Mobility enhancement and highly efficient gating of monolayer MoS2 transistors with Polymer Electrolyte

We report electrical characterization of monolayer molybdenum disulfide (MoS2) devices using a thin layer of polymer electrolyte consisting of poly(ethylene oxide) (PEO) and lithium perchlorate (LiClO4) as both a contact-barrier reducer and channel mobility booster. We find that bare MoS2 devices (without polymer electrolyte) fabricated on Si/SiO2 have low channel mobility and large contact resistance, both of which severely limit the field-effect mobility of the devices. A thin layer of PEO/ LiClO4 deposited on top of the devices not only substantially reduces the contact resistance but also boost the channel mobility, leading up to three-orders-of-magnitude enhancement of the field-effect mobility of the device. When the polymer electrolyte is used as a gate medium, the MoS2 field-effect transistors exhibit excellent device characteristics such as a near ideal subthreshold swing and an on/off ratio of 106 as a result of the strong gate-channel coupling.Comment: 17 pages, 4 figures, accepted by J. Phys.

A π-conjugated inorganic polymer constructed from boron difluoride formazanates and platinum(II) diynes

The first example of a π-conjugated polymer incorporating boron difluoride (BF2) formazanates is introduced. The film-forming properties, controllable reduction chemistry, and low optical band gap (ca. 1.4 eV) of the polymer make it an excellent candidate for use as a light-harvesting n-type semiconductor in organic electronics. Comparison of the polymer to model compounds confirmed that its unique optoelectronic properties can be directly attributed to the presence of the BF2 formazanate repeat unit and that the [Pt(PBu3)2]2+ unit must also be present to achieve the narrow band gaps observed

Association of ultra-rare coding variants with genetic generalized epilepsy: a case-control whole exome sequencing study

OBJECTIVE: We aimed to identify genes associated with genetic generalized epilepsy (GGE) by combining large cohorts enriched with individuals with a positive family history. Secondarily, we set out to compare the association of genes independently with familial and sporadic GGE. METHODS: We performed a case-control whole exome sequencing study in unrelated individuals of European descent diagnosed with GGE (previously recruited and sequenced through multiple international collaborations) and ancestry-matched controls. The association of ultra-rare variants (URVs; in 18 834 protein-coding genes) with epilepsy was examined in 1928 individuals with GGE (vs. 8578 controls), then separately in 945 individuals with familial GGE (vs. 8626 controls), and finally in 1005 individuals with sporadic GGE (vs. 8621 controls). We additionally examined the association of URVs with familial and sporadic GGE in two gene sets important for inhibitory signaling (19 genes encoding γ-aminobutyric acid type A [GABA(A)] receptors, 113 genes representing the GABAergic pathway). RESULTS: GABRG2 was associated with GGE (p = 1.8 × 10(-5)), approaching study-wide significance in familial GGE (p = 3.0 × 10(-6)), whereas no gene approached a significant association with sporadic GGE. Deleterious URVs in the most intolerant subgenic regions in genes encoding GABA(A) receptors were associated with familial GGE (odds ratio [OR] = 3.9, 95% confidence interval [CI] = 1.9-7.8, false discovery rate [FDR]-adjusted p = .0024), whereas their association with sporadic GGE had marginally lower odds (OR = 3.1, 95% CI = 1.3-6.7, FDR-adjusted p = .022). URVs in GABAergic pathway genes were associated with familial GGE (OR = 1.8, 95% CI = 1.3-2.5, FDR-adjusted p = .0024) but not with sporadic GGE (OR = 1.3, 95% CI = .9-1.9, FDR-adjusted p = .19). SIGNIFICANCE: URVs in GABRG2 are likely an important risk factor for familial GGE. The association of gene sets of GABAergic signaling with familial GGE is more prominent than with sporadic GGE

Selected reactive oxygen species and antioxidant enzymes in common bean after Pseudomonas syringae pv. phaseolicola and Botrytis cinerea infection

Phaseolus vulgaris cv. Korona plants were inoculated with the bacteria Pseudomonas syringae pv. phaseolicola (Psp), necrotrophic fungus Botrytis cinerea (Bc) or with both pathogens sequentially. The aim of the experiment was to determine how plants cope with multiple infection with pathogens having different attack strategy. Possible suppression of the non-specific infection with the necrotrophic fungus Bc by earlier Psp inoculation was examined. Concentration of reactive oxygen species (ROS), such as superoxide anion (O2 -) and H2O2 and activities of antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT) and peroxidase (POD) were determined 6, 12, 24 and 48 h after inoculation. The measurements were done for ROS cytosolic fraction and enzymatic cytosolic or apoplastic fraction. Infection with Psp caused significant increase in ROS levels since the beginning of experiment. Activity of the apoplastic enzymes also increased remarkably at the beginning of experiment in contrast to the cytosolic ones. Cytosolic SOD and guaiacol peroxidase (GPOD) activities achieved the maximum values 48 h after treatment. Additional forms of the examined enzymes after specific Psp infection were identified; however, they were not present after single Bc inoculation. Subsequent Bc infection resulted only in changes of H2O2 and SOD that occurred to be especially important during plant–pathogen interaction. Cultivar Korona of common bean is considered to be resistant to Psp and mobilises its system upon infection with these bacteria. We put forward a hypothesis that the extent of defence reaction was so great that subsequent infection did not trigger significant additional response

An experimental and numerical investigation of the use of liquid flow in serpentine microchannels for microelectronics cooling

This paper presents a combined experimental and numerical investigation of single-phase water flow and heat transfer in serpentine rectangular microchannels embedded in a heated copper block. The performance of four different microchannel heat sink (MCHS) configurations are investigated experimentally, the first having an array of straight rectangular microchannels (SRMs), while the other have single (SPSMs), double (DPSMs) and triple path multi-serpentine rectangular microchannels (TPSMs). Three-dimensional conjugate heat transfer models are developed for both laminar and turbulent single-phase water flows in each of these MCHSs and the governing flow and energy equations solved numerically using finite elements. The numerical predictions of pressure drop (∆P) and average Nusselt number (〖Nu〗_avg) are in good agreement with experimental data, and indicated that the single path serpentine microchannel (SPSM) leads to a 35% enhancement of the 〖Nu〗_avg at a volumetric flow rate of 0.5 l/min and a 19% reduction in total thermal resistance (R_th) compared to the conventional SRM heat sink. However, this enhancement is at the expense of a large (up to ten-fold) increase in ∆P compared to the SRM heat sink, so that a suitable compromise must be struck between heat transfer and pressure drop in practical MCHS designs

Whole-exome sequencing in undiagnosed genetic diseases: interpreting 119 trios

Purpose: Despite the recognized clinical value of exome-based diagnostics, methods for comprehensive genomic interpretation remain immature. Diagnoses are based on known or presumed pathogenic variants in genes already associated with a similar phenotype. Here, we extend this paradigm by evaluating novel bioinformatics approaches to aid identification of new gene–disease associations. Methods: We analyzed 119 trios to identify both diagnostic genotypes in known genes and candidate genotypes in novel genes. We considered qualifying genotypes based on their population frequency and in silico predicted effects we also characterized the patterns of genotypes enriched among this collection of patients. Results: We obtained a genetic diagnosis for 29 (24%) of our patients. We showed that patients carried an excess of damaging de novo mutations in intolerant genes, particularly those shown to be essential in mice (P = 3.4 × 10−8). This enrichment is only partially explained by mutations found in known disease-causing genes. Conclusion: This work indicates that the application of appropriate bioinformatics analyses to clinical sequence data can also help implicate novel disease genes and suggest expanded phenotypes for known disease genes. These analyses further suggest that some cases resolved by whole-exome sequencing will have direct therapeutic implications