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Biomedical subjects

R M Edwards

Publications and source records attributed to R M Edwards.

At least 127 records · Page 7Linked to original sources
PubMed1983

Central transmission time differences in the auditory brainstem response as a function of sex, age, and ear of stimulation.

Averaged auditory brainstem responses (ABRs) to monaural clicks were recorded from twenty-nine men and women and twenty children. Differences in the wave I to wave V transmission time, and wave I to wave III transmission time as a function of ear of stimulation and reference, sex, size and age were investigated. The wave I-V transmission time was shorter for the women compared to the men. Individual wave latencies were compared and the transmission time difference was found to be due to small, incremental differences between successive waves rather than to one particular wave component. Size differences, as measured by nasion-inion length and subject height, did not correlate to the transmission time difference and did not appear to contribute to the sex difference. An ear of stimulation difference was found in the women's group. The sex difference in transmission time was seen in the children's data, but the difference was not significant. Thus, sex differences, age differences, and ear of reference differences are seen in ABR transmission times.

Acoustic Stimulation↗
PubMed1982

Location of the gene for the low-affinity tryptophan-specific permease of Escherichia coli.

L-Tryptophan uptake was assayed under conditions in which the aroT gene had been inactivated by deletion and the product of the aroP permease was competitively inhibition. A mutant carrying a deletion from bgl through tnaA showed negligible L-tryptophan uptake, in contrast to a strain possessing an intact tna region or to strains carrying point mutations in tna. The ability to take up L-tryptophan was not restored by lysogenizing the tna-deleted strain with lambda tna+.

Amino Acid Transport Systems↗
PubMed1982

Auditory brainstem evoked responses in autistic children.

Auditory brainstem evoked responses (ABRs) were studied in 16 autistic children. Three children had severe delays in wave I latency, indicating defective functioning of the peripheral auditory pathway. The remaining subjects also had delayed wave I latency but only for right ear stimulation at the lowest stimulus intensity. Eight autistic children (and no control subjects) had ABR transmission time values 3 SDs beyond the normal mean, suggesting auditory processing defects peripheral to or within the brainstem auditory pathway. These findings (1) may have no causal relationship to the child's autistic handicaps, (2) may represent distortions in auditory input that impair the learning of language, and (3) may reflect an earlier state in which abnormal input directly caused maldevelopment of forebrain systems necessary for language and cognitive function.

Adolescent↗
PubMed1982

Electrophysiological studies of autism: the whisper of the bang.

Many neurophysiological hypotheses have focused upon the level of the central nervous system at which abnormal neural function may be present. Although some have argued that the type of language and cognitive defects shown by autistic children almost certainly reflects forebrain dysfunctions, current studies point to the possibility that some autistic children may have dysfunction of neural systems in the brainstem. One interpretation of these findings is that such abnormalities, occurring during a critical phase of early postnatal development, might themselves have acted directly as neuropathological agents, adversely influencing developing forebrain systems. A model for such an event has already been identified in animal research. If this be true, neurobiologists may not necessarily be identifying what is current pathology but may only be seeing a reflection of abnormal neural factors that once were important in development of the syndrome. Such a possibility suggests that investigators should consider extending their current studies to include young normal children as well as children with prototypic signs of abnormal language and interpersonal development.

Adolescent↗
PubMed1982

Sources of variability in auditory brain stem evoked potential measures over time.

Auditory brain stem EPs elicited in 10 normal adults by monaural clicks delivered at 72 dB HL, 20/sec showed no significant change in wave latencies or in the ratio of wave I to wave Y amplitude across 250 trial subsets, across 250 trial subsets, across 1500 trial blocks within a test session, or across two test sessions separated by several months. Sources of maximum variability were determined by using mean squared differences with all but one condition constant. 'Subjects' was shown to contribute the most variability followed by 'ears', 'sessions' and 'runs'; collapsing across conditions, wave III latencies were found to be the least variable, while wave II showed the most variability. Some EP morphologies showed extra peaks between waves II and IV, missing wave IV or wave IV fused with wave V. Such variations in wave form morphology were independent of EMG amplitude and were characteristic of certain individuals.

Adult↗
PubMed1982

Effect of potassium depletion on the vasopressin-sensitive cyclic AMP system in rat outer medullary tubules.

The effects of PDN on VP-sensitive cAMP metabolism were examined in MCT and MAL microdissected from the rat kidney. VP-sensitive adenylate cyclase activity was significantly reduced (delta -46%; p less than 0.05) in MAL of PDN rats but, in sharp contrast, was significantly increased (delta +79%; p less than 0.02) in MCT of PDN rats compared to controls. cAMP phosphodiesterase activity was significantly increased in both MAL (delta +59%; p less than 0.005) and MCT (delta +79%; p less than 0.001) of PDN rats compared to controls. The increase in cAMP accumulation in MAL measured in response to VP in intact tubules did not differ between PDN and controls, whereas cAMP accumulation in response to VP was significantly higher (delta +127%; p less than 0.001) in MCT of PDN rats compared to controls. The present results would indicate that the observed in vivo resistance to the antidiuretic effect of VP that occurs in PDN is not due to an impairment in VP-sensitive cAMP accumulation in MCT, but would rather suggest that a defect exists at a cellular step subsequent to cAMP generation. In addition, our results illustrate that the extent and directionality of in situ accumulation of cAMP measured in intact tubules cannot always be predicted from rhe activities of enzymes controlling its synthesis and degradation (adenylate cyclase and cAMP phosphodiesterase), which are measured in vitro in disrupted tubules.

Adenylyl Cyclases↗
PubMed1981

Synthesis of phosphatidylcholine from phosphatidylethanolamine by at least two methyltransferases in rat pituitary extracts.

Rat pituitary extracts contain at least two methyltransferases that methylate phosphatidylethanolamine to phosphatidylcholine using S-adenosylmethionine as the methyl donor. The first enzyme methylates phosphatidylethanolamine to phosphatidyl-N-monomethylethanolamine and has a high Km (40-42 microM) for S-adenosylmethionine, whereas the second enzyme(s) catalyzes two successive methylations of phosphatidyl-N-monomethylethanolamine to phosphatidyl-N,N-dimethylethanolamine and then to phosphatidylcholine and has a low Km (6.7 microM) for S-adenyl-L-methionine. The first enzyme is loosely bound to the membrane fraction; therefore it appears in both particulate (20,000 X g) and supernatant (20,000 X g) fractions, whereas the second enzyme(s) is tightly bound to the membrane and thus appears only in the particulate fraction. Both methyltransferases have two pH optima of 6.5 and 9.5 (9.5 activity greater than 6.5 activity) and they do not require Mg2+.

Animals↗
PubMed1981

ADH-sensitive cAMP system in papillary collecting duct: effect of osmolality and PGE2.

The papillary collecting duct (PCD) is considered to be of major importance in the final elaboration of the urine, but the metabolism of cyclic adenosine 3',5'-monophosphate (cAMP) has not yet been directly studied in the PCD. Therefore, in the present study we examined the basic properties of the cAMP system in isolated PCD microdissected from rat kidney. Vasopressin (VP) caused a marked (5- to 10-fold) stimulation of adenylate cyclase (AdC) but parathyroid hormone, calcitonin, isoproterenol, and bradykinin were without effect. A gradual increase in osmolality from 200 mosM had a biphasic effect on AdC, first enhancing (at 800 mosM) then inhibiting AdC activity at 2,000 mosM. cAMP-phosphodiesterase activity was inhibited as osmolality was increased from 200 to 800 mosM and the inhibition remained constant to 2,000 mosM. Incubation of intact PCD with VP resulted in a threefold increase in cAMP levels. As the osmolality of the incubation medium ws increased from 300 to 2,000 mosM, both basal and VP-stimulated cAMP levels continued to increase. Prostaglandin E2 (PGE2) (10(-5) M) alone (in the absence of vP) caused an increase in AdC activity, but the same dose of PGE2 had no effect on AdC activity stimulated by submaximal or maximal doses of VP. PGE2 (10(-5) M) caused a small increase in cAMP levels in intact PCD. On the other hand, PGE2 inhibited VP-stimulated cAMP levels by 50%. Incubation of PCD with PGE2 had no effect on cAMP-phosphodiesterase activity. The results demonstrate that osmolality in the physiologic range has a major influence on cAMP metabolism in the PCD and document an antagonism between PGE2 and VP at the level of cAMP accumulation in the PCD.

Adenylyl Cyclases↗
PubMed1980

Cerebral support for near-drowned children in a temperate environment.

The case histories of three children who were admitted to Modbury Hospital after immersion accidents in the northeastern suburbs of Adelaide during the period from November, 1978, to March, 1979, are presented. Hypothermia of moderate degree was found in one child. A Canadian treatment regimen is reviewed, and a plea made for a more vigorous management of the near-drowned victims of immersion accidents.

Barbiturates↗
PubMed1980

Cellular action of vasopressin in medullary tubules of mice with hereditary nephrogenic diabetes insipidus.

Our previous studies (1974. J. Clin. Invest.54: 753-762.) suggested that impaired metabolism of cyclic AMP (cAMP) may be involved in the renal unresponsiveness to vasopressin (VP) in mice with hereditary nephrogenic diabetes insipidus (NDI). To localize such a defect to specific segments of the nephron, we studied the activities of VP-sensitive adenylate cyclase, cAMP phosphodiesterase (cAMP-PDIE), as well as accumulation of cAMP in medullary collecting tubules (MCT) and in medullary thick ascending limbs of Henle's loop (MAL) microdissected from control mice with normal concentrating ability and from mice with hereditary NDI. Adenylate cyclase activity stimulated by VP or by NaF was only slightly lower (-24%) in MCT from NDI mice, compared with controls. In MAL of NDI mice, basal, VP-sensitive, and NaF-sensitive adenylate cyclase was markedly (> -60%) lower compared with MAL of controls. The specific activity of cAMP-PDIE was markedly higher in MCT of NDI mice compared with controls, but was not different between MAL of control and NDI mice. Under present in vitro conditions, incubation of intact MCT from control mice with VP caused a striking increase in cAMP levels (>10), but VP failed to elicit a change in cAMP levels in MCT from NDI mice. When the cAMP-PDIE inhibitor 1-methyl-3-isobutyl xanthine (MIX) was added to the above incubation, VP caused a significant increase in cAMP levels in MCT from both NDI mice and control mice. Under all tested conditions, cAMP levels in MCT of NDI mice were lower than corresponding values in control MCT. Under the present experimental setting, VP and other stimulating factors (MIX, cholera toxin) did not change cAMP levels in MAL from either control mice or from NDI mice. The results of the present in vitro experiments suggest that the functional unresponsiveness of NDI mice to VP is perhaps mainly the result of the inability of collecting tubules to increase intracellular cAMP levels in response to VP. In turn, this inability to increase cAMP in response to VP is at least partly the result of abnormally high activity of cAMP-PDIE, a somewhat lower activity of VP-sensitive adenylate cyclase in MCT of NDI mice, and perhaps to a deficiency of some other as yet unidentified factors. The possible contribution of low VP-sensitive adenylate cyclase activity in MAL of NDI mice to the renal resistance to VP remains to be defined.

Adenylyl Cyclases↗
PubMed1980

Lithium-induced polyuria: effect of lithium on adenylate cyclase and adenosine 3',5'-monophosphate phosphodiesterase in medullary ascending limb of Henle's loop and in medullary collecting tubules.

We investigated the effects of hyperosmolality, chronic treatment with lithium chloride (LiCl), and the addition of LiCl in vitro on vasopressin-sensitive (VP) adenylate cyclase (AdC) and cAMP phosphodiesterase (cAMP-PDIE) activities in the medullary thick ascending limb of Henle's loop (MAL) and medullary collecting tubule (MCT) microdissected from the outer medulla of the rat kidney. A hyperosmolar medium (800 mosmol) markedly enhanced AdC activity stimulated by 10(-6) M VP specifically in MCT, while having little effect or slightly decreasing VP-stimulated AdC in MAL, compared to activities under standard isotonic conditions. Hyperosmolality decreased cAMP-PDIE activity to about the same degree in MAL and MCT. Inclusion of LiCl in the incubation medium (15-20 mM) caused a significant dose-dependent inhibition of VP-stimulated AdC activity in both MAL and MCT, but had no effect on CAMP-PDIE in either segment. AdC and cAMP-PDIE activities in MAL and MCT from chronic LiCl-treated polyuric rats did not differ from controls when assayed under standard isotonic conditions. However, when assayed in a hyperosmolar (800 mosmol) medium, VP-sensitive AdC activity was significantly lower (P < 0.01) in MCT from LiCl-treated rats compared to control levels, while VP-sensitive AdC in MAL did not differ in LiCl-treated and control rats. The present results suggest that lowered VP-sensitive AdC activity in MCT of LiCl-treated polyuric rats may contribute to the observed lower concentrating ability and collecting tubule resistance to VP. Inhibition of VP-sensitive AdC in MAL as well as MCT by the acute addition of LiCl in vitro may explain the decreased urinary diluting ability observed with acute infusions of Li salts in vivo in the rat.

3',5'-Cyclic-AMP Phosphodiesterases↗