The analysis of protein biomarkers is of great importance in the diagnosis of diseases. Although many convenient and low-cost electrochemical approaches have been extensively investigated, they are not sensitive enough in the detection of protein biomarkers with low concentrations in physiological environments. Here, this study reports a novel organic-electrochemical-transistor-based biosensor that can successfully detect cancer protein biomarkers with ultrahigh sensitivity. The devices are operated by detecting electrochemical activity on gate electrodes, which is dependent on the concentrations of proteins labeled with catalytic nanoprobes. The protein sensors can specifically detect a cancer biomarker, human epidermal growth factor receptor 2, down to the concentration of 10 g mL , which is several orders of magnitude lower than the detection limits of previously reported electrochemical approaches. Moreover, the devices can successfully differentiate breast cancer cells from normal cells at various concentrations. The ultrahigh sensitivity of the protein sensors is attributed to the inherent amplification function of the organic electrochemical transistors. This work paves a way for developing highly sensitive and low-cost biosensors for the detection of various protein biomarkers in clinical analysis in the future.

Chitosan has been widely studied for use in many areas, such as for its applications in the biomedical, engineering and pharmaceutical fields, as well as in industry, because of its unique properties, including biodegradability, antimicrobial activity, polycationic nature and biocompatibility. Thanks to the rapid development of materials science, chitosan applications are now possible in textiles. However, there are still many limitations of chitosan fibers in terms of their high electrostaticity, poor mechanical properties and high cost, which are obstacles that inhibit potential applications of chitosan fiber in the industry. Generally, in order to achieve the best performance with chitosan and enhance its commercial value, chitosan fibers are usually blended with long cotton fibers in the textile industry. Therefore, based on preliminary experiments and feedback from the industry, this study was carried out to further investigate the relationship between fiber length, fiber interaction and yarn performance. The results of this study would therefore help to reduce the production cost of yarns with the blending parameters used and also expand the utilization and applications beyond medical applications to fashion-based functional wear. The sliver-blending method offers better tensile properties of yarn samples, while the fiber-blending method offers higher uniformity of fiber distribution. This study would help to reduce the production cost of yarns by blending and also to expand the utilization and application not limited to fashion-based functional wear.

ATP-sensitive K(+) channels (K(ATP)) couple the intermediary metabolism to cellular excitability and play an important role in the cardio-protective effect of ischemic preconditioning and the activity-dependent autoregulation of cerebral circulation. Although previous studies using PCR and Northern blot suggest that the vascular isoform may consist of Kir6.1 and SUR2B, their expression and precise distribution in various vasculatures remain unknown. To illustrate their vascular expression, we performed this study using in situ hybridization histochemistry. Antisense riboprobes were synthesized by in vitro transcription and labeled with digoxigenin. Distributions of these mRNAs in the various blood vessels were revealed under a bright-field microscope. The expression of Kir6.1 and SUR2B mRNAs was observed in small and intermediate arteries as well as arterioles in several tissues, including basilar, vertebral, mesenteric, coronary and renal arteries. The transcripts were found in arterial smooth muscles. Also, we observed Kir6.1/SUR2B expression in capillary beds. The Kir6.1 and SUR2B expression pattern showed clear overlap, suggesting that they may form heteromeric K(ATP) channels in these tissues. The Kir6.1 and SUR2B stains were detected in aorta and renal tubular cells although their expression level was extremely low. In contrast, the Kir6.1 and SUR2B mRNAs were not seen in vena cava, other small veins, myocardium and skeletal muscles. With their strong expression in small arteries and capillaries, it is very likely that the Kir6.1 and SUR2B form the vascular isoform of K(ATP) channels in these vasculatures.

The static and dynamic behavior of a developed electrothermal fabric was studied using an electrothermal model that considers the following fabric parameters: thermal conductivity coefficient, specific heat capacitance, fabric mass, and initial temperature. An experiment was set up to measure the average temperature of the knitted fabric of ordinary materials, namely wool, cotton, and acrylic. These materials were knitted with silver-coated conductive yarns in three loop densities each at an applied electric power of 4 W. The calculated coefficient of determination is greater than 0.98, and the fit standard error is smaller than 1.11. Therefore, the analytical equation could accurately model the electrothermal characteristics of the thermal fabrics under an applied electric current and compute the temperature at a certain time for the same fabric using known parameters.

Synaptic cleft acidification occurs following vesicle release. Such a pH change may affect synaptic transmissions in which G-protein-coupled inward rectifier K ؉ (GIRK) channels play a role. To elucidate the effect of extracellular pH (pH o ) on GIRK channels, we performed experiments on heteromeric GIRK1/GIRK4 channels expressed in Xenopus oocytes. A decrease in pH o to 6.2 augmented GIRK1/GIRK4 currents by ϳ30%. The channel activation was reversible and dependent on pH o levels. This effect was produced by selective augmentation of single channel conductance without change in the open-state probability. To determine which subunit was involved, we took advantage of homomeric expression of GIRK1 and GIRK4 by introducing a single mutation. We found that homomeric GIRK1-F137S and GIRK4-S143T channels were activated at pH o 6.2 by ϳ20 and ϳ70%, respectively. Such activation was eliminated when a histidine residue in the M1-H5 linker was mutated to a non-titratable glutamine, i.e. H116Q in GIRK1 and H120Q in GIRK4. Both of these histidines were required for pH sensing of the heteromeric channels, because the mutation of one of them diminished but not abolished the pH o sensitivity. The pH o sensitivity of the heteromeric channels was completely lost when both were mutated. Thus, these results suggest that the GIRK-mediated synaptic transmission is determined by both neurotransmitter and protons with the transmitter accounting for only 70% of the effect on postsynaptic cell and protons released together with the transmitter contributing to the other 30%.The G-protein-coupled inward rectifier K ϩ (GIRK) 1 channels are important players in cellular communications in several excitable tissues (1-3). The GIRK channels are activated by ␤␥-subunits of G-proteins, which are dissociated from the ␣␤␥-trimer as a result of receptor binding to neurotransmitters or hormones (3). Four members of GIRK channels have been identified in mammals with GIRK1/GIRK4 expressed abundantly in the heart and brain (4).GIRK channels are modulated by several intracellular signal molecules such as Na ϩ , ATP, and phospholipids (5-12). Extracellular molecules including hormones, neurotransmitters, and integrins directly or indirectly modulate GIRK channel activity through signaling transduction pathways (13-18). GIRK channels are also the major targets of ethanol, anesthetics, and opioids (19 -23). Another potentially important modulator of the GIRK channels is hydrogen ion. Increasing evidence indicates that H ϩ can act as a messenger modulating multiple cellular functions (24). In the central nervous system, protons have been shown to modulate synaptic transmission, neuronal plasticity, and membrane excitability (25). It is known that the pH level in synaptic vesicles is ϳ1.5 pH units lower than in cytosol (26). These protons are released from synaptic vesicles together with neurotransmitters during synaptic transmission, leading to extracellular acidification in the synaptic cleft (27). If the GIRK channels are sensitive to extracellular pH (pH...