)2As2 thin films (with nominal doping x = 0.08, 0.10 and 0.15) has been analyzed and compared with analogous measurements on single crystals taken from literature. The rho(T) of thin films looks different from that of single crystals, even when the cobalt content is the same. All rho(T) curves can be fitted by considering an effective two-band model (with holes and electrons bands) in which the electrons are more strongly coupled with the bosons (spin fluctuations) than holes, while the effect of impurities is mainly concentrated in the hole band. Within this model the mediating boson has the same characteristic energy in single crystals and thin films, but the shape of the transport spectral function at low energy has to be very different, leading to a "hardening" of the electron-boson spectral function in thin films, associated with the strain induced by the substrate.Comment: 13 pages, 4 figure

Point-contact Andreev-reflection spectroscopy in Fe(Te,Se) films: multiband superconductivity and electron-boson coupling

We report on a study of the superconducting order parameter in Fe(Te$_{1-x}$Se$_{x}$) thin films (with different Se contents: x=0.3, 0.4, 0.5) by means of point-contact Andreev-reflection spectroscopy (PCARS). The PCARS spectra show reproducible evidence of multiple structures, namely two clear conductance maxima associated to a superconducting gap of amplitude $\Delta_E \simeq 2.75 k_B T_c$ and additional shoulders at higher energy that, as we show, are the signature of the strong interaction of charge carriers with a bosonic mode whose characteristic energy coincides with the spin-resonance energy. The details of some PCARS spectra at low energy suggest the presence of a smaller and not easily discernible gap of amplitude $\Delta_H \simeq 1.75 k_B T_c$. The existence of this gap and its amplitude are confirmed by PCARS measurements in Fe(Te$_{1-x}$Se$_{x}$) single crystals. The values of the two gaps $\Delta_E$ and $\Delta_H$, once plotted as a function of the local critical temperature $T_c^A$, turn out to be in perfect agreement with the results obtained by various experimental techniques reported in literature.Comment: 8 pages, 6 figures. This is an author-created, un-copyedited version of an article published in Supercond. Sci. Technol. IOP Publishing Ltd is not responsible for any errors or omissions in this version of the manuscript or any version derived from it. The Version of Record is available online at 10.1088/0953-2048/27/12/12401

Therapeutically engineered induced neural stem cells are tumour-homing and inhibit progression of glioblastoma

Transdifferentiation (TD) is a recent advancement in somatic cell reprogramming. The direct conversion of TD eliminates the pluripotent intermediate state to create cells that are ideal for personalized cell therapy. Here we provide evidence that TD-derived induced neural stem cells (iNSCs) are an efficacious therapeutic strategy for brain cancer. We find that iNSCs genetically engineered with optical reporters and tumouricidal gene products retain the capacity to differentiate and induced apoptosis in co-cultured human glioblastoma cells. Time-lapse imaging shows that iNSCs are tumouritropic, homing rapidly to co-cultured glioblastoma cells and migrating extensively to distant tumour foci in the murine brain. Multimodality imaging reveals that iNSC delivery of the anticancer molecule TRAIL decreases the growth of established solid and diffuse patient-derived orthotopic glioblastoma xenografts 230- and 20-fold, respectively, while significantly prolonging the median mouse survival. These findings establish a strategy for creating autologous cell-based therapies to treat patients with aggressive forms of brain cancer

iPSC-derived neuronal models of PANK2-associated neurodegeneration reveal mitochondrial dysfunction contributing to early disease

Mutations in PANK2 lead to neurodegeneration with brain iron accumulation. PANK2 has a role in the biosynthesis of coenzyme A (CoA) from dietary vitamin B5, but the neuropathological mechanism and reasons for iron accumulation remain unknown. In this study, atypical patient-derived fibroblasts were reprogrammed into induced pluripotent stem cells (iPSCs) and subsequently differentiated into cortical neuronal cells for studying disease mechanisms in human neurons. We observed no changes in PANK2 expression between control and patient cells, but a reduction in protein levels was apparent in patient cells. CoA homeostasis and cellular iron handling were normal, mitochondrial function was affected; displaying activated NADH-related and inhibited FADH-related respiration, resulting in increased mitochondrial membrane potential. This led to increased reactive oxygen species generation and lipid peroxidation in patient-derived neurons. These data suggest that mitochondrial deficiency is an early feature of the disease process and can be explained by altered NADH/FADH substrate supply to oxidative phosphorylation. Intriguingly, iron chelation appeared to exacerbate the mitochondrial phenotype in both control and patient neuronal cells. This raises caution for the use iron chelation therapy in general when iron accumulation is absent

Insight from an Italian Delphi Consensus on EVAR feasibility outside the instruction for use: the SAFE EVAR Study

BACKGROUND: The SAfety and FEasibility of standard EVAR outside the instruction for use (SAFE-EVAR) Study was designed to define the attitude of Italian vascular surgeons towards the use of standard endovascular repair (EVAR) for infrarenal abdominal aortic aneurysm (AAA) outside the instruction for use (IFU) through a Delphi consensus endorsed by the Italian Society of Vascular and Endovascular Surgery (Societa Italiana di Chirurgia Vascolare ed Endovascolare - SICVE). METHODS: A questionnaire consisting of 26 statements was developed, validated by an 18 -member Advisory Board, and then sent to 600 Italian vascular surgeons. The Delphi process was structured in three subsequent rounds which took place between April and June 2023. In the first two rounds, respondents could indicate one of the following five degrees of agreement: 1) strongly agree; 2) partially agree; 3) neither agree nor disagree; 4) partially disagree; 5) strongly disagree; while in the third round only three different choices were proposed: 1) agree; 2) neither agree nor disagree; 3) disagree. We considered the consensus reached when >70% of respondents agreed on one of the options. After the conclusion of each round, a report describing the percentage distribution of the answers was sent to all the participants. RESULTS: Two -hundred -forty-four (40.6%) Italian Vascular Surgeons agreed to participate the first round of the Delphi Consensus; the second and the third rounds of the Delphi collected 230 responders (94.3% of the first -round responders). Four statements (15.4%) reached a consensus in the first rounds. Among the 22 remaining statements, one more consensus (3.8%) was achieved in the second round. Finally, seven more statements (26.9%) reached a consensus in the simplified last round. Globally, a consensus was reached for almost half of the proposed statements (46.1%). CONCLUSIONS: The relatively low consensus rate obtained in this Delphi seems to confirm the discrepancy between Guideline recommendations and daily clinical practice. The data collected could represent the source for a possible guidelines' revision and the proposal of specific Good Practice Points in all those aspects with only little evidence available

No evidence of association between prothrombotic gene polymorphisms and the development of acute myocardial infarction at a young age

Background : we investigated the association between 9 polymorphisms of genes encoding hemostasis factors and myocardial infarction in a large sample of young patients chosen because they have less coronary atherosclerosis than older patients, and thus their disease is more likely to be related to a genetic predisposition to a prothrombotic state Methods and Results : this nationwide case-control study involved 1210 patients who had survived a first myocardial infarction at an age of 45 years who underwent coronary arteriography in 125 coronary care units and 1210 healthy subjects matched for age, sex, and geographical origin. None of the 9 polymorphisms of genes encoding proteins involved in coagulation (G-455A -fibrinogen: OR, 1.0; CI, 0.8 to 1.2; G1691A factor V: OR, 1.1; CI, 0.6 to 2.1; G20210A factor II: OR, 1.0; CI, 0.5 to 1.9; and G10976A factor VII: OR, 1.0; CI, 0.8 to 1.3), platelet function (C807T glycoprotein Ia: OR, 1.1; CI, 0.9 to 1.3; and C1565T glycoprotein IIIa: OR, 0.9; CI, 0.8 to 1.2), fibrinolysis (G185T factor XIII: OR, 1.2; CI, 0.9 to 1.6; and 4G/5G plasminogen activator inhibitor type 1: OR, 0.9; CI, 0.7 to 1.2), or homocysteine metabolism (C677T methylenetetrahydrofolate reductase: OR, 0.9; CI, 0.8 to 1.1) were associated with an increased or decreased risk of myocardial infarction Conclusions : this study provides no evidence supporting an association between 9 polymorphisms of genes encoding proteins involved in hemostasis and the occurrence of premature myocardial infarction or protection against it