Fatigue properties of hollow zirconia implants.

The objective of this study was to clarify the fatigue behavior of hollow yttria-stabilized tetragonal zirconia polycrystals (Y-TZP) specimens assuming its use for two-piece implants. The fatigue properties of a solid specimen (which simulated a one-piece implant) and 3 types of hollow specimens (which simulated two-piece implants) were evaluated. Specimens were either solid with a diameter of 4.

Influence of surface treatment of yttria-stabilized tetragonal zirconia polycrystal with hot isostatic pressing on cyclic fatigue strength.

Hot isostatic pressing processed yttria-stabilized tetragonal zirconia polycrystal (HIP Y-TZP) has the potential for application to implants due to its high mechanical performance. The aim of this study was to investigate the influence of surface treatment of HIP Y-TZP on cyclic fatigue strength. HIP Y-TZP specimens were subjected to different surface treatments.

Cardiac T-type Ca(2+) channels in the heart.

Two different Ca(2+) channels exist in cardiac myocytes. While the L-type Ca(2+) channel is ubiquitous and the main source of Ca(2+) for excitation-contraction coupling and pacemaker activity, the functional role of the T-type Ca(2+) channel is diverse and depends on mammalian species, heart region, age and various cardiac diseases. Two isoforms of T-type Ca(2+) channel proteins in the heart, Ca(V)3.

Modified sympathetic nerve system activity with overexpression of the voltage-dependent calcium channel beta3 subunit.

N-type voltage-dependent calcium channels (VDCCs) play determining roles in calcium entry at sympathetic nerve terminals and trigger the release of the neurotransmitter norepinephrine. The accessory beta3 subunit of these channels preferentially forms N-type channels with a pore-forming CaV2.2 subunit.

Functional role of stromal interaction molecule 1 (STIM1) in vascular smooth muscle cells.

We investigated the functional role of STIM1, a Ca(2+) sensor in the endoplasmic reticulum (ER) that regulates store-operated Ca(2+) entry (SOCE), in vascular smooth muscle cells (VSMCs). STIM1 was mainly localized at the ER and plasma membrane. The knockdown of STIM1 expression by small interfering (si) RNA drastically decreased SOCE.

Modified behavioral characteristics following ablation of the voltage-dependent calcium channel beta3 subunit.

Voltage-dependent calcium channels are important for calcium influx and the ensuing intracellular calcium signal in various excitable membranes. The beta subunits of these channels modify calcium currents through pore-forming alpha1 subunits of the high-voltage- activated calcium channels. In the present study, beta3 subunit-null mice were used to investigate the importance of the beta3 subunit of the voltage-dependent calcium channel, which couples with the CaV2.

Essential role of the N-terminus of murine Orai1 in store-operated Ca2+ entry.

Store-operated Ca(2+) entry (SOCE) is a physiologically important process that is triggered by intracellular Ca(2+) depletion. Recently, human Orai1 (the channel-forming subunit) and STIM1 (the calcium sensor) were identified as essential molecules for SOCE. Here, we report the cloning and functional analysis of three murine orthologs of Orai1, termed Orai1, 2, and 3.

Involvement of the calcium channel beta3 subunit in olfactory signal transduction.

Despite the expression of voltage-dependent Ca2+ channels in nasal turbinate epithelium, their role in odorant chemosensation has remained obscure. Therefore, we investigated olfactory neurotransduction in beta3-deficient mice. RT-PCR and Western blots confirmed the expression of various types of Ca2+ channels in the nasal turbinate.

Involvement of transient receptor potential canonical 1 (TRPC1) in angiotensin II-induced vascular smooth muscle cell hypertrophy.

Angiotensin II (Ang II) induces vascular smooth muscle cell (VSMC) hypertrophy as one of the major events leading to atherosclerosis. Increased Ca(2+) entry is an important stimulus for VSMC hypertrophy, but the association with Ang II remains to be determined. Transient receptor potential canonical 1 (TRPC1) forms store-operated Ca(2+) (SOC) channels that are involved in Ca(2+) homeostasis.

Modified sympathetic regulation in N-type calcium channel null-mouse.

To elucidate the physiological importance of neuronal (N)-type calcium channels in sympathetic controls, we analyzed N-type channel-deficient (NKO) mice. Immunoprecipitation analysis revealed increased interaction between beta3 (a major accessory subunit of N-type channels) and R-type channel-forming CaV2.3 in NKO mice.

Upregulation of TRPC1 in the development of cardiac hypertrophy.

The importance of Ca(2+) entry in the cardiac hypertrophic response is well documented, but the actual Ca(2+) entry channels remain unknown. Transient receptor potential (TRP) proteins are thought to form either homo- or heteromeric Ca(2+) entry channels that are involved in the proliferation and differentiation of various cells. The purpose of this study was to explore the potential involvement of TRP channels in the development of cardiac hypertrophy.

Regulatory role of neuron-restrictive silencing factor in expression of TRPC1.

Neuron-restrictive silencer factor (NRSF) binds its consensus element to repress the transcription of various genes. The dominant-negative form (dnNRSF) has a hypertrophic effect on cardiogenesis through an unidentified mechanism. We examined the involvement of transient receptor potential (TRP) channel proteins, using transgenic mice overexpressing dnNRSF (dnNRSF mice).

Identification of a cardiac isoform of the murine calcium channel alpha1C (Cav1.2-a) subunit and its preferential binding with the beta2 subunit.

We describe a cardiac muscle isoform of the voltage-dependent calcium channel alpha1 subunit, which corresponds to the rabbit ortholog of alpha1C-a (Cav1.2a). We also cloned smooth muscle isoforms alpha1C-b (Cav1.

Involvement of voltage-dependent Ca(2+) channel beta(3) subunit in the autonomic control of heart rate variability.

Noradrenaline release from sympathetic nerve terminals is dependent on Ca(2+) entry through neuronal voltage-gated N-type Ca(2+) channels. The accessory beta(3) subunits of Ca(2+) channels (Ca(V)beta(3)) are preferentially associated with the alpha(1B) subunit to form N-type Ca(2+) channels, and are therefore expected to play a functional role in the stimulation-evoked release of noradrenaline. In this study, we employed Ca(V)beta(3)-null, Ca(V)beta(3)-overexpressing (Ca(V)beta(3)-Tg), and wild-type (WT) mice to investigate the possible roles of Ca(V)beta(3) in the sympathetic regulation of heart rate in vivo.

Pathophysiological significance of T-type Ca2+ channels: properties and functional roles of T-type Ca2+ channels in cardiac pacemaking.

Calcium channels are essential for excitation-contraction coupling and pacemaker activity in cardiac myocytes. While L-type Ca(2+) channels (LCC) have been extensively studied, functional roles of T-type channels (TCC) in native cardiac myocytes are still debatable. TCC are activated at more negative membrane potentials than LCC and therefore facilitate slow diastolic depolarization in sinoatrial node cells.

Thromboxane A2 and prostaglandin F2alpha mediate inflammatory tachycardia.

Systemic inflammation induces various adaptive responses including tachycardia. Although inflammation-associated tachycardia has been thought to result from increased sympathetic discharge caused by inflammatory signals of the immune system, definitive proof has been lacking. Prostanoids, including prostaglandin (PG) D(2), PGE(2), PGF(2alpha), PGI(2) and thromboxane (TX) A(2), exert their actions through specific receptors: DP, EP (EP(1), EP(2), EP(3), EP(4)), FP, IP and TP, respectively.

Effects of PFOS and PFOA on L-type Ca2+ currents in guinea-pig ventricular myocytes.

Perfluorooctane sulfonate (PFOS) and perfluorooctanoate (PFOA) are amphiphiles found ubiquitously in the environment, including wildlife and humans, and are known to have toxic effects on physiological functions of various tissues. We investigated the effects of PFOS and PFOA on action potentials and L-type Ca(2+) currents, I(CaL), in isolated guinea-pig ventricular myocytes using whole-cell patch-clamp recording. In current-clamp experiments, PFOS significantly decreased the rate of spike, action potential duration, and peak potential at doses over 10 microM.

Genomic organization and functional analysis of murine PKD2L1.

Mutations in genes that encode polycystins 1 or 2 cause polycystic kidney disease (PKD). Here, we report the genomic organization and functional expression of murine orthologue of human polycystin-2L1 (PKD2L1). The murine PKD2L1 gene comprises 15 exons in chromosome 19C3.

Antinociceptive effect of different types of calcium channel inhibitors and the distribution of various calcium channel alpha 1 subunits in the dorsal horn of spinal cord in mice.

To understand better which voltage-dependent calcium channels (VGCCs) are involved in nociceptive neurotransmission, we investigated the pharmacological properties and distribution of VGCCs in the mouse spinal cord. A behavioral assay revealed that intrathecal injections of omega-agatoxin TK, omega-agatoxin IVA, omega-conotoxin GVIA, and SNX-482, which block P/Q-, P/Q-, N-, and R-type calcium channels, respectively, produced analgesic effects, while an L-type channel blocker had no such effect. An electrophysiological study demonstrated the presence of various types of VGCCs within dorsal root ganglion (DRG) neurons.

Inhibitory effect of pranidipine on N-type voltage-dependent Ca2+ channels in mice.

We investigated the N-type voltage-dependent calcium channel blocking action of pranidipine, a novel dihydropyridine (DHP) derivative. Pranidipine significantly suppressed KCl-induced intracellular calcium changes ([Ca(2+)](i)) in a dose-dependent fashion in dorsal root ganglion neurons. A patch-clamp investigation revealed a dose-dependent blocking effect on N-type currents.

Sevoflurane inhibition of the slowly activating delayed rectifier K+ current in guinea pig ventricular cells.

Single ventricular cells were enzymatically isolated from guinea pig hearts and the effects of sevoflurane on the delayed rectifier K(+) current were investigated by the patch clamp method. The rapidly (I(Kr)) and slowly activating delayed rectifier K(+) current (I(Ks)) were isolated using chromanol 293B, a selective blocker for I(Ks) or E4031 (N-[4-[[1-[2-(6-methyl-2-pyridinyl)ethyl]-4-piperidinyl]carbonyl]phenyl]methanesulfonamide dihydrochloride), a blocker for I(Kr). Sevoflurane and halothane decreased I(Ks) in a concentration-dependent manner with an IC(50) value of 0.

Pacemaker mechanism of porcine sino-atrial node cells.

In cardiac sino-atrial node (SAN) cells, time- and voltage-dependent changes in the gating of various ionic currents provide spontaneous, stable and repetitive firing of action potentials. To address the ionic nature of the species-dependent heart rate, action potentials and membrane currents were recorded in single cells dissociated from the porcine SAN, and compared with those from SAN cells of rabbits, guinea-pigs and mice. The porcine SAN cells exhibited spontaneous activity with a frequency of 60-80 min(-1), which was much slower than that of rabbit SAN cells.

Genetic characterization of a new splice variant of the beta2 subunit of the voltage-dependent calcium channel.

This study reports a novel splice variant form of the voltage-dependent calcium channel beta2 subunit (beta2g). This variant is composed of the conserved amino-terminal sequences of the beta2a subunit, but lacks the beta-subunit interaction domain (BID), which is thought essential for interactions with the alpha1 subunit. Gene structure analysis revealed that this gene was composed of 13 translated exons spread over 107 kb of the genome.

Structures of the murine genes for the beta1- and beta4-subunits of the voltage-dependent calcium channel.

The structures of the genomic DNA of the murine beta1- and beta4-subunits of the voltage-dependent calcium channel were mapped by comparing genomic and cDNA sequences. The gene structure analysis revealed that the murine beta1 gene consists of 15 translated exons spread over 19 kb of the genome, whereas the beta4 gene consists of 13 translated exons spread over 124 kb of the genome. Alternative spliced transcripts of the beta1 gene were also characterized.