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Biomedical subjects

L E Nee

Publications and source records attributed to L E Nee.

47 records · Page 3Linked to original sources
PubMed1981

A double-blind controlled trial of lithium carbonate primary anorexia nervosa.

In this 4-week, double-blind, parallel group study, eight young women with primary anorexia nervosa were evaluated on lithium carbonate, and eight patients were treated with placebo and served as a control. All patients participated in a behavior modification treatment program. The lithium-treated and placebo groups were comparable on nearly all findings measured at baseline (t tests), with no significant differences observed except for calories per day, percent fat composition of the daily calories, "interpersonal sensitivity" on the Hopkins Symptom Checklist-90 (HSCL-90), "self-care" on the Goldberg Anorectic Attitude Questionnaires, (GAAQ) and "manipulation of others" on the physician-rated Psychiatric Rating Scale (PRS). The data were analyzed using repeated measures analysis of covariance (ANCOVA) with the baseline measure as the covariate. Group differences appeared in the areas of "denial or minimization of illness" on the GAAQ, "selective appetite" on the PRS, and weight. Although the repeated measures ANCOVA for weight revealed a significant group-by-time interaction, indicating nonparallelism and invalidating the test for group differences, ANCOVAs performed for each individual time point showed greater weight gain in the lithium group at weeks 3 and 4.

Adolescent↗
PubMed1980

Gilles de la Tourette syndrome: clinical and family study of 50 cases.

Fifty patients with Tourette syndrome were evaluated; data included family history, clinical characteristics, response to haloperidol, and side effects during haloperidol therapy. Sixteen patients had a family history of Tourette syndrome, and another 16 had a family history of tics. Twenty-four families had more than 2 members with Tourette syndrome or tics. There was no preponderance of families with a Jewish, Eastern European background in this sample. Thirty-four patients had obsessive-compulsive behavior. Among the 50 patients there was a high frequency of sleep disturbance, learning disability, self-destructive behavior, inappropriate sexual activity, and antisocial behavior. Family history was significantly related to the occurrence of sleep disturbance, obsessive-compulsive behavior, haloperidol response, and the frequency of side effects caused by haloperidol. The precise mode of genetic transmission in familial Tourette syndrome remains to be determined.

Female↗
PubMedDate not supplied

Alzheimer disease fibroblasts are hypersensitive to the lethal effects of a DNA-damaging chemical.

A group of fibroblast lines from three patients with the sporadic form of Alzheimer disease (AD) showed a small but statistically significant hypersensitivity to the lethal effects of the DNA-damaging chemical N-methyl-N'-nitro-nitrosoguanidine (MNNG) when compared with lines from eight normal control subjects. A fibroblast line from a patient with a dominantly inherited form of familial AD had a hypersensitivity similar to that of the three sporadic AD lines. However, fibroblast lines from a group of five patients with spinal muscular atrophy (SMA) were not hypersensitive to the chemical, demonstrating that not every primary neuronal degeneration manifests hypersensitivity to this chemical. These findings are consistent with the possibility that a defect in DNA-repair mechanisms may be the cause of the in vitro hypersensitivity, as well as the premature death of neurons in vivo, in both the sporadic and familial forms of AD.

Alzheimer Disease↗
PubMedDate not supplied

Serum- and bradykinin-induced calcium transients in familial Alzheimer's fibroblasts.

The calcium-sensitive photoprotein, aequorin, was used to examine serum- and bradykinin-induced transient increases in free cytosolic calcium ions in skin fibroblasts from 10 individuals with early onset familial AD (FAD), including four who were biopsied before their clinical symptoms would allow a diagnosis of AD, 2 individuals with late onset FAD, 8 at-risk but nonsymptomatic individuals, and 13 controls. The data show that (a) among controls, the peaks of the calcium transients increase in height as a function of donor age; (b) transients induced by 10% serum, 10 nM bradykinin (BK) or 100 nM BK were generally lower in FAD fibroblasts, including those from donors in the early stages of the disease, than in age-matched control cells; (c) such transients are reduced in cells from a proportion of the nonsymptomatic, at-risk individuals. Thus, serum- and BK-induced calcium transients are reduced in fibroblasts from both early and more advanced stage FAD donors and perhaps even from donors who are presymptomatic carriers of the defective gene. The data also suggest that changes in calcium transients in FAD fibroblasts neither mimic nor exaggerate the effects of normal aging.

Adult↗
PubMedDate not supplied

Distinguishable effects of presenilin-1 and APP717 mutations on amyloid plaque deposition.

Both APP and PS-1 are causal genes for early-onset familial Alzheimer's disease (AD) and their mutation effects on cerebral Abeta deposition in the senile plaques were examined in human brains of 29 familial AD (23 PS-1, 6 APP) cases and 14 sporadic AD cases in terms of Abeta40 and Abeta42. Abeta isoform data were evaluated using repeated measures analysis of variance which adjusted for within-subject measurement variation and confounding effects of individual APP and PS-1 mutations, age at onset, duration of illness and APOE genotype. We observed that mutations in both APP and PS-1 were associated with a significant increase of Abeta42 in plaques as been documented previously. In comparison to sporadic AD cases, both APP717 and PS-1 mutation cases had an increased density (measured as the number of plaques/mm(2)) and area (%) of Abeta42 plaques. However, we found an unexpected differential effect of PS-1 but not APP717 mutation cases. At least some of PS-1 but not APP717 mutation cases had the significant increase of density and area of Abeta40-plaques as compared to sporadic AD independently of APOE genotype. Our results suggest that PS-1 mutations affect cerebral accumulation of Abeta burden in a different fashion from APP717 mutations in their familial AD brains.

Adult↗
PubMedDate not supplied

Alzheimer's disease in 22 twin pairs--13-year follow-up: hormonal, infectious and traumatic factors.

We obtained follow-up data on 22 sets of twins where at least one twin had Alzheimer's disease (AD). The concordance rate for monozygotic twins (n = 17 pairs) was 59%, whereas that for dizygotic twins was 40%. In our series 8 monozygotic twins had hysterectomies; all had AD. The twins with hysterectomies also had a tendency to develop AD at an earlier age than their co-twin. Five twins with serious systemic infection developed AD, and they tended to have earlier onset than their corresponding twin. We found no strong evidence that head injury predisposed to AD.

Age of Onset↗
PubMedDate not supplied

Inherited Alzheimer's disease PS-1 olfactory function: a 10-year follow-up study.

This study was undertaken to evaluate smell tests as a clinical marker for identifying mutation carrier status and determining the clinical diagnosis of presenilin-1 Alzheimer's disease (AD) in family members of those afflicted with the disease. Ten years ago, we gave the self-administered, 40-question scratch and sniff University of Pennsylvania Smell Identification Test to 18 at-risk family members, individuals with dominantly-inherited Alzheimer's disease. Testing results were normal 10 years ago except in the case of one individual who had smoked three packs of cigarettes a day for more than 23 years. Four subjects tested in 1990 are now afflicted with Alzheimer's disease, including the smoker. The smell test in 1990 did not demonstrate predictive capabilities before clinical conversion to dementia. At follow-up, two subjects were too impaired to take the test. Two "converted" from normal smell function to abnormal function with a wide range in score. Study findings indicate that the smell test is too variable a measure to be used as a reliable test for predicting or verifying a diagnosis of presenilin-1 Alzheimer's disease.

Aged↗