scholarly journals Characteristic Flows on Signed Graphs and Short Circuit Covers

10.37236/4872 ◽  
2016 ◽  
Vol 23 (3) ◽  
Author(s):  
Edita Máčajová ◽  
Martin Škoviera

We generalise to signed graphs a classical result of Tutte [Canad. J. Math. 8 (1956), 13—28] stating that every integer flow can be expressed as a sum of characteristic flows of circuits. In our generalisation, the rôle of circuits is taken over by signed circuits of a signed graph which occur in two types — either balanced circuits or pairs of disjoint unbalanced circuits connected with a path intersecting them only at its ends. As an application of this result we show that a signed graph $G$ admitting a nowhere-zero $k$-flow has a covering with signed circuits of total length at most $2(k-1)|E(G)|$.

2020 ◽  
Vol 92 (2) ◽  
pp. 20901
Author(s):  
Abdul Kuddus ◽  
Md. Ferdous Rahman ◽  
Jaker Hossain ◽  
Abu Bakar Md. Ismail

This article presents the role of Bi-layer anti-reflection coating (ARC) of TiO2/ZnO and back surface field (BSF) of V2O5 for improving the photovoltaic performance of Cadmium Sulfide (CdS) and Cadmium Telluride (CdTe) based heterojunction solar cells (HJSCs). The simulation was performed at different concentrations, thickness, defect densities of each active materials and working temperatures to optimize the most excellent structure and working conditions for achieving the highest cell performance using obtained optical and electrical parameters value from the experimental investigation on spin-coated CdS, CdTe, ZnO, TiO2 and V2O5 thin films deposited on the glass substrate. The simulation results reveal that the designed CdS/CdTe based heterojunction cell offers the highest efficiency, η of ∼25% with an enhanced open-circuit voltage, Voc of 0.811 V, short circuit current density, Jsc of 38.51 mA cm−2, fill factor, FF of 80% with bi-layer ARC and BSF. Moreover, it appears that the TiO2/ZnO bi-layer ARC, as well as ETL and V2O5 as BSF, could be highly promising materials of choice for CdS/CdTe based heterojunction solar cell.


2004 ◽  
Vol 286 (5) ◽  
pp. G814-G821 ◽  
Author(s):  
Bi-Guang Tuo ◽  
Jimmy Y. C. Chow ◽  
Kim E. Barrett ◽  
Jon I. Isenberg

PKC has been shown to regulate epithelial Cl- secretion in a variety of models. However, the role of PKC in duodenal mucosal bicarbonate secretion is less clear. We aimed to investigate the role of PKC in regulation of duodenal mucosal bicarbonate secretion. Bicarbonate secretion by murine duodenal mucosa was examined in vitro in Ussing chambers using a pH-stat technique. PKC isoform expression and activity were assessed by Western blotting and in vitro kinase assays, respectively. PMA (an activator of PKC) alone had no effect on duodenal bicarbonate secretion or short-circuit current ( Isc). When PMA and dibutyryl-cAMP (db-cAMP) were added simultaneously, PMA failed to alter db-cAMP-stimulated duodenal bicarbonate secretion or Isc ( P > 0.05). However, a 1-h preincubation with PMA potentiated db-cAMP-stimulated duodenal bicarbonate secretion and Isc in a concentration-dependent manner (from 10-8 to 10-5M) ( P < 0.05). PMA preincubation had no effects on carbachol- or heat-stable toxin-stimulated bicarbonate secretion. Western blot analysis revealed that PKCα, -γ, -ϵ, -θ, -μ, and -ι/λ were expressed in murine duodenal mucosa. Ro 31–8220 (an inhibitor active against PKCϵ, -α, -β, and -γ), but not Gö 6983 (an inhibitor active against PKCα, -γ, -β, and -δ), reversed the potentiating effect of PMA on db-cAMP-stimulated bicarbonate secretion. PMA also time- and concentration-dependently increased the activity of PKCϵ, an effect that was prevented by Ro 31–8220 but not Gö 6983. These results demonstrate that activation of PKC potentiates cAMP-stimulated duodenal bicarbonate secretion, whereas it does not modify basal secretion. The effect of PKC on cAMP-stimulated bicarbonate secretion is mediated by the PKCϵ isoform.


2012 ◽  
Vol 303 (9) ◽  
pp. C936-C946 ◽  
Author(s):  
Veronika Gondzik ◽  
Wolf Michael Weber ◽  
Mouhamed S. Awayda

The mammalian collecting duct (CD) is continuously exposed to urinary proteases. The CD expresses an epithelial Na+ channel (ENaC) that is activated after cleavage by serine proteases. ENaC also exists at the plasma membrane in the uncleaved form, rendering activation by extracellular proteases an important mechanism for regulating Na+ transport. Many exogenous and a small number of endogenous extracellular serine proteases have been shown to activate the channel. Recently, kallikrein 1 (KLK1) was shown to increase γENaC cleavage in the native CD indicating a possible direct role of this endogenous protease in Na+ homeostasis. To explore this process, we examined the coordinated effect of this protease on Na+ and Cl− transport in a polarized renal epithelial cell line (Madin-Darby canine kidney). We also examined the role of native urinary proteases in this process. Short-circuit current ( Isc) was used to measure transport of these ions. The Isc exhibited an ENaC-dependent Na+ component that was amiloride blockable and a cystic fibrosis transmembrane conductance regulator (CFTR)-dependent Cl− component that was blocked by inhibitor 172. Apical application of trypsin, an exogenous S1 serine protease, activated IENaC but was without effects on ICFTR. Subtilisin an exogenous S8 protease that mimics endogenous furin-type proteases activated both currents. A similar activation was also observed with KLK1 and native rat urinary proteases. Activation with urinary proteases occurred within minutes and at protease concentrations similar to those in the CD indicating physiological significance of this process. ENaC activation was irreversible and mediated by enhanced cleavage of γENaC. The activation of CFTR was indirect and likely dependent on activation of an endogenous apical membrane protease receptor. Collectively, these data demonstrate coordinated stimulation of separate Na+ and Cl− transport pathways in renal epithelia by extracellular luminal proteases. They also indicate that baseline urinary proteolytic activity is sufficient to modify Na+ and Cl− transport in these epithelia.


1990 ◽  
Vol 258 (3) ◽  
pp. G432-G439 ◽  
Author(s):  
Y. Z. Wang ◽  
H. J. Cooke ◽  
H. C. Su ◽  
R. Fertel

We tested the hypothesis that the role of histamine in the control of intestinal secretion is mediated by prostaglandins (PGs). The effects of histamine on ion transport were examined in muscle-stripped sheets of mucosa/submucosa set up in flux chambers. Histamine evoked a transient concentration-dependent increase in short-circuit current (Isc) that was reduced by the Cl- transport inhibitor bumetanide. Histamine also caused the release of PGE2. The Isc response to histamine was reduced by indomethacin and piroxicam, which block PG formation, but not by nordihydroguaiaretic acid, which prevents production of lipoxygenase products. 2-Methylhistamine, but not dimaprit, evoked a concentration-dependent increase in Isc. The Isc response to histamine was reduced by the H1-blocker pyrilamine, but not by the H2-antagonist cimetidine. In addition to its direct effect, histamine augmented the responses of endogenously released neurotransmitters with and without indomethacin and hexamethonium. Tetrodotoxin (TTX) reduced the Isc response to 10(-3) M histamine. In the presence of TTX, exogenous histamine amplified the responses to PGs, vasoactive intestinal polypeptide, 2-chloroadenosine, bethanechol, and carbachol. These results suggest that histamine acts at H1-receptors on cells within the gut to mediate intestinal Cl- secretion in part by releasing PGs and by augmenting the actions of endogenously released neurotransmitters. Our results indicate that histamine has a role in the regulation of colonic transport function.


Author(s):  
Andrew J. Nickerson ◽  
Trey S. Rottgen ◽  
Vazhaikkurichi M. Rajendran

KV7 (KCNQ) K+ channels are expressed in many neuronal populations, and play an important role in regulating membrane potential by generating a hyper-polarizing K+ current and decreasing cell excitability. However, the role of KV7 channels in the neural regulation of intestinal epithelial Cl- secretion is not known. Cl- secretion in mouse distal colon was measured as a function of short circuit current (ISC), while pharmacological approaches were used to test the hypothesis that activation of KV7 channels in enteric neurons would inhibit epithelial Cl- secretion. Flupirtine, a non-selective KV7 activator, inhibited basal Cl- secretion in mouse distal colon and abolished or attenuated the effects of drugs that target various components of enteric neurotransmission, including tetrodotoxin (NaV channel blocker), Veratridine (NaV channel activator), Nicotine (nicotinic acetylcholine receptor agonist) and Hexamethonium (nicotinic antagonist). In contrast, flupritine did not block the response to epithelium-targeted agents VIP (endogenous VPAC receptor ligand) or carbachol (non-selective cholinergic agonist). Flupirtine inhibited Cl- secretion in both full-thickness and seromuscular-stripped distal colon (containing the submucosal, but not myenteric plexus), but generated no response in epithelial T84 cell monolayers. KV7.2 and KV7.3 channel proteins were detected by immunofluorescence in whole-mount preparations of the submucosa from mouse distal colon. ICA 110381 (KV7.2/7.3 specific activator) inhibited Cl- secretion comparably to flupirtine. We conclude that KV7 channel activators inhibit neurally-driven Cl- secretion in the colonic epithelium, and may therefore have therapeutic benefit in treating pathologies associated with hyper-excitable enteric nervous system, such as irritable bowel syndrome with diarrhea (IBS-D).


1980 ◽  
Vol 239 (6) ◽  
pp. G536-G542
Author(s):  
R. Schiessel ◽  
A. Merhav ◽  
J. B. Matthews ◽  
L. A. Fleischer ◽  
A. Barzilai ◽  
...  

In in vitro bullfrog fundic mucosa inhibited with 10(-3) M metiamide and exposed to a luminal pH of 2 a progressive slow decline in potential difference (PD) and short-circuit current (Isc) and a rise in resistance (R) were observed when the nutrient solution (N) contained 18 mM HCO3(-), but these changes were restored by an N containing 50 mM HCO3(-). Substitution of PO4(3-) or N-tris(hydroxymethyl)-methyl-2-aminoethanesulfonic acid for NHO3(-) in N caused a rapid drop in PD and Isc in inhibited tissues, changes that could be prevented by 10(-4) M histamine. Ulceration occurred more frequently in metiamide-inhibited gastric sacs exposed to artificial gastric juice with an N of 18 mMHCO3(-) than with 50 mM HCO3(-), but histamine prevented ulceration in the 18 mM HCO3(-) solution. JnetCl approximated Isc under most experimental conditions in inhibited mucosa and was reduced dramatically as were both Jn leads to sCl and Js leads to nCl when HCO3(-) was removed from N. In histamine-stimulated tissues, removal of nutrient HCO3(-) did not influence Cl- transport. Our results are consistent with the proposal that HCO3(-) in N supports normal Cl- flux and that the alkaline tide of actively secreting oxyntic cells can do the same in the absence of ambient HCO3(-).


2019 ◽  
Vol 970 ◽  
pp. 75-81
Author(s):  
Alexey Zavgorodniy ◽  
Aitbek Aimukhanov ◽  
Assylbek Zeinidenov ◽  
Galina Vavilova

The role of spin states in the process of charge carrier transport in copper phthalocyanine (CuPc) nanowires has been established. According to the data obtained, CuPc nanowires are in the η-phase. The current-voltage characteristics (IVC) of a photosensitive cell based on CuPc nanowires in a magnetic field are investigated. As a result of experiments, it was found that applying an external magnetic field, the spins of two positively charged polarons are oriented in one direction. The channel of formation of the bipolaron is blocked. As a result, a decrease in the short-circuit current of the photosensitive cell is observed by more than 61%.


2018 ◽  
Vol 67 ◽  
pp. 01021 ◽  
Author(s):  
Istighfari Dzikri ◽  
Michael Hariadi ◽  
Retno Wigajatri Purnamaningsih ◽  
Nji Raden Poespawati

Research in solar cells is needed to maximize Indonesia’s vast solar potential that can reach up to 207.898 MW with an average radiation of 4.8 kWh/m2/day. Organometallic perovskite solar cells (PSCs) have gained immense attention due to their rapid increase in efficiency and compatibility with low-cost fabrication methods. Understanding the role of hole transport layer is very important to obtain highly efficient PSCs. In this work, we studied the effect of Hole Transport Layer (HTL) to the performance of perovskite solar cell. The devices with HTL exhibit substantial increase in power conversion efficiency, open circuit voltage and short circuit current compared to the device without HTL. The best performing device is PSC with CuSCN as HTL layer, namely Voc of 0.24, Isc of 1.79 mA, 0.27 FF and efficiency of 0.09%.


1999 ◽  
Vol 276 (1) ◽  
pp. G28-G36 ◽  
Author(s):  
Anthony T. Blikslager ◽  
Malcolm C. Roberts ◽  
Robert A. Argenzio

We have previously shown that PGI2 and PGE2 have a synergistic role in restoring electrical transepithelial resistance ( R) in ischemia-injured porcine ileum via the second messengers Ca2+ and cAMP. Because Ca2+ and cAMP stimulate Cl− secretion, we assessed the role of PG-induced Cl−secretion in recovery of R. Mucosa from porcine ileum subjected to ischemia for 45 min was mounted in Ussing chambers and bathed in indomethacin and Ringer solution. Addition of PGs stimulated a twofold increase in R, which was preceded by elevations in short-circuit current (increase of 25 μA/cm2). The PG-induced effect on R was partially inhibited with bumetanide, an inhibitor of Cl− secretion. The remaining elevations in R were similar in magnitude to those induced in ischemic tissues by amiloride, an inhibitor of Na+ absorption. Treatment with 10−4 M 8-bromo-cGMP or 300 mosM mucosal urea resulted in elevations in R similar to those attained with PG treatment. PGs signal recovery of Rvia induction of Cl−secretion and inhibition of Na+absorption, possibly by establishing a transmucosal osmotic gradient.


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