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Biomedical subjects

K L Davis

Publications and source records attributed to K L Davis.

At least 379 records · Page 21Linked to original sources
PubMed1976

Pituitary response to thyrotropin-releasing hormone in depression.

Plasma thyrotropin (TSH) levels varied relatively little over minutes to days in the same individual not subjected to challenge with thyrotropin-releasing hormone (TRH). Thus, the TSH response to stimulation with TRH is not likely to be confounded by spontaneous changes of comparable degree. Variable numbers of depressed patients showed a blunted response to TRH stimulation of the pituitary, but the exact prevalence of this phenomenon remains to be clearly defined. In any case, the pituitary response to TRH stimulation was not correlated with the prevailing level of depression, nor did this response to an initial TRH challenge predict the degree of clinical change during a 15-day treatment during which three intravenous doses of 600 mug of TRH were given. Depressed patients, as do schizophrenics and normal patients, show diminished TSH responses to repeated challenges with TRH. Whether or not these three groups differ in regard to the rate at which the pituitary response can be abolished remains to be determined.

Administration, Oral↗
PubMed1976

Tardive dyskinesia and depressive illness.

Tardive dyskinesia has been regarded as a long-term complication of neuroleptic administration to patients with the diagnosis of schizophrenia. However, nine of the first fourteen patients evaluated for an investigation of tardive dyskinesia met diagnostic criteria for depression. Neuroleptics produce blockade of post-synaptic dopaminergic receptors. Tardive dyskinesia occurs when neuroleptics are discontinued, and is regarded as a manifestation of super-sensitive post-synaptic dopaminergic receptors. Tardive dyskinesia occurs when neuroleptics are discontinued, and is regarded as a manifestation of super-sensitive post-synaptic dopaminergic receptors. Chronically decreased neurotransmission in the synapse of a patient with depression may contribute to the development of a super-sensitive receptor and could explain the high proportion of patients with depression seen in this sample of patients with tardive dyskinesia.

Antidepressive Agents, Tricyclic↗
PubMed1975

Thyrotropin-releasing hormone in schizophrenia.

Oral administration of thyrotropin-releasing hormone (TRH) caused deterioration in the clinical status of seven out of nine schizophrenic men. This change was particularly apparent in the four patients diagnosed as paranoid schizophrenics. Such changes might be expected from a drug with properties similar to amphetamine.

Administration, Oral↗
PubMed1975

Cholinergic imbalance hypotheses of psychoses and movement disorders: strategies for evaluation.

It has been proposed that the etiologies of tardive dyskinesia and Huntington's chorea and of some forms of schizophrenia and the affective disorders involve a cholinergic imbalance with respect to a second neurotransmitter. This relative over- or underactivity of the cholinergic system could result from altered synthesis, storage, release, degradation, or reuptake or from a variety of receptor interactions. Under these hypotheses, clinical symptoms would reflect both the brain region in which the imbalance occurs and the neurotransmitter with which acetylcholine is interacting. Effective treatments could involve the correction of this hypothetical imbalance by changing the relative availability of either one or both of the neurotransmitters. Both precursor loading with choline or dimethylaminoethanol and cholinesterase inhibition may be useful in evaluating the effects of increased cholinergic activity in these disease states; the relative merits of these strategies are discussed.

Biogenic Amines↗
PubMed1975

Butaclamol hydrochloride in newly admitted schizophrenics.

Butaclamol hydrochloride, a new type of antipsychotic drug, was evaluated by an uncontrolled study of 13 newly admitted schizophrenic patients. The drug had antipsychotic effects as well as a strong propensity for evoking extrapyramidal side effects. With the maximal daily doses of 30 mg used in this study, therapeutic results obtained were probably somewhat less than optimal.

Clinical Trials as Topic↗
PubMedDate not supplied

Correlation between elevated levels of amyloid beta-peptide in the brain and cognitive decline.

CONTEXT: Alzheimer disease (AD) is characterized neuropathologically by the presence of amyloid beta-peptide (Abeta)-containing plaques and neurofibrillary tangles composed of abnormal tau protein. Considerable controversy exists as to whether the extent of accumulation of Abeta correlates with dementia and whether Abeta alterations precede or follow changes in tau. OBJECTIVES: To determine whether accumulation of Abeta correlates with the earliest signs of cognitive deterioration and to define the relationship between Abeta accumulation and early tau changes. DESIGN, SETTING, AND PATIENTS: Postmortem cross-sectional study of 79 nursing home residents with Clinical Dementia Rating (CDR) scale scores of 0.0 to 5.0 who died between 1986 and 1997, comparing the levels of Abeta variants in the cortices of the subjects with no (CDR score, 0.0 [n = 16]), questionable (CDR score, 0.5 [n = 11]), mild (CDR score, 1.0 [n = 22]), moderate (CDR score, 2.0 [n = 15]), or severe (CDR score, 4.0 or 5.0 [n = 15]) dementia. MAIN OUTCOME MEASURES: Levels of total Abeta peptides with intact or truncated amino termini and ending in either amino acid 40 (A(beta)x-40) or 42 (A(beta)x-42) in 5 neocortical brain regions as well as levels of tau protein undergoing early conformational changes in frontal cortex, as a function of CDR score. RESULTS: The levels of both A(beta)x-40 and A(beta)x-42 were elevated even in cases classified as having questionable dementia (CDR score = 0.5), and increases of both peptides correlated with progression of dementia. Levels of the more fibril-prone A(beta)x-42 peptide were higher than those of A(beta)x-40 in nondemented cases and remained higher throughout progression of disease in all regions examined. Finally, increases in A(beta)x-40 and A(beta)x-42 precede significant tau pathology at least in the frontal cortex, an area chosen for examination because of the absence of neuritic changes in the absence of disease. CONCLUSIONS: In this study, levels of total A(beta)x-40 and A(beta)x-42 were elevated early in dementia and levels of both peptides were strongly correlated with cognitive decline. Of particular interest, in the frontal cortex, Abeta was elevated before the occurrence of significant tau pathology. These results support an important role for Abeta in mediating initial pathogenic events in AD dementia and suggest that treatment strategies targeting the formation, accumulation, or cytotoxic effects of Abeta should be pursued.

Aged↗
PubMedDate not supplied

Antemortem markers of Alzheimer's disease.

This review examines various approaches to the development of antemortem markers of Alzheimer's disease. Among the procedures discussed are: neurochemical and histopathologic studies of the cholinergic system, concentrating on CSF and blood plasma; genetic studies; imaging and electrophysiological studies; and neuroendocrine studies.

Alzheimer Disease↗
PubMedDate not supplied

Toward a therapeutic strategy based on amyloid precursor protein: unanswered questions.

Undoubtedly, the future will see experimental therapeutics based on attempts to alter the processing of the amyloid precursor protein, and the formation of senile plaques. As these approaches evolve, it will become increasingly important to determine the role of amyloid precursor protein in normal and abnormal brain. Amyloid precursor protein may have beneficial therapeutic effects that need to be preserved. Any agent designed to alter the process of amyloid precursor protein would be designed to alter the course of Alzheimer's disease. Methodological problems abound in clinical studies designed to show the ability of a therapeutic agent to slow the progress of a degenerative brain disease. These difficulties and possible solutions are explored.

Alzheimer Disease↗
PubMedDate not supplied

Platelet phospholipid synthesis in Alzheimer's disease.

The rates of incorporation of [3H]choline and [3H]ethanolamine into membrane phospholipids of platelets from 22 drug-free Alzheimer's disease patients and 18 normal elderly controls were compared. No significant differences between groups were found. If alterations in lipid metabolism are involved in the pathophysiological processes underlying Alzheimer's disease, such alterations are not manifest in measures of radiolabeled base incorporation into platelet phospholipids.

Aged↗
PubMedDate not supplied

Computer-administration of questionnaires: a health screening system (HSS) developed for veterans.

The introduction of microcomputers in psychological research has spawned a burgeoning number of tests of psychological or behavioral function, but few computerized systems for administering questionnaires have been developed. A Health Screening System (HSS) is described that combines the benefits of the paper-and-pencil format (e.g., convenient navigation within test questions) and the added benefits of computer-implementation (e.g., efficiency, automated scoring). The HSS features; a) appealing test appearance (e.g., text in large-size fonts, color backgrounds); b) clear wording of tests and instructions (identical wording as original tests except when clarity is served by changes); c) limiting need for Examiner-Subject interaction (e.g., continuously available on-line training, navigation within test questions, answer review capability, durable 9-button response unit); d) options (e.g., question skipping, spoken instructions, test questions, and answers on command); e) modification capabilities (e.g., color, text, test layout editing, control of test order, automated breaks, addition of tests to system); and f) extras (e.g., kernel of main instruction on each test screen, digitized video, audio message from Examiner in training, copyright notification on each screen, raw and summary data outputs in spreadsheet formal). Ten HSS tests were administered to 22 US military veterans, who took slightly longer to complete them than did 10 veterans who were administered the same tests in their original paper-and-pencil format. User reaction to the computerized HSS was positive.

Adult↗
PubMedDate not supplied

Diagnostic issues in chronic schizophrenia: kraepelinian schizophrenia, undifferentiated schizophrenia, and state-independent negative symptoms.

Data are presented concerning three recent clinical distinctions in schizophrenia: kraepelinian versus non-kraepelinian patients; mixed versus simple undifferentiated subtypes; and state-dependent versus state-independent negative symptoms. Schizophrenic patients who have been ill and dependent on others for the past 5 years ('kraepelinians') were compared to other chronic schizophrenics. The kraepelinian patients met the criteria for schizophrenia by more diagnostic systems than other patients, were less responsive to haloperidol, had more severe negative symptoms and formal thought disorder, and had similarly severe positive symptoms. They also had cerebral ventricles that demonstrated more left-to-right asymmetry and a greater family history of schizophrenia spectrum disorders. Mixed undifferentiated schizophrenic patients, who met criteria for more than one schizophrenic subtype, were compared to simple undifferentiated schizophrenic patients, who met criteria for no subtype. The mixed group was characterized by more severe positive and negative symptoms and formal thought disorder, worse social functioning, and a worse response to haloperidol. In a subgroup of patients who were studied once while in a state of exacerbation and once while in a state of relative remission, the negative symptoms of inattention and affective flattening were state-dependent, while anhedonia-asociality was state-independent.

Adult↗