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Abstract To accelerate the practical application of water splitting in alkaline media, it is imperative to enhance the electrocatalytic performance for the Hydrogen Evolution Reaction (HER). In this context, we demonstrate that a simple (one‐pot, one‐step) electrodeposition process of nickel (Ni) in the presence of 3,5‐diamino1,2,4‐triazole (DAT) results in the formation of fractally structured Ni films with a significantly increased surface area. The Electrochemically active surface area (ECSA) increases with the electrodeposition charge passed, with the film electrodeposited at 14 C cm−2 achieving a reduction in overpotential at −10 mA cm−2 (η10) to 65.7 mV, coupled with a remarkable increase in ECSA (114‐fold greater than that of Ni‐foil). Additionally, nickel deposited in the presence of DAT effectively mitigates deactivation during electrolysis, exhibiting a 3.6‐fold lower overpotential degradation compared to that of the smooth Ni foil. This simple electrodeposition technique, applicable to a variety of conductive substrates, is distinguished by its high catalytic performance in the HER, a feature of considerable significance.

Metal-free hydrogen-bonding conductive polymer catalysts (HCPCs) are emerging alternatives to platinum-group-metals (PGMs) for electrocatalytic hydrogen evolution reaction (HER). In this study, electrodes coated with poly-neutral red (PNR) films were fabricated by oxidative chemical vapor deposition (oCVD) and electropolymerization deposition (EPD) to study their activities as HER-electrocatalysts in acidic media. PNR (EPD) exhibited a superior performance, i.e., an overpotential of 194 mV (at 10 mA cm−2) owing to a high exchange current density of 0.711 mA cm−2. The activity is substantiated by spectroelectrochemical measurements and time-dependent density functional theory (TDDFT) calculation unveiling a doubly reduced and doubly protonated PNRH2 as the reaction intermediate for the evolution of H2. It resulted in a first-order kinetic constant of k = 9.98 × 10−4 s−1 to indicate a slow dissociation of PNRH2 to release H2. Large Tafel slope of 176 mV dec−1 also limits the electrocatalytic activity of PNR.

We often come across differences in the severity of androgenetic alopecia (AGA) as assessed subjectively by the patients themselves and objectively by the attending physicians. For the purpose of examining the differences in the assessment of AGA between patients and physicians, we presented the Norwood classification to male patients and the Shiseido classification to female patients and asked them to assess the degree of hair loss by themselves. We compared the results with the severity as assessed by 2 specified dermatologists. The results show that the assessments of the severity of AGA were consistent between the patients and physicians in 42% (15/36) of cases, the physicians reported a higher grade of severity than the patients themselves in 30% (11/36) of cases, and the patients reported a higher grade of severity than the physicians in 28% (10/36) of cases; however, the Wilcoxon signed rank statistical analysis showed no significant difference between the patients and physicians assessments. AGA should be treated in accordance with individual symptoms and wishes and not a standardized treatment protocol.

The inwardly rectifying potassium (Kir) channel Kir4.1 in brain astrocytes mediates spatial K+ buffering and regulates neural activities. Recent studies have shown that loss-of-function mutations in the human gene KCNJ10 encoding Kir4.1 cause epileptic seizures, suggesting a close relationship between the Kir4.1 channel function and epileptogenesis. Here, we performed expressional analysis of Kir4.1 in a pilocarpine-induced rat model of temporal lobe epilepsy (TLE) to explore the role of Kir4.1 channels in modifyingTLE epileptogenesis. Treatment of rats with pilocarpine (350 mg/kg, i.p.) induced acute status epilepticus, which subsequently caused spontaneous seizures 7-8 weeks after the pilocarpine treatment. Western blot analysis revealed thatTLE rats (interictal condition) showed significantly higher levels of Kir4.1 than the control animals in the cerebral cortex, striatum, and hypothalamus. However, the expression of other Kir subunits, Kir5.1 and Kir2.1, remained unaltered. Immunohistochemical analysis illustrated that Kir4.1-immunoreactivity-positive astrocytes in the pilocarpine-induced TLE model were markedly increased in most of the brain regions examined, concomitant with an increase in the number of glial fibrillary acidic protein (GFAP)-positive astrocytes. In addition, Kir4.1 expression ratios relative to the number of astrocytes (Kir4.1-positive cells/GFAP-positive cells) were region-specifically elevated in the amygdala (i.e., medial and cortical amygdaloid nuclei) and sensory cortex. The present study demonstrated for the first time that the expression of astrocytic Kir4.1 channels was elevated in a pilocarpine-induced TLE model, especially in the amygdala, suggesting that astrocytic Kir4.1 channels play a role in modifying TLE epileptogenesis, possibly by acting as an inhibitory compensatory mechanism. [ABSTRACT FROM AUTHOR]