The teardrop appearance of the superior ophthalmic vein on computed tomography.
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Biomedical subjects
Publications and source records attributed to C Janus.
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Sixty-four patients with American Burkitt's lymphoma (AMBL) treated at the National Cancer Institute were reviewed to determine the frequency and characteristics of central nervous system (CNS) involvement. Patients with minimal or completely resected tumor never had CNS disease. Of the 45 patients with more extensive disease, 15 had CNS disease: nine presented with CNS disease, six of whom subsequently had recurrent CNS disease, and six developed CNS disease only at relapse. There was a significant association between CNS and bone-marrow disease at presentation. Therapy of CNS disease consisted of short courses of intrathecal chemotherapy with cytosine arabinoside and methotrexate. Cranial irradiation was given only to patients with CNS relapse. There are six long-term survivors (LTS) who have been disease free for four to six years post chemotherapy. Of these six LTS, three presented with CNS disease, two experienced isolated CNS relapse, and one had CNS disease both at presentation and at relapse. Three of the six LTS never received cranial irradiation. It is concluded that CNS involvement in AMBL can be effectively treated, and that long-term remission, which is probably cure, can be achieved.
Two hundred seventy-five patients with breast cancer and no axillary metastases had mastectomies and axillary node dissection performed during the period between 1970 and 1979 at The Fox Chase Cancer Center. They had a mean age of 60 years (range, 21-91) and 38 (14%) patients have had recurrence to date. Poor histologic differentiation and skin involvement were related to a high risk of recurrence. Those patients with skin infiltration by tumor or a poorly differentiated tumor had a 53 +/- 9% expected five-year tumor-free survival, whereas patients without these had a 90 +/- 2% expected five-year tumor-free survival. Tumor involvement of the lymphatic vessels within the breast and estrogen receptor protein positivity or negativity were not helpful for identifying a subpopulation at increased risk of recurrence. Large tumor size was not a poor prognostic indicator for a patient subpopulation. These factors should be considered as indicators for inclusion in clinical trials and adjuvant therapy and used as stratification points for the analysis of the data developed in these trials.
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As part of an investigation of the cellular origins of undifferentiated lymphomas of the Burkitt's and non-Burkitt's types, we have examined immunoglobulin secretion by cell lines and biopsy samples from these tumors and have compared it with other lymphoblastoid cell lines. The majority of American lymphoma cell lines and a smaller fraction of African lymphoma cell lines secreted monoclonal IgM. No other Ig classes were secreted. Ig secretion by the tumor samples was also found to be exclusively IgM. The secreted IgM was polymeric and associated with J chain. Secretion of free light chain by most of the tumor cell lines was observed. Quantitation by immunoassay demonstrated that the American lymphoma cell lines secreted significantly more IgM than the African lymphoma cell lines. We have proposed that the lymphoma cells represent an early stage of B cell differentiation, during which antigen-independent secretion occurs.
The term Krukenberg tumor refers to metastatic disease to the ovary and more specifically those metastases containing mucin-secreting signet cells. When this definition is used most of these tumors arise in the gastrointestinal tract although the term Krukenberg tumor has also been used more loosely to describe metastatic disease to the ovary from other sites such as breast and genital tract. On ultrasound examination, the Krukenberg tumor has been described as a complex type of mass showing both solid and cystic characteristics. When a mass with these echographic characteristics is found on pelvic sonography it is important to consider this entity in the differential diagnosis.
There is virtually nothing in the literature about patients' perceptions and misconceptions regarding sonography. From January to June, 1979, 204 patients at the Mount Sinai Hospital in New York City were asked to fill out questionnaires before and after their sonographic examinations. The results showed that many of the first-time patients did not know what to expect, had never heard of ultrasound, and were incorrectly prepared for the examination. Education of both patients and physicians is needed to prevent unnecessary patient anxiety and to encourage the use of this safe and accurate diagnostic modality.
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Dominant mutations in the Presenilin 1 gene are linked to an aggressive, early-onset form of familial Alzheimer's Disease (FAD). Spatial memory of transgenic (Tg) mice expressing either mutant (lines Tg(M146L)1, Tg(M146L)76, Tg(L286V)198) or wild type (line Tg(PS1wt)195) human PS1 transgenes was investigated in the Morris water maze (WM) test at 6 and 9 months of age. The results showed that the mutated Tg mice had increased swim speed when compared to non-Tg littermates or Tg PS1 wild type mice. The swim speed difference did not, however, significantly affect the spatial learning in the WM test and all groups showed comparable search paths during training and similar spatial bias during probe trials. When re-tested at 9 months, all mice showed significantly improved learning acquisition of spatial information. The lack of progressive spatial learning impairment in mice expressing the mutated human PS1 transgene in the WM does not preclude impairments in other cognitive tasks but suggests that full phenotypic expression of mutant PS1 alleles may require co-expression of human versions of other AD-associated genes.
Much evidence indicates that abnormal processing and extracellular deposition of amyloid-beta peptide (A beta), a proteolytic derivative of the beta-amyloid precursor protein (betaAPP), is central to the pathogenesis of Alzheimer's disease (reviewed in ref. 1). In the PDAPP transgenic mouse model of Alzheimer's disease, immunization with A beta causes a marked reduction in burden of the brain amyloid. Evidence that A beta immunization also reduces cognitive dysfunction in murine models of Alzheimer's disease would support the hypothesis that abnormal A beta processing is essential to the pathogenesis of Alzheimer's disease, and would encourage the development of other strategies directed at the 'amyloid cascade'. Here we show that A beta immunization reduces both deposition of cerebral fibrillar A beta and cognitive dysfunction in the TgCRND8 murine model of Alzheimer's disease without, however, altering total levels of A beta in the brain. This implies that either a approximately 50% reduction in dense-cored A beta plaques is sufficient to affect cognition, or that vaccination may modulate the activity/abundance of a small subpopulation of especially toxic A beta species.