Photon-Assisted Tunneling of High-Order Multiple Andreev Reflections in Epitaxial Nanowire Josephson Junctions.

Semiconductor/superconductor hybrids exhibit a range of phenomena that can be exploited for the study of novel physics and the development of new technologies. Understanding the origin of the energy spectrum of such hybrids is therefore a crucial goal. Here, we study Josephson junctions defined by shadow epitaxy on InAsSb/Al nanowires. The devices exhibit gate-tunable supercurrents at low temperatures and multiple Andreev reflections (MARs) at finite voltage bias. Under microwave irradiation, photon-assisted tunneling (PAT) of MARs produces characteristic oscillating sidebands at quantized energies, which depend on MAR order, n, in agreement with a recently suggested modification of the classical Tien-Gordon equation. The scaling of the quantized energy spacings with microwave frequency provides independent confirmation of the effective charge, ne, transferred by the nth-order tunneling process. The measurements suggest PAT as a powerful method for assigning the origin of low-energy spectral features in hybrid Josephson devices.

Signatures of Andreev Blockade in a Double Quantum Dot Coupled to a Superconductor.

We investigate an electron transport blockade regime in which a spin triplet localized in the path of current is forbidden from entering a spin-singlet superconductor. To stabilize the triplet, a double quantum dot is created electrostatically near a superconducting Al lead in an InAs nanowire. The quantum dot closest to the normal lead exhibits Coulomb diamonds, and the dot closest to the superconducting lead exhibits Andreev bound states and an induced gap. The experimental observations compare favorably to a theoretical model of Andreev blockade, named so because the triplet double dot configuration suppresses Andreev reflections. Observed leakage currents can be accounted for by finite temperature. We observe the predicted quadruple level degeneracy points of high current and a periodic conductance pattern controlled by the occupation of the normal dot. Even-odd transport asymmetry is lifted with increased temperature and magnetic field. This blockade phenomenon can be used to study spin structure of superconductors. It may also find utility in quantum computing devices that use Andreev or Majorana states.

Semiconductor-Ferromagnetic Insulator-Superconductor Nanowires: Stray Field and Exchange Field.

Nanowires can serve as flexible substrates for hybrid epitaxial growth on selected facets, allowing for the design of heterostructures with complex material combinations and geometries. In this work we report on hybrid epitaxy of freestanding vapor-liquid-solid grown and in-plane selective area grown semiconductor-ferromagnetic insulator-superconductor (InAs/EuS/Al) nanowire heterostructures. We study the crystal growth and complex epitaxial matching of wurtzite and zinc-blende InAs/rock-salt EuS interfaces as well as rock-salt EuS/face-centered cubic Al interfaces. Because of the magnetic anisotropy originating from the nanowire shape, the magnetic structure of the EuS phase is easily tuned into single magnetic domains. This effect efficiently ejects the stray field lines along the nanowires. With tunnel spectroscopy measurements of the density of states, we show that the material has a hard induced superconducting gap, and magnetic hysteretic evolution which indicates that the magnetic exchange fields are not negligible. These hybrid nanowires fulfill key material requirements for serving as a platform for spin-based quantum applications, such as scalable topological quantum computing.

Flame Retardants-Mediated Interferon Signaling in the Pathogenesis of Nonalcoholic Fatty Liver Disease.

Nonalcoholic fatty liver disease (NAFLD) is a growing concern worldwide, affecting 25% of the global population. NAFLD is a multifactorial disease with a broad spectrum of pathology includes steatosis, which gradually progresses to a more severe condition such as nonalcoholic steatohepatitis (NASH), fibrosis, cirrhosis, and eventually leads to hepatic cancer. Several risk factors, including exposure to environmental toxicants, are involved in the development and progression of NAFLD. Environmental factors may promote the development and progression of NAFLD by various biological alterations, including mitochondrial dysfunction, reactive oxygen species production, nuclear receptors dysregulation, and interference in inflammatory and immune-mediated signaling. Moreover, environmental contaminants can influence immune responses by impairing the immune system's components and, ultimately, disease susceptibility. Flame retardants (FRs) are anthropogenic chemicals or mixtures that are being used to inhibit or delay the spread of fire. FRs have been employed in several household and outdoor products; therefore, human exposure is unavoidable. In this review, we summarized the potential mechanisms of FRs-associated immune and inflammatory signaling and their possible contribution to the development and progression of NAFLD, with an emphasis on FRs-mediated interferon signaling. Knowledge gaps are identified, and emerging pharmacotherapeutic molecules targeting the immune and inflammatory signaling for NAFLD are also discussed.

Nicotinamide attenuates cyclophosphamide-induced hepatotoxicity in SD rats by reducing oxidative stress and apoptosis.

Cyclophosphamide (CP) is a widely used anticancer and immunosuppressant drug. Nevertheless, clinical utilization of CP is limited due to considerable adverse effects and toxicities. Nicotinamide (NMD) is a micronutrient and the effect of NMD against CP-induced hepatotoxicity is yet unexplored. The present study was designed to evaluate the chemoprotective effect of NMD against CP-induced hepatic injury in Sprague-Dawley rats. Hepatotoxicity was induced by the administration of CP (30 mg/kg/day) for 10 consecutive days by intraperitoneal injection. The chemoprotective effect of NMD treatment (200 mg/kg) against CP-induced hepatotoxicity was evaluated by the oxidative stress, liver function, histopathological changes, and DNA damage. NMD cotreatment significantly reduced CP-induced oxidative stress, histological changes, and apoptosis in the liver. The present study demonstrated that NMD treatment ameliorated CP-induced hepatic damage by improving the antioxidant system and reducing DNA damage. The present findings revealed that NMD supplementation might be useful to reduce CP-associated hepatotoxicity, and thereby can increase the therapeutic utility of CP.

Role of Neutrophils and Myeloid-Derived Suppressor Cells in Glioma Progression and Treatment Resistance.

Recent efforts in brain tumor research have been directed towards the modulation of the immune system for therapeutic interventions. Several human cancers, including gliomas, are infiltrated with immune cell types-including neutrophils and myeloid-derived suppressor cells-that contribute to tumor progression, invasiveness, and treatment resistance. The role of tumor-associated neutrophils and myeloid-derived suppressor cells in cancer biology remains elusive, as these cells can exert a multitude of pro-tumor and antitumor effects. In this review, we provide the current understanding and novel insights on the role of neutrophils and myeloid-derived suppressor cells in glioma progression and treatment resistance, as well as the mechanisms of pleiotropic behaviors in these cells during disease progression, with an emphasis on possible strategies to reprogram these cells towards their antitumor actions.

Direct Synthesis of Colorful Single-Walled Carbon Nanotube Thin Films.

In floating catalyst chemical vapor deposition (FC-CVD), tuning chirality distribution and obtaining narrow chirality distribution of single-walled carbon nanotubes (SWCNTs) is challenging. Herein, by introducing various amount of CO2 in FC-CVD using CO as a carbon source, we have succeeded in directly synthesizing SWCNT films with tunable chirality distribution as well as tunable colors. In particular, with 0.25 and 0.37 volume percent of CO2, the SWCNT films display green and brown colors, respectively. We ascribed various colors to suitable diameter and narrow chirality distribution of SWCNTs. Additionally, by optimizing reactor temperature, we achieved much narrower ( n, m) distribution clustered around (11,9) with extremely narrow diameter range (>98% between 1.2 and 1.5 nm). We propose that CO2 may affect CO disproportionation and nucleation modes of SWCNTs, resulting in SWCNTs' various diameter ranges. Our work could provide a new route for high-yield and direct synthesis of SWCNTs with narrow chirality distribution and offer potential applications in electronics, such as touch sensors or transistors.

CD36 mediates lipid accumulation in pancreatic beta cells under the duress of glucolipotoxic conditions: Novel roles of lysine deacetylases.

The cluster of differentiation 36 (CD36) is implicated in the intake of long-chain fatty acids and fat storage in various cell types including the pancreatic beta cell, thus contributing to the pathogenesis of metabolic stress and diabetes. Recent evidence indicates that CD36 undergoes post-translational modifications such as acetylation-deacetylation. However, putative roles of such modifications in its functional activation and onset of beta cell dysregulation under the duress of glucolipotoxicity (GLT) remain largely unknown. Using pharmacological approaches, we validated, herein, the hypothesis that acetylation-deacetylation signaling steps are involved in CD36-mediated lipid accumulation and downstream apoptotic signaling in pancreatic beta (INS-1832/13) cells under GLT. Exposure of these cells to GLT resulted in significant lipid accumulation without affecting the CD36 expression. Sulfo-n-succinimidyl oleate (SSO), an irreversible inhibitor of CD36, significantly attenuated lipid accumulation under GLT conditions, thus implicating CD36 in this metabolic step. Furthermore, trichostatin A (TSA) or valproic acid (VPA), known inhibitors of lysine deacetylases, markedly suppressed GLT-associated lipid accumulation with no discernible effects on CD36 expression. Lastly, SSO or TSA prevented caspase 3 activation in INS-1832/13 cells exposed to GLT conditions. Based on these findings, we conclude that an acetylation-deacetylation signaling step might regulate CD36 functional activity and subsequent lipid accumulation and caspase 3 activation in pancreatic beta cells exposed to GLT conditions. Identification of specific lysine deacetylases that control CD36 function should provide novel clues for the prevention of beta-cell dysfunction under GLT.

Valproic Acid Improves Glucose Homeostasis by Increasing Beta-Cell Proliferation, Function, and Reducing its Apoptosis through HDAC Inhibition in Juvenile Diabetic Rat.

Recent evidence highlighted that there is a link between type-1 diabetes mellitus and histone deacetylases (HDACs) due to their involvement in beta-cell differentiation, proliferation, and function. The present study aimed to investigate the protective role of valproic acid (VPA) on beta-cell proliferation, function, and apoptosis in juvenile diabetic rat. Diabetes was induced in juvenile Sprague-Dawley rats by streptozotocin (75 mg/kg, i.p.) and VPA was administered at the doses of 150 and 300 mg/kg/day for 3 weeks by oral route. Various biochemical parameters, cellular alterations, and protein expression as well as apoptosis were assessed using different assays. VPA treatment significantly decreased plasma glucose, beta-cell damage, and apoptosis as well as increased the beta-cell function, insulin level/expression. The present study demonstrated that VPA improves beta-cell proliferation and function as well as reduces beta-cell apoptosis through HDAC inhibition. Our findings provide evidence that VPA may be useful for the treatment of juvenile diabetes.

Sodium valproate ameliorates diabetes-induced fibrosis and renal damage by the inhibition of histone deacetylases in diabetic rat.

Recent reports emphasize the contribution of histone deacetylases (HDACs) in the pathogenesis of diabetic renal injury and fibrosis. Valproic acid (VPA) is a first-line drug used for the treatment of epilepsy and migraine as well as established as a HDAC inhibitor. The present study was aimed to evaluate the anti-fibrotic and renoprotective effects of VPA in diabetic nephropathy (DN). Diabetes was induced by single injection of STZ (50mg/kg), whereas VPA at the doses of 150 and 300mg/kg/day was administered for 8 consecutive weeks by oral route in Sprague Dawley rats. The renal injuries and fibrosis were assessed by histology, fibrosis specific staining and fibroblast activation by a transmission electron microscope, while expression of proteins of interest was evaluated by western blotting and immunohistochemistry. VPA treatment ameliorated the histological alterations as well as fibrosis, and decreased the expression of TGF-ß1, CTGF, α-SMA, fibronectin, collagen I, COX-2, ICAM-1 and HDAC4/5/7. Further, VPA treatment significantly increased histone H3 acetylation and MMP-2 expression. The present study clearly established that VPA treatment ameliorates the renal injury and fibrosis in diabetic kidney by preventing the myofibroblast activation and fibrogenesis by HDAC inhibition and associated mechanisms, thereby improving the profibrotic and anti-fibrotic protein balance.

Sodium Butyrate Ameliorates L-Arginine-Induced Pancreatitis and Associated Fibrosis in Wistar Rat: Role of Inflammation and Nitrosative Stress.

Several reports indicated that histone deacetylases (HDACs) play a crucial role in inflammation and fibrogenesis. Sodium butyrate (SB) is a short-chain fatty acid having HDAC inhibition potential. The present study aimed to evaluate the protective effect of SB against L-arginine (L-Arg)-induced pancreatic fibrosis in Wistar rats. Pancreatic fibrosis was induced by twice intraperitoneal (i.p.) injections of 20% L-Arg (250 mg/100 g) at 2-h interval on day 1, 4, 7, and 10, whereas SB (800 mg/kg/day) was administrated for 10 days. At the end of the study, biochemical estimations, histological alterations, DNA damage, and the expression of various proteins were evaluated. Posttreatment of SB decreased L-Arg-induced oxidative and nitrosative stress, DNA damage, histological alterations, and fibrosis. Interestingly, posttreatment of SB significantly decreased the expression of α-smooth muscle actin, interleukin-1ß, inducible nitric oxide synthase, and 3-nitrotyrosine. The present study demonstrated that posttreatment of SB alleviates L-Arg-induced pancreatic damage and fibrosis in rat.

Zinc protects cyclophosphamide-induced testicular damage in rat: involvement of metallothionein, tesmin and Nrf2.

The role of zinc (Zn) in the protection of germ cells against testicular toxicants has long been elucidated, but the exact molecular mechanisms have not yet been explored. Cyclophosphamide (CP), one of the most commonly used anticancer drugs survived ages of treatment, but the unwanted toxicity limits its clinical usage. The present investigation was aimed to explore the role of Zn and its associated pathways in CP-induced testicular toxicity in S.D. rat. CP was administered in saline 30 mg/kg 5× weekly for 3 weeks (total dose of 450 mg/kg) by i.p. route, while Zn was supplemented by oral route at the doses of 1, 3, 10mg/kg/day for 3 weeks. CP significantly reduced Zn levels in serum and testes, body and testicular weight, sperm count and motility, spermiogenic cells, plasma testosterone and significantly increased the oxidative stress, sperm head abnormalities, sperm DNA damage with decreased chromatin and acrosome integrity; while Zn supplementation ameliorated the same. The present results demonstrated that Zn supplementation protected against CP-induced testicular damages by modulating metallothionein (MT), tesmin and Nrf2 associated pathways. Thus Zn supplementation during anticancer therapy might be potentially beneficial in reducing the off target effects associated with oxidative stress.

3-Aminobenzamide--a PARP inhibitor enhances the sensitivity of peripheral blood micronucleus and comet assays in mice.

CONTEXT: DNA repair is an essential outcome of DNA damage, which may compromise the end point of various in vitro and in vivo test systems of the genotoxicity evaluation. poly(ADP-ribose) polymerase (PARP) enzymes have an essential role in DNA repair. Here, we investigated the effect of 3-AB, a PARP inhibitor on the sensitivity of comet and PBMN assays. OBJECTIVE: This study aimed to enhance the sensitivity of the comet and peripheral blood micronucleus (PBMN) assays using 3-aminobenzamide (3-AB), a well-characterized PARP inhibitor. MATERIALS AND METHODS: Cyclophosphamide (CP, 50 mg/kg), 5-flourouracil (5-FU, 25 mg/kg), zidovudine (AZT, 400 mg/kg) and furosemide (FUR, 60 mg/kg) were selected as genotoxins. 3-AB was given every 8 h with the first dose given 2 h before the genotoxin treatment. For the PBMN assay, small amount of blood was taken from the tail tip of each animal and smears were prepared. The comet assay was performed in PBL, bone marrow and liver. RESULTS: In the comet as well as PBMN assay, 3-AB pre-treatment enhanced the extent of DNA damage in all the combination groups (3-AB + CP, 3-AB + 5-FU and 3-AB + AZT) compared to CP, 5-FU and AZT per se. 3-AB also enhanced the DNA damage caused by FUR in the bone marrow and liver. DISCUSSION: This study results clearly demonstrate that the pretreatment with 3-AB (30 mg/kg) significantly enhances the sensitivity of the PBMN and comet assays. This model may be useful for the detection of marginally active DNA damaging agents.

Pre-pubertal exposure of cytarabine-induced testicular atrophy, impaired spermatogenesis and germ cell DNA damage in SD rats.

CONTEXT: Cytarabine (Ara-C) is an effective chemotherapeutic drug for the treatment of acute leukaemias. It inhibits the DNA synthesis and repair, thereby causes cytotoxicity in the proliferating cells. OBJECTIVE: This study was aimed to investigate the effects of pre-pubertal exposure of Ara-C on testesticular development in juvenile SD rats and their function at puberty. MATERIALS AND METHODS: Ara-C was injected at the doses of 50, 100 and 200 mg/kg/day from postnatal day (PND) 29-42 (14 days) by intraperitoneal (i.p.) route. Half of the animals were sacrificed on PND 43 and remaining on PND 70. End points of the evaluation included gross pathological examination, histomorphometric analysis, sperm count and sperm head morphology, cell proliferation and DNA damage as well as apoptosis analysis. RESULTS: Ara-C treatment significantly decreased food and water intake, weight gain, testes and epididymis weight and increased histological alterations in the seminiferous tubule. Furthermore, Ara-C treatment significantly decreased the PCNA-positive cells and sperm count in a dose-dependent manner. Ara-C treatment also increased the DNA damage and apoptosis in testes and sperm as evident from the comet and TUNEL assays results. DISCUSSION: The present study results clearly indicated that Ara-C treatment impaired spermatogenesis and adversely affects the testicular development and its function in rats by reducing the germ cell proliferation and the inducing DNA damage and apoptosis.

MGMT function determines the differential response of ATR inhibitors with DNA-damaging agents in glioma stem cells for GBM therapy.

Background: The most prevalent cancer treatments cause cell death through DNA damage. However, DNA damage response (DDR) repair pathways, initiated by tumor cells, can withstand the effects of anticancer drugs, providing justification for combining DDR inhibitors with DNA-damaging anticancer treatments. Methods: Cell viability assays were performed with CellTiter-Glo assay. DNA damage was evaluated using Western blotting analysis. RNA-seq and single-cell level expression were used to identify the DDR signatures. In vivo, studies were conducted in mice to determine the effect of ATris on TMZ sensitization. Results: We found a subpopulation of glioma sphere-forming cells (GSCs) with substantial synergism with temozolomide (TMZ) using a panel of 3 clinical-grade ataxia-telangiectasia- and Rad3-related kinase inhibitors (ATRis), (elimusertib, berzosertib, and ceralasertib). Interestingly, most synergistic cell lines had O6-methylguanine-DNA methyltransferase (MGMT) promoter methylation, indicating that ATRi mainly benefits tumors with no MGMT repair. Further, TMZ activated the ATR-checkpoint kinase 1 (Chk1) axis in an MGMT-dependent way. TMZ caused ATR-dependent Chk1 phosphorylation and DNA double-strand breaks as shown by increased γH2AX. Increased DNA damage and decreased Chk1 phosphorylation were observed upon the addition of ATRis to TMZ in MGMT-methylated (MGMT-) GSCs. TMZ also improved sensitivity to ATRis in vivo, as shown by increased mouse survival with the TMZ and ATRi combination treatment. Conclusions: This research provides a rationale for selectively targeting MGMT-methylated cells using ATRis and TMZ combination. Overall, we believe that MGMT methylation status in GBM could serve as a robust biomarker for patient selection for ATRi combined with TMZ.

Mechanisms of NLRP3 inflammasome-mediated hepatic stellate cell activation: Therapeutic potential for liver fibrosis.

The liver injury leads to an inflammatory response, which causes the activation of hepatic stellate cells (HSCs) that further secrete ECM proteins and play an important role in liver fibrosis. Moreover, the inflammatory response is a driving force for fibrogenesis, which is triggered by many types of injuries. Exaggerated inflammatory immune responses are mediated by cytoplasmic protein complexes known as inflammasomes, which are involved in many chronic liver diseases. Inflammasomes are pattern recognition receptors (PRRs) that can sense any microbial motifs known as pathogen-associated molecular patterns (PAMPs), and host- or environmental-derived stress signals known as damage-associated molecular patterns (DAMPs). The inflammasomes cause caspase-mediated proteolytic cleavage of pro-IL-1ß and pro-IL-18 into active IL-1ß and IL-18. In this review, we provide a comprehensive summary of the important roles of NLRP3 inflammasome in the pathogenesis of liver fibrosis with an emphasis on several direct and indirect pathways responsible for the NLRP3 inflammasome-mediated HSCs activation and fibrogenesis. In addition, we discuss the general pharmacological and genetics strategies for the inhibition of NLRP3 inflammasome activation and its downstream signaling with examples of emerging pharmacotherapeutics, targeting the NLRP3 inflammasome signaling as well as a possible way to develop effective and safer NLRP3 inflammasome inhibitors.

Epitaxially Driven Phase Selectivity of Sn in Hybrid Quantum Nanowires.

Hybrid semiconductor-superconductor nanowires constitute a pervasive platform for studying gate-tunable superconductivity and the emergence of topological behavior. Their low dimensionality and crystal structure flexibility facilitate unique heterostructure growth and efficient material optimization, crucial prerequisites for accurately constructing complex multicomponent quantum materials. Here, we present an extensive study of Sn growth on InSb, InAsSb, and InAs nanowires and demonstrate how the crystal structure of the nanowires drives the formation of either semimetallic α-Sn or superconducting ß-Sn. For InAs nanowires, we observe phase-pure superconducting ß-Sn shells. However, for InSb and InAsSb nanowires, an initial epitaxial α-Sn phase evolves into a polycrystalline shell of coexisting α and ß phases, where the ß/α volume ratio increases with Sn shell thickness. Whether these nanowires exhibit superconductivity or not critically relies on the ß-Sn content. Therefore, this work provides key insights into Sn phases on a variety of semiconductors with consequences for the yield of superconducting hybrids suitable for generating topological systems.

Neuronal differentiation drives the antitumor activity of mitogen-activated protein kinase kinase (MEK) inhibition in glioblastoma.

Background: Epidermal growth factor receptor (EGFR) amplification is found in nearly 40%-50% of glioblastoma cases. Several EGFR inhibitors have been tested in glioblastoma but have failed to demonstrate long-term therapeutic benefit, presumably because of acquired resistance. Targeting EGFR downstream signaling with mitogen-activated protein kinase kinase 1 and 2 (MEK1/2) inhibitors would be a more effective approach to glioblastoma treatment. We tested the therapeutic potential of MEK1/2 inhibitors in glioblastoma using 3D cultures of glioma stem-like cells (GSCs) and mouse models of glioblastoma. Methods: Several MEK inhibitors were screened in an unbiased high-throughput platform using GSCs. Cell death was evaluated using flow cytometry and Western blotting (WB) analysis. RNA-seq, real-time quantitative polymerase chain reaction, immunofluorescence, and WB analysis were used to identify and validate neuronal differentiation. Results: Unbiased screening of multiple MEK inhibitors in GSCs showed antiproliferative and apoptotic cell death in sensitive cell lines. An RNA-seq analysis of cells treated with trametinib, a potent MEK inhibitor, revealed upregulation of neurogenesis and neuronal differentiation genes, such as achaete-scute homolog 1 (ASCL1), delta-like 3 (DLL3), and neurogenic differentiation 4 (NeuroD4). We validated the neuronal differentiation phenotypes in vitro and in vivo using selected differentiation markers (ß-III-tubulin, ASCL1, DLL3, and NeuroD4). Oral treatment with trametinib in an orthotopic GSC xenograft model significantly improved animal survival, with 25%-30% of mice being long-term survivors. Conclusions: Our findings demonstrated that MEK1/2 inhibition promotes neuronal differentiation in glioblastoma, a potential additional mechanism of action of MEK1/2 inhibitors. Thus, MEK inhibitors could be efficacious in glioblastoma patients with activated EGFR/MAPK signaling.

Developmental and reproductive toxic effects of exposure to microplastics: A review of associated signaling pathways.

Microplastics (MPs), small pieces of plastic (∼5 mm), are released into the environment not only as a result of the decomposition of large-sized plastics but also from day-to-day use of plastic products. Chronic exposure to MPs has been attributed to harmful effects on aquatic organisms and rodents. Effects include gastrointestinal toxicity, hepatotoxicity, neurotoxicity, and reproductive and developmental toxicities. Exposure to MPs may also potentially affect human health. Herein, we reviewed the impact of MPs on male and female reproductive systems and the associated mechanisms involved in the reproductive and developmental toxicities of MPs. We performed a literature search in Google Scholar and PubMed using the following keywords: MPs and reproductive toxicity; MPs and developmental studies; MPs and infertility; MPs and aquatics; and MPs and rodents. Evidence of MPs accumulation has been reported in many organs of humans and experimental models. The harmful effects of MPs have been manifested in male and female reproductive systems of mammalian and aquatic animals, including developmental effects on gametes, embryos, and their offspring. This review describes various signaling pathways involved in MPs-associated male and female reproductive and developmental toxicities.

Andreev Interference in the Surface Accumulation Layer of Half-Shell InAsSb/Al Hybrid Nanowires.

Understanding the spatial distribution of charge carriers in III-V nanowires proximity coupled to superconductors is important for the design and interpretation of experiments based on hybrid quantum devices. In this letter, the gate-dependent surface accumulation layer of half-shell InAsSb/Al nanowires is studied by means of Andreev interference in a parallel magnetic field. Both uniform hybrid nanowires and devices featuring a short Josephson junction fabricated by shadow lithography, exhibit periodic modulation of the switching current. The period corresponds to a flux quantum through the nanowire diameter and is consistent with Andreev bound states occupying a cylindrical surface accumulation layer. The spatial distribution is tunable by a gate potential as expected from electrostatic models.