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Biomedical subjects

A B Joseph

Publications and source records attributed to A B Joseph.

At least 37 records · Page 2Linked to original sources
PubMed1986

Brain atrophy and interhemispheric fissure enlargement in Cotard's syndrome.

The hallmark of Cotard's syndrome is the delusion of being dead. The literature indicates that it is often associated with parietal lobe lesions. This association was investigated by blindly comparing the computed tomographic scans of eight patients who had Cotard's syndrome (one of whom is described) with those of eight controls matched as closely as possible for age, sex, race, and principal psychiatric diagnosis. Two trends emerged. Compared with controls, patients with Cotard's syndrome had more brain atrophy in general and more median frontal lobe atrophy in particular. Parietal disease did not discriminate between the index and control groups. Cotard's syndrome may be associated with multifocal brain atrophy and medial frontal lobe disease.

Adolescent↗
PubMed1986

Cotard's syndrome in a patient with coexistent Capgras' syndrome, syndrome of subjective doubles, and palinopsia.

The hallmark of Cotard's syndrome is the delusion of being dead. It is usually seen in affective disorders, and its existence as a separate entity is controversial. A patient is described who presented with paranoid schizophrenia, Cotard's syndrome, the misidentification syndromes of Capgras and subjective doubles, and palinopsia (visual perseveration). Focal theories for these conditions are briefly outlined and the patient is discussed with reference to them. It is proposed that this case supports the concept that Cotard's syndrome is a distinct disorder. The possibility of cerebral dysfunction in the confluence of the parietal, temporal, and occipital regions accounting for this specific clinical presentation is considered.

Adult↗
PubMed1985

Design considerations for the brain-machine interface.

Implantation of prosthetic devices designed to complement the function of the human brain is a rare but well recognized innovative treatment for some patients. If this technique is to become clinically useful special attention will have to be paid to the bio-engineering requirements of the prosthesis-brain interface.

Biomedical Engineering↗
PubMed1985

Brainstem and vermis atrophy in catatonia.

The computerized tomographic scans of five catatonic patients and five matched controls were blindly assessed. The catatonic patients showed preponderant atrophy of the brainstem and cerebellar vermis. Catatonia may be associated with lesions in these areas.

Aged↗
PubMed1984

Startle disease.

Explore the source record for details and available documents.

Afferent Pathways↗
PubMed1981

Restoration of nervous system function after permanent injury.

Permanent injury to the nervous system can occur in a number of ways and lead to profound residual disability. Attempts to restore function are being made by many different groups. They range from prosthetic repair to pharmacological intervention. A theoretical framework within which injuries can be analysed and understood is desirable. One is proposed. From it a rational set of approaches to the restoration of nervous system function is generated. These are outlined.

Hearing Disorders↗
PubMed1981

A murine model for multiple laparoscopies: I. Early lymphoid response to intraperitoneal insufflation of CO2.

In a model for multiple laparoscopies proliferation of T-lymphocytes was an early, but transitory, immunologic reaction in the spleen to intraperitoneal CO2 insufflation. Intraperitoneal insufflations of approximately 3.5 ml of CO2 were given daily to three groups of BALB/c mice for 11, 20, and 32 consecutive days, respectively. Air insufflation was given to experimental controls. The observations in the insufflation model are summarized as follows: 1) Multiple CO2 insufflation approximately doubled the number of splenic T lymphocytes. 2) The percentage value was highest on the day of the last insufflation. The difference between this value in each of the three groups was statistically not significant; ie, there was no dose-response relationship in the range of 11-32 insufflations. 3) There was a dose-response effect in the range of 3-9 insufflations. 4) The number of splenic T lymphocytes decreased with each day after the end of treatment. Untreated control values were reached in 12-16 days. 5) Air insufflation had only a minimal effect on the proliferation of T lymphocytes in the spleen. In this model there is correlation between early proliferation of T lymphocytes in the spleen and the late occurrence of a high incidence of malignant lymphoma (approximately 60%). The long-term survivors of CO2 insufflation also developed a wide spectrum of intraabdominal malignancies. It was speculated that CO2 insufflation provided an abnormal internal environment that affected a variety of target tissues. Prolonged CO2 accumulation might have modified nucleic acid structure via chronic intracellular acidosis. Could the neoplastic sequelae in this model be a clue to a similar sequel in humans after multiple laparoscopies?

Animals↗
PubMed1980

Post-transplantation development of malignant lymphoma, an experimental model: syngeneic lymph node transplants.

Previously, malignant lymphomas in mice have been found to be the late sequelae of the autologous transplantation of skin grafts pretreated with CO(2); these did not occur with grafts cultured in air alone. The clinical result in this autologous system reflects environmental differences in vitro (Goldsmith & Narvaez 1975). In the present study the syngeneic transplantation in BALB/c mice of lymph node tissue resulted in the late appearance of malignant lymphomas (48-69%), irrespective of the pretransplantation treatment of the grafts. Lymph node grafts were exposed to three different environments before transplantation into syngeneic hosts: (1) to culture in air (24 hours); (2) to culture in an atmosphere of 45% CO(2) in air (24 hours); (3) direct transplantation without in vitro exposure. Transplantation of these three groups of differently treated grafts was followed by the same clinical results in their recipients. These were: (1) The development of lymphoma whereas the spontaneous incidence was zero. (2) The proliferation of T-lymphocytes in the spleen; the incidence of this abnormality correlates with the lymphoma incidence. (3) A higher than normal occurence of immune-associated lesions (amyloidosis, interstitial nephritis and myocarditis). Both syngeneic and autologous transplantations may serve as animal models for the study of clinical malignant lymphoma.

Animals↗
PubMed1980

Metabolic carcinogenesis--induction of murine lymphoma by CO2-treatment in vivo and in vitro.

Metabolic carcinogenesis may be viewed as a process in which a chronic disturbance of metabolic homeostasis leads to malignancy. Fluctuation in the CO2 tension in tissues is accompanied by changes in the intracellular pH. This prompted investigations into the long-term clinical effects of high CO2 tensions on various normal tissues in mice by two different methods. The first consisted of exposing different tissues in vitro to a high CO2% in air before transplantation into syngeneic or autologous hosts. The second method consisted of exposing intraperitoneal tissues in vivo to CO2-infusion, thus avoiding graft-host interactions. This is a report of the most significant findings in the series of investigations analyzed, 1. High incidences of malignant lymphoma in strains of mice with a low or zero spontaneous incidence followed: (a) syngeneic transplantation, (b) autologous transplantation, (c) in vivo exposure to CO2-infusion. 2. Syngeneic graft recipients developed similar high lymphoma incidences, irrespective of the tissue grafted or the pretransplantation treatment of the graft. 3. In the autologous system, however, the clinical results reflect the differences in the pretransplantation treatment, in contrast to those in the syngeneic system. 4. Whereas intraperitoneal CO2-infusion induced lymphoma, air-infusion did not. 5. Non-lymphoid grafts exposed in vitro to elevated CO2 induced only lymphoid malignancies. But non-lymphoid tissues exposed in vivo to elevated CO2 developed tumors of other tissues, such as lung tumor, in addition to lymphoid malignancies. 6. The same morphological lymphoid abnormalities occurred in all lymphoma-developing animals in these three experimental models. Hyperplasia in the splenic T-cell areas appeared most frequently. 7. The presence of immune-associated lesions in experimental animals (amyloidosis, interstitial nephritis and myocarditis) points to the activation of immune mechanisms in this lymphoma development. The evidence as a whole suggests the possibility that chronic immunological stimulation of host lymphoid tissue may be involved in the development of lymphoid malignancies in these animal models.

Animals↗