Asymmetric Supercapacitive Characteristics of PANI Embedded Holey Graphene Nanoribbons

In the present study, graphene oxide nanoribbons (GONR) and reduced graphene oxide nanoribbons (RGONR) supported polyaniline (PANI) nanocomposites are synthesized via an <i>in situ</i> chemical polymerization method and investigated for supercapacitor electrodes. Electrochemical studies performed by cyclic voltammetry and galvanostatic charge–discharge (GCD) measurements suggest that both nanocomposites possess enhanced specific capacitance (<i>C</i>_sp as 740 F/g for GONR/PANI and 1180 F/g for RGONR/PANI at 5 mV/s). GONR/PANI and RGONR/PANI nanocomposites show good rate capability with high <i>C</i>_sp upon increasing the current density from 2 to 20 A/g in GCD measurements, approximately 55% decay in <i>C</i>_sp value of the nanocomposites is observed compared to pristine PANI (∼70%). The undertaken study signifies enhanced electrical and electrochemical properties of GONR/RGONR supported PANI nanocomposites due to a synergistic effect of GONR/RGONR and PANI. Furthermore, asymmetric devices are fabricated using GONR/RGONR as the negative electrode, while GONR/PANI and RGONR/PANI are used as the positive electrode, which exhibit significant enhancement in energy density and device performance

Additional file 1: Table S1. of Disorders of sex development: insights from targeted gene sequencing of a large international patient cohort

DSD gene variants. Each variant found in a diagnostic gene (after the filtering and curation process) is shown. In some cases where the gene is inherited in an autosomal recessive manner, two variants are grouped together. Inheritance has been indicated where familial samples were available: negative indicates negative for variant and N/A sample not available. De novo events have only been noted where both parental samples were available and found to be negative for the change. Previously reported refers to a variant being described in either ClinVar, HGMD, or a publication in a peer-reviewed journal via a PubMed search. Variants were classified consistent with previous MPS publications of DSD cohorts [8, 10] which were based on ACMG guidelines [15]. VUS were called for three reasons: 1 = fits phenotype but predicted to be benign; 2 = damaging but doesn’t fit phenotype; or 3 = variant in the AR repetitive region. Patients marked with an asterisk were identified to have two or more diagnostic gene variants. Null variants (frameshifts, splice sites mutations, and premature stop codons) are shown in bold. Patients have been classified based on clinical notes provided, according to the recommended classification of DSD in the Chicago consensus report. Classifications: CGD complete gonadal dysgenesis, DASA disorders of androgen synthesis or action, DSD DSD of “unknown” origin; hypospadias, LCH Leydig cell hypoplasia, OT ovotesticular DSD, PGD partial gonadal dysgenesis, PMDS persistent Müllerian duct syndrome; syndromic, T testicular DSD. Related affected individuals are indicated. File is in Excel spreadsheet format. (XLSX 47 kb