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Biomedical subjects

B J Carroll

Publications and source records attributed to B J Carroll.

At least 109 records · Page 6Linked to original sources
PubMed1986

Regulation of the soybean-Rhizobium nodule symbiosis by shoot and root factors.

The availability of soybean mutants with altered symbiotic properties allowed an investigation of the shoot or root control of the relevant phenotype. By means of grafts between these mutants and wild-type plants (cultivar Bragg and Williams), we demonstrated that supernodulation as well as hypernodulation (nitrate tolerance in nodulation and lack of autoregulation) is shoot controlled in two mutants (nts382 and nts1116) belonging most likely to two separate complementation groups. The supernodulation phenotype was expressed on roots of the parent cultivar Bragg as well as the roots of cultivar Williams. Likewise it was shown that non-nodulation (resistance to Bradyrhizobium) is root controlled in mutant nod49. The shoot control of nodule initiation is epistatically suppressed by the non-nodulation, root-expressed mutation. These findings suggest that different plant organs can influence the expression of the nodulation phenotype.

Journal Article↗
PubMed1986

Depression, urinary free cortisol excretion and lymphocyte function.

An impairment in lymphocyte response to mitogen stimulation, a correlate of cell-mediated immunity, has been reported in patients with depressive illness. To investigate whether such impairment in lymphocyte function is related to excessive secretion of cortisol, an immunosuppressive hormone, we compared mitogen-induced lymphocyte proliferation in three groups of subjects: depressed patients with elevated 24-hour urinary free cortisol (UFC) excretion; depressed patients with normal UFC excretion; and normal controls. Depressed patients in both groups showed significant reductions in lymphocyte mitogenic activity, in comparison with the normal controls, but the two depressive groups did not significantly differ from each other in their lymphocytic responses to any of the mitogens used. Furthermore, no significant correlations were found, within depressed patients, between UFC excretion and lymphocyte mitogenic responses. Depression is therefore associated with an impairment in lymphocyte function that cannot be explained solely on the basis of increased cortisol secretion.

Depressive Disorder↗
PubMed1986

Informed use of the dexamethasone suppression test.

Like all laboratory tests, the dexamethasone suppression test (DST) should be used as an aid to diagnosis in specified clinical contexts. The test is not appropriate for routine screening for all psychiatric patients; it is most useful in those with a clinical picture of endogenous or melancholic depression for whom treatment with antidepressant drugs or ECT is being considered. In such cases, normalization of the DST may precede and be prognostic of clinical improvement. By contrast, failure of the DST to normalize in hospitalized patients being considered for discharge may be an indicator of possible relapse. Factors that can invalidate the DST, producing spurious false-positive results, are described, and the general principles for sound clinical use of the DST as a laboratory test in psychiatry are summarized.

Bipolar Disorder↗
PubMed1985

Opioid regulation of hypothalamic-pituitary-adrenal function in depression.

A morphine infusion paradigm was used to investigate opioid mechanisms in the regulation of the hypothalamic-pituitary-adrenal (HPA) axis in depression. The subjects were unmedicated psychiatric inpatients and healthy volunteers. Morphine suppressed cortisol secretion. Early resumption of cortisol secretion was associated with a diagnosis of major depression and abnormal dexamethasone suppression test results. Our data suggest that the hyperactivity of the HPA axis observed in depression is abnormally resistant to opioid inhibition as well as glucocorticoid feedback.

Adult↗
PubMed1985

Plasma cortisol determination for the dexamethasone suppression test. Comparison of competitive protein-binding and commercial radioimmunoassay methods.

Quality control serum samples and postdexamethasone plasma pools were used to compare 16 commercial cortisol radioimmunoassay kits with the competitive protein-binding assay for plasma glucocorticoids that we used to standardize the dexamethasone suppression test (DST). Thirteen radioimmunoassays gave higher criterion values for the DST than those established using the competitive protein-binding assay. The range of radioimmunoassay criterion values was 4.34 to 8.70 mu mg/dL. Possible explanations are given for these findings, and their importance to the clinical utility of the DST are emphasized. Each laboratory should validate its own criterion cortisol value for depression based on local data, including appropriate control groups.

Depressive Disorder↗
PubMed1985

Prolactin response to morphine in depression.

Twenty-two unmedicated inpatients with major depression and 18 healthy volunteers of either sex were given an intravenous injection of 5 mg morphine. Blood samples were drawn immediately before and at intervals for 3 hrs after the injection and assayed for prolactin. Morphine stimulated prolactin secretion. The prolactin response of females was significantly greater than the response of male subjects. There were no significant differences in the prolactin response to morphine between depressed and healthy subjects. The implications of these findings for the hypothesized role of the opioid system in the pathophysiology of depression are discussed.

Adult↗
PubMed1985

Cortisol escape from morphine suppression.

Twenty-one unmedicated, sequentially admitted psychiatric patients of either sex and four male healthy volunteers were given an intravenous injection of 2.5 mg morphine. Blood samples were drawn immediately before and at 30-minute intervals for 3 hours after the injection and assayed for cortisol. Morphine suppressed cortisol secretion. Early resumption of cortisol secretion (escape) was more frequent in patients with a diagnosis of major depressive disorder and with abnormal dexamethasone suppression test results. The sensitivity of this infusion paradigm for the diagnosis of major depressive disorder was 40%, and the specificity was 82%. The implications of these findings for the pathophysiology of depression are discussed.

Adult↗
PubMed1985

Isolation and properties of soybean [Glycine max (L.) Merr.] mutants that nodulate in the presence of high nitrate concentrations.

Soybean seeds [Glycine max (L.) Merr. ev. Bragg] were mutagenized with ethyl methanesulfonate. The M(2) progeny (i.e., the first generation after mutagenesis) of these seeds were screened for increased nodulation under high nitrate culture conditions. Fifteen independent nitrate-tolerant symbiotic (nts) mutants were obtained from 2500 M(2) families. In culture on sand with KNO(3), nodule mass and nodule number in mutant lines were several-fold those of the wild type cultured under the same conditions. Inheritance of the nts character through to subsequent generations was observed in the 10 mutants tested. Mutant nts382 also nodulated more than the wild type in the absence of nitrate. Furthermore, nitrate stimulated growth in both the wild type and nts382, and these lines had similar nitrate reductase activity. These results indicate that nts382 is affected in a nodule-development regulatory gene and not in a gene related to nitrate assimilation.

Journal Article↗
PubMed1985

A Supernodulation and Nitrate-Tolerant Symbiotic (nts) Soybean Mutant.

The nodulation characteristics of soybean (Glycine max) mutant nts382 are described. The mutant nodulated significantly more than the parent cultivar Bragg in the presence and absence of several combined nitrogen sources (KNO(3), urea, NH(4)Cl, and NH(4)NO(3)). The number of nodules on the tap root and on lateral roots was increased in the mutant line. In the presence of KNO(3) and urea, nitrogenase activity was considerably higher in nts382 than in Bragg. Mutant plants were generally smaller than wild-type plants. Although nts382 is a supernodulator, inoculation with Rhizobium japonicum was necessary to induce nodule formation and both trial strains CB1809 (= USDA136) and USDA110 elicited the mutant phenotype. Segregation of M(3) progeny derived from a M(2) wild-type plant indicated that the mutant character is inherited as a Mendelian recessive. The mutant is discussed in the context of regulation of nodulation and of hypotheses that have been proposed to explain nitrate inhibition of nodulation.

Journal Article↗
PubMed1985

Dexamethasone suppression test: a review of contemporary confusion.

Reasons for the current controversy and confusion about the dexamethasone suppression test (DST) are reviewed, and basic axioms regarding use and interpretation of the test are reiterated. Problems with reliability and validity of current diagnostic systems limit their use as "gold standards" for evaluating the DST; accurate evaluation must await follow-up and treatment response studies. Interpretation of DST results in specific patients requires common sense, consideration of the clinical context, and attention to technical factors. While its ultimate significance is not yet known, the DST, like other laboratory tests, may help to resolve uncertainty in clinical diagnosis. Perhaps most important, it may help to refine current paradigms for psychiatric nosology and diagnosis.

Acute Disease↗
PubMed1984

Biological 'markers' for endogenous depression. Effect of age, severity of illness, weight loss, and polarity.

The dexamethasone suppression test (DST) can differentiate between endogenous and nonendogenous depression. Similarly, EEG sleep patterns can differentiate primary from secondary depression, and this technique has also been used to make the endogenous-nonendogenous discrimination. However, a number of physiological variables associated with this diagnostic distinction may also affect the DST results and sleep architecture. With the use of multivariate statistical procedures, we found that although age and weight loss affect the results of both tests, both the DST and sleep EEG differentiate endogenous from nonendogenous depression when these variables are taken into account. Severity of illness affected both proposed diagnostic markers, but did not account for the differences between diagnostic groups, alone or when added to the physiological variables. The DST was more sensitive in unipolar than in bipolar endogenous depression, but there were no significant differences in the sleep of unipolar and bipolar patients.

Adult↗
PubMed1984

Hypothalamic-pituitary-adrenocortical activity in patients with diabetes mellitus.

Several clinical and physiologic associations between depression and diabetes mellitus have been reported. In this study, a potential neuroendocrine association was studied by measuring hypothalamic-pituitary-adrenocortical (HPA) axis activity in patients with diabetes mellitus. Plasma cortisol levels and response to dexamethasone administration were determined in 54 diabetics. Twenty-three (55%) of forty-two 1-mg dexamethasone suppression tests (DSTs) performed in 34 subjects, with eight repeated tests, and two (10%) of twenty 2-mg DSTs demonstrated a blunting of normal suppression. None of a variety of potential demographic, physiologic, or mood factors predicted nonsuppression. This study replicates prior findings that HPA dysfunction occurs in association with diabetes, and invalidates the use of the 1-mg DST as a diagnostic marker for melancholia in patients with diabetes.

Adult↗
PubMed1984

A psychoendocrine study of premenstrual tension syndrome. A model for endogenous depression?

We studied 42 women with severe Premenstrual Tension Syndrome (PMTS) and compared their clinical features and adrenocortical function with those seen in major depressive disorders. Self-report scales demonstrated that PMTS was very distressing, but the disturbance did not meet the RDC for Major Depressive Disorder -- endogenous subtype. Twenty-four hour urinary free cortisol estimation did not indicate cortisol hypersecretion and abnormal Dexamethasone Suppression Test results occurred much less frequently than is usual in endogenous depression. Adrenocortical function did not differ significantly between follicular and premenstrual phases. PMTS does not appear to be a psychoendocrine model for endogenous depression.

Adult↗
PubMed1984

Plasma prolactin and severe premenstrual tension.

It has been suggested that elevated luteal phase prolactin (PRL) levels may have an important role in causing some of the symptoms of the premenstrual tension syndrome (PMTS). Thirty-seven women suffering from severe premenstrual dysphoria were selected for this study. Single morning and afternoon serum PRL evaluations were performed during the follicular (day 9) and late luteal (day 26) phases of the menstrual cycle. PRL was measured by an established double antibody radioimmunoassay technique. All mean PRL values were within the normal range. Only afternoon mean PRL levels showed a tendency for a premenstrual increase. The significance of this statistical finding is unclear, since one-third of the subjects showed a decrease in premenstrual PRL levels. Twenty-four hour PRL secretory profiles recorded on days 9 and 26 in two women with extremely severe PMTS and in two asymptomatic matched control subjects also failed to show a significant correlation between PRL levels and PMTS. Thirty subjects participated in a treatment trial using bromocriptine. A marked rebound hyperprolactinemia was observed in a subgroup of women nine days after cessation of bromocriptine. This was associated with no detectable effect on mood, behavior, or menstrual regularity. Thus, our data fail to show any specific relationship between PRL and PMTS.

Adult↗
PubMed1984

Comparison of plasma cortisol and corticosterone in the dexamethasone suppression test for melancholia.

The suppression of plasma corticosterone (B), measured by radioimmunoassay (RIA), was compared to simultaneous suppression of plasma cortisol (F), measured as total corticoids by a competitive protein binding (CPB) assay, in the overnight dexamethasone suppression test (DST). Baseline plasma B concentrations in 10 control subjects were 4.04 +/- 1.07 ng/ml (X +/- S.D.) at 0800 hr and 1.51 +/- 0.68 ng/ml at 1600 hr. Post-dexamethasone 1600 hr B levels in the controls were 0.46 +/- 0.29 ng/ml. An early escape of plasma B (greater than 1.2 ng/ml), like that of F (greater than 5 micrograms/dl), during the overnight 24 hr 1.0 mg dose DST was noted in patients with melancholia (endogenous depression). Half-hourly catheter samples in a normal subject stimulated to escape from dexamethasone suppression showed that in general, plasma B concentrations parallel plasma F concentrations over a 12 hr period. Repeated weekly DSTs on two patients with different psychiatric diagnoses resulted in B : F correlations of 0.74 and 0.60. Overall agreement between B- and F-DST outcomes in all categories tested at 1600 and 2300 hr was 93%; the agreement in the melancholic and non-endogenous depressed groups was 100%. Post-dexamethasone, both B and F were suppressed 55-60% below the criterion level in controls. In those patients who escaped from dexamethasone suppression, the percentage increase in plasma B above the criterion level was significantly greater (+55%) than the corresponding percentage change in plasma F. Most patients with borderline abnormal F-DSTs (3.5 - 4.9 micrograms/dl) exhibited clearly abnormal B-DSTs (greater than 1.2 ng/ml). We conclude that the use of dexamethasone suppression of plasma B (using 1.2 ng/ml as the abnormal criterion value) is an additional indicator of an abnormal DST in depressed patients.

Bipolar Disorder↗
PubMed1984

Morphine inhibits cortisol and stimulates prolactin secretion in man.

The role of opioids in endocrine regulation has been the subject of numerous studies. Surprisingly, however, the acute endocrine effects of morphine on basal hormonal levels in man have not been adequately documented. We report here the effects of intravenous morphine (5 mg) on plasma cortisol and prolactin. Fourteen healthy volunteers (nine male, five female) received morphine at 0930 hr. Blood samples were collected immediately before and 30, 60, 90, 120 and 180 min after the injection. In six of the male subjects the procedure was repeated with a placebo (normal saline) injection. Morphine stimulated prolactin release. There was a trend for a greater response in females compared to male subjects. Cortisol secretion was markedly suppressed by morphine. In sharp contrast to the results obtained with placebo, cortisol levels following morphine declined progressively at a rate consistent with the half-life of cortisol. This downward trend of cortisol values continued uninterrupted for the duration of the experiment in all 14 subjects. These results are consistent with the presence of an inhibitory opioid mechanism in the human hypothalamo-pituitary-adrenal axis.

Adrenal Cortex↗
PubMed1984

Circadian hormone secretory profiles in women with severe premenstrual tension syndrome.

The circadian secretory profiles of serum prolactin, growth hormone and cortisol were measured in two women suffering from severe premenstrual tension syndrome and in two asymptomatic control subjects. Subjects and controls were screened and included after a rigorous selection process. Blood samples were obtained every 30 min over a period of 24 h in each woman both on day 9 (follicular phase) and day 26 (luteal phase) of the menstrual cycle. There was no relationship between the hormonal secretory profiles and the premenstrual tension syndrome.

Adult↗