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Two-dimensional transition metal dichalcogenides (TMDs) offer numerous advantages over silicon-based application in terms of atomically thin geometry, excellent opto-electrical properties, layer-number dependence, band gap variability, and lack of dangling bonds. The production of high-quality and large-scale TMD films is required with consideration of practical technology. However, the performance of scalable devices is affected by problems such as contamination and patterning arising from device processing; this is followed by an etching step, which normally damages the TMD film. Herein, we report the direct growth of MoSe2films on selective pattern areas via a surface-mediated liquid-phase promoter using a solution-based approach. Our growth process utilizes the promoter on the selective pattern area by enhancing wettability, resulting in a highly uniform MoSe2film. Moreover, our approach can produce other TMD films such as WSe2films as well as control various pattern shapes, sizes, and large-scale areas, thus improving their applicability in various devices in the future. Our patterned MoSe2field-effect transistor device exhibits a p-type dominant conduction behavior with a high on/off current ratio of ∼106. Thus, our study provides general guidance for direct selective pattern growth via a solution-based approach and the future design of integrated devices for a large-scale application.

Two-dimensional (2D) layered materials with properties such as a large surface-to-volume ratio, strong light interaction, and transparency are expected to be used in future optoelectronic applications. Many studies have focused on ways to increase absorption of 2D-layered materials for use in photodetectors. In this work, we demonstrate another strategy for improving photodetector performance using a graphene/MoS2heterojunction phototransistor with a short channel length and a tunable Schottky barrier. The channel length of sub-30 nm, shorter than the diffusion length, decreases carrier recombination and carrier transit time in the channel and improves phototransistor performance. Furthermore, our graphene/MoS2heterojunction phototransistor employed a tunable Schottky barrier that is only controlled by light and gate bias. It maintains a low dark current and an increased photocurrent. As a result, our graphene/MoS2heterojunction phototransistor showed ultrahigh responsivity and detectivity of 2.2 × 105A/W and 3.5 × 1013Jones, respectively. This is a considerable improvement compared to previous pristine MoS2phototransistors. We confirmed an effective method to develop phototransistors based on 2D materials and obtained ultrahigh performance of our phototransistor, which is promising for high-performance optoelectronic applications.

Graphene is one of the most promising materials for photodetectors due to its ability to convert photons into hot carriers within approximately 50 fs and generate long-lived thermalized states with lifetimes longer than 1 ps. In this study, we demonstrate a wide range of vertical photodetectors having a graphene/h-BN/Au heterostructure in which an hexagonal boron nitride (h-BN) insulating layer is inserted between an Au electrode and graphene photoabsorber. The photocarriers effectively tunnel through the small hole barrier (1.93 eV) at the Au/h-BN junction while the dark carriers are highly suppressed by a large electron barrier (2.27 eV) at the graphene/h-BN junction. Thus, an extremely low dark current of ∼10–13A is achieved, which is 8 orders of magnitude lower than that of graphene lateral photodetector devices (∼10–5A). Also, our device displays an asymmetric photoresponse behavior due to photothermionic emission at the graphene/h-BN and Au/h-BN junctions. The asymmetric behavior generates additional thermal carriers (hot carriers) to enable our device to generate photocurrents that can overcome the Schottky barrier. Furthermore, our device shows the highest value of the Iph/Idarkratio of ∼225 at 7 nm thick h-BN insulating layer, which is 3 orders of magnitude larger than that of the previously reported graphene lateral photodetectors without any active materials. In addition, we achieve a fast response speed of 12 μs of rise time and 5 μs of fall time, which are about 100 times faster than those of other graphene integrated photodetectors.

Piezoelectricity of transition metal dichalcogenides (TMDs) under mechanical strain has been theoretically and experimentally studied. Powerful strain sensors using Schottky barrier variation in TMD/metal junctions as a result of the strain-induced lattice distortion and associated ion-charge polarization were demonstrated. However, the nearly fixed work function of metal electrodes limits the variation range of a Schottky barrier. We demonstrate a highly sensitive strain sensor using a variable Schottky barrier in a MoS2/graphene heterostructure field effect transistor (FET). The low density of states near the Dirac point in graphene allows large modulation of the graphene Fermi level and corresponding Schottky barrier in a MoS2/graphene junction by strain-induced polarized charges of MoS2. Our theoretical simulations and temperature-dependent electrical measurements show that the Schottky barrier change is maximized by placing the Fermi level of the graphene at the charge neutral (Dirac) point by applying gate voltage. As a result, the maximum Schottky barrier change (ΔΦSB) and corresponding current change ratio under 0.17% strain reach 118 meV and 978, respectively, resulting in an ultrahigh gauge factor of 575 294, which is approximately 500 times higher than that of metal/TMD junction strain sensors (1160) and 140 times higher than the conventional strain sensors (4036). The ultrahigh sensitivity of graphene/MoS2heterostructure FETs can be developed for next-generation electronic and mechanical–electronic devices.

In this report, a screening-engineered carbon nanotube (CNT) network/MoS2/metal heterojunction vertical field effect transistor (CNT-VFET) is fabricated for an efficient gate modulation independent of the drain voltage. The gate field in the CNT-VFET transports through the empty space of the CNT network without any screening layer and directly modulates the MoS2semiconductor energy band, while the gate field from the Si back gate is mostly screened by the graphene layer. Consequently, the on/off ratio of CNT-VFET maintained 103in overall drain voltages, which is 10 times and 1000 times higher than that of the graphene (Gr) VFET at Vsd= 0.1 (ratio = 81.9) and 1 V (ratio = 3), respectively. An energy band diagram simulation shows that the Schottky barrier modulation of CNT/MoS2contact along the sweeping gate bias is independent of the drain voltage. On the other hand, the gate modulation of Gr/MoS2is considerably reduced with increased drain voltage because more electrons are drawn into the graphene electrode and screens the gate field by applying a higher drain voltage to the graphene/MoS2/metal capacitor.

Two dimensional (2D) layered materials and their heterojunctions with other materials are attracted because of their remarkable electrical and optical properties. In particular, graphene/semiconductor Schottky heterojunction is used for high performance solar cells. Here, we demonstrated very high open circuit voltage (Voc)in graphene/silicon heterojunction solar cell by dual-gate electric field application. The low density of states near Dirac point in graphene allows large modulation of graphene Fermi-level and corresponding Schottky barrier in a graphene/silicon junction. The top and bottom gate electric fields independently adjust the built-in potentials of respective upper and lower silicon energy band to induce higher band bending (1.22 eV) than the bandgap (1.12 eV). As a result, a maximum Vocof 0.94 V is achieved at the − 8 V of top-gate voltage and 10 V of bottom-gate voltage, exceeding highest known Vocfor previous graphene/silicon solar cell (Voc= 0.61 V) and the S-Q Limit (0.84 V) of conventional silicon solar cell – a thermodynamic limit for the energy conversion efficiency of solar cells with a single band gap energy. The ratio of output power gain to input gate power (ΔPG/ΔPC) is approximately 1012–1014with negligible power consumption in the gate (PC= 1 fW/cm2–10 pW/cm2), resulting in the significant advances in the power generation (PG= 40 mW/cm2).

ABSTRACT‘Location, location, location’ are treated as three sacred words in the lodging industry because location plays a significant role in the industry’s success. However, little attention has been paid to understanding hotel locations in regional contexts. The purpose of this study was to investigate spatial clustering patterns of hotels over time in relation to hotel locations and regions in the U.S. The Smith Travel Research (STR) Hotel Census Data from 1985 to 2017 were used for the study, and a series of statistical analyses was carried out to examine the relationships among the identified patterns. The results indicated that hotel locations and development were concentrated in specific geographical regions during the study periods. The implications of the study are discussed.

The hysteresis of the solution-processed oxide thin-film transistors (TFTs) is fatal issue to interrupt stable operation. So, we came up with uni-directional pre-annealing to solve the problem. There are inevitable defects when solution-processed oxide TFTs are fabricated, due to the porosities by the solvent volatilization. Also oxygen vacancies needed for carrier generation in metal oxide semiconductor can be trap states inducing charge carrier trapping. Uni-directional pre-annealing improved the hysteresis, preventing randomly solvent evaporation and decreased the defects of the film. We can result in advanced stability of the solution-processed oxide TFTs, at the same time showing that the field effect mobility was enhanced from 3.35 cm2/Vs to 4.78 cm2/Vs simultaneously, and exhibiting better subthreshold swing from 0.89 V/dec to 0.23 V/dec.

The voltage-gated cardiac Na+channel (Nav1.5), encoded by the SCN5A gene, conducts the inward depolarizing cardiac Na+current (INa) and is vital for normal cardiac electrical activity. Inherited loss-of-function mutations in SCN5A lead to defects in the generation and conduction of the cardiac electrical impulse and are associated with various arrhythmia phenotypes. Here we show that sirtuin 1 deacetylase (Sirt1) deacetylates Nav1.5 at lysine 1479 (K1479) and stimulates INavia lysine-deacetylation-mediated trafficking of Nav1.5 to the plasma membrane. Cardiac Sirt1 deficiency in mice induces hyperacetylation of K1479 in Nav1.5, decreases expression of Nav1.5 on the cardiomyocyte membrane, reduces INaand leads to cardiac conduction abnormalities and premature death owing to arrhythmia. The arrhythmic phenotype of cardiac-Sirt1-deficient mice recapitulated human cardiac arrhythmias resulting from loss of function of Nav1.5. Increased Sirt1 activity or expression results in decreased lysine acetylation of Nav1.5, which promotes the trafficking of Nav1.5 to the plasma membrane and stimulation of INa. As compared to wild-type Nav1.5, Nav1.5 with K1479 mutated to a nonacetylatable residue increases peak INaand is not regulated by Sirt1, whereas Nav1.5 with K1479 mutated to mimic acetylation decreases INa. Nav1.5 is hyperacetylated on K1479 in the hearts of patients with cardiomyopathy and clinical conduction disease. Thus, Sirt1, by deacetylating Nav1.5, plays an essential part in the regulation of INaand cardiac electrical activity.

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Herein, the energy level alignment and electron recombination kinetics in solid state dye-sensitized solar cells (DSCs) employing a solid polymer electrolyte (SPE) have been quantitatively characterized. In order to determine the microscopic origin of the enhanced characteristics in polymer electrolytes, we carried out an extensive study of the photovoltaic properties with respect to the electrolyte type and composition, including a liquid electrolyte (LE) and various salt types and concentrations. We observed a smaller downward shift in the conduction band energy of the TiO2layer upon contact with the SPE as well as a retarded electron recombination rate. These led to an increase in the Vocfor DSCs with an SPE, which is mostly attributable to the coordinative interactions of the ethylene oxide (EO) units in poly(ethylene oxide) (PEO) and poly(ethylene glycol) dimethyl ether (PEGDME) with metallic Li+ions and Ti atoms. Such coordinative interactions induce 1) the capture of Li+cations in the bulk of the polymer electrolyte, thereby reducing their effective concentration and 2) the facile formation of a PEO passivation layer on top of the TiO2layer. Therefore, it was concluded that the high Vocin solid state DSCs employing a polymer electrolyte is attributable to the coordinative properties of the EO units in PEO and PEGDME in the SPE.

The origin of the differences between the performance parameters found for dye-sensitized solar cells (DSCs) using liquid and poly(ethylene oxide)-based solid polymer electrolytes has been investigated. Limitations associated with poor polymer electrolyte penetration and ionic diffusion have been analyzed together with other effects such as the dye regeneration rate, the conduction band edge shift, and the electron recombination kinetics occurring in the solid polymer electrolyte. We have found that dye regeneration was faster for sensitized TiO2films fully wetted with polymer electrolyte than that with liquid cells. This new result was attributed to a 0.2 eV decrease in the dye highest occupied molecular orbital energy yielding to an increase in the driving force for dye regeneration. These understandings may contribute to a further increase in the energy-conversion efficiency of DSCs employing solid polymer electrolyte.

This work presents formation of single-layered Pt islands on Au electrodes using the CO route, and the electrochemical behavior of CO, hydrogen, and ethanol was investigated with scanning tunneling microscopy (STM), X-ray photoelectron spectroscopy (XPS), and cyclic voltammetry. The conventional route, consisting of irreversible adsorption of Pt precursor ions (10–3M PtCl42–in 0.05 M H2SO4) and subsequent electrochemical reduction, resulted in multiple-layered Pt islands; the CO route, utilizing CO adsorption to protect pre-existing Pt islands from irreversible adsorption of Pt, exclusively produced single-layered Pt islands. Furthermore, STM results implied that single-layered Pt islands on Au(111) were islands of alloyed Pt in a (√3 × √3)R30° arrangement, while multiple-layered islands were stacked layers of Pt in an (1 × 1) array. The coverages of deposited Pt estimated from STM and XPS measurements were quantitatively consistent with each other to confirm existence of the single-layered Pt islands. Coulometric analyses of adsorbed CO and hydrogen indicated lower adsorption stoichiometry of hydrogen on Pt islands prepared by the two deposition routes, especially when the deposited amount of Pt was small. Comparison of the coulometric coverages of CO and hydrogen with electrochemically active Pt coverages estimated with STM results supported that the adsorption stoichiometries of CO and hydrogen were higher on single-layered Pt islands than on multiple-layered ones, roughly by a factor of ∼1.8. Also, ethanol oxidation was enhanced on single-layered Pt islands approximately ∼4 times on average referring to Pt(poly), while the enhancement factor on multiple-layered ones was ∼1.5. Thus, this work demonstrated that the CO route exclusively produced single-layered Pt islands on Au, contrasting with multiple-layered islands in various electrochemical aspects.

New thiolate/disulfide redox couples (M−/M2) were introduced and also combined with T−/T2, resulting in more efficient binary redox couples. The binary redox couples, in particular M−/T2, yielded a high energy conversion efficiency and reasonably stable performance with the carbon black counter electrode for dye-sensitized solar cells.

The blood levels of microRNA-122 (miR-122) is associated with the severity of cardiovascular disorders, and targeting it with efficient and safer miR inhibitors could be a promising approach. Here, we report the generation of a γ-peptide nucleic acid (γPNA)-based miR-122 inhibitor (γP-122-I) that rescues vascular endothelial dysfunction in mice fed a high-fat diet. We synthesized diethylene glycol-containing γP-122-I and found that its systemic administration counteracted high-fat diet (HFD)-feeding-associated increase in blood and aortic miR-122 levels, impaired endothelial function, and reduced glycemic control. A comprehensive safety analysis established that γP-122-I affects neither the complete blood count nor biochemical tests of liver and kidney functions during acute exposure. In addition, long-term exposure to γP-122-I did not change the overall adiposity, or histology of the kidney, liver, and heart. Thus, γP-122-I rescues endothelial dysfunction without any evidence of toxicity in vivoand demonstrates the suitability of γPNA technology in generating efficient and safer miR inhibitors.

DNA-dependent protein kinase (DNA-PK) is involved in joining DNA double-strand breaks induced by ionizing radiation or V(D)J recombination and is activated by DNA ends and composed of a DNA binding subunit, Ku, and a catalytic subunit, DNA-PKcs. It has been suggested that DNA-PK might be 2ndupstream kinase for protein kinase B (PKB). In this report, we showed that Ser473 phosphorylation in the hydrophobic-motif of PKB is blocked in DNA-PK knockout mouse embryonic fibroblast cells (MEFs) following insulin stimulation, while there is no effect on Ser473 phosphorylation in DNA-PK wild type MEF cells. The observation is further confirmed in human glioblastoma cells expressing a mutant form of DNA-PK (M059J) and a wild-type of DNA-PK (M059K), indicating that DNA-PK is indeed important for PKB activation. Furthermore, the treatment of cells with doxorubicin, DNA-damage inducing agent, leads to PKB phosphorylation on Ser473 in control MEF cells while there is no response in DNA-PK knockout MEF cells. Together, these results proposed that DNA-PK has a potential role in insulin signaling as well as DNA-repair signaling pathway.

Rottlerin is widely used as a protein kinase C-δ inhibitor. Recently, several reports have shown the possible apoptosis-inducing effect of rottlerin in some cancer cell lines. Here we report that rottlerin induces not only apoptosis but also autophagy via a PKC- δ-independent pathway in HT1080 human fibrosarcoma cells. Rottlerin treatment induced a dose- and time-dependent inhibition of cell growth, and cytoplasmic vacuolations were markedly shown. These vacuoles were identified as acidic autolysosomes by electron microscopy, acidic vesicular organelle (AVO) staining and transfection of green fluorescent protein-LC3. The LC3-II protein level also increased after treatment with rottlerin. Prolonged exposure to rottlerin eventually caused apoptosis via loss of mitochondrial membrane potential and translocation of AIF from mitochondria to the nucleus. However, the activities of caspase-3, -8, and -9 were not changed, and PARP did not show signs of cleavage. Interestingly, the pretreatment of cells with a specific inhibitor of autophagy (3-methyladenine) accelerated rottlerin-induced apoptosis as revealed by an analysis of the subdiploid fraction and TUNEL assay. Nevertheless, the knockdown of PKC-δ by RNA interference neither affected cell growth nor acidic vacuole formation. Similarly, rottlerin-induced cell death was not prevented by PKC-δ overexpression. Taken together, these findings suggest that rottlerin induces early autophagy and late apoptosis in a PKC-δ-independent manner, and the rottlerin-induced early autophagy may act as a survival mechanism against late apoptosis in HT1080 human fibrosarcoma cells.

Previous studies have demonstrated that rottlerin, a specific PKCd inhibitor, potentiates death receptormediated apoptosis through a cytochrome c-dependent or -independent pathway. However, its ability to regulate necrotic cell death, as well as the underlying mechanism, remains unknown. We found that in murine fibrosarcoma L929 cells, treatment with rottlerin protected the cells against TNF-induced necrosis, whereas it sensitized the cells to apoptosis induced by co-treatment with Hsp90 inhibitor geldanamycin and TNF, in a manner independent of its ability to inhibit PKC-d. TNF treatment induced rapid accumulation of mitochondrial superoxide (O2-) through the Nox1 NADPH oxidase when cells undergo necrosis. Moreover, pretreatment with rottlerin failed to induce the GTP-bound form of small GTPase Rac1 by TNF treatment, and subsequently suppressed mitochondrial O2-production and poly(ADP-ribose) polymerase activation, thus inhibiting necrotic cell death. Therefore, our study suggests that Nox1 NADPH oxidase is a new molecular target for anti-necrotic activity of rottlerin upon death-receptor ligation.

There is a commonly shared concern among Koreans that Korean politics is much too costly yet inefficient. The issue of money politics and corruption therefore has repeatedly dominated the media and public debate, especially during the election years. Despite repeated reform attempts, many weaknesses in the regulatory system still remain and the opaque nature of political financing persists. This paper argues that one of the major contributing factors to these policy failures is that previous reform measures were undertaken without a knowledge or understanding of the facts regarding the financing of political funds in Korea. This paper will bringing to show that analyses of the official NEC data on political funds are useful in light many of the problems embedded in both the legal and institutional aspects of Korea's political finance system. For instance, the presence of significant advantages for the incumbent in accessing political funds limits competition and fairness, and leads to the entrenchment of elected officials who are detached from their constituents. The official data also reveal evidence of strong linkages between the politicians and moneyed interests, making the political system vulnerable to corruption. In addition, Korea's party system's weak grass‐root support base allows domination by central party bosses; hence, the party system is weak in providing accountability, responsibility, deliberation, and competition. Finally, the most telling signal that Korea's political system is in need of reform comes ironically, not from what the official funds data are able to tell, but from what they are unable to tell. That is, the lack of transparency itself can be seen as an indicator that Korea's political finance system lacks credibility and accountability.

Pervanadate, a complex of vanadate and H2O2, has an insulin mimetic effect, and acts as an inhibitor of protein tyrosine phosphatase. Pervanadate-induced phospholipase D (PLD) activation is known to be dependent on the tyrosine phosphorylation of cellular proteins and protein kinase C (PKC) activation, and yet underlying molecular mechanisms are not clearly understood. Here, we investigated the signaling pathway of pervanadate-induced PLD activation in Rat2 fibroblasts. Pervanadate increased PLD activity in dose- and time- dependent manner. Protein tyrosine kinase inhibitor, genistein, blocked PLD activation. Interestingly, AG-1478, a specific inhibitor of the tyrosine kinase activity of epidermal growth factor receptor (EGFR) blocked not only the PLD activation completely but also phosphorylation of p38 mitogen- activated protein kinase (MAPK). However, AG-1295, an inhibitor specific for the tyrosine kinase activity of pletlet drived growth factor receptor (PDGFR) did not show any effect on the PLD activation by pervanadate. We further found that pervanadate increased phosphorylation levels of p38, extracellular signal-regulated kinase (ERK) and c-Jun NH2-terminal kinase (JNK). SB203580, a p38 MAPK inhibitor, blocked the PLD activation completely. However, the inhibitions of ERK by the treatment of PD98059 or of JNK by the overexpression of JNK interacting peptide JBD did not show any effect on pervanadate-induced PLD activation. Inhibition or down-regulation of PKC did not alter the pervanadate-induced PLD activation in Rat2 cells. Thus, these results suggest that pervanadate-induced PLD activation is coupled to the transactivation of EGFR by pervanadate resulting in the activation of p38 MAP kinase.

We made stable cell lines overexpressing PLD1 (GP-PLD1) from GP+envAm12 cell, a derivative of NIH 3T3 cell. PLD1 activity and extracellular signal-regulated kinase (ERK) phosphorylation were enhanced in GP-PLD1 cells by the treatment of lysophosphatidic acid (LPA). In contrast, these LPA-induced effects were attenuated with the pretreatment of pertussis toxin (PTX) or protein kinase C (PKC) inhibitor. Moreover, accumulation of phosphatidic acid (PA), a product of PLD action, potentiated the LPA-induced ERK activation in GP-PLD1 cells while blocking of PA production with the treatment of 1-butanol attenuated LPA-induced ERK phosphorylation. From these results, we suggest that LPA activate PLD1 through pertussis toxin-sensitive G protein and PKC-dependent pathways, then PA produced from PLD1 activation facilitate ERK phosphorylation.

The article discusses spring flowers in Korea. Pasqueflowers, ginger plant flowers and dandelions are described. The origins of names of flowers are detailed including the "roe deer's ear," the Anemone, and the "hyeonhosaek." Also discussed is the composer Gustav Mahler's third symphony in D minor which is dedicated to nature and the earth.

Introduction:The sodium current (INa) controlling cardiac cell excitability is conducted via the Na+channel NaV1.5 (encoded by SCN5A). Dysregulation of NaV1.5 has been implicated in arrhythmia, with increased late NaV1.5 current (INa,L) causing long QT type 3. Many NaV1.5 post-translational modifications have been reported by us and others, including SUMOylation, the addition of a Small Ubiquitin-like MOdifier (SUMO) at K442-NaV1.5. Plant et al. (2020) recently reported that hypoxia increases INa,Lby increased NaV1.5 SUMOylation.Hypothesis:SUMOylation modifies peak but not late NaV1.5 currents through membrane localization.Methods:SUMOylation of NaV1.5 by SUMO1 was detected by immunoprecipitation and immunoblot. The effects of SUMOylation on peak INaand INa,Lwere measured using patch clamp in HEK293 cells transfected with wild type (WT) or mutant K442R-NaV1.5 with/without the β1 subunit and in neonatal rat cardiac myocytes (NRCMs). Tetrodotoxin (TTX) was used to quantitate INa,Lin NRCMs. NaV1.5 trafficking was detected by immunofluorescence.Results:NaV1.5 was SUMOylated by SUMO1 in HEK cells, NRCMs, and human heart samples. Overexpressing or directly applying SUMO1 induced hyperSUMOylation of NaV1.5 at K442 and increased the amplitude of peak INain NRCMs and in HEK cells overexpressing WT but not K442R-Nav1.5. SUMOylation did not affect INa,Lin HEK293 cells expressing NaV1.5 with/without the β1 subunit or in NRCMs (Fig. 1A, B). SUMO1 enhanced membrane localization of NaV1.5 in HEK293 cells (Fig. 1C) with minimal changes to steady state activation, inactivation or channel kinetics.Conclusion:SUMOylation of Nav1.5 at K442 increases peak INawithout changing INa,L, at least in part by altering membrane abundance. Our findings do not support SUMOylation as a mechanism for changes in INa,L.

van der Waals heterostructures (vdWHs) of metallic (m-) and semiconducting (s-) transition-metal dichalcogenides (TMDs) exhibit an ideal metal/semiconductor (M/S) contact in a field-effect transistor. However, in the current two-step chemical vapor deposition process, the synthesis of m-TMD on pregrown s-TMD contaminates the van der Waals (vdW) interface and hinders the doping of s-TMD. Here, NbSe2/Nb-doped-WSe2metal-doped-semiconductor (M/d-S) vdWHs are created via a one-step synthesis approach using a niobium molar ratio-controlled solution-phase precursor. The one-step growth approach synthesizes Nb-doped WSe2with a controllable doping concentration and metal/doped-semiconductor vdWHs. The hole carrier concentration can be precisely controlled by controlling the Nb/(W + Nb) molar ratio in the precursor solution from ∼3 × 1011/cm2at Nb-0% to ∼1.38 × 1012/cm2at Nb-60%; correspondingly, the contact resistance RCvalue decreases from 10 888.78 at Nb-0% to 70.60 kΩ.μm at Nb-60%. The Schottky barrier height measurement in the Arrhenius plots of ln(Isat/T2) versus q/KBTdemonstrated an ohmic contact in the NbSe2/WxNb1–xSe2vdWHs. Combining p-doping in WSe2and M/d-S vdWHs, the mobility (27.24 cm2V–1s–1) and on/off ratio (2.2 × 107) are increased 1238 and 4400 times, respectively, compared to that using the Cr/pure-WSe2contact (0.022 cm2V–1s–1and 5 × 103, respectively). Together, the RCvalue using the NbSe2contact shows 2.46 kΩ.μm, which is ∼29 times lower than that of using a metal contact. This method is expected to guide the synthesis of various M/d-S vdWHs and applications in future high-performance integrated circuits.

Introduction:SUMOylation, the addition of a Small Ubiquitin-like MOdifier (SUMO), is a post-translational modification that modulates an array of proteins in various cellular processes. Cardiac Na+channel NaV1.5, encoded by SCN5A, critically controls cell excitability, and altered channel gating has been implicated in both inherited and acquired arrhythmias.Hypothesis:We tested whether SUMOylation of the cardiac sodium channel NaV1.5 modifies the inward Na+current (INa) and influences cardiac electrical activity.Methods:SUMOylation of NaV1.5 by SUMO1 was detected by immunoprecipitation and immunoblotting. The effects of SUMOylation/de-SUMOylation on the amplitude and properties of INain HEK293 cells transiently transfected with wild type (WT) and mutant (K442R) NaV1.5 and in neonatal rat cardiac myocytes (NRCMs) were measured using whole-cell and inside-out patch clamp. The role of SUMOylation in vivowas studied using electrocardiograms (EKGs) and ambulatory telemetry on Scn5a heterozygous knockout (SCN5A+/-) mice treated with adeno-associated virus overexpression of the de-SUMOylating protein SENP2 (AAV-SENP2) or the SUMOylation inhibitor anacardic acid.Results:NaV1.5 in HEK cells, NRCMs and human heart samples is SUMOylated by SUMO1. Overexpression or direct application of SUMO1 induced hyperSUMOylation of NaV1.5 at K442 and increased the amplitude of INain NRCMs and in HEK cells overexpressing WT but not K442R-Nav1.5 (Fig 1A). Forcing hypoSUMOylation in SCN5A+/-mice by AAV9-SENP2 overexpression or by treatment with anacardic acid led to decreased INain cardiac myocytes (Fig 1B), QRS prolongation (Fig 1C), heart block and ventricular arrhythmias.Conclusion:SUMO1-mediated SUMOylation of Nav1.5 at K442 increases INa, while deSUMOylation produces conduction defects and arrhythmias in mice. SUMOylation of Nav1.5 may modify arrhythmic risk in disease states and represents a potential target for pharmacological manipulation.