Helical Strips Research Articles

A novel miniature monopole tag antenna for passive UHF RFID applications

A novel miniature monopole tag antenna for passive Ultra-High Frequency (UHF) radio frequency identification (RFID) operation is presented.The antenna possesses a two-sided structure that is printed on an FR4 substrate and fed by a 50-Ω microstrip line. By properly using helical strips and vias, the antenna size can be reduced to a small volume of 10 (L) × 9.5 (W) × 0.8 (H) mm3 to be easily integrated within various portable devices. A miniaturized quasi-lumped circuit is also designed to attain a good impedance matching between the antenna and the chip. Experimental results demonstrate that the antenna has a suitable operating band about 914–939 MHz and also quite omnidirectional radiation pattern with appreciable gain. Moreover, the proposed compact tag antenna, capable of achieving a maximum readable range of about 5.6 m with an EIRP equal to 4 W, is well suited for RFID applications. © 2010 Wiley Periodicals, Inc. Microwave Opt Technol Lett 52:2770–2772, 2010; View this article online at wileyonlinelibrary.com. DOI 10.1002/mop.25596

Novel Miniature Monopole Tag Antenna for UHF RFID Applications

A novel miniature monopole tag antenna for passive UHF radio frequency identification (RFID) operation is presented. The antenna possesses a two-sided structure that is printed on an FR4 substrate and fed by a 50-? microstrip line. By properly using helical strips and vias, the antenna size can be reduced to a small volume of 10 (L) × 9.5 (W) × 0.8 (H) mm3 to be easily integrated within various portable devices. A miniaturized quasi-lumped circuit is also designed to achieve a good impedance matching between the antenna and the tag chip. Experimental results demonstrate that the antenna has a suitable operating band about 914-939 MHz and also nearly omnidirectional radiation patterns with proper gain. Moreover, the proposed compact tag antenna, capable of achieving a maximum readable range about 5.6 m with an effective isotropic radiated power (EIRP) equal to 4 W, is well suitable for RFID applications.

Thromboxane A2-induced Bi-directional Regulation of Cerebral Arterial Tone

Myosin light chain phosphatase plays a critical role in modulating smooth muscle contraction in response to a variety of physiologic stimuli. A downstream target of the RhoA/Rho-kinase and nitric oxide (NO)/cGMP/cyclic GMP-dependent kinase (cGKI) pathways, myosin light chain phosphatase activity reflects the sum of both calcium sensitization and desensitization pathways through phosphorylation and dephosphorylation of the myosin phosphatase targeting subunit (MYPT1). As cerebral blood flow is highly spatio-temporally modulated under normal physiologic conditions, severe perturbations in normal cerebral blood flow, such as in cerebral vasospasm, can induce neurological deficits. In nonpermeabilized cerebral vessels stimulated with U-46619, a stable mimetic of endogenous thromboxane A2 implicated in the etiology of cerebral vasospasm, we observed significant increases in contractile force, RhoA activation, regulatory light chain phosphorylation, as well as phosphorylation of MYPT1 at Thr-696, Thr-853, and surprisingly Ser-695. Inhibition of nitric oxide signaling completely abrogated basal MYPT1 Ser-695 phosphorylation and significantly increased and potentiated U-46619-induced MYPT1 Thr-853 phosphorylation and contractile force, indicating that NO/cGMP/cGKI signaling maintains basal vascular tone through active inhibition of calcium sensitization. Surprisingly, a fall in Ser-695 phosphorylation did not result in an increase in phosphorylation of the Thr-696 site. Although activation of cGKI with exogenous cyclic nucleotides inhibited thromboxane A2-induced MYPT1 membrane association, RhoA activation, contractile force, and regulatory light chain phosphorylation, the anticipated decreases in MYPT1 phosphorylation at Thr-696/Thr-853 were not observed, indicating that the vasorelaxant effects of cGKI are not through dephosphorylation of MYPT1. Thus, thromboxane A2 signaling within the intact cerebral vasculature induces "buffered" vasoconstrictions, in which both the RhoA/Rho-kinase calcium-sensitizing and the NO/cGMP/cGKI calcium-desensitizing pathways are activated.

Reduced Landau–de Gennes functional and surface smectic state of liquid crystals

In [X.B. Pan, Landau–de Gennes model of liquid crystals and critical wave number, Comm. Math. Phys. 239 (1–2) (2003) 343–382], based on the de Gennes analogy between liquid crystals and superconductivity [P.G. de Gennes, An analogy between superconductors and smectics A, Solid State Commun. 10 (1972) 753–756], the second author introduced the critical wave number Q c 3 (which is an analog of the upper critical field H c 3 for superconductors) and predicted the existence of a surface smectic state, which was supposed to be an analogy of the surface superconducting state. In a surface smectic state, the bulk liquid crystal is in the nematic state, and a thin layer of smectic appears in a helical strip on the surface of the sample. In this paper we study an approximate form of the Landau–de Gennes model of liquid crystals, and examine the behavior of minimizers, in particular the boundary layer behavior. Our work shows the importance of the joint chirality constant qτ, which is the product of wave number q and chirality τ and also appears in the work of [P. Bauman, M. Calderer, C. Liu, D. Phillips, The phase transition between chiral nematic and smectic A ∗ liquid crystals, Arch. Rational Mech. Anal. 165 (2002) 161–186] and [X.B. Pan, Landau–de Gennes model of liquid crystals and critical wave number, Comm. Math. Phys. 239 (1–2) (2003) 343–382]. The joint chirality constant of a liquid crystal is useful to predict whether the liquid crystal is of type I or type II, and it is also useful to examine whether the liquid crystal is in a surface smectic state. The results in this paper suggest that a liquid crystal with large Ginzburg–Landau parameter κ and large joint chirality constant qτ exhibits type II behavior, and it will be in the surface smectic state if q τ ∼ b κ 2 for some β 0 < b < 1 , where β 0 is the lowest eigenvalue of the Schrödinger operator with a unit magnetic field in the half space, and 0 < β 0 < 1 . We also show that a liquid crystal with small qτ exhibits type I behavior.

ELECTROMAGNETIC SCATTERING FROM CONDUCTING CIRCULAR CYLINDER COATED BY META-MATERIALS AND LOADED WITH HELICAL STRIPS UNDER OBLIQUE INCIDENCE

The asymptotic strip boundary condition (ASBC) is applied to analyze the solution of the electromagnetic scattering from a conducting cylinder coated with a homogeneous linear material layer and loaded with conducting helical strips. Such homogeneous material layer can be implemented by a conventional dielectric material, a single negative (SNG) or double negative (DNG) meta-material layer. A study of different materials’ constitutive parameters is presented with accordance to Drude and Lorentz material modeling. The boundary condition assumes that the strips are rounded around the coated cylinder in a helical form and both the strip’s period and the spacing between the helix turns are very small and mathematically approaching the zero. Scattering due to normal and oblique incident plane waves (θi, φi) of arbitrary polarization using the series solution is also computed. A number of parametric studies were investigated to illustrate the advantages of using metamaterials compared with conventional coating materials in terms of strip’s rounding pitch angle and coating layer electrical thickness variations. It is also shown that for SNG materials, modified Bessel functions are used to accept negative arguments. Coating with metamaterials proves to achieve higher forward scattering compared with conventional materials for the same electrical coating thickness.

Pkd2+/− Vascular Smooth Muscles Develop Exaggerated Vasocontraction in Response to Phenylephrine Stimulation

Vascular complications are the leading cause of morbidity and mortality in autosomal dominant polycystic kidney disease. Although evidence suggests an abnormal vascular reactivity, contractile function in Pkd mutant vessels has not been studied previously. Contractile response to phenylephrine (PE; 10(-10) to 10(-4)M), an alpha1-adrenergic receptor agonist, was examined. De-endothelialized Pkd2(+/-) aortic rings generated a higher maximum force (F(max)) than that in wild-type (wt; 5.78 +/- 0.73 versus 2.69 +/- 0.43 mN; P < 0.001) and a significant left shift in PE dosage-response curve. On simultaneous recordings, Pkd2(+/-) aortic helical strips also responded to PE with a greater F(max) but a lesser [Ca(2+)](i) rise, resulting in a greatly enhanced Deltaforce/DeltaCa(2+) ratio than that in wt. At F(max), a higher elevation in the phosphorylated regulatory myosin light chain was observed in Pkd2(+/-) strips. Ca(2+)-dependent calmodulin/myosin light-chain kinase-mediated contraction was examined by direct Ca(2+) (pCa8-5) stimulation to beta-escin permeabilized aortic strips; the pCa-force curve in Pkd2(+/-) strips was not shifted, thereby indicating that PE induced dosage-response alteration that resulted from Ca(2+)-independent mechanisms. Quantitative analyses of contractile proteins demonstrated elevated expressions in smooth muscle alpha-actin and myosin heavy chain in Pkd2(+/-) arteries, changes that likely contribute to the higher F(max). Similar to those in aortas, de-endothelialized Pkd2(+/-) resistance (fourth-order mesenteric) arteries responded to PE with a stronger contraction but a lesser [Ca(2+)](i) rise than in wt. Taken together, the arterial vasculature in Pkd2(+/-) mice exhibits an exaggerated contractile response and increased sensitivity to PE. An enhanced Ca(2+)-independent force generation and elevated contractile protein expression likely contribute to these abnormalities.

Effects of big endothelin-1 in comparison with endothelin-1 on the microvascular blood flow velocity and diameter of rat mesentery in vivo

Synthetic big endothelin-1 (ET-1), a 39-residue precursor of ET-1, has been reported to elicit potent contractile action on helical strip specimens obtained from the porcine coronary artery, but its molar potency was found to be 140-fold lower than that of ET-1 [Saito, Y., Nakao, K., Mukoyama, M., Imura, H., 1990. Increased plasma endothelin level in patients with essential hypertension. N. Engl. J. Med. 322, 205]. It has been hypothesized that the increased rate of production and/or release of ET-1 from the vascular endothelium may contribute to the pathogenesis of hypertension. However, the effects of big ET-1 in comparison with ET-1 on the macrocirculation and microcirculation of the rat mesentery have not been well documented. Thus, our main purpose for this study was to examine the effects of both big ET-1 and ET-1 to clarify the role of phosphoramidon in inhibiting the conversion of big ET-1 to ET-1, by investigating the systemic blood pressure, microvascular blood flow velocity, and diameters of arterioles and venules of the rat mesentery. For this purpose, two groups of experiments were performed. In these experiments, the mesentery was arranged for in situ intravital microscopic observation under transillumination. In the first group of experiments, intravenous cumulative injections of big ET-1 or ET-1 were infused through a catheter inserted into the right jugular vein. Infusion of big ET-1 (1–8 nmol/kg) elicited a long-lasting significant pressor effect. Infusion of big ET-1 (1–2 nmol/kg) elicited a significant dose-dependent increase in the microvascular blood flow velocity both in arterioles (20–30 μm) and venules (30–40 μm). Microvascular diameters exhibited a slight but significant vasodilator effect. However, the infusion of big ET-1 (4–8 nmol/kg) elicited a dose-dependent significant decrease in the blood flow velocities, and diameters returned to control measurements. The administration of ET-1 (0.25–2 nmol/kg) induced a dose-dependent significant decrease in the blood flow velocity of arterioles and venules, and their diameters exhibited a vasoconstrictive effect more prominent in arterioles than in venules. In the second group of experiments, cumulative injections of phosphoramidon (30 mg/kg/10 min) were administered 10 min prior to the infusion of big ET-1. Phosphoramidon significantly suppressed the long-lasting significant pressor effect and significantly inhibited the dose-dependent increase and dose-dependent decrease in the microvascular blood flow velocity produced by big ET-1 in the rat mesenteric microcirculation. This study observed differences in the effects big ET-1 and ET-1 have on the rat mesenteric microcirculation and proposes a possible mechanism explaining these differences. Moreover, phosphoramidon markedly inhibited the conversion of big ET-1 to ET-1 in the rat mesenteric microcirculation, which may suggest an inhibition of the enzyme which converts big ET-1 to ET-1.

Preclinical Profile of PF9404C, a Nitric Oxide Donor with β Receptor Blocking Properties

PF9404C ((2'S),(2S)-3-isopropylamine, 1-[4-(2,3-dinitroxy)propoxymethyl]-phenoxy-2'-propranol) is the S-S diesteroisomer of a novel blocker of beta-adrenergic receptors with vasorelaxing properties. It causes a concentration-dependent relaxation of rat aorta helical strips precontracted with 10(-6) M norepinephrine (NE; IC50 33 nM). It is equipotent to nitroglycerin (NTG; IC50 49 nM), but much more potent than isosorbide dinitrate (ISD; IC50 15,000 nM). In rat aorta smooth muscle cells, at 10 microM, PF9404C increased the formation of cGMP from 3 pmol/mg protein in basal conditions to 53 pmol/mg protein, suggesting that the mechanism of its vasorelaxing effects involves the slow generation of NO. This is supported by the facts that (i) ODQ (a blocker of guanylate cyclase) inhibited the vasodilatory effects of PF9404C; and (ii) PF9404C generates NO, as indirectly measured by the Griess reaction. In the electrically driven guinea pig left atrium, PF9404C blocks the inotropic effects of isoproterenol in a concentration-dependent manner. Its IC50 (30 nM) was similar to that of S-propranolol (22.4 nM) and lower than that of metoprolol (120 nM) or atenolol (192 nM). The beta adrenergic ligand (-)-[3H]-CGP12177 (4-[3-[(1,1-dimethylethyl)amino]-2-hydroxypropoxy]-1,3-dihydro-2H-benzimidazol-2-one hydrochloride) (0.2 nM) is displaced from its binding sites in rat brain membranes with a K(i) of 7, 17, 170, and 1200 nM for PF9404C, S-(-)propranolol, metoprolol, and atenolol, respectively. PF9404C blocks 45Ca2+ entry into bovine adrenal chromaffin cells induced by direct depolarization with 70 mM K+ or by the nicotinic agonist dimethylphenylpiperazinium (DMPP). PF9404C exhibits about 3-fold higher potency than NTG to relax the majority of the vessels studied, especially when they were contracted with K+, and shows a certain selectivity of action for the renal artery. It produces auto-tolerance that is ca. 20-fold less pronounced than that observed with NTG. Cross-tolerance in preparations pre-exposed to PF9404C and later relaxed with NTG, was much greater than auto-tolerance. This makes PF9404C a useful pharmacological tool for the development of novel NO-donor compounds with a lesser degree of vascular tolerance than those currently available.

Evidence that inward rectifier K+ channels mediate relaxation by the PGI2 receptor agonist cicaprost via a cyclic AMP-independent mechanism

We investigated the role of the inward rectifier potassium (KIR) channel and the cyclic AMP-dependent pathway in mediating vasorelaxation induced by the prostacyclin analogue cicaprost. Small vessel myography was used to assess responses to cicaprost in segments of rat tail artery contracted with phenylephrine. Microelectrode recordings were made from helical strips to assess effects on membrane potential. Cicaprost caused relaxation and hyperpolarisation that were significantly inhibited by Ba2+ (30-100 microM), a known blocker of KIR channels. Raising extracellular K+ from 5 to 15 mM elicited membrane hyperpolarisation and an endothelium-independent relaxation that was blocked by Ba2+ (30-100 microM), suggesting the existence of functional KIR channels on the smooth muscle. In contrast, neither glibenclamide (10 microM), a blocker of ATP-sensitive K+ channels, nor fluoxetine hydrochloride (100 microM), a blocker of G-protein-gated inward rectifier K+ channels, nor pertussis toxin (PTX; 1 microg/ml), which irreversibly inhibits Gi/Go, reduced relaxation to cicaprost. Indeed, PTX significantly potentiated responses. Relaxation to cicaprost was not mediated by NO but was partially endothelium-dependent, consistent with a similar inhibition by a combination of charybdotoxin (0.1 microM) and apamin (0.5 microM), blockers of endothelium-derived hyperpolarising factor (EDHF). However, relaxation was unaffected by adenylyl cyclase (SQ22536, dideoxyadenosine) or protein kinase A (Rp-2-O-monobutyryl-cAMP) inhibitors, consistent also with Ba2+ only weakly inhibiting relaxation to the adenylyl cyclase activator forskolin. We conclude that cicaprost relaxes rat tail artery by activating KIR channels with some involvement from EDHF. The mechanism appears to be largely independent of cyclic AMP and Gi/Go, although the latter appears to counteract relaxation through an unknown pathway and/or receptor.

Optimization of the crushing characteristics of triangulated aluminum beverage cans

In this study, a cylindrical shell body of the aluminum cans is triangulated and optimized for being folded down easily and safely for recycling. The triangulated cylindrical shell is constructed by a family of triangular surfaces based on one set of helical strips and circles lying on a cylindrical side surface. The intersections of helical strips and circles are used as the vertexes of the triangular surfaces. By changing the helical angle of the strips, the number of the strips, and the number of the circles, various triangulated cylindrical shells with different crushing characteristics can be developed. On the basis of the numerical simulation, the minimization problem of the crushing force of the triangulated cylindrical shells is solved using the crashworthiness maximization technique for tubular structures that combines the techniques of design of experiment, response surface approximation as well as usual mathematical programming.

Increased contractile responses to 5-hydroxytryptamine and Angiotensin II in high fat diet fed rat thoracic aorta

BackgroundFeeding normal rats with high dietary levels of saturated fat leads to pathological conditions, which are quite similar to syndrome X in humans. These conditions such as hypertriglyceridemia, hypercholesterolemia, obesity, and hyperglycemia might induce hypertension through various mechanisms. Metabolic syndrome and the resulting NIDDM represent a major clinical challenge because implementation of treatment strategies is difficult. Vascular abnormalities probably contribute to the etiology of many diabetic complications including nephropathy, neuropathy, retinopathy, and cardiomyopathy. It has been shown that in Streptozotocin induced diabetic animals there is an increase in maximal responses to 5-Hydroxytryptamine and Angiotensin II. The purpose of this study was to evaluate High fat diet fed rats for the development of hypertriglyceridemia, hypercholesterolemia, hyperinsulinemia and hyperglycemia and to assess their vascular responses to 5-Hydroxytryptamine and Angiotensin II.MethodsMale Sprague Dawley rats were used for this study and were divided into two equal groups. One of the groups was fed with normal pellet diet and they served as the control group, whereas the other group was on a high fat diet for 4 weeks. Body weight, plasma triglycerides, plasma cholesterol, and plasma glucose were measured every week. Intraperitoneal glucose tolerance test was performed after 4 weeks of feeding. At the end of fourth week of high fat diet feeding, thoracic aortae were removed, and cut into helical strips for vascular reactivity studies. Dose-response curves of 5-Hydroxytryptamine and Angiotensin II were obtained.ResultsThere was no significant difference in pD2, with 5-Hydroxytryptamine and Angiotensin II in both groups but Emax was increased.ConclusionsThese results suggest that hypertension in high fat diet rats is associated with increased in vitro vascular reactivity to 5-HT and Ang II.

Analysis of hard surfaces of cylindrical structures of arbitrarily shaped cross section using asymptotic boundary conditions

The surface equivalence principle is used to formulate the problem of infinitely long cylindrical structures of arbitrary cross section and loaded with metallic strips. The strips are tilted by an angle with respect to the cross section plane. Special cases are considered when the strips are directed along or transverse to the cylinder axis. The excitation is an oblique plane wave incident with arbitrary polarization. The asymptotic strip boundary condition (ASBC) is used to simplify the problem. The surface integral equations are solved using the method of moments. The numerical solution is verified with the series solutions of the circular cylinders loaded with helical strips. Several applications of hard surfaces are presented for structures loaded with tilted strips such as the struts loaded with tilted strips to reduce the equivalent blockage width of the struts and make it polarization independent.

A DIELECTRIC ROD GUIDE LOADED WITH HELICAL STRIPS ANALYZED WITH ASYMPTOTIC BOUNDARY CONDITIONS

A study of the propagation characteristics of a dielectric rod guide loaded with helical strips is presented. The analysis is based on the use of the asymptotic strip boundary condition (ASBC). The boundary condition assumes that the strip's period approaches zero. The eigenvalues of the modes are computed and plotted for different pitch angles. The special cases of periodic circumferential strips and longitudinal strips are also considered. It is found that the dominant mode is a hybrid type for all pitch angles except for the case when the strips are oriented along the rod axis. In this case, the dominant mode is the TE z type and has zero cutoff frequency. It is found also that there exist modes that have a cessation frequency where it ceases to propagate thereafter. The cessation frequency increases by increasing the pitch angle.

Vascular effects of singlet oxygen (1O2) generated by photo-excitation on adrenergic neurotransmission in isolated rabbit mesenteric vein

It has been suggested that reactive oxygen species (ROS) may be involved in the regulation of vascular tone. However, the nature of ROS effects on vascular sensitivity remains to be elucidated. The present study was designed to investigate the effects of ROS, especially 1O2, on neurotransmission at the sympathetic neurovascular junction. Basal noradrenaline (NA) release, release of NA induced by electrical stimulation (ES), and resting NA release at the sympathetic nerve terminals were determined using a superfusion technique. The amount of NA was determined by HPLC; isometric tension changes evoked by ES were also recorded simultaneously. 1O2 was generated from Rose Bengal by photo-activation. The generation of 1O2 in the superfusate was monitored by electron spin resonance (ESR) using the spin trap 2,2,6,6-tetramethyl-4-piperidinol throughout the experimental time course. The ESR results confirmed that 1O2 was generated by photo-activation of Rose Bengal via the formation of 2,2,6,6-tetramethyl-4-hydroxyl-piperidinyloxy. Exposure of helical strips of rabbit mesenteric vein to 1O2 induced a significant increase in tension and NA release during the basal period, but had no effect on ES-induced release. L-histidine, an 1O2 scavenger, significantly inhibited the observed effects on vascular tension and NA release in response to 1O2. These results suggest that 1O2 may induce NA-mediated vasoconstriction at the postjunctional site, and may be associated with Ca2+-independent NA release from the prejunctional site of adrenergic neurotransmission.

Regulation of vascular reactivity by E. coli endotoxin in vitro

The regulatory role of Escherichia coli endotoxin on the reactivity of goat thoracic aorta to different vasoactive agents was examined in vitro. Helical strips of the aorta exhibited slow, sustained and dose-dependent contractile responses to exogenous norepinephrine (NE, 10 −7 to 10 −4 M), high potassium (80 mM) and high calcium (0.1–300 mM). Endotoxin exposure did not elicit any intrinsic effect on the aortic strips, which were otherwise quiescent. However, incubation of the tissue with different concentrations of endotoxin (1, 3 or 10 μg/ml) inhibited the NE-induced contractions in a dose-dependent manner, as was also evidenced by the increasing effective concentration-50 (EC 50) values for NE. The contractile responses to hypertonic K + and Ca 2+ were also significantly inhibited in tissue incubated with endotoxin. This effect was independent of the concentration of endotoxin in the bathing fluid. The contractile responses of aortic strips to NE, K + and Ca 2+ were restored to normal values by removing the endotoxin after several washes with Krebs–Henseliet (K–H) solution. The effect of acetylcholine (ACh, 10 −5 M) on the maintained tonic contracture of NE (10 −5 M) was assessed to investigate the role of nitric oxide (NO). The study suggests that the vascular hypo-reactivity induced by E. coli endotoxin may be partially due to α-adrenoceptor blocking action and to decreased uptake of Ca 2+ by microsomes and mitochondria in the presence of endotoxin. This regulatory effect of endotoxin was only transient in nature and did not permanently impair the contractility of vascular smooth muscles (VSMs). The involvement of nitric oxide was precluded since ACh failed to relax the NE-precontracted tissues with intact endothelium.

Melatonin suppresses homocysteine enhancement of serotonin-induced vasoconstriction in the human umbilical artery.

Hyperhomocysteinemia is a major and independent risk factor for vascular disease. Oxidative stress is a possible mechanism for homocysteine (Hcy)-induced endothelial dysfunction. Herein, we evaluated the antioxidant property of melatonin as related to the vasospastic effect of Hcy on the human umbilical artery. Helical strips of human umbilical arteries with intact endothelium were obtained at elective Caesarean delivery between 37 and 39 wks of gestation. Changes in 5-hydroxytryptamine (5-HT)-induced vasoconstriction were measured. Arterial strips were treated with FeSO4 (10 microM) and Hcy (10 or 100 microM) or pre-treated with a hydroxyl radical (.OH) scavenger (mannitol, 20 mM), a cyclooxygenase inhibitor (indomethacin, 20 microM), nitric oxide (NO) synthesis inhibitor (L-NG-monomethylarginine, LNMA, 200 microM), or melatonin (1 or 10 microM). Hcy potentiated 5-HT-induced constriction in a concentration-dependent manner. Pre-treatment with mannitol significantly suppressed the vasospastic effect of Hcy. LNMA augmented the vasospastic effect of Hcy, but indomethacin did not. Melatonin significantly suppressed the vasospastic effect of Hcy in a concentration-dependent manner. These findings suggest that Hcy potentiates 5-HT-induced vasoconstriction in the human umbilical artery, possibly by suppressing bioavailable NO. Melatonin protects against the vasospastic effect of Hcy, most likely by scavenging.OH arising from Hcy autooxidation.

Role of Ca2+-sensitive protein kinase C in phenylephrine enhancement of Ca2+ sensitivity in rat tail artery.

We investigated the role of protein kinase C (PKC) isoforms on changes in sensitivity of contractile mechanisms to intracellular Ca(2+) (force /[Ca(2+)]i) by phenylephrine (0.1-100 microM) in rat tail arterial helical strips using simultaneous measurements of force and [Ca(2+)]i. Force/[Ca(2+)]Ii induced by phenylephrine was greater than that induced by 80 mM K+. Force/[Ca(2+)]i induced by phenylephrine in physiologic saline solution or low Ca(2+) solution was dependent on the agonist concentration. Removal of Ca(2+) completely abolished the phenylephrine-induced contraction. The PKC inhibitors staurosporine and calphostin C inhibited the increase in force/[Ca(2+)]i induced by phenylephrine to a much greater extent than that induced by 80 mM K+. LY379196, a specific PKCbeta inhibitor, did not inhibit the increase of calcium sensitivity due to phenylephrine. The classic PKC isoforms, alpha, betaI, and II not gamma were demonstrated in the artery by immunohistochemistry. These results suggest that in rat tail arterial smooth muscle, PKCalpha, and not beta or gamma, mediates the increase of changes in sensitivity of contractile mechanisms to intracellular Ca(2+) to high dose of alpha1 receptor stimulation (phenylephrine 100 microM) on nonphysiologic conditions.

Quadrifilar helix antenna with parasitic helical strips

AbstractAn omnidirectional quadrifilar helix antenna (QHA) with parasitic helical strips for circular polarization (CP) is proposed and experimentally investigated for handheld mobile terminals. This antenna is small in size, low cost, and lightweight. The mutual coupling effect between the grounded helical strips and the feeding helical arms provides a good impedance match, a smaller axial ratio, and wider hemispherical coverage. The impedance bandwidth corresponding to SWR&lt;2 and bandwidth with respect to the axial ratio &lt;3 dB are found to be 39% and 160 MHz at 3.64 GHz, respectively. © 2001 John Wiley &amp; Sons, Inc. Microwave Opt Technol Lett 30: 128–130, 2001.

Melatonin Counteracts Potentiation by Homocysteine of KCl-Induced Vasoconstriction in Human Umbilical Artery: Relation to Calcium Influx

Homocysteinemia is a major and independent risk factor for vascular disease. Oxidative stress is a possible mechanism for homocysteine (HCY)-induced vascular disease. Herein, we evaluated the antioxidant property of melatonin (MLT) in relation to the vasoconstrictive effect of HCY on the human umbilical artery. Helical umbilical arterial strips without endothelium were obtained at elective Cesarean delivery near term. Changes in potassium chloride (KCl)-induced vasoconstriction were measured. Arterial strips were treated with HCY (10 or 100 μM) plus FeSO4 (10 μM) alone or pretreated with a hydroxyl radical (•OH) scavenger, mannitol (20 mM), or MLT (1 or 10 μM). The effect of HCY on the response of arterial strips to external calcium (Ca2+) in the presence of KCl (20 mM) was determined. HCY plus FeSO4 potentiated KCl-induced vasoconstriction in a concentration-dependent manner; pretreatment with mannitol significantly reduced this vasospastic effect. HCY (100 μM) significantly augmented the contractile response to external Ca2+. MLT (10 μM) significantly suppressed the contractile response to external Ca2+. These results suggest that HCY potentiates KCl-induced umbilical artery vasoconstriction, in part by increasing Ca2+ influx in vascular smooth muscle cells via activation of Ca2+ channels. MLT significantly suppressed the vasoconstrictive effect of HCY, probably by scavenging •OH arising from HCY autooxidation.

Optimization of the Crushing Characteristic of Triangulated Cans.

The axial crushing behavior of a triangulated cylindrical shell constructed by one set of helical strips and circles lying on the surface, is simulated by the finite element method. This paper also discusses the affection to the crushing characteristic of the angle and the number of the helix as well as the number of the circles along the axial direction of the cylinder. Based on the numerical analyses, minimizing problems of the axial crushing force of triangulated cylindrical shells are solved by using the crashworthiness maximization technique for tubular structures which combined the techniques of design-of-experiment, response surface approximation as well as usual mathematical programming. Moreover, the behavior of the triangulated cylinders when subjected simultaneously to axial crushing and twisting forces is optimized.