Restoration of Range of Motion in the Cervical Spine through Single-Segment Artificial Disc Replacement Using the Baguera®C Prosthesis.

Background: Anterior cervical discectomy and fusion (ACDF) is a standard procedure for degenerative diseases of the cervical spine, providing nerve decompression and spinal stabilization. However, it limits cervical spine motility, restricts fused segment activity, and may lead to adjacent degeneration. Cervical disc arthroplasty (CDA) is an accepted alternative that preserves the structure and flexibility of the cervical spine. This study aimed to explore the dynamic changes in the range of motion (ROM) of the cervical spine after CDA using a viscoelastic artificial disc, as well as the factors affecting mobility restoration. Methods: A retrospective analysis was conducted on 132 patients who underwent single-level anterior cervical discectomy and CDA from January 2015 to June 2022. Result: Analysis of data from 132 patients revealed a significant improvement in clinical outcomes. The mean ROM of C2-C7 and functional spinal unit (FSU) segments significantly increased from 2 to 36 months post-operatively. Cervical spine flexibility was preserved and enhanced after prosthesis implantation. However, it took six months for the cervical spine motility to stabilize. In addition, sex and age were found to impact motility restoration, with female and younger patients exhibiting larger ROMs post-surgery. Additionally, CDA at the C5-C6 level resulted in the greatest increase in ROM, potentially improving overall kinematic ability. Conclusions: Single-segment artificial disc arthroplasty effectively restores the ROM in degenerative cervical spine conditions.

Pachymeningeal en plaque metastasis from gastric cancer mimicking subdural hematoma: illustrative case.

BACKGROUND: Pachymeningeal metastasis associated with gastric cancer, especially in its early stages, is extremely rare. OBSERVATIONS: The authors describe a 77-year-old man with a past medical history of lung cancer and previously treated chronic subdural hematoma who was admitted to their hospital because of hematemesis and newly diagnosed gastric cancer. He became unconscious during the hospitalization. The preoperative brain imaging studies had the appearance of recurrent subdural hematoma and extracranial tumor with skull invasion. Craniotomy revealed pachymeningeal carcinomatosis and en plaque metastasis of tumor. The histopathology of the tumors was consistent with metastatic gastric adenocarcinoma. LESSONS: This is the first reported case of metastatic gastric cancer as a pachymeninges-based en plaque entity. This report highlights the rare radiological presentation and operative findings in this case. The authors also summarize those case reports associated with dural metastasis arising from gastric cancer.

Baicalein Exerts Therapeutic Effects against Endotoxin-Induced Depression-like Behavior in Mice by Decreasing Inflammatory Cytokines and Increasing Brain-Derived Neurotrophic Factor Levels.

Inflammation plays an important role in the pathophysiology of depression. This study aims to elucidate the antidepressant effect of baicalein, an anti-inflammatory component of a traditional Chinese herbal medicine (Scutellaria baicalensis), on lipopolysaccharide (LPS)-induced depression-like behavior in mice, and to investigate the underlying mechanisms. In vitro, baicalein exhibited antioxidant activity and protected macrophages from LPS-induced damage. The results of the tail suspension test and forced swimming test (tests for despair potential in mice) showed the antidepressant effect of baicalein on LPS-treated mice. It also substantially decreased the production of pro-inflammatory cytokines, including IL-6, TNF-α, MCP-1, and eotaxin, elicited by LPS in the plasma. Baicalein downregulated NF-κB-p65 and iNOS protein levels in the hippocampus, demonstrated its ability to mitigate neuroinflammation. Additionally, baicalein increased the levels of the mature brain-derived neurotrophic factor (mBDNF) in the hippocampus of LPS-treated mice, and elevated the ratio of mBDNF/proBDNF, which regulates neuronal survival and synaptic plasticity. Baicalein also promoted the expression of CREB, which plays a role in a variety of signaling pathways. In summary, the findings of this study demonstrate that the administration of baicalein can attenuate LPS-induced depression-like behavior by suppressing neuroinflammation and inflammation induced by the peripheral immune response.

The relationship between theory of mind and the executive functions: Evidence from patients with frontal lobe damage.

"Theory of mind" (ToM) refers to the ability to predict others' thoughts, intentions, beliefs, and feelings. Evidence from neuropsychology and functional imaging indicates that ToM is a domain-specific or modular architecture; however, research in development psychology has suggested that ToM is the full development of the executive functions in individuals. Therefore, the relationship between ToM and the executive functions needs to be clarified. Since the frontal lobe plays a critical role in the abilities of ToM and the executive functions, patients with frontal lobe damage were recruited for the present study. Assessments of ToM and the executive functions were performed on 23 patients with frontal lobe damage and 20 healthy controls. When controlling for the executive functions, significant differences between the patient and normal groups were found in the affective component of ToM, but not in the cognitive component. The present study suggests that in various social situations, executing ToM abilities requires logical reasoning processes provided by the executive functions. However, the reasoning processes of affective ToM are independent of executive functions.

Mentalizing ability in patients with prefrontal cortex damage.

INTRODUCTION: Mentalizing ability is the issue in the social cognition of patients with brain injury that has received the most attention. The present study investigated mentalization ability in patients with prefrontal cortex damage. The aims of this study were to investigate: (a) whether patients with prefrontal cortex damage are impaired in mentalizing ability, including theory of mind (ToM) and empathy; (b) whether patients with ventromedial prefrontal cortex damage are impaired in different aspects of ToM; (c) whether patients with ventromedial prefrontal cortex damage are impaired in different aspects of empathy; and (d) whether impairment of mentalizing ability in patients with prefrontal cortex damage can be explained by executive dysfunction. METHOD: Mini-Mental State Examination (MMSE), Matrix Reasoning subtest, working memory, executive function, theory of mind, and empathy assessments were conducted on eight patients with ventromedial prefrontal cortex damage, 15 patients with dorsolateral prefrontal cortex damage, and 19 normal comparisons matched for level of education and intelligence. RESULTS: The results showed that performance on affective and nonverbal theory of mind was significantly lower in patients with dorsolateral prefrontal cortex damage than in the comparison group. Performance on personal distress items of empathy was significantly lower in the ventromedial prefrontal cortex damage group than in the dorsolateral prefrontal cortex damage group. In addition, further multiple regression analysis showed that affective theory of mind could be explained by the Wisconsin Card Sorting Test-Modified (WCST-M), with an explained variance of up to 44%. CONCLUSION: The present study suggests that the impairment of mentalizing ability in patients with prefrontal cortex damage is partially the result of executive dysfunction.

(±)3,4-methylenedioxyamphetamine inhibits the TEA-sensitive K⁺ current in the hippocampal neuron and the Kv2.1 current expressed in H1355 cells.

The whole-cell patch clamp method was used to study the effects of (±)3,4-methylenedioxyamphetamine (MDA) in hippocampal CA1 neurons from neonatal rats and in lung epithelial H1355 cells expressing Kv2.1. Extracellular application of MDA (30 µM) induced bursts of action potentials in hippocampal CA1 neurons exhibiting single spike action potentials without a bursting firing pattern, and promoted action potential bursts in hippocampal CA1 neurons exhibiting bursting firing of action potentials. Whereas MDA (30 and 100 µM) markedly decreased the delayed outward current in hippocampal CA1 neurons, MDA (100 µM) only slightly decreased the fast-inactivating K(+) current (I(A)) current. Furthermore, MDA (100 µM) substantially decreased the delayed outward current in the presence of 4-aminopyridine (4-AP; 3 mM), but did not significantly decrease the delayed outward current in the presence of tetraethylammonium (TEA; 30 mM). MDA (100 µM) also inhibited the current in H1355 cells expressing Kv2.1. Our results have shown that MDA inhibits the TEA-sensitive K(+) current in the hippocampus and the Kv2.1 current expressed in H1355 cells. These effects may contribute to the pharmacological and toxicological effects of MDA.

Non-Hodgkin's B-cell lymphoma of a lumbar nerve root: a rare cause of lumbar radiculopathy.

Non-Hodgkin's lymphoma involving the spinal nerve roots is rare. The presentation of nerve root lymphoma mimics other forms of radiculopathy. In vivo, nerve root lymphomas are difficult to differentiate from nerve sheath tumors by imaging studies. The nature of the tumor can be determined best by histological examination. Surgical removal of nerve root lymphomas commonly produces trauma to the nerve roots. Hence, we prefer to use surgical decompression of nerve roots rather than tumor enucleation. Here, we present a patient with a lumbar nerve root lymphoma to remind clinicians of the possibility of non-Hodgkin's lymphoma in instances of lumbar radiculopathy.

Evidence of D-phenylglycine as delivering tool for improving L-dopa absorption.

BACKGROUND: L-dopa has been used for Parkinson's disease management for a long time. However, its wide variety in the rate and the extent of absorption remained challenge in designing suitable therapeutic regime. We report here a design of using D-phenylglycine to guard L-dopa for better absorption in the intestine via intestinal peptide transporter I (PepT1). METHODS: D-phenylglycine was chemically attached on L-dopa to form D-phenylglycine-L-dopa as a dipeptide prodrug of L-dopa. The cross-membrane transport of this dipeptide and L-dopa via PepT1 was compared in brush-boarder membrane vesicle (BBMV) prepared from rat intestine. The intestinal absorption was compared by in situ jejunal perfusion in rats. The pharmacokinetics after i.v. and p.o. administration of both compounds were also compared in Wistar rats. The striatal dopamine released after i.v. administration of D-phenylglycine-L-dopa was collected by brain microdialysis and monitored by HPLC. Anti-Parkinsonism effect was determined by counting the rotation of 6-OHDA-treated unilateral striatal lesioned rats elicited rotation with (+)-methamphetamine (MA). RESULTS: The BBMV uptake of D-phenylglycine-L-dopa was inhibited by Gly-Pro, Gly-Phe and cephradine, the typical PepT1 substrates, but not by amino acids Phe or L-dopa. The cross-membrane permeability (Pm*) determined in rat jejunal perfusion of D-phenylglycine-L-dopa was higher than that of L-dopa (2.58 ± 0.14 vs. 0.94 ± 0.10). The oral bioavailability of D-phenylglycine-L-dopa was 31.7 times higher than that of L-dopa in rats. A sustained releasing profile of striatal dopamine was demonstrated after i. v. injection of D-phenylglycine-L-dopa (50 mg/kg), indicated that D-phenylglycine-L-dopa might be a prodrug of dopamine. D-phenylglycine-L-dopa was more efficient than L-dopa in lowering the rotation of unilateral striatal lesioned rats (19.1 ± 1.7% vs. 9.9 ± 1.4%). CONCLUSION: The BBMV uptake studies indicated that D-phenylglycine facilitated the transport of L-dopa through the intestinal PepT1 transporter. The higher jejunal permeability and the improved systemic bioavailability of D-phenylglycine-L-dopa in comparison to that of l-dopa suggested that D-phenylglycine is an effective delivery tool for improving the oral absorption of drugs like L-dopa with unsatisfactory pharmacokinetics. The gradual release of dopamine in brain striatum rendered this dipeptide as a potential dopamine sustained-releasing prodrug.

Action potential bursts in central snail neurons elicited by procaine: roles of ionic currents.

The role of ionic currents on procaine-elicited action potential bursts was studied in an identifiable RP1 neuron of the African snail, Achatina fulica Ferussac, using the two-electrode voltage clamp method. The RP1 neuron generated spontaneous action potentials and bath application of procaine at 10 mM reversibly elicited action potential bursts in a concentration-dependent manner. Voltage clamp studies revealed that procaine at 10 mM decreased [1] the Ca2+ current, [2] the Na+ current, [3] the delayed rectifying K+ current I(KD), and [4] the fast-inactivating K+ current (I(A)). Action potential bursts were not elicited by 4-aminopyridine (4-AP), an inhibitor of I(A), whereas they were seen after application of tetraethylammonium chloride (TEA), a blocker of the I(K)(Ca) and I(KD) currents, and tacrine, an inhibitor of I(KD). Pretreatment with U73122, a phospholipase C inhibitor, blocked the action potential bursts elicited by procaine. U73122 did not affect the I(KD) of the RP1 neuron; however, U73122 decreased the inhibitory effect of procaine on the I(KD). Tacrine decreased the TEA-sensitive I(KD) of RP1 neuron but did not significantly affect the I(A). Tacrine also successfully induced action potential bursts in the RP1 neuron. It is concluded that the inhibition on the I(KD) is responsible for the generation of action potential bursts in the central snail RP1 neuron. Further, phospholipase C activity is involved in the procaine-elicited I(KD) inhibition and action potential bursts.

Ecstasy and methamphetamine elicit action potential bursts via different mechanisms in a central snail neuron.

This study sought to determine the effects of (+) methamphetamine (METH) and its ring-substituted analog (+/-)3,4-methylenedioxymethamphetamine (MDMA; ecstasy) on electrophysiological behavior and their relationships to second messenger systems in an identifiable RP4 neuron of the African snail, Achatina fulica Ferussac. Extracellular application of MDMA at 1mM and METH at 3mM elicited action potential bursts that were not blocked after immersing the neurons in Ca(2+)-free solution. Notably, MDMA- (1mM) elicited action potential bursts were blocked by pretreatment with the protein kinase C (PKC) inhibitors chelerythrine (20 microM) and Ro 31-8220 (20 microM), but not by the PKA inhibitors KT-5720 (10 microM) and H89 (10 microM). The PKC activator phorbol 12,13-dibutyrate (PDBu; 3 microM), but not the PKA activator forskolin (50 microM), facilitated the induction of bursts elicited by MDMA at a lower concentration (0.3mM). In contrast, METH- (3mM) elicited action potential bursts were blocked by pretreatment with KT-5720 (10 microM) and H89 (10 microM), but not by chelerythrine (20 microM) and Ro 31-8220 (20 microM). Forskolin (50 microM), but not PDBu (3 microM) facilitated the induction of bursts elicited by METH at a lower concentration (1mM). Tetraethylammonium chloride (TEA), a blocker of the delayed rectifying K(+) current (I(KD)), did not elicit bursts at a concentration of 5mM but did facilitate the induction of action potential bursts elicited by both METH and MDMA. Voltage clamp studies revealed that both METH and MDMA decreased the TEA-sensitive I(KD) of the RP4 neuron. Forskolin (50 microM) or dibutyryl cAMP (1mM), a membrane-permeable cAMP analog, alone did not elicit action potential bursts. However, co-administration with forskolin (50 microM) and TEA (5mM) or co-administration with dibutyryl cAMP (1mM) and TEA (50mM) elicited action potential bursts in the presence of the PKC inhibitor chelerythrine (20 microM). Similarly, PDBu (10 microM) or phorbol 12-myristate 13-acetate (PMA; 3 microM) alone did not elicit action potential bursts. However, co-administration with PDBu (10 microM) and TEA (5mM) or co-administration with PMA (3 microM) and TEA (5mM) elicited action potential bursts in the presence of the PKA inhibitor KT-5720 (10 microM). These data suggest that action potential bursts in the RP4 neuron were not due to Ca(2+)-dependent synaptic effects. Rather, action potential bursts may be elicited through (1) combined activation of the cAMP-PKA signaling pathway and inhibition of the I(KD) and (2) combined activation of PKC and inhibition of the I(KD).

An unusual primitive neuroectodermal tumor in the thoracic epidural space.

Primitive neuroectodermal tumor (PNET) is a generic term used to describe a group of histologically indistinguishable neoplasms, including cerebellar medulloblastomas, which are located at various sites in the central nervous system. Primary epidural PNETs are rare and few patients have been reported. We report a 15-year-old girl who presented with gradual onset, over 1 month, of upper back pain and bilateral lower leg weakness. A thoracic spine MRI showed a dumbbell-shaped epidural mass at T2-4 with right paraspinal and posterior mediastinal extension. Surgical resection of the epidural tumor for decompression was performed. The pathologic examination revealed a PNET. Primary spinal PNETs typically have a poor prognosis and optimal therapy has not yet been defined. Surgical resection, with the combination of chemo-radiotherapy or radiotherapy, leads to better outcomes. However, primary epidural PNETs may be classified as a subtype of spinal PNETs because they are free from intrathecal invasion. For these patients, surgery alone and surgery combined with radiotherapy or chemo-radiotherapy remain controversial. Our patient received surgery alone and, 1y ear later, has experienced no local recurrence within the epidural space but the mediastinal part of the tumor has enlarged.

Arsenic trioxide modulates the central snail neuron action potential.

BACKGROUND/PURPOSE: The electropharmacological effect of arsenic trioxide (As2O3) is unknown. The present study investigated the effects of As2O3 on spontaneous neuronal impulse activity. METHODS: Intracellular recordings and the two-electrode voltage clamp method were used to study the effect of As2O3 on the RP4 neuron, the number 4 neuron in the right partial ganglion of the giant African snail (Achatina fulica Ferussac). RESULTS: The RP4 neuron generated spontaneous action potentials, which were affected by As2O3 in a concentration-dependent manner. Extracellular application of 1 or 3 mM As2O3 decreased the frequency of spontaneously generated action potentials. At 10 mM, As2O3 first depolarized and then elicited irreversible bursts of potential (BoPs) at 60 minutes after administration. At 30 mM, As2O3 depolarized the resting membrane potential and abolished the spontaneous action potentials. The BoPs elicited by 10mM As2O3 were blocked when neurons were pretreated with phospholipase C (PLC) inhibitors (10 microM U73122 or 3mM neomycin). The BoPs elicited by As2O3 remained unchanged in the presence of KT5720, verapamil, or calcium replacement solution. Voltage-clamp studies revealed that 10mM As2O3 decreased the fast inward current and had no effect on the steady-state outward current of the neuron. CONCLUSION: As2O3 at 10 mM elicits BoPs in central snail neurons and this effect may relate to the PLC activity of the neuron, rather than protein kinase A activity, or calcium influxes of the neuron. As2O3 at higher concentration irreversibly abolishes the spontaneous action potentials of the neuron.

Inflammatory mediators of cerebrospinal fluid from patients with spinal cord injury.

BACKGROUND: The guidelines of MP treatment for acute SCI are still under debate. We examined the inflammatory mediators of CSF in patients with SCI and assessed the effect of MP treatment. METHODS: We studied 7 patients with acute SCI at the cervical level and examined the mediators of CSF in patients by cytokine antibody array, ELISA and gelatin zymography. RESULTS: We found that levels of IL-6, IL-8, monocyte chemoattractant protein-1, neutrophil-activating peptide 2, intracellular adhesion molecule-1, soluble Fas, tissue inhibitors of metalloproteinase 1, and matrix metalloproteinases-2 and -9 were upregulated in patients with complete SCI without MP treatment as compared to patients with MP treatments, incomplete SCI, or controls. Nerve growth factor was upregulated in patients with MP treatment. CONCLUSIONS: We suggest that a neuroinflammatory CSF profile after complete SCI could be suppressed with MP treatment via downregulating the expression of various cytokines.

Analgesic effect of lidocaine patch 5% in the treatment of acute herpes zoster: a double-blind and vehicle-controlled study.

BACKGROUND AND OBJECTIVES: Although lidocaine patch 5% has been widely used for postherpetic neuralgia, its analgesic effect on the intense pain associated with acute herpes zoster has not been investigated because of its potential hazard to damaged skin. METHODS: Forty-six patients suffering from moderate to severe pain caused by acute herpes zoster infection (within 4 weeks of onset) were enrolled in a randomized, double-blind, vehicle-controlled, parallel study. Lidocaine patch 5% or vehicle patch were applied to the intact portion of the painful skin area without blisters at 12-hour intervals twice a day for 2 consecutive days. Analgesic efficacy and side effect profiles were assessed before and 48 hours after patch application. RESULTS: We found that both groups of patients experienced significant pain relief during rest and movement. Differences of mean reduction of pain intensity between the two groups were 14.7 (4.7-24.8, P = 0.005) during rest and 10.4 (1.6-19.3, P = 0.007) during movement, favoring the lidocaine patch. The lidocaine patch produced a greater percentage change in a patient's global impression than the vehicle patch. The incidence and severity of adverse events were low with both treatments. CONCLUSIONS: This study demonstrates that lidocaine patch 5%, applied twice a day, could serve as a well tolerated and effective modality to relieve moderate to severe pain associated with acute herpes zoster presumably through its pharmacological action and physical barrier effect on sensitized skin.

Effects of sodium azide, barium ion, d-amphetamine and procaine on inward rectifying potassium channel 6.2 expressed in Xenopus oocytes.

BACKGROUND/PURPOSE: Inward rectifying potassium channel 6.2 (Kir6.2DelataC26 channel) is closely related to ATP-sensitive potassium channels. Whether sodium azide, barium ion, d-amphetamine or procaine acts directly on the Kir6.2DeltaC26 channel remains unclear. We studied the effects of these compounds on Kir6.2DeltaC26 channel expressed in Xenopus oocytes. METHODS: The coding sequence of a truncated form of mouse Kir6.2 (GenBank accession number NP_034732.1), Kir6.2(1-364) (i.e. Kir6.2DeltaC26), was subcloned into the pET20b(+) vector. Plasmid containing the correct T7 promoter-Kir6.2(1-364) cDNA fragment [Kir6.2/pET20b(+)] was then subject to NotI digestion to generate the templates for in vitro run-off transcriptions. The channel was expressed in Xenopus laevis oocytes. Two-electrode voltage clamping was used to measure the effects of sodium azide, barium ion, d-amphetamine and procaine on Kir6.2DeltaC26 channel current. RESULTS: Sodium azide activated and barium ion and d-amphetamine inhibited the Kir6.2DeltaC26 channel. Procaine did not have any significant effect on the Kir6.2DeltaC26 channel. CONCLUSION: Kir6.2DeltaC26 channel expressed in Xenopus oocytes can be used as a pharmacological tool for the study of inward rectifying potassium channels.

Effects of penicillin on procaine-elicited bursts of potential in central neuron of snail, Achatina fulica.

Effects of penicillin on changes in procaine-elicited bursts of potential (BoP) were studied in a central neuron (RP4) of snail, Achatina fulica Ferussac. Procaine elicited BoP in the RP4 neuron while penicillin elicited depolarization of the neuron. Penicillin decreased the BoP elicited by procaine in a concentration-dependent manner. The effect of penicillin on the procaine-elicited BoP was not altered in the preparations treated with ascorbate or L-NAME (N-nitro-L-arginine methyl ester). However, the inhibitory effect of penicillin on the procaine-elicited BoP was enhanced with a decrease in extracellular sodium ion. Sodium ion was one of the important ions contributing to the action potential of the neuron. Two-electrode voltage-clamp studies revealed that penicillin decreased the fast sodium inward current of the neuron. It is concluded that penicillin inhibited the BoP elicited by procaine and sodium ion altered the effect of penicillin on procaine-elicited BoP.

d-Amphetamine inhibits inwardly rectifying potassium channels in Xenopus oocytes expression system.

Effects of d-amphetamine on the renal outer medullary potassium (ROMK1) channels were tested in the Xenopus oocytes expression system. Xenopus oocytes were injected with mRNA coding for wild-type or mutant ROMK1 channels. Giant inside-out patch-clamp recordings were performed. d-Amphetamine inhibited the activity of ROMK1 channels in a manner that was concentration-dependent but voltage-independent. ROMK1 channels are regulated by intracellular pH (pH i) and protein kinase A (PKA). d-Amphetamine decreased the activity of wild-type and pH i gating residue mutant (K80M) channels over a range of pH i values. However, d-amphetamine failed to reduce channel activity in the presence of PKA inhibitors (H89 and KT 5720) and had no inhibitory effect on the mutants of PKA-phosphorylation sites (S44A, S219A, or S313A), mutants that mimicked the negative charge carried by a phosphate group bound to a serine (S44D, S219D, or S313D), or mutant channels with a positive charge (S219R). These findings suggest that d-amphetamine inhibits ROMK1 channels independently of the pH i. The effects of d-amphetamine on ROMK1 channels may be due to a conformational change induced by PKA-mediated phosphorylation, but not to charge-charge interactions.

Neurotoxicity of a novel local anesthetic agent, ropivacaine: the possible roles of bursts of potential and cytoplasmic second messenger.

BACKGROUND/PURPOSE: Ropivacaine has been shown to induce convulsion following overdose or accidental intravenous injection, but the mechanisms are poorly understood. Using an identifiable central neuron from giant African snail, the authors studied the mechanism of ropivacaine-elicited bursts of potential and explored the possible mechanisms of ropivacaine-induced neurotoxicity. METHODS: Ropivacaine action on a central neuron (RP4) of the giant African snail (Achatina fulica Ferussac) was recorded by conventional electrophysiologic technique. Interactions between ropivacaine and prazosin, propranolol, atropine, d-tubocurarine, calcium-free solution, H89, U73,122, neomycin, high-magnesium solution, and chelerythrine were also observed. RESULTS: The RP4 neuron showed spontaneous firing of action potentials. Extracellular application of ropivacaine (900 microM) reversibly elicited bursts of potential in the RP4 neuron. The bursts of potential elicited by ropivacaine were not blocked after administration of: (1) prazosin, propranolol, atropine, d-tubocurarine; (2) calcium-free solution; and (3) pretreatment with H89 or chelerythrine. The bursts of potential elicited by ropivacaine were blocked by pretreatment with U73122 (30 microM) or by adding neomycin (3.5 mM) or high-magnesium solution (30 mM). CONCLUSION: Ropivacaine reversibly elicited bursts of potential in the central snail neuron. The ropivacaine-elicited bursts of potential were associated with phospholipase C activity in the RP4 snail neuron. Our results suggest that ropivacaine-induced neurotoxicity is highly associated with phospholipase C activity and phospholipase C inhibitor may offer a novel therapeutic approach for managing local anesthetic-induced convulsion or other transient neurologic toxicity.

Bursts of potential elicited by d-amphetamine in central snail neuron: effect of sodium azide.

Effects of sodium azide (NaN(3)) on spontaneously generated action potential and bursts of potential elicited by d-amphetamine (d-amphetamine-elicited BoP) were studied on the right parietal 4 (RP4) neuron of the snail Achatina fulica Ferussac in vitro. Sodium azide altered the spontaneous action potential of RP4 neuron in a concentration-dependent manner. In lower concentrations, neither NaN(3) (30, 100, 300 microM; 1 and 3 mM) nor d-amphetamine (135 microM) affect the resting membrane potential, amplitude and frequency of RP4 neurons, while in the higher concentrations NaN(3) (30 mM) did abolish the spontaneous action potential on RP4 neurons and depolarized the RP4 neurons reversibly. At lower concentration, NaN(3) (30 microM) facilitated the d-amphetamine-elicited BoP. The BoP elicited by NaN(3) (30 microM) and d-amphetamine (135 microM) were decreased following treatment with KT5720 (protein kinase A inhibitor), or intracellular injection of EGTA [ethylene glycol-bis(2-aminoethyl ether)-N,N,N',N'-tetraacetic acid]. However, the BoP was not affected by applying U73122 (1-[6-[((17beta)-3-methoxyestra-1,3,5[10]-trien-17-yl)amino]hexyl]-1H-pyrrole-2,5-dione) or neomycin (phospholipase inhibitors). Voltage clamp studies revealed that NaN(3) (30 microM) did not alter the total fast inwards currents (70 msec.) and the steady-state outwards currents (5 sec.). It appeared that the BoP elicited by NaN(3) (30 microM) and d-amphetamine (135 microM) was mainly due to protein kinase A-related messenger system and intracellular calcium. It is concluded that d-amphetamine-elicited BoP was not mainly due to inhibition of the function of mitochondria in the neuron while the function of mitochondria did alter the BoP elicited by amphetamine.

Phylogenetic characterization of Newcastle disease viruses isolated in Taiwan during 2003-2006.

Isolates of Newcastle disease virus (NDV) from chicken cases were obtained from various locations in Taiwan during 2003-2006 and were genotypically analyzed by using reverse transcription polymerase chain reaction (RT-PCR) with primers specific to the viral fusion (F) protein gene (534 bp). Part of the amplified F protein DNA product (nucleotide sequence 47-418) and the deduced amino acid sequences were compared phylogenetically with those from strains previously reported in Taiwan and other geographic regions. Our results showed that all Taiwanese isolates (n=20) collected during 2003-2006, according to the phylogenetic tree, belong to the genotype VIId. In addition, all the six Taiwanese isolates obtained in 2003, carry the motif (112)R-R-Q-K-R(116) and have the amino acid L(23) replaced by F(23) (assigned as Group 1). On the other hand, 12 out of the 14 Taiwanese isolates obtained during 2004-2006 possess the motif (112)R-R-K-K-R(116) and have the amino acid G(74), instead of E(74) (assigned as Group 2). To our best knowledge, this is the first reported VIId isolates that possess the sequences of G(74)/(112)R-R-K-K-R(116) within the F0 protein. Since a high mortality, severe clinical signs, typical postmortem lesions, and a high intra-cerebral pathogenicity index (ICPI) were observed in the NDV-infected chickens, these isolates acquired between 2003 and 2006 are considered as the velogenic type. The Group 2 viruses have become dominant and responsible for the majority of Taiwanese outbreaks during recent years. Based on our phylogenetic analysis, it can be postulated that these isolates were evolved from previously reported local strains, and the Group 2 family emerged the latest in the genotype VIId. The information is fundamental to improving the efficiency of controlling strategies and vaccine development for NDV.