Kv Currents Research Articles

Tannic Acid Modulates Voltage-gated K+ Channels to Promote Neuritogenesis in Neuronal N2A Cells.

In a previous report, we showed that voltage-gated K+ (Kv) Kv1 and Kv2 channels are involved in cAMP-induced neuritogenesis of mouse neuronal N2A cells. In this report, we examined the effects of tannic acid (TA) on Kv channels and neuritogenesis in N2A cells. TA (15 μM) mildly enhanced Kv currents at -30 to -20 mV but strongly inhibited Kv currents at higher voltages, causing a preferential activation of currents at low voltages. When enhancement and suppression of Kv currents (at -20 and +70 mV, respectively) by different concentrations of TA were analyzed, TA at 4 μM produced strong enhancement at -20 mV with relatively mild suppression at + 70 mV. TA (4 μM) also promoted neuritogenesis; such promotion was suppressed by a Kv channel blocker tetraethylammonium ion, or a combination of hongotoxin-1 (blocker of Kv1.1), UK 78282 (blocker of Kv1.4) and guangxitoxin 1E (blocker of Kv2.1). Our results demonstrate, for the first time, TA at low concentrations could modulate Kv channels and thereby promote neuritogenesis.

Blockade of Voltage-Gated K+ Channels in Rabbit Coronary Arterial Smooth Muscle Cells by the Antipsychotic Drug Zotepine.

Zotepine is a second-generation antipsychotic that demonstrates significant efficacy in antagonizing D2 and 5-HT2A receptors. Although clinical investigations have shown that administering zotepine is associated with an increased prevalence of hyperglycemia and a heightened risk of cardiovascular disease, the side effects of zotepine on voltage-gated K+ (Kv) channels have not been established. Zotepine suppressed the vascular Kv channels in rabbit coronary arterial smooth muscle cells in a concentration-dependent manner, with an IC50 of 5.3 ± 0.4 μM and a Hill coefficient of 1.6 ± 0.2. The decay rate of inactivation was significantly accelerated by zotepine. Applying zotepine (10 μM) shifted the steady-state inactivation curve in a negative direction. Applying train pulses at 1 and 2 Hz resulted in a progressive increase in blockage of the Kv currents by zotepine. Furthermore, zotepine prolonged the recovery time from inactivation. Although pretreatment with the Kv2.1 subtype inhibitor stromatoxin-1 and the Kv7 subtype inhibitor linopirdine did not change the degree of zotepine-induced inhibition of Kv currents, pretreatment with the Kv1.5 channel inhibitor DPO-1 decreased the inhibitory effects of zotepine on Kv currents. Zotepine also induced membrane depolarization. These results indicate that zotepine inhibits Kv currents (mainly Kv1.5 subtype) in dose-, time-, and use (state)-dependent manners by changing the steady-state inactivation curve.

Melatonin inhibits voltage-gated potassium KV4.2 channels and negatively regulates melatonin secretion in rat pineal glands.

Melatonin is synthesized in and secreted from the pineal glands and regulates circadian rhythms. Although melatonin has been reported to modulate the activity of ion channels in several tissues, its effects on pineal ion channels remain unclear. In the present study, the effects of melatonin on voltage-gated K+ (KV) channels, which play a role in regulating the resting membrane potential, were examined in rat pinealocytes. The application of melatonin reduced pineal KV currents in a concentration-dependent manner (IC50 = 309 µM). An expression analysis revealed that KV4.2 channels were highly expressed in rat pineal glands. Melatonin-sensitive currents were abolished by the small interfering RNA knockdown of KV4.2 channels in rat pinealocytes. In human embryonic kidney 293 (HEK293) cells expressing KV4.2 channels, melatonin decreased outward currents (IC50 = 479 µM). Inhibitory effects were mediated by a shift in the voltage dependence of steady-state inactivation in a hyperpolarizing direction. This inhibition was observed even in the presence of 100 nM luzindole, an antagonist of melatonin receptors. Melatonin also blocked the activity of KV4.3, KV1.1, and KV1.5 channels in reconstituted HEK293 cells. The application of 1 mM melatonin caused membrane depolarization in rat pinealocytes. Furthermore, KV4.2 channel inhibition by 5 mM 4-aminopyridine attenuated melatonin secretion induced by 1 µM noradrenaline in rat pineal glands. These results strongly suggest that melatonin directly inhibited KV4.2 channels and caused membrane depolarization in pinealocytes, resulting in a decrease in melatonin secretion through parasympathetic signaling pathway. This mechanism may function as a negative-feedback mechanism of melatonin secretion in pineal glands. NEW & NOTEWORTHY Melatonin is a hormone that is synthesized in and secreted from the pineal glands, which regulates circadian rhythms. However, the effects of melatonin on pineal ion channels remain unclear. The present study demonstrated that melatonin directly inhibited voltage-gated potassium KV4.2 channels, which are highly expressed in rat pinealocytes, and induced membrane depolarization, resulting in a decrease in melatonin secretion. This mechanism may function as a negative-feedback mechanism of melatonin secretion in pineal glands.

Second-generation antipsychotic quetiapine blocks voltage-dependent potassium channels in coronary arterial smooth muscle cells.

Voltage-dependent K+ (Kv) channels play an important role in restoring the membrane potential to its resting state, thereby maintaining vascular tone. In this study, native smooth muscle cells from rabbit coronary arteries were used to investigate the inhibitory effect of quetiapine, an atypical antipsychotic agent, on Kv channels. Quetiapine showed a concentration-dependent inhibition of Kv channels, with an IC50 of 47.98 ± 9.46 μM. Although quetiapine (50 μM) did not alter the steady-state activation curve, it caused a negative shift in the steady-state inactivation curve. The application of 1 and 2Hz train steps in the presence of quetiapine significantly increased the inhibition of Kv current. Moreover, the recovery time constants from inactivation were prolonged in the presence of quetiapine, suggesting that its inhibitory action on Kv channels is use (state)-dependent. The inhibitory effects of quetiapine were not significantly affected by pretreatment with Kv1.5, Kv2.1, and Kv7 subtype inhibitors. Based on these findings, we conclude that quetiapine inhibits Kv channels in both a concentration- and use (state)-dependent manner. Given the physiological significance of Kv channels, caution is advised in the use of quetiapine as an antipsychotic due to its potential side effects on cardiovascular Kv channels.

Kv3.1 Interaction with UBR5 Is Required for Chronic Inflammatory Pain.

Chronic inflammatory pain caused by neuronal hyperactivity is a common and refractory disease. Kv3.1, a member of the Kv3 family of voltage-dependent K+ channels, is a major determinant of the ability of neurons to generate high-frequency action potentials. However, little is known about its role in chronic inflammatory pain. Here, we show that although Kv3.1 mRNA expression was unchanged, Kv3.1 protein expression was decreased in the dorsal spinal horn of mice after plantar injection of complete Freund's adjuvant (CFA), a mouse model of inflammatory pain. Upregulating Kv3.1 expression alleviated CFA-induced mechanical allodynia and heat hyperalgesia, whereas downregulating Kv3.1 induced nociception-like behaviors. Additionally, we found that ubiquitin protein ligase E3 component n-recognin 5 (UBR5), a key factor in the initiation of chronic pain, binds directly to Kv3.1 to drive its ubiquitin degradation. Intrathecal injection of the peptide TP-CH-401, a Kv3.1 ubiquitination motif sequence, rescued the decrease in Kv3.1 expression and Kv currents through competitive binding to UBR5, and consequently attenuated mechanical and thermal hypersensitivity. These findings demonstrate a previously unrecognized pathway of Kv3.1 abrogation by UBR5 and indicate that Kv3.1 is critically involved in the regulation of nociceptive behavior. Kv3.1 is thus a promising new target for treating inflammatory pain.

Simulation investigations of an efficient L-band bi-frequency MILO with ridged-disk-loaded interaction structure

This article presents simulation studies of an L-band bi-frequency magnetically insulated line oscillator for its efficiency enhancement using a ridged-disk-loaded radio frequency (RF) interaction structure. The electromagnetic (EM) properties of the RF interaction structure implemented with conventional and ridged disk have been investigated with the aid of CST microwave studio suite. A comparative study between the EM properties of conventional slow-wave structures and ridged-slow-wave structures (RSWS) is presented. The impact of adding ridges at the tip of disks has been examined for its influence on the dispersion curve, phase velocity, and coupling impedance. The coupling impedance of the RSWS with ridged-disk-loaded vanes was found to be greater than that of the conventional SWS. Furthermore, influence on output power of the device is observed for different ridge's parameters. With the optimum dimension of ridge parameters, particle-in-cell simulation detects an high-power microwave at frequencies of 1.20 and 1.40 GHz, producing 3.8 GW of cumulative peak RF power with a conversion efficiency of 23.8%, when operated with a 420 kV input DC voltage and current of 38 kA.

Design, modelling and experiments on a multisource energy harvester based on a single ferroelectric ceramic

Abstract Energy harvesting is a promising technique that can provide renewable and clean energy for the wireless sensor nodes. However, the solar, mechanical and thermal energies in our living environment are not always available due to the day/night, the weather and working conditions. Therefore, energy harvesting for a single energy source cannot provide a stable and continuous energy supply. Here, a multisource energy harvester based on a single material/structure (PLZT-Sb) is presented for scavenging solar, thermal, and mechanical energies simultaneously or individually. And then the output energy mathematical model is established and proved experimentally. The enhanced energy generations with the peak voltage of 1.9kV and peak current of 200nA are achieved by the unique integration of multi-effects, which can drive 139 LEDs. This work demonstrates an innovative approach for developing multisource energy harvester in a single ferroelectric material on the basis of the coupled multi-physics fields.

Testosterone Enhances KV Currents and Airway Smooth Muscle Relaxation Induced by ATP and UTP through P2Y4 Receptors and Adenylyl Cyclase Pathway.

Numerous studies suggest the involvement of adenosine-5'-triphosphate (ATP) and similar nucleotides in the pathophysiology of asthma. Androgens, such as testosterone (TES), are proposed to alleviate asthma symptoms in young men. ATP and uridine-5'-triphosphate (UTP) relax the airway smooth muscle (ASM) via purinergic P2Y2 and P2Y4 receptors and K+ channel opening. We previously demonstrated that TES increased the expression of voltage-dependent K+ (KV) channels in ASM. This study investigates how TES may potentiate ASM relaxation induced by ATP and UTP. Tracheal tissues treated with or without TES (control group) from young male guinea pigs were used. In organ baths, tracheas exposed to TES (40 nM for 48 h) showed enhanced ATP- and UTP-evoked relaxation. Tetraethylammonium, a K+ channel blocker, annulled this effect. Patch-clamp experiments in tracheal myocytes showed that TES also increased ATP- and UTP-induced K+ currents, and this effect was abolished with flutamide (an androgen receptor antagonist). KV channels were involved in this phenomenon, which was demonstrated by inhibition with 4-aminopyridine. RB2 (an antagonist of almost all P2Y receptors except for P2Y2), as well as N-ethylmaleimide and SQ 22,536 (inhibitors of G proteins and adenylyl cyclase, respectively), attenuated the enhancement of the K+ currents induced by TES. Immunofluorescence and immunohistochemistry studies revealed that TES did not modify the expression of P2Y4 receptors or COX-1 and COX-2, while we have demonstrated that this androgen augmented the expression of KV1.2 and KV1.5 channels in ASM. Thus, TES leads to the upregulation of P2Y4 signaling and KV channels in guinea pig ASM, enhancing ATP and UTP relaxation responses, which likely limits the severity of bronchospasm in young males.

Inhibition of voltage-gated potassium channel by aripiprazole in rabbit coronary arterial smooth muscle cells

Aripiprazole, a third-generation antipsychotic, has been widely used to treat schizophrenia. In this study, we evaluated the effect of aripiprazole on voltage-gated potassium (Kv) channels in rabbit coronary arterial smooth muscle cells using the patch clamp technique. Aripiprazole reduced the Kv current in a concentration-dependent manner with a half-maximal inhibitory concentration of 0.89 ± 0.20 μM and a Hill coefficient of 1.30 ± 0.25. The inhibitory effect of aripiprazole on Kv channels was voltage-dependent, and an additional aripiprazole-induced decrease in the Kv current was observed in the voltage range of full channel activation. The decay rate of Kv channel inactivation was accelerated by aripiprazole. Aripiprazole shifted the steady-state activation curve to the right and the inactivation curve to the left. Application of a repetitive train of pulses (1 and 2 Hz) promoted inhibition of the Kv current by aripiprazole. Furthermore, the recovery time constant from inactivation increased in the presence of aripiprazole. Pretreatment of Kv1.5 subtype inhibitor reduced the inhibitory effect of aripiprazole. However, pretreatment with Kv 7 and Kv2.1 subtype inhibitors did not change the degree of aripiprazole-induced inhibition of the Kv current. We conclude that aripiprazole inhibits Kv channels in a concentration-, voltage-, time-, and use (state)-dependent manner by affecting the gating properties of the channels.

Performance improvement studies of axially partitioned dual band magnetically insulated line oscillator

In magnetically insulated line oscillator (MILO)s, a proportion of device current is responsible for the self-generated magnetic field that aids electron flow confinement in the anode cathode gap, thereby suitable RF generation. The device currents should not be high due to its direct impact on device efficiency, and electron energy depositions at load can lead to anode plasma formation. Also, the lower currents can facilitate the device to operate at larger voltages and/or for longer operational times. In this article, couple of axially partitioned dual band MILOs (DBMILO) designs that operate at lower device currents in comparison with the existing axially partitioned DBMILOs in the literature is presented. For one design with the radius of the slow wave structure (SWS), i.e., RSWS = 40 mm, the injection of the DC electron beam parameters 505 kV and 49 kA, generated an output RF power of ∼5.8 GW oscillating at 3.71 and 10.16 GHz (S-and X- bands) concurrently with ∼23.8% conversion efficiency. However, the other design (RSWS = 40.6 mm) at beam voltage 505 kV and device current of 47 kA generated an output RF power of >3.85 GW oscillating at 3.5 and 10.5 GHz, concurrently, where the frequencies are harmonically related. Thus, the proposed designs yielded significant device current reduction to ∼47 and ∼49 kA from ∼56 kA (existed), respectively, thereby drop of 16% and 12.5% to its counter designs, respectively. Also, there is substantial reduction in the electron energy depositions, thus the occurrence of anode plasma formations. Moreover, the peak conversion efficiency is enhanced to 23.4% and 16.4%, from 12.8%.

Characterisation of GFAP-Expressing Glial Cells in the Dorsal Root Ganglion after Spared Nerve Injury.

Satellite glial cells (SGCs), enveloping primary sensory neurons' somas in the dorsal root ganglion (DRG), contribute to neuropathic pain upon nerve injury. Glial fibrillary acidic protein (GFAP) serves as an SGC activation marker, though its DRG satellite cell specificity is debated. We employed the hGFAP-CFP transgenic mouse line, designed for astrocyte studies, to explore its expression within the peripheral nervous system (PNS) after spared nerve injury (SNI). We used diverse immunostaining techniques, Western blot analysis, and electrophysiology to evaluate GFAP+ cell changes. Post-SNI, GFAP+ cell numbers increased without proliferation, and were found near injured ATF3+ neurons. GFAP+ FABP7+ SGCs increased, yet 75.5% of DRG GFAP+ cells lacked FABP7 expression. This suggests a significant subset of GFAP+ cells are non-myelinating Schwann cells (nmSC), indicated by their presence in the dorsal root but not in the ventral root which lacks unmyelinated fibres. Additionally, patch clamp recordings from GFAP+ FABP7-cells lacked SGC-specific Kir4.1 currents, instead displaying outward Kv currents expressing Kv1.1 and Kv1.6 channels specific to nmSCs. In conclusion, this study demonstrates increased GFAP expression in two DRG glial cell subpopulations post-SNI: GFAP+ FABP7+ SGCs and GFAP+ FABP7- nmSCs, shedding light on GFAP's specificity as an SGC marker after SNI.

Inhibition of voltage-dependent K+ currents of rabbit coronary arterial smooth muscle cells by the atypical antipsychotic paliperidone.

Paliperidone, an atypical antipsychotic, is widely used to treat schizophrenia. In this study, we explored whether paliperidone inhibited the voltage-dependent K+ (Kv) channels of rabbit coronary arterial smooth muscle cells. Paliperidone reduced Kv channel activity in a concentration-dependent manner with a half-maximal inhibitory concentration (IC50 ) of 16.58 ± 3.03 μM and a Hill coefficient of 0.60 ±0.04. It did not significantly shift the steady-state activation or inactivation curves, suggesting that the drug did not affect the gating properties of Kv channels. In the presence of paliperidone, the application of 20 repetitive depolarizing pulses at 1 and 2Hz gradually increased the inhibition of the Kv current. Further, the recovery time constant after Kv channel inactivation was increased by paliperidone, indicating that it inhibited the Kv channel in a use (state)-dependent manner. Its inhibitory effects were reduced by pretreatment with a Kv1.5 subtype inhibitor. However, pretreatment with a Kv2.1 or Kv7 inhibitor did not reduce its inhibitory effect. We conclude that paliperidone inhibits Kv channels (mainly Kv1.5 subtype channels) in a concentration- and use (state)-dependent manner without changing channel gating.

Kv2.1 Channels Prevent Vasomotion and Safeguard Myogenic Reactivity in Rat Small Superior Cerebellar Arteries.

Vascular smooth muscle voltage-gated potassium (Kv) channels have been proposed to contribute to myogenic autoregulation. Surprisingly, in initial experiments, we observed that the Kv2 channel inhibitor stromatoxin induced vasomotion without affecting myogenic tone. Thus, we tested the hypothesis that Kv2 channels contribute to myogenic autoregulation by fine-tuning the myogenic response. Expression of Kv2 channel mRNA was determined using real-time PCR and 'multiplex' single-cell RT-PCR. Potassium currents were measured using the patch-clamp technique. Contractile responses of intact arteries were studied using isobaric myography. Expression of Kv2.1 but not Kv2.2 channels was detected in intact rat superior cerebellar arteries and in single smooth muscle cells. Stromatoxin, a high-affinity inhibitor of Kv2 channels, reduced smooth muscle Kv currents by 61% at saturating concentrations (EC50 36 nmol/L). Further, stromatoxin (10-100 nmol/L) induced pronounced vasomotion in 48% of the vessels studied. In vessels not exhibiting vasomotion, stromatoxin did not affect myogenic reactivity. Notably, in vessels exhibiting stromatoxin-induced vasomotion, pressure increases evoked two effects: First, they facilitated the occurrence of random vasodilations and/or vasoconstrictions, disturbing the myogenic response (24% of the vessels). Second, they modified the vasomotion by decreasing its amplitude and increasing its frequency, thereby destabilizing myogenic tone (76% of the vessels). Our study demonstrates that (i) Kv2.1 channels are the predominantly expressed Kv channels in smooth muscle cells of rat superior cerebellar arteries, and (ii) Kv2.1 channels provide a novel type of negative feedback mechanism in myogenic autoregulation by preventing vasomotion and thereby safeguarding the myogenic response.

Receptor-specific contributions of caveolae, PKC, and Src tyrosine kinase to serotonergic and adrenergic regulation of Kv channels and vasoconstriction

AimsCaveolae are invaginated, Ω-shaped membrane structures. They are now recognized as portals for signal transduction of multiple chemical and mechanical stimuli. Notably, the contribution of caveolae has been reported to be receptor-specific. However, details of how they differentially contribute to receptor signaling remain unclear. Main methodsUsing isometric tension measurements, patch-clamping, and western blotting, we examined the contribution of caveolae and their related signaling pathways to serotonergic (5-HT2A receptor-mediated) and adrenergic (α1-adrenoceptor-mediated) signaling in rat mesenteric arteries. Key findingsDisruption of caveolae by methyl-β-cyclodextrin effectively blocked vasoconstriction mediated by the 5-HT2A receptor (5-HT2AR), but not by the α1-adrenoceptor. Caveolar disruption selectively impaired 5-HT2AR-mediated voltage-dependent K+ channel (Kv) inhibition, but not α1-adrenoceptor-mediated Kv inhibition. In contrast, both serotonergic and α1-adrenergic effects on vasoconstriction, as well as Kv currents, were similarly blocked by the Src tyrosine kinase inhibitor PP2. However, inhibition of protein kinase C (PKC) by either GO6976 or chelerythrine selectively attenuated the effects mediated by the α1-adrenoceptor, but not by 5-HT2AR. Disruption of caveolae decreased 5-HT2AR-mediated Src phosphorylation, but not α1-adrenoceptor-mediated Src phosphorylation. Finally, the PKC inhibitor GO6976 blocked Src phosphorylation by the α1-adrenoceptor, but not by 5-HT2AR. Significance5-HT2AR-mediated Kv inhibition and vasoconstriction are dependent on caveolar integrity and Src tyrosine kinase, but not on PKC. In contrast, α1-adrenoceptor-mediated Kv inhibition and vasoconstriction are not dependent on caveolar integrity, but rather on PKC and Src tyrosine kinase. Caveolae-independent PKC is upstream of Src activation for α1-adrenoceptor-mediated Kv inhibition and vasoconstriction.

The novel KV7 channel activator URO-K10 exerts enhanced pulmonary vascular effects independent of the KCNE4 regulatory subunit

KV7 channels exert a pivotal role regulating vascular tone in several vascular beds. In this context, KV7 channel agonists represent an attractive strategy for the treatment of pulmonary arterial hypertension (PAH). Therefore, in this study, we have explored the pulmonary vascular effects of the novel KV7 channel agonist URO-K10. Consequently, the vasodilator and electrophysiological effects of URO-K10 were tested in rat and human pulmonary arteries (PA) and PA smooth muscle cells (PASMC) using myography and patch-clamp techniques. Protein expression was also determined by Western blot. Morpholino-induced knockdown of KCNE4 was assessed in isolated PA. PASMC proliferation was measured by BrdU incorporation assay. In summary, our data show that URO-K10 is a more effective relaxant of PA than the classical KV7 activators retigabine and flupirtine. URO-K10 enhanced KV currents in PASMC and its electrophysiological and relaxant effects were inhibited by the KV7 channel blocker XE991. The effects of URO-K10 were confirmed in human PA. URO-K10 also exhibited antiproliferative effects in human PASMC. Unlike retigabine and flupirtine, URO-K10-induced pulmonary vasodilation was not affected by morpholino-induced knockdown of the KCNE4 regulatory subunit. Noteworthy, the pulmonary vasodilator efficacy of this compound was considerably increased under conditions mimicking the ionic remodelling (as an in vitro model of PAH) and in PA from monocrotaline-induced pulmonary hypertensive rats. Taking all together, URO-K10 behaves as a KCNE4-independent KV7 channel activator with much increased pulmonary vascular effects compared to classical KV7 channel activators. Our study identifies a promising new drug in the context of PAH.

Evaluation of the Image Quality of Ultra-Low-Dose Paranasal Sinus Computed Tomography Scans

Objective: We aimed to investigate the image quality of paranasal sinus computed tomography (CT) scans obtained with the “Advanced intelligent Clear-IQ Engine” (AICE) software and ultra-low dose parameters in patients with prediagnosed rhinitis, sinusitis or nasal septum deviation. Methods: The first 50 patients (31 men and 19 women, aged 18-70 years) who agreed to participate in our prospectively planned study were included in the study. Imaging of the patients was performed with a 160-slice multidetector CT device Canon Aquilion Prime SP (Canon Medical Systems, Otawara, Japan). Tube voltage of 80 kV and tube current of 40 mA were chosen. The effective radiation dose (ED) was calculated based on the “dose-length product” (DLP) information of each patient. Evaluation of images was made on reformat images made with “AiCE Bone” filter in the axial and coronal planes. All images were double-blindly evaluated by 2 radiologists out of 5 points (5 = very good; 1 = not diagnostic). The visibility of 17 bilateral important anatomical landmarks examined on paranasal sinus CT was scored (0 = not visible; 2 = completely visible). In the evaluation of images, the agreement between radiologists was evaluated with Kappa statistics. Results: The median ED value of the CT protocol was 0.015±0.001 mSv [range 0.012-0.017 mSv]. The overall image quality of the images in our study was interpreted as 4 (good) or 3 (moderate) for all patients. Inter-research agreement was 92%. Most of the anatomical landmarks evaluated were completely visible. Six (bilateral of three) anatomical landmarks could be partially visible in some patients. Conclusion: Combining the ultra-low dose CT protocol and the AiCE reconstruction algorithm makes it possible to achieve very low ED values ​​in paranasal sinus CT scans and still obtain sufficient image quality in indications such as septum deviation and sinusitis.

Design and experimental results of a 28 GHz, 400 kW gyrotron for electron cyclotron resonance heating

A high-power 28 GHz gyrotron has been successfully developed at the Institute of Applied Electronics, China Academy of Engineering Physics. This gyrotron was designed for electron cyclotron resonance heating (ECRH) in the spherical tokamak XL-50. A diode magnetron injection gun was designed to produce the required gyrating electron beam. The gyrotron operates in the TE8,3 mode in a cylindrical open cavity. An internal quasi-optical mode converter was designed to convert the operating mode into a fundamental Gaussian wave beam and separate the spent electron beam from the outgoing microwave power. A tube has been built and successfully tested. The operational frequency of the tube is 28.1 GHz. For beam parameters at an accelerating voltage of 71 kV and beam current of 16 A, the gyrotron has delivered an output power of 400 kW, with a pulse length of 5 s. The output efficiency is about 50% with a single-stage depressed collector. The gyrotron has been installed on the XL-50 and has played an important role in the ECRH experiments.

The Quantitative Effect of Noise and Object Diameter on Low-Contrast Detectability of AAPM CT Performance Phantom Images

Parameters for determining computed tomography (CT) image quality include noise and low-contrast detectability. Studies on low-contrast detectability using the AAPM CT performance phantom have several limitations, such as the absence of quantitative information on the effect of noise and object size on low-contrast detectability. In this study, the quantitative effect of noise and object diameter on low-contrast detectability were investigated. Images of the American Association of Physicists in Medicine (AAPM) CT performance phantom model 610 were acquired with a tube voltage of 120 kV and tube currents of 50, 100, 150, and 200 mA. The low-contrast section of the AAPM CT performance phantom model 610 has objects with diameters between 2.5 and 7.5 mm. We analysed the mean CT number, noise level, signal-to noise ratio (SNR), and contrast-to-noise ratio (CNR), acquired using MatLab software. The results obtained indicate that noise and object size affect low-contrast detectability. The CNRs increase linearly with increasing of object diameter with R2 of 0.88, 0.67, 0.75, and 0.83 for tube currents of 50, 100, 150 and 200 mA, respectively.

An elliptical beam-tunnel sine waveguide slow wave structure for G-band elliptical beam traveling wave tube

In order to improve the performance of sine waveguide (SW) traveling wave tube (TWT), an elliptical beam-tunnel sine waveguide (EBTSW) slow wave structure (SWS) is proposed. EBTSW-SWS not only has high interaction impedance in a relatively wide frequency band but also has an elliptical beam-tunnel. The simulation results of high-frequency characteristics show that, under the same dispersion, the passband of EBTSW-SWS increases by 30% compared to the SW-SWS, and the average interaction impedance of EBTSW-SWS is higher than that of SW-SWS in almost the whole passband. Moreover, the particle-in-cell (PIC) simulation results reveal that under the operating voltage of 20.8 kV and beam current of 150 mA, EBTSW-TWT can provide more than 70 W of saturated output power in the frequency range of 200-260 GHz, reaching the maximum power of 151 W at 220 GHz with the maximum electronic efficiency of 4.85%.

Splitting CO2 in Intense Pulsed Plasma Jets.

The splitting of CO2 was studied in a pulsed plasma discharge produced in a coaxial gun at voltages between ~1 and 2 kV and peak discharge currents of 7 to 14 kA. The plasma was ejected from the gun at a speed of a few km/s and had electron temperatures between 11 and 14 eV with peak electron densities ~2.4 × 1021 particles m-3. Spectroscopic measurements were carried out in the plasma plume produced at pressures between 1 and 5 Torr, and evidence of CO2 dissociation into oxygen and CO was found. An increased discharge current led to the observation of more intense spectra lines and the presence of new oxygen lines, which implies more dissociation channels. Several dissociation mechanisms are discussed, the main candidate being the splitting of the molecule by direct electron impact. Estimates of dissociation rates are made based on measured plasma parameters and interaction cross-sections available in the literature. A possible application of this technique is in future Mars missions where the coaxial plasma gun running in the atmosphere could be able to produce oxygen at a rate of the order of over 100 g per hour in a highly repetitive regime.