Search Results - (Author, Cooperation:R. Schiff)

2011-12-14

American Association for the Advancement of Science (AAAS)

0036-8075

1095-9203

Biology

Chemistry and Pharmacology

Computer Science

Medicine

Natural Sciences in General

Physics

Animals ; Breast Neoplasms/*genetics/metabolism/mortality/pathology ; Cell Cycle ; Cell Line, Tumor ; *Cell Transformation, Neoplastic ; Female ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; *Genes, myc ; Humans ; Mammary Neoplasms, Experimental/genetics/metabolism/mortality/pathology ; Mice ; Mice, Nude ; Mitosis ; Neoplasm Transplantation ; Proto-Oncogene Proteins c-myc/*metabolism ; RNA Interference ; RNA, Small Interfering ; Spindle Apparatus/physiology ; Sumoylation ; *Transcription, Genetic ; Transplantation, Heterologous ; Ubiquitin-Activating Enzymes/antagonists & inhibitors/*genetics/metabolism

1399-3038

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

Electronic Resource

1399-3038

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

We describe a patient with severe combined immunodeficiency and transplacental transfer of maternal T cells who received an unfractionated HLA-identical sibling bone marrow transplant without prior conditioning. He presented prior to transplantation with a dermatitis later diagnosed as mild graft versus host disease. He had a normal absolute lymphocyte count, but proliferative responses to mitogens were very low. Antigens of the noninherited maternal HLA haplotype were detected on his blood lymphocytes. After transplantation, he developed a severe reaction including fever, cutaneous erythema and hepatosplenomegaly. Lymphocytes carrying the noninherited maternal HLA haplotype disappeared from his circulation, and his unprimed mononuclear cells became spontaneously cytotoxic to maternal lymphoblasts. He subsequently developed a lymphocytosis of 69,000/mm3, diarrhea, elevated transaminases and a worsening rash, necessitating treatment with immunosuppressive agents. Full T-cell engraftment and evidence of B-cell function later ensued and spontaneously cytotoxic lymphocytes against maternal cells disappeared by 47 days post-transplantation. We postulate that the patient's constellation of signs and symptoms after transplantation represented a combination of severe graft versus graft and mild graft versus host reactions.

Electronic Resource

0922-3371

Elsevier Journal Backfiles on ScienceDirect 1907 - 2002

Biology

Electronic Resource

0014-4827

Elsevier Journal Backfiles on ScienceDirect 1907 - 2002

Biology

Medicine

Electronic Resource

1432-1998

Springer Online Journal Archives 1860-2000

Medicine

Abstract Current imaging modalities are accurate in establishing the diagnosis and extent of thoracic Hodgkin disease. After treatment, however, it is extremely difficult to differentiate potential residual active neoplastic disease from scar tissue, or identify early recurrence. We evaluated the contribution of MRI in the assessment of the response to treatment of thoracic Hodgkin disease in the assumption that scar formation would be characterized by low signal intensity in all pulse sequences, whereas active tumor should maintain a degree of high signal intensity on T2-weighted images. In 47 occasions (23 patients) both CT and MRI were able to identify correctly active disease, but had low specificity in confirming remission because of residual tissues masses. High signal intensity on T2-weighted MR images often persisted despite remission, probably because of edema, necrosis, granulation or other factors. MRI was somewhat more specific than CT and may be quite valuable to confirm remission in patients with residual masses that no longer appear hyperintense on T2 after treatment.

Electronic Resource

1432-1998

Springer Online Journal Archives 1860-2000

Medicine

Abstract We studied the thyroid gland in 18 long term survivors of Hodgkin Disease, all of whom received radiation therapy (2400–4000 cGy, mean 3434). Evaluation included clinical examination, thyroid function tests, ultrasound, as well as selective use of nuclear scintigraphy. The time interval post radiation was 1–16 years (mean 6.4 years). Clinical evaluation and thyroid function tests were insensitive in detecting abnormalities and most nodules were non palpable. Ultrasound detected abnormalities in 16 patients (89%) including diffuse atrophy (n=6), solitary nodules (n=4), multiple nodules (n=5) and gland heterogeneity with calcification in one patient. Cold nodules on nuclear scintigraphy (n=4) were subjected to biopsy. Multiple foci of papillary carcinoma were found in one patient. There was a tendency for nodules to increase in number as the post radiation interval also increased. We recommend frequent sonographic evaluation and early suppression of thyroid stimulation in an attempt to arrest the development of neoplastic changes.

Electronic Resource

1573-2592

Adenosine deaminase deficiency ; purine nucleoside phosphorylase deficiency ; severe combined immunodeficiency

Springer Online Journal Archives 1860-2000

Medicine

Abstract The courses of six patients with adenosine deaminase (ADA) and two with purine nucleoside phosphorylase (PNP) deficiencies were evaluated before and after therapy. The heterogeneity of immunologic and clinical parameters was striking in each enzyme deficiency. In both PNP and ADA deficiency, some patients had very low immunoglobulin levels, while others had normal levels. T-cell function was always low in patients with ADA deficiency. In the two patients with PNP deficiency, contrary to the classical descriptions of this disorder, T-cell function fluctuated with time. Five ADA-deficient patients were treated with irradiated normal red-cell transfusions as a form of enzyme replacement and showed no lasting benefit. Three of the ADA-deficient patients and one of the PNP-deficient patients were given transplants of haploidentical parental bone marrow stem cells without pretransplant immunosuppression. In the PNP-deficient patient, chimerism has not been documented on enzymatic testing. One ADA-deficient patient has demonstrated long-term engraftment with good B-and T-cell function. Haploidentical bone marrow transplantation is currently the preferred therapy for enzyme-deficient patients with absent T-cell function who do not have an HLA-identical donor, as it may result in a lasting reconstitution of immune function. In those patients with unsatisfactory responses to transplantation, however, specific enzyme replacement or gene therapy may be considered in the future.

Electronic Resource

1618-2650

Springer Online Journal Archives 1860-2000

Chemistry and Pharmacology

Electronic Resource

1573-7381

Springer Online Journal Archives 1860-2000

Medicine

Summary Previous attempts to generate myelin in the myelin-deficient rat spinal cord by transplanting mouse glia were not successful. In order to determine whether this result was due to graft rejection or to interspecies mismatch of cellular or molecular components at the axoglial junction, we have repeated the experiment in cyclosporine-treated rats. Our results show that in the immunosuppressed hosts, foetal glial xenografts form an abundance of myelin within the dorsal columns at or near the injection site about two weeks after the operation. In some cases, myelination extends virtually across the entire width of the dorsal columns. Ultrastructurally, the myelin sheaths are normal in all respects, including the presence of the ‘radial component’. The lateral edges of the myelin lamellae form typical paranodal axoglial junctions, some displaying periodic ‘transverse bands’. We infer that previous mouse to rat xenograft failures reflect host immune response rather than mismatch of heterologous junctional components. We also compared foetal, early post-natal and adult xenografts. Foetal donor cells, containing an abundance of precursors but virtually no mature oligodendrocytes, are more effective than neonatal donor cells in forming myelin, and after adult grafts, we found no myelin formation. Thus, in xenografts, as in allografts, foetal precursor cells are far more suitable than glia from mature donors in generating significant amounts of myelin.

Electronic Resource

1573-7381

Springer Online Journal Archives 1860-2000

Medicine

Summary Implantation of hybridoma cells that secrete a monoclonal antigalactocerebroside into the dorsal columns of ⩽ 9-day-old rat spinal cord results in failure of development of dorsal column myelin in the vicinity of the implant. Clusters of apparently undamaged amyelinated axons remain among the hybridoma cells. Ventral myelin is unaffected. These in vivo results support antibody-mediated inhibition of myelin formation as a potential mechanism underlying failure of remyelination in multiple sclerosis.

Electronic Resource

1573-7381

Springer Online Journal Archives 1860-2000

Medicine

Summary O1 hybridoma cells, which produce a monocolonal IgM antigalactocerebroside, were implanted into the spinal cords of immature and mature rats and the cords examined 5–24 days later. Study of the younger group, in which myelin was developing at the time of implantation, revealed examples of abnormal myelin sheaths in which the repeat period was markedly increased. The paranodal regions of these abnormal sheaths were superficially normal in configuration; i.e. myelin lamellae terminated one by one as ‘terminal loops’ that indented the axolemma and formed normal axoglial junctions displaying periodic ‘transverse bands’. Neighbouring terminal loops are normally joined by tight junctions that block passage of tracers from the paranodal periaxonal space into the compact myelin, as seen after implantation of a control hybridoma. In the abnormal sheaths that developed after O1 implantation, in contrast, terminal loops were usually widely separated from each other. As a result, multiple pathways from the paranodal periaxonal space into the myelin sheath remained patent, forming potential routes for shunting nodal action currents. This subtle abnormality could thus compromise conduction, even though the sheaths might appear to be normally myelinated at the histological level. Equivalent abnormalities in human neurological diseases, including multiple sclerosis and paraproteinemic neuropathies, could underlie functional loss in the absence of frank demyelination.

Electronic Resource

0538-8066

Chemistry ; Physical Chemistry

Wiley InterScience Backfile Collection 1832-2000

Chemistry and Pharmacology

The reactions of hydroxyl radicals with eight substituted aromatic hydrocarbons and four olefins were studied utilizing the flash photolysis-resonance fluorescence technique. The rate constants were measured at 298°K using either Ar or He as the diluent gas. The values of the rate constants (k × 1012) in the units of cm3/molec. sec are (a) OH + o-xylene → products: (12.9±3.8), 20 torr He; (13.0±0.3), 20 torr Ar; (12.4±0.1), 200 torr He;(b) OH + m-xylene → products: (15.6±1.4), 3 torr Ar; (19.4±0.8), 20 torr Ar; (21.4±0.2), 20 torr He; (20.3±1.9), 200 torr Ar; (20.6±1.3), 200 Torr He;(c) OH + p-xylene → products: (8.8±1.2), 3 torr Ar; (10.1±1.0), 20 torr He; (10.5±0.6), 200 torr He;(d) OH + ethyl benzene → products: (7.50±0.38), 3 torr He; (7.06±0.26), 20 torr He; (7.95±0.28), 200 torr He;(e) OH + n-propylbenzene → products: (6.40±0.36), 20 torr He; (5.86±0.16), 200 torr He;(f) OH + isopropylbenzene → products: (7.79±0.40), 200 torr He;(g) OH + hexafluorobenzene → products: (0.221±0.020), 20 torr He; (0.219±0.016) 200 torr He;(h) OH + n-propyl pentafluorobenzene → products: (2.52±0.54), 3 torr He; (3.01±0.76), 20 torr He; (3.06±0.24), 200 torr He;(i) OH + propylene → products: (25.6±1.2), 20 torr He; (26.3±1.2), 200 torr He;(j) OH + 1-butene → products: (29.6±1.9), 3 torr He; (29.4±1.4), 20 torr He;(k) OH + cis-2-butene → products: (43.2±4.1), 3 torr He; (42.6±2.5), 20 torr He;(l) OH + tetramethylethylene → products: (56.9±1.3), 20 torr He.

15 Tab.

Electronic Resource