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Biomedical subjects

D Gottlieb

Publications and source records attributed to D Gottlieb.

At least 55 records · Page 3Linked to original sources
PubMed1991

Passive listening and task related P300 measurement for the evaluation of dementia and pseudodementia.

The late evoked potential P300 was tested in three groups of subjects. These consisted of 25 patients suffering from dementia (Group I), 14 patients suffering from pseudodementia due to severe depressive disease (Group II), and 24 age-matched normal controls (Group III). Since patients suffering from dementia frequently have difficulties in counting targets in the "oddball" paradigm, we evaluated the usefulness of a Passive Listening condition. With the classical "oddball" paradigm, 78% of the subjects were correctly related to one of the three groups examined. The "P300-like" wave form produced in the Passive Listening condition was not found to be sensitive enough to allow such a distinction.

Adult↗
PubMed1991

Reappearance of the visual percept after intentional blinking in a patient with Balint's syndrome.

We present a patient with Balint's syndrome who complained of fading of the scenes under visual fixation. When he intentionally blinked, the faded visual percept reappeared. The disappearance of the visual percept may be explained as the result of either unstable visual fixation or of saturation of the visual pathways. The role of blinking in reviving the visual percept may be explained accordingly as causing a refixation of the target under visual fixation or as resetting the visual pathways for visual processing.

Aged↗
PubMed1990

Requirements for the adoptive transfer of antibody responses to a priming antigen in man.

Antibody responses to recall vaccines can be adoptively transferred after marrow transplantation in man. Transfer of responses to priming Ag has not been successful, although this would broaden the range of organisms to which recipients could be protected. To investigate the importance of T cells and Ag in such transfer we primed marrow donors with keyhole limpet hemocyanin (KLH) 1 or 3 wk before marrow harvesting. B cells secreting IgM and IgG anti-KLH antibody were present in donor marrow at both 1 and 3 wk after immunization. After T cell depletion, donor marrow was infused into chemo-irradiated recipients, half of whom were immunized pretransplant with KLH. We found no evidence for the transfer of the IgM component of the response. Clonal expansion of the transferred IgG antibody-secreting cells with a corresponding rise in recipient serum IgG antibody levels was seen only when donors were primed 3 wk before marrow harvest and when the recipients were also immunized. IEF and immunoblotting demonstrated that successful transfer coincided with maturation of the IgG primary response from a polyclonal to an oligoclonal pattern and confirmed that donor oligoclonal bands appeared in the recipient serum. We conclude that the immunization protocols required for the transfer of antibody responses to priming Ag reflect the initial dependence of unprimed B cells on T cell help and on prolonged Ag stimulation. Ag-stimulated primary B cells in T cell-depleted marrow respond only to the noncognate growth and differentiation signals available in the chemo-irradiated recipient after an initial period of clonal selection and expansion in the donor which is both T cell and Ag dependent. Even after this initial selection, continued expansion of antibody-secreting clones in recipients retains an absolute dependence on Ag stimulation. Immunization techniques to protect transplant recipients against organisms such as Pseudomonas and CMV may need to be modified accordingly.

Antibody Formation↗
PubMed1989

Endogenously generated activated killer cells circulate after autologous and allogeneic marrow transplantation but not after chemotherapy.

After marrow transplantation, major histocompatibility complex (MHC)-unrestricted natural killer (NK) lymphocytes are among the first cells to appear in the circulation. After T-cell-depleted bone marrow transplantation (TD-BMT), these cells have an activated pattern of target cell killing; they also secrete lymphokines including gamma-interferon (gamma-IFN), interleukin-2 (IL-2), and tumor necrosis factor (TNF) and may have a significant role as a primary defense against viral reactivation and in the elimination of residual host malignancy. We studied 43 patients with hematologic malignancy, treated by allogeneic TD-BMT, autologous nondepleted BMT, or chemotherapy alone to investigate (a) the mechanisms underlying the generation of these activated killer cells, (b) the range of conditions under which they are produced, and (c) their surface phenotype. We showed that gamma-IFN-secreting activated killer cells with the capacity to kill MHC-nonidentical NK-resistant targets are generated 4 to 6 weeks after either allogeneic TD-BMT or autologous BMT but do not appear after treatment with chemotherapy. Production therefore is not owing to T-cell depletion per se or to host donor alloreactivity, nor is it caused by stimulation by alloantigens contained in blood product support since no significant difference exists between allograft and chemotherapy patients in the number of units of blood platelet support given in the posttreatment period. Because most patients had no evidence of stimulation from virus reactivation/infection, the phenomenon of activation therefore appears to represent posttransplant immune disregulation following repopulation of the host immune system with lymphoid subsets derived exclusively from blood and marrow. Activated killing is predominantly mediated by the CD16+ CD3- subset, but substantial activity remains in the CD16- CD3+ cell fraction. Monoclonal antibodies (MoAbs) that block interaction with class-I MHC molecules at the level of target cell (W6/32 anti-HLA class I) or effector cell (CD8) do not inhibit killing by CD16- CD3+ cells. Activated killer cells may contribute to the lower risk of relapse after marrow transplantation as compared with intensive chemotherapy.

Adolescent↗
PubMed1987

The neurotoxicity of high-dose cytosine arabinoside is age-related.

Fifteen patients with acute myeloid leukaemia were given a total of 17 courses of high-dose cytosine arabinoside (Ara-C). The median age of the patients was 37 years. Four patients developed severe irreversible neurotoxicity, three developed mild to moderate, reversible neurotoxicity, whereas eight patients had no toxicity. Of five patients over the age of 55 years given high dose Ara-C, four developed severe, irreversible neurotoxicity, but there were no severe episodes in nine patients aged 55 years or less. (P less than 0.01). At a dose of 3 g/m2 given intravenously every 12 hours for 3 days, three cases of severe irreversible neurotoxicity were noted in elderly patients. Neurotoxicity at this total dose has previously been considered unusual. Administration of high dose Ara-C at total doses of 18 g/m2 and over carries a risk of severe irreversible cerebellar toxicity that increases with age.

Activities of Daily Living↗
PubMed1987

Aryl sulfatase A deficiency in psychiatric and neurologic patients.

Two hundred ninety-five psychiatric and neurologic patients were randomly screened for aryl sulfatase A (ASA) activity in lymphocyte extracts. Two of these patients showed very low ASA activity, in the range of metachromatic leukodystrophy (MLD)-affected patients. The residual activity in these low ASA patients showed normal enzyme behavior with regard to ASA kinetic features and the ability to catabolize 14C labeled sulfatide by intact fibroblasts. Taking into account that approximately 3% of the general population are homozygous for the pseudo-aryl sulfatase A gene and are clinically unaffected, the data obtained here indicate that the patients studied in this work, as well as most psychiatric patients reported in the literature with low ASA activity, represent the normal ASA polymorphism. Thus, the very low ASA activity patients are in fact homozygous for the pseudo-deficient allele, which does not result in clinical abnormalities. The clinical symptoms in these psychiatric patients and probably other "variant" MLD patients are therefore not related to low ASA activity.

Bipolar Disorder↗
PubMed1987

The regional cerebral blood flow in patients under chronic hemodialytic treatment.

Regional cerebral blood flow (rCBF) was measured by the xenon-133 inhalation method in an unselected group of nine chronic hemodialysis patients before and after a single hemodialytic treatment. All patients underwent neurological, neuropsychological, and biochemical evaluations on the same occasions. Predialysis rCBF values did not differ from those obtained in age-matched normal controls. Following hemodialysis, there was a mild reduction in the rCBF by a mean of 7 +/- 2.6% (p = 0.02). The posthemodialysis rCBF reduction was not associated with any neurological or cognitive dysfunction. The causes of hemodialysis-induced rCBF decreases are unknown, but increased blood viscosity and biochemical changes, such as urea reduction and blood alkalinization, may play a role.

Adult↗
PubMed1987

Central neurogenic hyperventilation in a patient with medulloblastoma.

Central neurogenic hyperventilation is a rare but important cause of the frequently observed phenomenon of hyperventilation. Its diagnosis demands that primary respiratory or metabolic causes, as well as cerebrospinal fluid abnormalities, be ruled out. We hereby describe a patient whose attacks of hyperventilation were the presenting sign of her disease and might be consistent with the central neurogenic mechanism. This patient suffered from a medulloblastoma which compressed the pons. After removal of the tumor the hyperventilation attacks ceased.

Adult↗