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Biomedical subjects

J C Nelson

Publications and source records attributed to J C Nelson.

At least 199 records · Page 11Linked to original sources
PubMed1981

Anterior pituitary hormone levels in the cerebrospinal fluid of patients with pituitary and parasellar tumors.

Cerebrospinal fluid (CSF) concentrations of growth hormone, prolactin (PRL), adrenocorticotropin, thyroid-stimulating hormone, follicle-stimulating hormone, luteinizing hormone, and the glycoprotein hormone alpha subunit were determined in 30 patients with pituitary and parasellar tumors. Although many of the patients had elevated hormone levels, no differentiation between patients with intrasellar tumors and those with pituitary tumors with suprasellar extension or primary suprasellar tumors could be made based upon the absolute CSF hormone concentration. A highly significant correlation between serum and CSF PRL concentrations was found (r = 0.87; P less than 0.001), suggesting that CSF PRL is derived from the serum. No correlation was found between the serum and CSF concentrations of the other anterior pituitary hormones.

Adrenocorticotropic Hormone↗
PubMed1981

Psychosis and depression arising in the midlife period. A comparison.

Two groups of hospitalized psychotic patients were compared to a hospitalized nonpsychotic group composed mainly of major unipolar depressives. In the main, demographic and historical dimensions did not differ. Interpersonal and social role development favored the nonpsychotic group, but only employment history and maternal function reached significance. All groups were judged to be under substantial stress in association with the index hospitalization. Loss of a supportive relationship was the most frequent stress category for all groups but was relatively more frequent in the nonpsychotic (depressive) group. Medical stress was significantly higher in the psychotic groups.

Adult↗
PubMed1981

The symptoms of major depressive illness.

The authors suggest that the common characteristics of various descriptions of major depressive illness--endogenous, endogenomorphic, psychotic, and melancholic--are an autonomous course, a need for biological treatment, and a presumed alteration in neurochemistry. The literature is reviewed to determine those symptoms which best characterize this syndrome. These symptoms may prove useful in developing valid diagnostic criteria for major depressive illness.

Antidepressive Agents, Tricyclic↗
PubMed1981

Personality traits and disorder in depression.

The authors examined the relationship of personality traits and personality disorder to depressive subtype, descriptive characteristics, and outcome in 160 depressed inpatients. Personality disorder was significantly more common in unipolar nonmelancholic depressed patients (61%) than in unipolar melancholic (14%) or bipolar depressed patients (23%). Personality disorder did not affect symptom manifestation but was related to earlier onset of depressive illness and worse outcome within the unipolar nonmelancholic group. Obsessive traits were most common in the unipolar melancholic patients, while histrionic, hostile, and borderline traits predominated in the nonmelancholic patients. The authors discuss the usefulness of a multiaxial diagnostic system and the importance of separating trait and disorder in personality assessment.

Adult↗
PubMed1981

Delusional and nondelusional unipolar depression: further evidence for distinct subtypes.

In a retrospective analysis, the course, symptoms, treatment response, and personality of 54 delusional and 66 nondelusional unipolar depressed patients were compared. The delusional patients had more guilt feelings and were more ruminative, agitated, and referential than the nondelusional patients. They had a poor response to a tricyclic antidepressant therapy but good treatment outcome with a tricyclic-antipsychotic combination or ECT. The form and content of prior episodes were remarkably similar to the index episode in both groups. The authors believe that these findings support the conception of unipolar delusional depression as a distinct subtype of depressive illness.

Adult↗
PubMed1981

16 Alpha-[125I]-beta-estradiol compared with [3H]-beta-estradiol as the tracer in estradiol receptor assays.

We assessed the potential usefulness of 16 alpha-[125I]-beta-estradiol in estradiol receptor assays as compared with a long-used [3H]-beta-estradiol dextran-coated charcoal method, measuring 472 consecutive human breast-cancer cytosols by both procedures. Six different preparations of 16 alpha-[125I]-beta-estradiol were used. Nonspecific binding in five batches was similar and comparable to [3H]-beta-estradiol. Although the sixth batch had increased nonspecific binding, this did not affect results. Dissociation constants were virtually identical (r = 0.94). Results were concordant for 98.5% of cytosols: 161 were negative and 304 positive by both methods and seven were positive by one method, negative by the other. Four were positive with the 125I procedure and undetectable with [3H]-beta-estradiol. Three were measurable by both methods, but were above the cut-off value in one and below it in the other. We find 16 alpha-[125I]-beta-estradiol to be an adequate substitute for [3H]-beta-estradiol in estradiol receptor assays.

Breast Neoplasms↗
PubMed1980

Primary affective disorder criteria and the endogenous-reactive distinction.

Seventy-six patients hospitalized during the course of one year with a depressive episode and without prior history of other psychiatric illness were evaluated retrospectively using the primary affective disorder criteria. Symptom ratings were made by two raters uninvolved in the treatment of the patient and blind to the discharge diagnosis, hospital course, and treatment response. The patients were designated "endogenous" or reactive" based on whether the depressive syndrome was autonomous or responsive to environmental changes. Ninety-two percent of the patients with endogenous depression and 45% of those with reactive depression met the criteria for definite primary affective disorder. We suggest that the primary affective disorder criteria define a heterogeneous group of patients with respect to the endogenous-reactive distinction. The value of criteria that would identify a homogeneous group with an endogenous depressive state is discussed. The primary affective disorder symptoms that did identify patients with endogenous depression were psychomotor change, self-reproach, and decreased concentration.

Adjustment Disorders↗
PubMed1980

Characteristics of autonomous depression.

The records of 172 depressed inpatients were examined retrospectively to determine the presenting symptoms, history of stress, clinical course, and personality features characteristic of patients whose depressive syndrome had become autonomous. The autonomous distinction was based on observation of a lack of responsiveness of the syndrome to environmental events during the first week of hospitalization prior to drug treatment. The autonomous criterion was selected since it is a central characteristic of recent psychobiological models of depression and it could be operationally defined, reliably rated, and assessed independently of other patient characteristics. Sixty-eight autonomous patients were identified and compared with 104 patients who were responsive to hospitalization. The characteristics of the autonomous patients are discussed in relation to the previous literature, other diagnostic systems, and the criteria proposed for the diagnosis of melancholia in DSM-III.

Adjustment Disorders↗
PubMed1980

Induced fetal hyperthyroidism: cardiac output and oxygen consumption.

In 13 chronically catheterized fetal lambs, we inserted a subcutaneous osmotic minipump that released triiodothyronine (T3) at a rate of 5.9 microgram x h-1. Five days postoperatively, fetal plasma T3 concentration had increased 10-fold from a control value of 18.4 ng x dl-1; reverse T3 and thyroxine had decreased 83 and 61% from control values of 524 ng x dl-1, and 9.5 microgram x dl-1, respectively. Fetal heart rate increased 29% to 210 from 163 beats x min-1, and blood pressure remained constant. Cardiac output measured with radioactive-labeled microspheres increased 22% to 678 +/- 33 from a control value obtained from another group of animals of 554 +/- 16 ml x min-1 x kg-1. Umbilical blood flow also increased 22%, while coronary flow increased 35%, and pulmonary flow increased 90%. In contrast, flow to the thyroid gland decreased 52%. Fetal oxygen consumption increased 28% to 10.5 +/- 0.5 from 8.2 +/- 1.1 ml x min-1 x kg-1. Placental carbon monoxide diffusing capacity and venous and arterial blood gas values remained unchanged. We conclude that 1) sustained fetal T3 infusion is one of the few factors that can increase fetal cardiac output, and may play a role in increasing cardiac output in the newborn infant, 2) T3 infusion results in an increased rate of metabolism with increased oxygen consumption, and 3) placental reserve for oxygen diffusion exceeds normal oxygen requirements.

Animals↗
PubMed1980

Neuroloeptic effect on desipramine steady-state plasma concentratins.

The authors examined the effect of neuroleptic drugs on desipramine steady-state plasma concentration in 30 patients who received similar milligram per kilogram doses of desipramine. Fifteen of these patients also received a neuroloeptic drug and had desipramine plasma levels twice that of the 15 patients who received dispiramine alone. The authros discuss the implications of the magnitude of this difference for therapeutic response and incidence of side effects.

Adult↗
PubMed1979

Surgical treatment of chronic visceral ischemia.

Our experience with the operative repair for chronic visceral ischemia in eight patients, including two patients without visceral ischemic symptoms, is described. We prefer revascularization of as many vessels as possible and have used a small diameter Dacron bifurcation graft directed cephalad from the infrarenal aorta to the superior mesenteric artery and hepatic or splenic artery in four patients. One patient died postoperatively of an arrhythmia. Three patients died of unrelated causes 7 to 36 months after surgery. Four patients are alive 8 to 48 months after surgery. All patients were relieved of the intestinal ischemic symptoms by surgery.

Aorta, Abdominal↗
PubMed1979

Somnambulistic-like episodes secondary to combined lithium-neuroleptic treatment.

Ten of 114 psychiatric patients undergoing combined lithium-neuroleptic treatment exhibited somnambulistic-like episodes. These episodes are differentiated from nocturnal wanderings and epileptic attacks during sleep; they occurred within two to three hours after sleep onset and were characterized by the patients appearing confused and walking about in a quiet, detached and clumsy manner. Generally, there was amnesia for the event. Since sleepwalking occurs out of slow wave sleep, the increase in slow wave sleep induced by lithium and certain neuroleptics may represent a neurophysiological mechanism responsible for these patients' somnambulistic behaviour. The occurrence of grand mal seizures in two patients was probably unrelated to the somnambulistic-like episodes. However, persistence of the latter appears to be associated with drug-induced EEG irregularity.

Adolescent↗
PubMed1979

Exacerbation of psychosis by tricyclic antidepressants in delusional depression.

The authors describe three patients with delusional unipolar depression whose delusional thinking worsened markedly following administration of tricyclic antidepressant drugs. The patients had met Research Diagnostic Criteria for major depressive episode and had no evidence of schizophrenia or mania. Since tricyclic antidepressants are known to exacerbate psychosis in schizophrenic patients, it is sometimes suggested that the exacerbation of psychotic thinking in depressed patients indicates schizophrenia. The authors suggest that such an exacerbation does not in itself indicate schizophrenia but may occur in patients with an affective disorder who are prone to depressive delusions. The authors discuss the use of antipsychotic medication in this patient group and present a neurochemical hypothesis to explain the interaction of the drug with the illness, which results in exacerbation of psychotic thinking.

Antidepressive Agents, Tricyclic↗
PubMed1978

Disseminated intravascular coagulation. Complication of LeVeen peritoneovenous shunts.

Disseminated intravascular coagulation (DIC) occurred in three of five patients after insertion of a LeVeen shunt for intractable ascites. Four episodes of DIC in these patients ranged in severity from progressive and life-threatening to transient and asymptomatic. Interruption of the shunt in two patients stopped the DIC. Careful monitoring for DIC following shunt insertion allows rational decisions to protect the patient against life-threatening hemorrhage or thrombosis. Disseminated intravascular coagulation occurred in two patients during a trial intravenous infusion of ascites and occurred in one patient even when the surgical procedure was modified to minimize the volume and rate of the infused ascites.

Aged↗
PubMed1978

Delusional unipolar depression: description and drug response.

This retrospective study describes the response of 13 delusional unipolar depressives to combination antipsychotic-tricyclic antidepressant drug therapy. The Research Diagnostic Criteria were used by two independent raters to verify the presence of a delusional, primary, unipolar, major depressive disorder. Thirteen patients met the criteria and received combined antipsychotic-antidepressant pharmacotherapy. Twelve of the 13 responded. This contrasts sharply with the low response rate described for delusional depressives when treated with tricyclic antidepressants alone. Descriptive characteristics of the delusional depressives were compared with those of a group of nondelusional unipolar depressives. Delusional depressives had histories of a greater number of prior depressive episodes and more of the delusional depressives demonstrated a psychomotor disturbance.

Adult↗
PubMed1978

Reduced thyroid function after thyrotropin stimulation.

The course of serum T4 and T3 return to baseline after TSH stimulation was studied in two groups at six normal subjects over 28 days after im bovine TSH (b TSH; 0.15 U/kg). In the first group of six subjects, serum bTSH rose from undetectable levels to a mean peak of 5.6 +/- 0.5 ng/ml (mean +/- SE) at 2 h, and fell below detectable levels by 24 h with a t1/2 of 7 +/- 1 h. T4 rose to a peak 59 +/- 10% above basal levels within 24 h, returned to basal levels on day 7, then dropped below basal levels on days 9-24, with a nadir of -16 +/- 4% on day 14. Free T4 paralleled T4 levels. T3 rose to a peak 104 +/- 28% above basal at 24 h, then fell faster than T4, reaching basal levels by day 4. During the period of low T4, T3 was at or below basal levels. Human TSH (h TSH) concentration dropped when T4 and T3 rose, but did not rise above basal levels when T4 and T3 fell below basal levels. Neither a T3 elevation nor an increased percentage of free T4 was present during the time of reduced T4 levels. The same pattern of thyroidal response was seen in the second group of six subjects. In this second group, hTSH response to repeated TRH challenge was studied. During the period of reduced T4 and T3, hTSH response to TRH was diminished. On day 28, T4, T3, hTSH, and hTSH response to TRH returned to basal levels. We conclude that the brief elevation of T4 and T3 after bTSH stimulation exerts a suppressive effect on the pituitary which extends beyond the period of elevated thyroid hormone levels, and that delay in pituitary recovery is the mechanism of the decreased thyroid function after acute bTSH stimulation.

Adult↗
PubMed1978

Heparin-induced thrombocytopenia.

Two patients with underlying thromboembolic disorders developed severe thrombocytopenia while receiving heparin sodium; one of these patients developed recurrence of the thrombocytopenia and possible heparin-induced pulmonary emboli when heparin was restarted. In a prospective study of patients receiving heparin in a coronary care unit (CCU), nine of 37 patients developed transient mild thrombocytopenia (platelet counts ranging from 88,000 to 150,000/cu mm). Heparin added to citrated platelet-rich plasma caused platelet aggregation in the two original patients. In three of six CCU patients tested, and in 17 of 87 other subjects, with maximum aggregation at concentrations of heparin likely to be present in vivo during therapy. We herein discuss evidence that suggests that heparin may cause or aggravate thrombosis by causing platelet aggregation. The occurrence of severe heparin-induced thrombocytopenia is well documented, and mild transient thrombocytopenia may be more common than has been recognized. Studies of heparin efficacy should take these responses into account.

Dose-Response Relationship, Drug↗