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Biomedical subjects

D L Roberts

Publications and source records attributed to D L Roberts.

At least 73 records · Page 4Linked to original sources
PubMed1990

Malignant melanoma in West Glamorgan--increasing incidence and improving prognosis, 1986-88.

A prospective 3-year epidemiological study, from 1986 to 1988, of malignant melanoma (MM) in West Glamorgan has shown an increase in the number of patients presenting with this condition associated with a significant trend towards thinner lesions. A total of 116 cases was recorded with an annual crude incidence per 100,000 population of 7.4 for males, 13.7 for females and 10.6 overall. Although the numbers are relatively small and must be interpreted with caution, these are the highest incidence rates for MM recorded to date in the United Kingdom. These figures are almost double those recorded by the Welsh Cancer Registry for West Glamorgan (1979-83), wherein the corresponding rates recorded were 3.8 for males, 7.4 for females and 5.6 overall. The mean age of diagnosis was 56.9 years for males and 57 years for females. The mean depth of invasion measured on the Breslow scale was 2.68 mm for males and 1.55 mm for females. There was no change in depth of invasion for males, which was consistently higher than in females throughout, the mean depth being 2.77 mm in 1986 and 2.74 mm in 1988 for males, and 2.00 mm in 1986 and 1.36 mm in 1988 for females. Overall there was a statistically significant trend towards thinner lesions over the 3-year period. It is suggested that the incidence of MM continues to rise and that a very limited public education programme in England and Scotland has had a measurable effect by increasing the frequency of early presentation, gauged indirectly by depth of invasion of melanoma in female patients in areas geographically quite distinct from the original public education campaign centres.

Adolescent↗
PubMed1990

Placebo-controlled dose-ranging trial designs in phase II development of nefazodone.

Nefazodone is a selective 5-HT2 receptor antagonist. Nefazodone has a pharmacologic profile similar to trazodone and other phenylpiperazine antidepressants, but distinct from nonselective first-generation agents and other selectively acting second-generation agents. Results of a multicenter, double-blind, fixed-dose trial indicate nefazodone is effective in improving depressive symptoms of outpatients with major depressive disorder treated with daily doses of 100 mg to 200 mg. A comparison of the fixed-dose trial design with an alternative design permitting dose titration within fixed ranges is presented. The relative merits of each design for establishing therapeutic dose ranges are discussed.

Depressive Disorder↗
PubMed1989

Cloning and expression of the gene cluster encoding key proteins involved in acetyl-CoA synthesis in Clostridium thermoaceticum: CO dehydrogenase, the corrinoid/Fe-S protein, and methyltransferase.

Acetogenic bacteria fix CO or CO2 by a pathway of autotrophic growth called the acetyl-CoA (or Wood) pathway. Key enzymes in the pathway are a methyltransferase, a corrinoid/Fe-S protein, a disulfide reductase, and a carbon monoxide dehydrogenase. This manuscript describes the isolation of the genes that code for the methyltransferase, the two subunits of the corrinoid/Fe-S protein, and the two subunits of carbon monoxide dehydrogenase. These five genes were found to be clustered within an approximately 10-kilobase segment on the Clostridium thermoaceticum genome. The proteins were expressed at up to 5-10% of Escherichia coli cell protein, and isopropyl beta-D-thiogalactopyranoside had no effect on the levels of expression, implying that the C. thermoaceticum inserts contained transcriptional and translational signals that were recognized by E. coli. The methyltransferase is expressed in E. coli in a fully active dimeric form with a specific activity and heat stability similar to the enzyme expressed in C. thermoaceticum. However, both the corrinoid/Fe-S protein and carbon dioxide dehydrogenase, although expressed in high amounts and with identical subunit molecular weights in E. coli, are inactive and less heat stable than are the native enzymes from C. thermoaceticum.

Acetyl Coenzyme A↗
PubMed1984

Ehlers-Danlos syndrome type IV mimicking non-accidental injury in a child.

This case report describes a child in whom non-accidental injury was initially suspected, but who was later shown to have autosomal dominant Ehlers-Danlos syndrome (EDS) type IV. Her mother and brother were also type III collagen deficient. This syndrome may be commoner than the small number of reported cases suggested and may sometimes explain previously undiagnosed easy bruising. The importance of recognizing this syndrome is stressed as it may save a great deal of embarrassment, frustration and anger for the family wrongly suspected of causing injury to their child.

Adult↗
PubMed1983

Monoaminergic antagonists which block naloxone-induced release of luteinizing hormone bind selectively to hypothalamic opiate receptors.

The possibility that adrenergic receptor antagonists which prevent naloxone-induced release of luteinizing hormone (LH) in vivo exert their action by direct competition with naloxone for hypothalamic opiate receptors was investigated in vitro in immature female rats. First, 26-day-old rats were injected with prazosin, an alpha 1-adrenergic blocker, or yohimbine, an alpha 2-adrenergic blocker, before receiving naloxone (2.5 mg/kg body wt.). Both adrenergic antagonists prevented naloxone-provoked LH secretion in a dose-dependent manner with yohimbine exhibiting a slightly greater potency. In a separate experiment hypothalami from 26-day-old rats were removed, membrane pellets prepared and incubated with [3H]naloxone in the presence of increasing concentrations of naloxone or various monoamine-active substances. Phentolamine, prazosin and yohimbine were the most effective competitors for naloxone binding sites while pronethalol, methysergide and metergoline were far less effective. These findings parallel the relative inhibitory potencies of these compounds in vivo for preventing naloxone-induced LH release as shown here and in a previous report. Clonidine and L-phenylephrine, both alpha-adrenergic agonists, also showed activity in the binding assay. Surprisingly, alpha-methyl-p-tyrosine and 5-hydroxytryptophan, substances which substitute for monoamine precursors early in the biosynthetic pathway, also displaced [3H]naloxone from hypothalamic receptors. These results offer a mechanism for the modulating effects of monoamine-active drugs on opiate antagonist-induced LH release and may have significance for inhibition of LH secretion by endogenous opiates.

Animals↗
PubMed1982

A comparative study of polylactic acid, Gelfoam, and Surgicel in healing extraction sites.

The search for a biodegradable material which may be placed in a fresh extraction socket to facilitate healing and prevent localized osteitis is a project which continues to hold much interest for oral surgeons. Polylactic acid is a biodegradable material which appears to have some promise in this area. The present study was devised to compare polylactic acid with two commonly used biodegradable substances and natural healing in order to determine the tissue response and suitability of polylactic acid as a treatment modality in fresh extraction sites. The over-all results were very satisfactory. The polylactic acid was well tolerated and did not interfere with the healing process.

Alveolar Process↗
PubMed1982

Antagonist of gonadotropin-releasing hormone blocks naloxone-induced elevations in serum luteinizing hormone.

Administration of a gonadotropin-releasing hormone (GnRH) antagonist, [D-Phe, D-Trp3.6]-GnRH, to immature female rats blocks the equivalent elevations in serum luteinizing hormone (LH) which are provoked by exogenous, natural GnRH (8 ng/100 g BW) or naloxone (0.25 mg/100 g BW), a specific opiate antagonist. A significant inhibition of GnRH- or naloxone-induced release of LH is obtained when rats are pretreated for 0, 15, 30 or 60 min with 5,000 ng/100 g BW of GnRH antagonist but no inhibition is evident when the antagonist is injected 180 min before either stimulant of LH secretion. A similar time-course is observed for GnRH antagonist inhibition of basal LH levels. The minimally effective dose of GnRH antagonist for suppressing both GnRH- and naloxone-induced LH release is 1,000 ng/100 g BW. More than 80% of the LH response to GnRH or naloxone is blocked by the highest tested dose (10,000 ng/100 g BW) of GnRH antagonist. Since naloxone has no direct influence on pituitary release of LH, these similar influences of GnRH antagonist on the LH-releasing properties of natural GnRH and naloxone, strongly suggest that the systemic administration of the opiate antagonist, naloxone, stimulates the release of endogenous GnRH.

Animals↗