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This paper presents a new model of elastic articulated objects based on revolving conic surface. The model includes three-dimensional object skeleton and deformable surfaces that can represent the deformation of human body surfaces. In each limb, surface deformation is represented by adjusting only two deformation parameters. Then, the deformation parameters are determined by corresponding two-dimensional image contours from a sequence of stereo images. The three-dimensional motion parameters are estimated based on the skeleton points. The algorithm presented in this paper includes skeleton-based parameter estimation of motion and parameter determination of deformable surfaces. [ABSTRACT FROM AUTHOR]

This paper presents a new model of elastic articulated objects based on revolving conic surface. The model includes 3D object skeleton and deformable surfaces that can represent the deformation of human body surfaces. In each limb, surface deformation is represented by adjusting only one deformation parameter. Then, the 3D deformation parameters are determined by corresponding 2D image points from a sequence of stereo images. The 3D motion parameters are estimated based on the skeleton points. The algorithm presented in this paper includes skeleton-based parameter estimation of motion and parameter determination of deformable surfaces. [ABSTRACT FROM AUTHOR]

Abstract: The hypothalamic paraventricular (PVN) neurons projecting to the spinal cord and brainstem play an important role in the control of homeostasis and the sympathetic nervous system. Although GABAB receptors are present in the PVN, their function in the control of synaptic inputs to PVN presympathetic neurons is not clear. Using retrograde tracing and whole-cell patch-clamp recordings in rat brain slices, we determined the role of presynaptic GABAB receptors in regulation of glutamatergic and GABAergic inputs to spinally projecting PVN neurons. The GABAB receptor agonist baclofen (1–50 μM) dose-dependently decreased the frequency but not the amplitude of spontaneous excitatory postsynaptic currents (sEPSCs) and inhibitory postsynaptic currents (sIPSCs). The effect of baclofen on sEPSCs and sIPSCs was completely blocked by 10 μM CGP52432, a selective GABAB receptor antagonist. Baclofen also significantly reduced the frequency of both miniature excitatory and miniature inhibitory postsynaptic currents (mEPSCs and mIPSCs). Furthermore, uncoupling pertussis toxin-sensitive Gi/o proteins with N-ethylmaleimide abolished baclofen-induced inhibition of mEPSCs and mIPSCs. However, the inhibitory effect of baclofen on the frequency of mIPSCs and mEPSCs persisted in the presence of either Cd2+, a voltage-gated Ca2+ channel blocker, or 4-aminopyridine, a blocker of voltage-gated K+ channels. Our results suggest that activation of presynaptic GABAB receptors inhibits synaptic GABA and glutamate release to PVN presympathetic neurons. This presynaptic action of GABAB receptors is mediated by the N-ethylmaleimide-sensitive Gi/o proteins, but independent of voltage-gated Ca2+ and K+ channels. [Copyright &y& Elsevier]

Spinally administered muscarinic receptor agonists or acetylcholinesterase inhibitors produce efficacious analgesia. However, the mechanisms of the antinociceptive actions of muscarinic agonists in the spinal cord are not fully known. Previous in vitro studies have shown that muscarinic agonists increase GABA release and reduce the glutamatergic synaptic input to lamina II interneurons through GABAB receptors in the spinal cord. In the present study, we studied the effect of muscarinic agents on dorsal horn projection neurons and the role of spinal GABAB receptors in their action. Single-unit activity of ascending dorsal horn neurons was recorded in the lumbar spinal cord of anesthetized rats. The responses of dorsal horn neurons to graded mechanical stimuli were determined before and after topical spinal application of muscarine and neostigmine. We found that topical application of 0.1–5 μM muscarine or 0.5–5 μM neostigmine significantly suppressed the evoked response of dorsal horn neurons in a concentration-dependent manner. The inhibitory effect of muscarine or neostigmine on dorsal horn neurons was completely abolished in the presence of 1 μM atropine and by intrathecal pretreatment with 1 μg pertussis toxin to inactivate inhibitory G proteins. Furthermore, the inhibitory effect of both muscarine and neostigmine on the evoked response of dorsal horn neurons was significantly attenuated in the presence of 1 μM CGP55845, a GABAB receptor antagonist. Collectively, these data suggest that muscarinic agents inhibit dorsal horn projection neurons through muscarinic receptors coupled to pertussis toxin-sensitive Gi/o proteins. The inhibitory action of muscarinic agonists on these dorsal horn neurons is mediated in part by spinal GABAB receptors. [Copyright &y& Elsevier]

Single wurtzite p-type Zn1-yCuyO1-xSx alloy films with 0.081≤x≤0.186 and 0.09≤y≤0.159 were grown on quartz reproducibly by magnetron sputtering. The alloys show very stable p-type conductivity with a hole concentration of 4.31-5.78×1019 cm-3, a resistivity of 0.29-0.34 Ω cm and a mobility of 0.32-0.49 cm2 V-1 s-1. The p-type conductivity is attributed to substitution of Cu+1 for the Zn site, and the ionization energy of the Cu+1 acceptor is measured to be 53 meV, much less than that of Cu-doped ZnO reported previously. The small ionization energy is due to Cu heavy doping and increase in valence band maximum of ZnO induced by alloying with S. [ABSTRACT FROM AUTHOR]

In the cold rolling process, the expansion and coalescence of micro-defects can make steel sheet quality descend and create edge crack in the steel sheet. And the edge crack can cause the strip rupture completely. In this research, the cohesive zone model (CZM) was used to analyse the initiation and propagation of edge crack in the cold rolling process with the non-reversing two-high mill. A bi-linear traction-separation law was utilized which is primarily given by the CZM parameters including the cohesive stress, T, and the cohesive energy, Γ. Compared with other popular models such as the Gurson-Tvergaard-Needleman (GTN) model, the CZM presents certain advantages because it requires a smaller number of parameters to be defined. Comparison results of the experiments and simulation illustrated that the CZM can provide accurate prediction for the propagation of edge crack in the cold rolling process. Parametric analysis was carried out and showed that the extent of the crack propagation increases with the increasing of the reduction ratio. [ABSTRACT FROM AUTHOR]

We report room temperature ferromagnetism enhancement of Cu-doped ZnOS (Zn1−xCuxO1−ySy) alloy thin films with high hole concentration. The Zn0.91Cu0.09O0.92S0.08 alloy thin films with a hole concentration of 4.3 × 1019 cm−3 show the strongest magnetization of 1.5μB/Cu. First-principles calculation shows that high hole concentration stabilizes the ferromagnetic ordering in the Zn1−xCuxO1−ySy system, indicating a strong correlation between ferromagnetic stability and hole concentration. These results suggest that the Zn1−xCuxO1−ySy alloy with high hole concentration is promising to find applications in spintronic devices. [ABSTRACT FROM AUTHOR]

CuBe composite wires of 100 µm in diameter coated with a layer of NiCoP were prepared by a chemical plating method under DC current (CPUDC). The influences of DC current on coating morphology, deposition rate, composition, giant magneto-impedance (GMI) effect and magnetic properties were investigated. It was shown that the circumferential domain structure of coating layer was induced by the DC current going through the wires. A maximum GMI ratio of 870% was obtained in the composite wire prepared under 150 mA and tested at 180 kHz. It is 30 times higher than that of the composite wire plated in the same condition by conventional chemical plating method, indicating that CPUDC is an easy and effective approach to obtain composite wires and its applications will be further extended on magnetic sensors. [ABSTRACT FROM AUTHOR]

Abstract: Chronic neuropathic pain remains an unmet clinical problem because it is often resistant to conventional analgesics. Metabotropic glutamate receptors (mGluRs) are involved in nociceptive processing at the spinal level, but their functions in neuropathic pain are not fully known. In this study, we investigated the role of group III mGluRs in the control of spinal excitatory and inhibitory synaptic transmission in a rat model of neuropathic pain induced by L5/L6 spinal nerve ligation. Whole-cell recording of lamina II neurons was performed in spinal cord slices from control and nerve-ligated rats. The baseline amplitude of glutamatergic EPSCs evoked from primary afferents was significantly larger in nerve-injured rats than in control rats. However, the baseline frequency of GABAergic and glycinergic inhibitory postsynaptic currents (IPSCs) was much lower in nerve-injured rats than in control rats. The group III mGluR agonist l(+)-2-amino-4-phosphonbutyric acid (l-AP4) produced a greater inhibition of the amplitude of monosynaptic and polysynaptic evoked EPSCs in nerve-injured rats than in control rats. l-AP4 inhibited the frequency of miniature EPSCs in 66.7% of neurons in control rats but its inhibitory effect was observed in all neurons tested in nerve-injured rats. Furthermore, l-AP4 similarly inhibited the frequency of GABAergic and glycinergic IPSCs in control and nerve-injured rats. Our study suggests that spinal nerve injury augments glutamatergic input from primary afferents but decreases GABAergic and glycinergic input to spinal dorsal horn neurons. Activation of group III mGluRs attenuates glutamatergic input from primary afferents in nerve-injured rats, which could explain the antinociceptive effect of group III mGluR agonists on neuropathic pain. [Copyright &y& Elsevier]

Abstract: Both μ- and δ-opioid agonists selectively inhibit nociception but have little effect on other sensory modalities. Voltage-activated Ca2+ channels in the primary sensory neurons are important for the regulation of nociceptive transmission. In this study, we determined the effect of δ-opioid agonists on voltage-activated Ca2+ channel currents (ICa) in small-diameter rat dorsal root ganglion (DRG) neurons that do and do not bind isolectin B4 (IB4). The δ-opioid agonists [d-Pen2,d-Pen5]-enkephalin (DPDPE) and deltorphin II produced a greater inhibition of high voltage–activated ICa in IB4-negative than IB4-positive neurons. Furthermore, DPDPE produced a greater inhibition of N-, P/Q-, and L-type ICa in IB4-negative than IB4-positive neurons. However, DPDPE had no significant effect on the R-type ICa in either type of cells. We were surprised to find that DPDPE failed to inhibit either the T-type or high voltage–activated ICa in all the DRG neurons with T-type ICa. Double immunofluorescence labeling showed that the majority of the δ-opioid receptor-immunoreactive DRG neurons had IB4 labeling, while all DRG neurons immunoreactive to δ-opioid receptors exhibited Cav3.2 immunoreactivity. Additionally, DPDPE significantly inhibited high voltage–activated ICa in Tyrode''s or N-methyl-d-glucamine solution but not in tetraethylammonium solution. This study provides new information that δ-opioid agonists have a distinct effect on voltage-activated Ca2+ channels in different phenotypes of primary sensory neurons. High voltage–activated Ca2+ channels are more sensitive to inhibition by δ-opioid agonists in IB4-negative than IB4-positive neurons, and this opioid effect is restricted to DRG neurons devoid of functional T-type Ca2+ currents. [Copyright &y& Elsevier]

Abstract: Olvanil ((N-vanillyl)-9-oleamide), a non-pungent transient receptor potential vanilloid type 1 agonist, desensitizes nociceptors and alleviates pain. But its molecular targets and signaling mechanisms are little known. Calcium influx through voltage-activated Ca2+ channels plays an important role in neurotransmitter release and synaptic transmission. Here we determined the effect of olvanil on voltage-activated Ca2+ channel currents and the signaling pathways in primary sensory neurons. Whole-cell voltage-clamp recordings were performed in acutely isolated rat dorsal root ganglion neurons. Olvanil (1 μM) elicited a delayed but sustained inward current, and caused a profound inhibition (∼60%) of N-, P/Q-, L-, and R-type voltage-activated Ca2+ channel current. Pretreatment with a specific transient receptor potential vanilloid type 1 antagonist or intracellular application of 1,2-bis(2-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid abolished the inhibitory effect of olvanil on voltage-activated Ca2+ channel current. Calmodulin antagonists (ophiobolin-A and calmodulin inhibitory peptide) largely blocked the effect of olvanil and capsaicin on voltage-activated Ca2+ channel current. Furthermore, calcineurin (protein phosphatase 2B) inhibitors (deltamethrin and FK-506) eliminated the effect of olvanil on voltage-activated Ca2+ channel current. Notably, 1,2-bis(2-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid, calmodulin antagonists, and calcineurin inhibitors each alone significantly increased the amplitude of voltage-activated Ca2+ channel current. In addition, double immunofluorescence labeling revealed that olvanil induced a rapid internalization of CaV2.2 immunoreactivity from the membrane surface of dorsal root ganglion neurons. Collectively, this study suggests that stimulation of non-pungent transient receptor potential vanilloid type 1 inhibits voltage-activated Ca2+ channels through a biochemical pathway involving intracellular Ca2+-calmodulin and calcineurin in nociceptive neurons. This new information is important for our understanding of the signaling mechanisms of desensitization of nociceptors by transient receptor potential vanilloid type 1 analogues and the feedback regulation of intracellular Ca2+ and voltage-activated Ca2+ channels in nociceptive sensory neurons. [Copyright &y& Elsevier]

Abstract: Longitudinal wave velocity is used to characterize the point defects in crystalline solids. High purity Al single crystal was selected for both the finite element analysis and experimental work. Since the jog motions of dislocations caused by intersected slides such as cross slips induce point defects, the total amount of cross slips was calculated instead of calculating directly from the point defects. The effect of crystal orientations on total amount of cross slips under pure shear was also investigated via the finite element method. The result suggest that if the initial shear stress direction is located at the inner side of stereographic triangle, only single slip activities occurred at the beginning of plastic deformation and no effects due to point defects were present. However, as the shear stress direction rotates along the slip direction, point defects are induced by cross slips between primary and secondary slip systems due to work-hardening. This phenomenon was then examined by measuring longitudinal wave velocity changes propagating in Al single crystal subjected to the combination loads of equi-biaxial tension and compression (a pure shear state). Good qualitative agreement between the finite element result and measured data suggest that the longitudinal wave velocity can be used as an index to characterize point defects in crystalline materials. [Copyright &y& Elsevier]

Both myelinated and unmyelinated afferents are implicated in transmitting diabetic neuropathic pain. Although unmyelinated afferents are generally considered to play a significant role in diabetic neuropathic pain, pathological changes in diabetic neuropathy occur mostly in myelinated A-fibers. In the present study, we first examined the role of capsaicin-sensitive C-fibers in the development of allodynia induced by diabetic neuropathy. We then studied the functional changes of afferent nerves pertinent to diabetic neuropathic pain. Diabetes was induced in rats by i.p. streptozotocin. To deplete capsaicin-sensitive C-fibers, rats were treated with i.p. resiniferatoxin (300 μg/kg). Mechanical and thermal sensitivities were measured using von Frey filaments and a radiant heat stimulus. Single-unit activity of afferents was recorded from the tibial nerve. Tactile allodynia, but not thermal hyperalgesia, developed in diabetic rats. Resiniferatoxin treatment did not alter significantly the degree and time course of allodynia. Post-treatment with resiniferatoxin also failed to attenuate allodynia in diabetic rats. The electrophysiological recordings revealed ectopic discharges and a higher spontaneous activity mainly in Aδ- and Aβ-fiber afferents in diabetic rats regardless of resiniferatoxin treatment. Furthermore, these afferent fibers had a lower threshold for activation and augmented responses to mechanical stimuli. Thus, our study suggests that capsaicin-sensitive C-fiber afferents are not required in the development of allodynia in this rat model of diabetes. Our electrophysiological data provide substantial new evidence that the abnormal sensory input from Aδ- and Aβ-fiber afferents may play an important role in diabetic neuropathic pain. [Copyright &y& Elsevier]

Glasses in SiO2-Al2O3-B2O3-RO system doped with different Re2O3 (Re = La, Ce, Nd and Sm) at 4·5 mol.-% were prepared by conventional melt quenching technique. Structural, thermal durability and dielectric properties were investigated by using differential thermal analysis, Fourier transform infrared spectroscopy and precision impedance analyser respectively. Chemical durability was evaluated by weight losses of samples after immersion in HCl solution for varying times. The results showed that with increasing ionic radius of Re3+ ions (La3+Ce2O3>Nd2O3>Sm2O3. [ABSTRACT FROM AUTHOR]

Abstract: Activation of the descending noradrenergic system inhibits nociceptive transmission in the spinal cord. Although both α1- and α2-adrenoceptors in the spinal cord are involved in the modulation of nociceptive transmission, it is not clear how α1-adrenoceptors regulate excitatory and inhibitory synaptic transmission at the spinal level. In this study, inhibitory and excitatory postsynaptic currents (IPSCs and EPSCs, respectively) were recorded from lamina II neurons in rat spinal cord slices. The specific α1-adrenoceptor agonist phenylephrine significantly increased the frequency of GABAergic spontaneous IPSCs in a concentration dependent manner, and this effect was abolished by the α1-adrenoceptor antagonist 2-(2,6-dimethoxyphenoxy)ethylaminomethyl-1,4-benzodioxane (WB4101). Phenylephrine also significantly reduced the amplitude of monosynaptic and polysynaptic EPSCs evoked from primary afferents. The inhibitory effect of phenylephrine on evoked monosynaptic glutamatergic EPSCs was largely blocked by the GABAA receptor antagonist picrotoxin and, to a lesser extent, by the GABAB receptor antagonist CGP55845. Furthermore, blocking T-type Ca2+ channels with amiloride or mibefradil diminished the inhibitory effect produced by phenylephrine or the GABAA receptor agonist muscimol on monosynaptic EPSCs evoked from primary afferents. Collectively, these findings suggest that activation of α1-adrenoceptors in the spinal cord increases synaptic GABA release, which attenuates glutamatergic input from primary afferents mainly through GABAA receptors and T-type Ca2+ channels. This mechanism of presynaptic inhibition in the spinal cord may be involved in the regulation of nociception by the descending noradrenergic system. [Copyright &y& Elsevier]

Abstract: Activation of muscarinic acetylcholine receptors (mAChRs) inhibits spinal nociceptive transmission by potentiation of GABAergic tone through M2, M3, and M4 subtypes. To study the signaling mechanisms involved in this unique mAChR action, GABAergic spontaneous inhibitory postsynaptic currents (sIPSCs) of lamina II neurons were recorded using whole-cell patch clamp techniques in rat spinal cord slices. The mAChR agonist oxotremorine-M caused a profound increase in the frequency of GABAergic sIPSCs, which was abolished in the Ca2+-free solution. Inhibition of voltage-gated Ca2+ channels with Cd2+ and Ni2+ largely reduced the effect of oxotremorine-M on sIPSCs. Blocking nonselective cation channels (NSCCs) with SKF96365 or 2-APB also largely attenuated the effect of oxotremorine-M. However, the KCNQ channel blocker XE991 and the adenylyl cyclase inhibitor MDL12330A had no significant effect on oxotremorine-M-induced increases in sIPSCs. Furthermore, the phosphoinositide-3-kinase (PI3K) inhibitor wortmannin or LY294002 significantly reduced the potentiating effect of oxotremorine-M on sIPSCs. In the spinal cord in which the M3 subtype was specifically knocked down by intrathecal small interfering RNA (siRNA) treatment, SKF96365 and wortmannin still significantly attenuated the effect of oxotremorine-M. In contrast, SKF96365 and wortmannin both failed to alter the effect of oxotremorine-M on sIPSCs when the M2/M4 mAChRs were blocked. Therefore, our study provides new evidence that activation of mAChRs increases synaptic GABA release through Ca2+ influx and voltage-gated Ca2+ channels. The PI3K–NSCC signaling cascade is primarily involved in the excitation of GABAergic interneurons by the M2/M4 mAChRs in the spinal dorsal horn. [Copyright &y& Elsevier]

Abstract: The paraventricular nucleus (PVN) of the hypothalamus is important for the neural regulation of cardiovascular function. Nitric oxide (NO) increases synaptic GABA release to presympathetic PVN neurons through the cyclic guanosine monophosphate (cGMP)/protein kinase G signaling pathway. However, the downstream signaling mechanisms underlying the effect of NO on synaptic GABA release remain unclear. In this study, whole-cell voltage-clamp recordings were performed on retrograde-labeled spinally projecting PVN neurons in rat brain slices. Bath application of the NO precursor l-arginine or the NO donor S-nitroso-N-acetylpenicillamine (SNAP) significantly increased the frequency of GABAergic miniature inhibitory postsynaptic currents (mIPSCs) in labeled PVN neurons. A specific antagonist of cyclic ADP ribose, 8-bromo-cyclic ADP ribose (8-Br-cADPR), had no significant effect on l-arginine-induced potentiation of mIPSCs. Surprisingly, blocking of voltage-gated potassium channels (Kv) with 4-aminopyridine or α-dendrotoxin eliminated the effect of l-arginine on mIPSCs in all labeled PVN neurons tested. The membrane permeable cGMP analog mimicked the effect of l-arginine on mIPSCs, and this effect was blocked by α-dendrotoxin. Furthermore, the specific Kv channel blocker for Kv1.1 (dendrotoxin-K) or Kv1.2 (tityustoxin-Kα) abolished the effect of l-arginine on mIPSCs in all neurons tested. SNAP failed to inhibit the firing activity of labeled PVN neurons in the presence of dendrotoxin-K, Kα. Additionally, the immunoreactivity of Kv1.1 and Kv1.2 subunits was colocalized extensively with synaptophysin in the PVN. These findings suggest that NO increases GABAergic input to PVN presympathetic neurons through a downstream mechanism involving the Kv1.1 and Kv1.2 channels at the nerve terminals. [Copyright &y& Elsevier]

Abstract: Deletion of transient receptor potential vanilloid type 1 (TRPV1)-expressing afferent neurons reduces presynaptic μ opioid receptors but paradoxically potentiates the analgesic efficacy of μ opioid agonists. In this study, we determined if removal of TRPV1-expressing afferent neurons by resiniferatoxin (RTX), an ultrapotent capsaicin analog, influences the development of opioid analgesic tolerance. Morphine tolerance was induced by daily intrathecal injections of 10 μg of morphine for 14 consecutive days or by daily i.p. injections of 10 mg/kg of morphine for 10 days. In vehicle-treated rats, the effect of intrathecal or systemic morphine on the mechanical withdrawal threshold was gradually diminished within 7 days. However, the analgesic effect of intrathecal and systemic morphine was sustained in RTX-treated rats at the time the morphine effect was lost in the vehicle group. Furthermore, the μ opioid receptor-G protein coupling in the spinal cord was significantly decreased (∼22%) in vehicle-treated morphine tolerant rats, but was not significantly altered in RTX-treated rats receiving the same treatment with morphine. Additionally, there was a large reduction in protein kinase Cγ-immunoreactive afferent terminals in the spinal dorsal horn of RTX-treated rats. These findings suggest that loss of TRPV1-expressing sensory neurons attenuates the development of morphine analgesic tolerance possibly by reducing μ opioid receptor desensitization through protein kinase Cγ in the spinal cord. These data also suggest that the function of presynaptic μ opioid receptors on TRPV1-expressing sensory neurons is particularly sensitive to down-regulation by μ opioid agonists during opioid tolerance development. [Copyright &y& Elsevier]

The Climate Forecast System (CFS), the fully coupled ocean–land–atmosphere dynamical seasonal prediction system, which became operational at NCEP in August 2004, is described and evaluated in this paper. The CFS provides important advances in operational seasonal prediction on a number of fronts. For the first time in the history of U.S. operational seasonal prediction, a dynamical modeling system has demonstrated a level of skill in forecasting U.S. surface temperature and precipitation that is comparable to the skill of the statistical methods used by the NCEP Climate Prediction Center (CPC). This represents a significant improvement over the previous dynamical modeling system used at NCEP. Furthermore, the skill provided by the CFS spatially and temporally complements the skill provided by the statistical tools. The availability of a dynamical modeling tool with demonstrated skill should result in overall improvement in the operational seasonal forecasts produced by CPC. The atmospheric component of the CFS is a lower-resolution version of the Global Forecast System (GFS) that was the operational global weather prediction model at NCEP during 2003. The ocean component is the GFDL Modular Ocean Model version 3 (MOM3). There are several important improvements inherent in the new CFS relative to the previous dynamical forecast system. These include (i) the atmosphere–ocean coupling spans almost all of the globe (as opposed to the tropical Pacific only); (ii) the CFS is a fully coupled modeling system with no flux correction (as opposed to the previous uncoupled “tier-2” system, which employed multiple bias and flux corrections); and (iii) a set of fully coupled retrospective forecasts covering a 24-yr period (1981–2004), with 15 forecasts per calendar month out to nine months into the future, have been produced with the CFS. These 24 years of fully coupled retrospective forecasts are of paramount importance to the proper calibration (bias correction) of subsequent operational seasonal forecasts. They provide a meaningful a priori estimate of model skill that is critical in determining the utility of the real-time dynamical forecast in the operational framework. The retrospective dataset also provides a wealth of information for researchers to study interactive atmosphere–land–ocean processes. [ABSTRACT FROM AUTHOR]