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Biomedical subjects

Vernon M S Oh

Publications and source records attributed to Vernon M S Oh.

7 recordsLinked to original sources
PubMed2006

Where has all the botox gone? (how) will we ever learn... using monoclonal antibodies to track botulinum toxin.

Botulinum toxin (BTX) is an important therapeutic tool in the treatment of overactive skeletal and smooth muscles, as well as hypersecretory and painful disorders. Despite advances in our understanding of how BTX works, much remains to be elucidated, such as how BTX ameliorates pain, how it produces weakness remote from the site of injection and the fate of the heavy and light chain components of the BTX molecule following endocytosis into the presynaptic membrane. BTX, conjugated to radionuclides, allows investigators to track the molecule both in vitro and in vivo. However, altering the BTX molecule may cause structural changes or pharmacokinetic and pharmacodynamic alterations, and disrupt its normal action. We propose instead to bind the biomarkers (appropriate dyes, radionuclides or MRI contrast agents) to monoclonal antibodies directed against either heavy or light chain components of BTX, thus allowing administration of native (i.e. unaltered) BTX.

Animals↗
PubMed2006

Topical botulinum toxin to treat hyperhidrosis? No sweat!

Palmar, plantar and axillary hyperhidrosis, though benign, may be burdensome and occupationally restrictive, even hazardous. Treatment modalities range from topical antiperspirants, iontophoresis, systemic medications such as anticholinergics and benzodiazepines and injections of botulinum toxin, to thoracic sympathectomy. Intradermal injections of botulinum toxin (BTX), though effective, are painful especially when multiple injections are required. Iontophoretic administration of BTX has been described, the BTX entering the eccrine sweat glands via the sweat pores and through the sweat ducts. We postulate that BTX can be administered topically, either unassisted or assisted by application of an electrical gradient, low-frequency ultrasound or excipients such as dimethylsulfoxide. We examine the rationale and feasibility for such a treatment modality and route of administration.

Administration, Topical↗
PubMed2006

Expression of neuronal nitric oxide synthase in the internal thoracic artery and saphenous vein.

OBJECTIVES: Endothelial nitric oxide synthase (type III) generates nitric oxide, which dilates blood vessels. Recently, it was discovered that arterial smooth muscle cells express neuronal nitric oxide synthase (type I). The purpose of this study was to determine the relative amounts of neuronal nitric oxide synthase in the human internal thoracic artery and saphenous vein. METHODS: Remainder segments of internal thoracic arteries and saphenous veins were obtained from 45 patients during coronary artery bypass grafting. Western blotting used specific antibodies against the 3 isoforms of human nitric oxide synthase and beta-actin (for normalization) to measure the relative amounts of the 3 isoforms of nitric oxide synthase proteins in vessel specimens. Immunohistochemistry was used to localize the 3 proteins in specific cells. RESULTS: Western blotting detected all 3 isoforms of nitric oxide synthase in the human internal thoracic artery. The band density (normalized to beta-actin) of neuronal nitric oxide synthase was not significantly different from the band density of endothelial nitric oxide synthase. The amounts of neuronal nitric oxide synthase in arteries and veins were equal. Immunohistochemistry showed that the highest expression of endothelial nitric oxide synthase was in endothelial cells, but some expression was also seen in smooth muscle cells. Most of the neuronal nitric oxide synthase was in smooth muscle cells. The location and relative amounts of inducible nitric oxide synthase were variable. CONCLUSIONS: Neuronal nitric oxide synthase is expressed in the vascular smooth muscle of patients undergoing bypass, and the amount in the internal thoracic artery is the same as in the saphenous vein.

Actins↗
PubMed2006

Botulinum toxin: a novel therapeutic option for bronchial asthma?

Two components are essential for the development of an attack of bronchial asthma: inflammation and bronchoconstriction, the latter being mediated by smooth muscle contraction. Despite the efficacy of chronic therapy, many asthmatics relapse. Measures to inhibit contraction of the airway smooth muscle, such as vagotomy and thermoablation, may decrease the bronchoconstrictor component of the asthma attack and help to decrease morbidity and mortality from the disease. Botulinum toxin acts to weaken skeletal and smooth muscle by preventing the docking of the acetylcholine vesicle on the inner surface of the presynaptic membrane, thus causing chemical denervation and paresis of skeletal or smooth muscle. We explore the possibility that administration of botulinum toxin may achieve the same effect in bronchial asthma and examine the evidence to support this hypothesis.

Asthma↗
PubMed2004

Haplotypes of the beta2-adrenergic receptor gene are associated with essential hypertension in a Singaporean Chinese population.

OBJECTIVE: To investigate the relation between the gene encoding the beta2-adrenergic receptor (B2AR) and essential hypertension in a Singaporean Chinese cohort. METHODS: Three single nucleotide polymorphisms (SNPs) were genotyped in 190 cases and 323 controls, and eight haplotypes were determined and tested for association using the likelihood test statistic. RESULTS: We observed a significant difference in haplotype frequency distributions between the cases and the controls (P <0.00001). A logistic regression model fitted to the data supported this finding. CONCLUSION: The results suggest that variants at the B2AR locus may play a role in the pathophysiology of hypertension in this population.

Adult↗
PubMedDate not supplied

Singapore's experience of SARS.

The coronavirus that causes severe acute respiratory syndrome (SARS) is transmitted mainly via respiratory droplets. Typical presenting symptoms are akin to those of ordinary pneumonia. Young patients start with fever, chills, malaise, headache, or myalgia; cough and dyspnoea follow. Older persons and those taking corticosteroids may have neither fever nor respiratory symptoms. Exceptional suspicion is needed to identify SARS early in the illness. During an outbreak, even patients with low suspicion of SARS should be promptly isolated, and all contacts quarantined. Health workers need training in the use of appropriate barriers against droplets and other body fluids. Any fever cluster in patients or carers requires immediate action: discharges, visits, and transfers between wards and hospitals should be stopped. Halting hospital admissions and ten-day quarantine of suspected cases create wide buffer zones. To counter a possible resurgence of SARS, a system of prepared isolation and quarantine facilities is important.

Disease Outbreaks↗