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Biomedical subjects

R H Roth

Publications and source records attributed to R H Roth.

At least 325 records · Page 18Linked to original sources
PubMed1976

The maintenance system and occlusal dynamics.

We have discussed the maintenance system and its relationship to occlusal dynamics and occlusion function. The premise has been set forth that to avoid untoward sequelae post-orthodontically in the areas of relapse of tooth positions, occlusal wear, periodontal disease, and temporomandibular pain-dysfunction, it is best to have an occlusion free from centric and excursive interferences. The practical approach to the desired goal for the orthodontist lies in an understanding and familiarity of occlusal dynamics that allows him to look at detailing of tooth positions with insight into their ramifications from a functional standpoint. The insight can only be gained by hard work and self-discipline in the study of occlusion. A knowledge of these concepts will alert the orthodontist ot the true severity of the cases he is treating, allow him to position teeth so as not to create problems and , lastly, to be able to competently handle those cases that do develop posttreatment problems.

Bruxism↗
PubMed1976

Free and conjugated dihydroxyphenylacetic acid: effect of alterations in impulse flow in rat neostriatum and frontal cortex.

Stimulation of the nigro-neostriatal dopamine pathway results in an accumulation of both free and conjugated dihydroxy-phenylacetic acid (DOPAC) in the rat neostriatum. Drugs which have previously been shown to alter impulse flow in central dopaminergic neurons also produce predictable changes in the levels of both free and conjugated DOPAC in both the neostriatum and, in most cases, in the frontal cortex. Drugs such as the antipsychotics which increase impulse flow in the nigro-neostriatal dopamine neurons increase both free and conjugated DOPAC levels in both the neostriatum and frontal cortex. Drugs which reduce impulse flow, such as d-amphetamine and apomorphine, cause a reduction in free DOPAC in both the neostriatum and frontal cortex but reduce DOPAC conjugate only in the neostriatum. Pargyline, a monoamine oxidase inhibitor, causes an extensive depletion of free and conjugated DOPAC in both the striatum and frontal cortex, indicating that these metabolites are rapidly cleared from both of these brain areas.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1976

14C-homovanillic acid in the cerebrospinal fluid of parkinsonian patients after intravenous 14C-L-dopa.

Six patients with Parkinson's disease and five controls were premedicated with probenecid and the peripheral decarboxylase inhibitor alpha-methyldopathydrazine (Carbidopa) before intravenous administration of 50 muc of 14C-L-dopa in tracer quantity. Seven-and-one-half hours later lumbar CSF was obtained. 14C-homovanillic acid (HVA), a major metabolite of brain dopamine, was isolated by thin-layer chromatography and measured. The statistically significant positive correlation between endogenous HVA and 14C-HVA in the entire patient group and the slightly lower values of endogenous HVA and 14C-HVA in the CSF of the parkinsonians support the assumption that the concentration of HVA in the CSF after probenecid treatment reflects brain dopamine turnover. Measurement of labeled HVA here seems to have little advantage over measurement of endogenous HVA alone.

Aged↗
PubMed1975

Evidence for involvement of protein kinase in the activation by adenosine 3':5'-monophosphate of brain tyrosine 3-monooxygenase.

Addition of adenosine 3':5'-monophosphate (cAMP) to high speed supernatant preparations obtained from rat brain caused a 3- to 4-fold increase in tyrosine 3-monooxygenase (tyrosine hydroxylase) activity. The tyrosine 3-monooxygenase remained in an activated state upon removal of the cAMP by passing the enzyme through a Sephadex G-25 column. Substances which inhibit cAMP-dependent protein kinase, namely, EDTA, ADP, and adenosine, and protein kinase modulator, each antagonized the activation of tyrosine 3-monooxygenase produced by cAMP. Furthermore, addition of partially purified brain cAMP-dependent protein kinase caused a several-fold increase in tyrosin 3-monooxygenase activity. The activation of tyrosine 3-monooxygenase by added cAMP and protein kinase required the presence of ATP and Mg-2+. These data suggests that the cAMP activation of tyrosine 3-monooxygenase may be mediated by a cAMP-dependent protein kinase.

Adenosine↗
PubMed1975

Norepinephrine release from nerve terminals within the rabbit superior cervical ganglion.

Norepinephrine-3H (NE-3H) and its metabolic normetanephrine-3H were released from the superfused rabbit SCG incubated in tyrosine-3H in response to preganglionic stimulation. Neither dopamine-3H nor its metabolite, 3-methoxy-tyrosine could be detected in the superfusate from "control" or "nerve stimulated" tissues. Nerve stimulated NE-3H release a) was calcium dependent, b) had a stimulus threshold similar to that of C fibers, c) was not blocked by either 50 micromolar curare or 100 micromolar atropine, d) was abolished by chronic decentralization and e) was elicited by stimulation of both the cervical sympathetic and internal carotid nerves. These results suggest that there is a here-to-for undescribed, noradrenergic pathway which originates elsewhere in the sympathetic chain but terminates in the superior cervical ganglion.

Animals↗
PubMed1975

Some physiological and pharmalogical characteristics of the stimulus induced release of norepinephrine from the rabbit superior cervical ganglion.

The cervical sympathetic nerve stimulated release of norepinephrine (NE) from the rabbit superior cervical ganglion (SCG) was characterized. The quantity of NE released per impulse declined with increasing stimulation frequency over the range of 3/sec to 15/sec. Nerve stimulated NE release was potentiated by 1 micromolar desmethylimipramine and 25 micromolar phenoxylbenzamine and inhibited by 1 micromolar bretylium, 25 micromolar methoxamine and 1 micromolar prostaglandin E1. These results suggest that nerve stimulated NE release in the rabbit SCG occurs from sympathetic fibers which are subject to the same neurosecretory control mechanisms as sympathetic fibers elsewhere in the autonomic nervous system.

Animals↗