Biomedical subjects

Daniel D Truong

Publications and source records attributed to Daniel D Truong.

9 recordsLinked to original sources

PubMed2006

NMDA receptor-mediated excitotoxicity contributes to the cerebral hypoxic injury of a rat model of posthypoxic myoclonus.

Cardiac arrest-induced cerebral hypoxic injury could induce posthypoxic movement disorders. Here we investigated the effects of memantine, an NMDA receptor channel blocker, on the neurodegeneration occurred in an established rat model of posthypoxic myoclonus. We found that administration of memantine for 7 days significantly reduced cerebral hypoxia-induced neurodegeneration in the CA1 of the hippocampus, the reticular thalamic nucleus (RTN) and the primary fissure of the cerebellum of the posthypoxic animals. The results suggest that the neurodegeneration observed in specific areas of the brain of the posthypoxic rats is contributed by NMDA receptor-mediated excitotoxicity.

Animals↗

PubMed2006

Molecular defects of the dystonia-causing torsinA mutation.

The DeltaGAG deletion mutation in DYT1, causing a loss of a glutamic acid near the carboxyl terminus of torsinA protein (torsinADeltaE), is dominantly inherited and tends to result in a severe generalized form of dystonia with childhood onset. We have used a yeast two-hybrid interaction assay to examine torsinA and its mutant torsinADeltaE interactions. Our data showed that torsinA monomers are capable of interacting with themselves and that mutant torsinADeltaE fails to interact with itself or with torsinA. We also demonstrated that purified torsinA protein is an ATPase, which forms a multimeric complex in vitro and that the DeltaGAG mutation disrupts the formation of multimeric complex and decreases torsinA's ATPase activity.

Adenosine Triphosphatases↗

PubMed2006

Botulinum toxin: clinical use.

Since its development for the use of blepharospasm and strabismus more than 2.5 decades ago, botulinum neurotoxin (BoNT) has become a versatile drug in various fields of medicine. It is the standard of care in different disorders such as cervical dystonia, hemifacial spasm, focal spasticity, hyperhidrosis, ophthalmological and otolaryngeal disorders. It has also found widespread use in cosmetic applications. Many other indications are currently under investigation, including gastroenterologic and urologic indications, analgesic management and migraine. This paper is an extensive review of the spectrum of BoNT clinical applications.

Animals↗

PubMed2005

Post-hypoxic myoclonus induces Fos expression in the reticular thalamic nucleus and neurons in the brainstem.

Post-hypoxic myoclonus is a movement disorder characterized by brief, sudden involuntary muscle jerks. Although the mechanism underlying this disorder remains unclear, earlier pharmacological studies indicated that aberrant activity of specific neuronal circuitry in the central nervous system causes this disorder. In the present study, Fos protein, an immediate-early gene product, was used as a marker of neuronal activity to identify the brain nuclei possibly involved in post-hypoxic myoclonus. We found that Fos protein was immunologically detected in the reticular thalamic nucleus (RT), the medial longitudinal fasciculus (MLF) as well as in the locus coeruleus (LC) and the periventricular gray substance (PVG) in post-hypoxic rats that developed myoclonus in response to auditory stimuli. Fos was not detected in these nuclei from rats that underwent 4 min of cardiac arrest without myoclonus. Electrolytic lesions of the RT or MLF but not the LC/PVG significantly reduced auditory stimulated myoclonus in the post-hypoxic rats. The results suggest that neuronal activity in the RT and the MLF plays a contributing role in post-hypoxic myoclonus.

Analysis of Variance↗

PubMed2005

Expanding use of botulinum toxin.

Botulinum toxin type A (BTX-A) is best known to neurologists as a treatment for neuromuscular conditions such as dystonias and spasticity and has recently been publicized for the management of facial wrinkles. The property that makes botulinum toxin type A useful for these various conditions is the inhibition of acetylcholine release at the neuromuscular junction. Although botulinum toxin types A and B (BTX-A and BTX-B) continue to find new uses in neuromuscular conditions involving the somatic nervous system, it has also been recognized that the effects of these medications are not confined to cholinergic neurons at the neuromuscular junction. Acceptors for BTX-A and BTX-B are also found on autonomic nerve terminals, where they inhibit acetylcholine release at glands and smooth muscle. This observation led to trials of botulinum neurotoxins in various conditions involving autonomic innervation. The article reviews the emerging use of botulinum neurotoxins in these and selected other conditions, including sialorrhea, primary focal hyperhidrosis, pathological pain and primary headache disorders that may be of interest to neurologists and related specialists.

Botulinum Toxins↗

PubMed2004

Natural history of posttraumatic cervical dystonia.

We studied a case series of 9 patients with posttraumatic cervical dystonia, in whom involuntary muscle spasms and abnormal head postures occurred within 7 days after cervical injury. Patients were examined, treated with botulinum toxin as necessary, and were followed up to 5 years. Based on our observations of these cases, we propose that complex regional pain syndrome (CRPS) could represent a variant of posttraumatic cervical dystonia that may develop over time after the initiation of dystonia.

Adult↗

PubMed2003

Randomized trial of the adenosine A(2A) receptor antagonist istradefylline in advanced PD.

OBJECTIVE: To evaluate the safety and efficacy of the adenosine A(2A) receptor antagonist istradefylline (KW-6002) in patients with levodopa-treated Parkinson's disease (PD) with both motor fluctuations and peak-dose dyskinesias. METHODS: This was a 12-week, double-blind, randomized, placebo-controlled, exploratory study in which PD subjects with both motor fluctuations and peak-dose dyskinesias were randomized to treatment with placebo (n = 29), istradefylline up to 20 mg/day (n = 26), or istradefylline up to 40 mg/day (n = 28). There was no prespecified primary outcome measure, and 19 outcome variables were analyzed. RESULTS: As assessed by home diaries, subjects assigned to istradefylline experienced a mean (+/- SE) reduction in the proportion of awake time spent in the "off" state of 7.1 +/- 2.0% compared with an increase of 2.2 +/- 2.7% in the placebo group (p = 0.008). There was a decrease in "off" time of 1.2 +/- 0.3 hours in the istradefylline group compared with an increase of 0.5 +/- 0.5 hour in the placebo group (p = 0.004). Dyskinesia severity was unchanged, but "on" time with dyskinesia increased in the istradefylline group compared with the placebo group (percent, p = 0.002; hours, p = 0.001). No differences were observed in change in Unified Parkinson's Disease Rating Scale scores or Clinical Global Impression of Change. Twenty-four percent of placebo-assigned subjects and 20% of istradefylline-assigned subjects withdrew from the study. Both dose regimens of istradefylline were generally well tolerated, and nausea was the most common adverse event. CONCLUSION: Istradefylline was generally well tolerated and reduced "off" time as assessed by home diaries. Severity of dyskinesia was unchanged, but "on" time with dyskinesia increased.

Adenosine A2 Receptor Antagonists↗

PubMed2002

Activation of adenosine triphosphate-sensitive potassium channels confers protection against rotenone-induced cell death: therapeutic implications for Parkinson's disease.

It is anticipated that further understanding of the protective mechanism induced by ischemic preconditioning will improve prognosis for patients of ischemic injury. It is not known whether preconditioning exerts beneficial actions in neurodegenerative diseases, in which ischemic injury plays a causative role. Here we show that transient activation of ATP-sensitive potassium channels, a trigger in ischemic preconditioning signaling, confers protection in PC12 cells and SH-SY5Y cells against neurotoxic effect of rotenone and MPTP, mitochondrial complex I inhibitors that have been implicated in the pathogenesis of Parkinson's disease. The degree of protection is in proportion to the bouts of exposure to an ATP-sensitive potassium channel opener, a feature reminiscent of ischemic tolerance in vivo. Protection is sensitive to a protein synthesis inhibitor, indicating the involvement of de novo protein synthesis in the protective processes. Pretreatment of PC12 cells with preconditioning stimuli FeSO(4) or xanthine/xanthine oxidase also confers protection against rotenone-induced cell death. Our results demonstrate for the first time the protective role of ATP-sensitive potassium channels in a dopaminergic neuronal cell line against rotenone-induced neurotoxicity and conceptually support the view that ischemic preconditioning-derived therapeutic strategies may have potential and feasibility in therapy for Parkinson's disease.

Adenosine Triphosphate↗

PubMed2002

Posthypoxic myoclonus animal models.

The animal model presented here resembles several of the key features of human myoclonus. Further study of the neuropathology and pharmacology of this animal model will hopefully increase our knowledge of the brain structures and systems affected in this disease and permit testing of therapeutic agents for the significant number of patients who do not respond to current treatments.

Acoustic Stimulation↗