A Highly Sensitive and Stretchable Core-Shell Fiber Sensor for Gesture Recognition and Surface Pressure Distribution Monitoring.

This work reports a highly-strain flexible fiber sensor with a core-shell structure utilizes a unique swelling diffusion technique to infiltrate carbon nanotubes (CNTs) into the surface layer of Ecoflex fibers. Compared with traditional blended Ecoflex/CNTs fibers, this manufacturing process ensures that the sensor maintains the mechanical properties (923% strain) of the Ecoflex fiber while also improving sensitivity (gauge factor is up to 3716). By adjusting the penetration time during fabrication, the sensor can be customized for different uses. As an application demonstration, the fiber sensor is integrated into the glove to develop a wearable gesture language recognition system with high sensitivity and precision. Additionally, the authors successfully monitor the pressure distribution on the curved surface of a soccer ball by winding the fiber sensor along the ball's surface.

Digital mapping of surface turbulence status and aerodynamic stall on wings of a flying aircraft.

Real-time monitoring of flow turbulence is very difficult but extremely important in fluid dynamics, which plays an important role in flight safety and control. Turbulence can cause airflow to detach at the end of the wings, potentially resulting in the aerodynamic stall of aircraft and causing flight accidents. Here, we developed a lightweight and conformable system on the wing surface of aircraft for stall sensing. Quantitative data about airflow turbulence and the degree of boundary layer separation are provided in situ using conjunct signals provided by both triboelectric and piezoelectric effects. Thus, the system can visualize and directly measure the airflow detaching process on the airfoil, and senses the degree of airflow separation during and after a stall for large aircraft and unmanned aerial vehicles.

Fractal structured charge-excitation triboelectric nanogenerators for powering portable electronic devices.

Effective power management on the outputs of triboelectric nanogenerators (TENGs) is critical for their practical applications due to the large impedance and unbalanced load matching. Recently proposed voltage multiplying circuits for external-charge excitation and self-charge excitation are usually unstable and require reversal for device restarting and common switched-capacitor-converters usually cause large switching losses. In this work, we fabricated a fractal structured charge-excitation circuit for TENGs using diodes and capacitors. The fractal switched-capacitor-converter coupled with voltage regulator diodes can greatly boost the output charge and current of the TENG without reverse starting. The managed output performance of the TENG can be controlled by the electronic component parameters and external operating frequency. Through the component and condition optimization, the fractal structured charge-excitation TENG (FSC-TENG) can achieve nearly 5.8 times charge boosting and almost 16.8 times power boosting in the pulsed mode. Furthermore, the FSC-TENG successfully drove a hygrothermograph and was integrated into a yoga mat for harvesting human-body motion energy to power an electronic watch and a pedometer. The FSC-TENG with good charge accumulation properties and stability is a promising candidate for practical self-powered applications.

Upregulation of renal sodium transporters in D5 dopamine receptor-deficient mice.

D(5) dopamine receptor (D(5)R)-deficient (D(5)(-/-)) mice have hypertension that is aggravated by an increase in sodium intake. The present experiments were designed to test the hypothesis that a dysregulation of renal sodium transporters is related to the salt sensitivity in D(5)(-/-) mice. D(5)R was expressed in the renal proximal tubule, thick ascending limb, distal convoluted tubule, and cortical and outer medullary collecting ducts in D(5)(+/+) mice. On a control Na(+) diet, renal protein expressions of NKCC2 (sodium-potassium-2 chloride cotransporter), sodium chloride cotransporter, and alpha and gamma subunits of the epithelial sodium channel were greater in D(5)(-/-) than in D(5)(+/+) mice. Renal renin abundance and urine aldosterone levels were similar but renal angiotensin II type 1 receptor (AT(1)R) protein expression was increased in D(5)(-/-) mice. An elevated Na(+) diet increased further the elevated blood pressure of D(5)(-/-) mice but did not affect the normal blood pressure of D(5)(+/+) mice. The increased levels of NKCC2, sodium chloride cotransporter, and alpha and gamma subunits of the epithelial sodium channel persisted with the elevated Na(+) diet and unaffected by chronic AT(1)R blockade (losartan) in D(5)(-/-) mice. The expressions of proximal sodium transporters NHE3 (sodium hydrogen exchanger type 3) and NaPi2 (sodium phosphate cotransporter type 2) were increased by the elevated Na(+) diet in D(5)(-/-) mice; the increased expression of NHE3 but not NaPi2 was abolished by AT(1)R blockade. Our findings suggest that the increased protein expression of sodium transporters/channels in distal nephron segments may be the direct consequence of the disruption of D(5)R, independent of the renin-angiotensin aldosterone system.

G protein-coupled receptor kinase 4 (GRK4) regulates the phosphorylation and function of the dopamine D3 receptor.

During conditions of moderate sodium excess, the dopaminergic system regulates blood pressure and water and electrolyte balance by engendering natriuresis. Dopamine exerts its effects on dopamine receptors, including the dopamine D(3) receptor. G protein-coupled receptor kinase 4 (GRK4), whose gene locus (4p16.3) is linked to essential hypertension, desensitizes the D(1) receptor, another dopamine receptor. This study evaluated the role of GRK4 on D(3) receptor function in human proximal tubule cells. D(3) receptor co-segregated in lipid rafts and co-immunoprecipitated and co-localized in human proximal tubule cells and in proximal and distal tubules and glomeruli of kidneys of Wistar Kyoto rats. Bimolecular fluorescence complementation and confocal microscopy revealed that agonist activation of the receptor initiated the interaction between D(3) receptor and GRK4 at the cell membrane and promoted it intracellularly, presumably en route to endosomal trafficking. Of the four GRK4 splice variants, GRK4-gamma and GRK4-alpha mediated a 3- and 2-fold increase in the phosphorylation of agonist-activated D(3) receptor, respectively. Inhibition of GRK activity with heparin or knockdown of GRK4 expression via RNA interference completely abolished p44/42 phosphorylation and mitogenesis induced by D(3) receptor stimulation. These data demonstrate that GRK4, specifically the GRK4-gamma and GRK4-alpha isoforms, phosphorylates the D(3) receptor and is crucial for its signaling in human proximal tubule cells.

Renal D3 dopamine receptor stimulation induces natriuresis by endothelin B receptor interactions.

Dopaminergic and endothelin systems participate in the control blood pressure by regulating sodium transport in the renal proximal tubule. Disruption of either the endothelin B receptor (ETB) or D(3) dopamine receptor gene in mice produces hypertension. To examine whether these two receptors interact we studied the Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) rats by selectively infusing reagents into the right kidney of anesthetized rats. The D(3) receptor agonist (PD128907) caused natriuresis in WKY rats which was partially blocked by the ETB receptor antagonist. In contrast, PD128907 blunted sodium excretion in the SHRs. We found using laser confocal microscopy that the ETB receptor was mainly located in the cell membrane in control WKY cells. Treatment with the D(3) receptor antagonist caused its internalization into intracellular compartments that contained the D(3) receptors. Combined use of D(3) and ETB antagonists failed to internalize ETB receptors in cells from WKY rats. In contrast in SHR cells, ETB receptors were found mainly in internal compartments under basal condition and thus were likely prevented from interacting with the agonist-stimulated, membrane-bound D(3) receptors. Our studies suggest that D(3) receptors physically interact with proximal tubule ETB receptors and that the blunted natriuretic effect of dopamine in SHRs may be explained, in part, by abnormal D(3)/ETB receptor interactions.

Dysregulation of dopamine-dependent mechanisms as a determinant of hypertension: studies in dopamine receptor knockout mice.

Dopamine plays an important role in the pathogenesis of hypertension by regulating epithelial sodium transport and by interacting with vasoactive hormones/humoral factors, such as aldosterone, angiotensin, catecholamines, endothelin, oxytocin, prolactin pro-opiomelancortin, reactive oxygen species, renin, and vasopressin. Dopamine receptors are classified into D(1)-like (D(1) and D(5)) and D(2)-like (D(2), D(3), and D(4)) subtypes based on their structure and pharmacology. In recent years, mice deficient in one or more of the five dopamine receptor subtypes have been generated, leading to a better understanding of the physiological role of each of the dopamine receptor subtypes. This review summarizes the results from studies of various dopamine receptor mutant mice on the role of individual dopamine receptor subtypes and their interactions with other G protein-coupled receptors in the regulation of blood pressure.

Dopamine D1-like receptor-mediated inhibition of Cl/HCO3- exchanger activity in rat intestinal epithelial IEC-6 cells is regulated by G protein-coupled receptor kinase 6 (GRK 6).

The present study investigated the effect of dopamine D1-like receptor stimulation on the Cl-/HCO3- exchange activity in rat intestinal epithelial IEC-6 cells. The Cl-/HCO3- exchange activity was found to be a chloride-dependent, DIDS-sensitive and niflumate-insensitive process. The presence of the SLC26A6 anion exchanger was detected by both RT-PCR and immunoblotting analysis in IEC-6 cells, in which three different small interfering RNAs (siRNAs) targeting SLC26A6 markedly inhibited Cl-/HCO3- exchange. Activation of dopamine D1-like receptors with SKF 38393 inhibited Cl-/HCO3- exchanger activity, this being antagonized by the D1 selective antagonist SKF 83566. However, effects of SKF 38393 were maximal at 5 min of exposure to the agonist and rapidly diminished with no effect at 15 min, suggestive of agonist-induced desensitization of D1-like receptors. Pretreatment of cells with heparin, a non-selective inhibitor of G protein-coupled receptor kinases (GRKs), prevented the observed attenuation of SKF 38393-induced inhibition of Cl-/HCO3- exchange. Overnight pretreatment with anti-GRK6A and anti-GRK6B, but not with anti-GRK4 antibodies, prevented the loss of SKF 38393-mediated effects. Both PKA and PKC signaling pathways participate in SKF 38393-mediated inhibition of Cl-/HCO3- exchange. These findings suggest that SLC26A6 is at least one of the anion exchanger's family members responsible for Cl-/HCO3- exchange in IEC-6 cells. Dopamine D1 receptors in IEC-6 rapidly desensitize to D1-like agonist stimulation and GRK 6, but not GRK 4, appear to be involved in agonist-mediated responsiveness and desensitization.

Amelioration of genetic hypertension by suppression of renal G protein-coupled receptor kinase type 4 expression.

Abnormalities in D1 dopamine receptor function in the kidney are present in some types of human essential and rodent genetic hypertension. We hypothesize that increased activity of G protein-coupled receptor kinase type 4 (GRK4) causes the impaired renal D1 receptor function in hypertension. We measured renal GRK4 and D1 and serine-phosphorylated D1 receptors and determined the effect of decreasing renal GRK4 protein by the chronic renal cortical interstitial infusion (4 weeks) of GRK4 antisense oligodeoxynucleotides (As-Odns) in conscious- uninephrectomized spontaneously hypertensive rats (SHRs) and their normotensive controls, Wistar-Kyoto (WKY) rats. Basal GRK4 expression and serine-phosphorylated D1 receptors were &90% higher in SHRs than in WKY rats and were decreased to a greater extent in SHRs than in WKY rats with GRK4 As-Odns treatment. Basal renal D1 receptor protein was similar in both rat strains. GRK4 As-Odns, but not scrambled oligodeoxynucleotides, increased sodium excretion and urine volume, attenuated the increase in arterial blood pressure with age, and decreased protein excretion in SHRs, effects that were not observed in WKY rats. These studies provide direct evidence of a crucial role of renal GRK4 in the D1 receptor control of sodium excretion and blood pressure in genetic hypertension.

Perturbation of D1 dopamine and AT1 receptor interaction in spontaneously hypertensive rats.

The dopaminergic and renin-angiotensin systems interact to regulate blood pressure. Because this interaction may be perturbed in genetic hypertension, we studied D1 dopamine and AT1 angiotensin receptors in immortalized renal proximal tubule (RPT) and A10 aortic vascular smooth muscle cells. In normotensive Wistar-Kyoto (WKY) rats, the D1-like agonist fenoldopam increased D1 receptors but decreased AT1 receptors. These effects were blocked by the D1-like antagonist SCH 23390 (10(-7) mol/L per 24 hours). In spontaneously hypertensive rat (SHR) RPT cells, fenoldopam also decreased AT1 receptors but no longer stimulated D1 receptor expression. Basal levels of AT1/D1 receptor coimmunoprecipitation were greater in WKY RPT cells (29+/-2 density units, DU) than in SHR RPT cells (21+/-2 DU, n=7 per group, P<0.05). The coimmunoprecipitation of D1 and AT1 receptors was increased by fenoldopam (10(-7) mol/L per 24 hours) in WKY RPT cells but decreased in SHR RPT cells. The effects of fenoldopam in RPT cells from WKY rats were similar in aortic vascular smooth muscle cells from normotensive BD IX rats, that is, fenoldopam decreased AT1 receptors and increased D1 receptors. Our studies show differential regulation of the expression of D1 and AT1 receptors in RPT cells from WKY and SHR. This regulation and D1/AT1 receptor interaction are different in RPT cells of WKY and SHR. An altered interaction of D1 and AT1 receptors may play a role in the impaired sodium excretion and enhanced vasoconstriction in hypertension.