[Expression of HLA-DR antigens (Ia-like antigens) in the cornea].
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Biomedical subjects
Publications and source records attributed to H Stein.
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In 1958, a medium-sized cell was recognized in human lymph nodes and found to occur in clusters in about one out of every 10 cases of reactive hyperplasia. At first, it was interpreted as a lymphoblast. Later, electron-microscopic investigations revealed that the cell contained abundant rough endoplasmic reticulum and was apparently restricted to T-regions of lymph nodes. Recently, it was possible to analyze a malignant lymphoma uniformly composed of such cells with a panel of monoclonal antibodies. The cells proved to be Leu-1+, OKT4+, Leu-3a+, HLA-DR+, and weakly reactive with VIL-A1 (antibody to common ALL antigen) and clone F8-11-13, but negative for OKT3, OKT11, OKT8, cytoplasmic immunoglobulin, common B-cell antigen, and C3b receptors. Short-term, in vitro cultures of lymphoma cells showed weak responses to phytohemagglutinin and Interleukin 2 (IL2), but no IL2 production. Lymphoma cells had a low spontaneous proliferation rate (about 2% Ki-67+ cells). In view of these findings, the term "plasma-cytoid T-cell" is proposed. A functional relationship between these cells and the myeloid system was suggested because the patient developed a myelomonocytic leukemia 3 months after the diagnosis of malignant lymphoma was made.
It's no secret the eye care field, which lay dormant for the most part in the gentle hands of the three Os, is being dressed up and marketed by big business who recognize the financial potential. You are in competition with this element in this 6 billion dollar vision care area, but you should be competing on a different level. Surveys still indicate price is the 7th reason patients choose their doctor on a scale of 1 to 10. To be financially successful in the future, fortunately or unfortunately, will require more of the O.D. than being professionally competent. It's going to take a combination of all the prerequisites that make for success in any business. Sound principles in planning, marketing, management, personnel, communications, education, public relations, and finance. Doctors must be willing to hire the support talent in areas they lack to accomplish their goal. It is not necessary for a practice to grow bigger, but it is necessary that it constantly grow better. Where to begin? The doctor and his staff must be able to answer the question, "Why should a patient come to this office for vision care, rather than the ophthalmologist three blocks away, or the optical chain in the Mail?" Don't answer, "quality." It's relative.(ABSTRACT TRUNCATED AT 250 WORDS)
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In osteoporosis, a pathologic state of diminution of bone mass, radiography is the most widely used diagnostic method, but it is only descriptive and mainly depicts changes in the compacta. Based on the Compton photon-scattering phenomenon, a noninvasive yet quantitative measuring method for analyzing bone density was developed. The values of repeated measurements taken at identical locations did not vary by more than 2%. Using this technique, bone density of the lower tibia was measured in 39 men and 36 women; 14 had been affected by an injury to a knee or calf and immobilized five to eight years prior to this investigation. The measured values demonstrated an impressive equality between the tibiae of each individual and between the two sexes up to 50 years of age. However, these values correlated poorly with the bone density of the distal radius. In women older than 50 years of age, bone density decreased. Bone density was also low in all postinjury limbs. When compared with radiographic and bone mineral content (BMC) measurements of the same limb at the same location, the bone density measurements were useful and reduced the range of uncertainty of diagnosing osteoporosis by radiography only. Little or no correlation was found between bone density values and BMC measurements. The Compton scattering technique may become a precise and sensitive method for the clinical diagnosis of postinjury osteoporosis and quantitation of the long-term effects of limb injuries.
Posterior dislocation of the hip joint is the result of severe trauma and leaves those affected with a significant degree of morbidity. Avascular necrosis of the femoral head is its most feared, and yet difficult to diagnose, complication, mainly in the immediate postinjury period. Intraarticular (slice) fractures of the posteroinferior and inferomedial aspects of the femoral head associated with such dislocations may cause the same clinical symptomatology as the sequelae of avascular necrosis, yet need a different approach and have a different prognosis. Since these slice fractures occur in a blind spot area for routine radiographic examinations of the hip, they are often missed and consequently underdiagnosed. Computerized tomography of the hip following posterior dislocation has become a most useful tool in ascertaining the diagnosis in these patients because it very clearly delineates such "slice" fractures, thus enhancing the correct assessment of this severe and often crippling injury.
Electron micrographs of fracture callus obtained ten days after injury show typical primary matrix vesicle mineralization. In remodeling haversian canals distant from the fracture sites, matrix vesicles and calcifying nodules were observed. The occurrence of these elements was also found to control unfractured tibiae with intramedullary nails but not normal bone. These observations suggest that during haversian remodeling, mineralization after osseous or marrow tissue damage is associated with matrix vesicles.
A case is presented of local recurrence of tuberculosis after successful hip arthrodesis, in a patient subsequently found to have active asymptomatic renal tuberculosis. The possibility of hematogenous spread is raised, and the importance of thorough genitourinary evaluation in cases of reactivated skeletal tuberculosis is discussed.
In this study the antigenic profile of Hodgkin (H) and Sternberg-Reed (SR) cells from cases of Hodgkin's disease was analysed using a large panel of monoclonal and polyclonal antibodies reactive with cells of lymphoid and haemotopoietic origin. The aim of this investigation was, firstly, to throw light on the origin of H and SR cells and, secondly, to determine whether there is any evidence to support recent suggestions that H and SR cells differ antigenically between different histological categories of Hodgkin's disease. Frozen sections (from 24 cases) and paraffin sections (83 cases) were stained by immunoenzymatic methods and the results compared with those obtained from staining a wide variety of reactive and neoplastic tissue samples (including examples of tuberculosis, sarcoidosis, malignant histiocytosis, histiocytosis X, osteomyelosclerosis and non-Hodgkin's lymphoma). The results revealed that H and SR cells of all types of Hodgkin's disease consistently lack markers found on null cells, B cells, T cells, cells of monocyte/macrophage series, interdigitating reticulum cells, dendritic reticulum cells and erythropoietic and thrombopoietic cells. However, H and SR cells constantly expressed an antigen detectable with the recently produced monoclonal antibody Ki-I. The vast majority of typical and lacunar type H and SR cells contained the granulocyte-related antigens detected by monoclonal antibodies TU5, TU6, TU9 and 3C4, whereas other more or less specific granulopoietic cell markers (such as peroxidase, chloroacetate esterade, lysozyme, cationic leukocyte antigen and OKMI) were consistently absent. H and SR cells in cases of nodular paragranuloma (nodular type of Hodgkin's disease with lymphocyte predominance) were not monotypic in light chain type (as has been previously reported), but rather contained chi and lambda chains within the same cells, as do typical and lacunar type H and SR cells. Immunostaining of normal and hyperplastic lymphoid tissue with the Ki-I antibody led to the detection of a new, as yet unidentified, small-cell population of unknown origin and function, which is present between, around, and within cortical follicles. It is concluded from these findings that H and SR cells constitute a unique cell type that differs in many properties from all other known cell types. Furthermore, H and SR cells of the various histological types of Hodgkin's disease are more closely related than previously believed. It is suggested that the hitherto unknown cell population detected with the monoclonal antibody Ki-I in normal lymphoid tissue is the normal equivalent of H and SR cells.
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Antisera directed at human C3 receptors were prepared by 2 different methods. In method I rabbits were immunized with EAC coated with C3 receptors of tonsil cells (AC3RS type I). In method II rabbits were immunized with insoluble aggregates of tonsil membrane constituents containing significant amounts of C3 receptors. After appropriate absorptions both types of AC3RS showed a selective reactivity with those cells known to express C3 receptors. With the EAC rosette inhibition test it is demonstrated that both types of AC3RS contain antibodies against the binding sites of C3b, C3bi and C3d receptors. The antibody titer was consistently higher in AC3RS of type II.
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The results of a recent investigation, in which an antiserum specifically directed against Hodgkin (H) and Sternberg-Reed (SR) cells was prepared, indicated the existence of a granulocytic cell-specific antigen on H and SR cells. In the present study, a large series of biopsies from patients with Hodgkin's disease were subjected to immunostaining with monoclonal mouse antibodies raised against acute myelomonocytic leukemia (AMML) cells. Among seven hybrids that secreted antibodies showing reactivity to AMML cells but not to Daudi cells, there were three (TU5, TU6 and TU9) whose antibodies selectively stained formalin resistant antigens in cells of granulopoiesis. The strongest staining was found in the more mature cells; only a few promyelocytes stained very faintly with TU9, H and SR cells showed distinct staining for TU9 in 57 (76%) of the 75 tested cases of Hodgkin's disease, whereas TU5 and TU6-reactive H and SR cells were found in only 35 cases (47%). All cases of the nodular sclerosis type and almost all cases of the mixed cellularity type contained TU9-reactive H and SR cells, although the percentage varied from case to case. TU9-reactive H and SR cells were demonstrated in nine of 12 cases of the lymphocyte depletion type and in eight of 21 cases of the lymphocyte predominance type. The presence of granulocytic cell-specific antigens in H and SR cells in most of the cases of Hodgkin's disease suggest that (1) H and SR cells (including the lacunar cell variant) are not heterogeneous, but rather homogeneous in origin and nature, at least in a majority of cases, and (2) H and SR cells are more closely related to cells of the granulocytic cell lineage than to any other type of cell of the hemato-lymphoid system.
Monoclonal antibodies OKT11 (gamma 1) and OKT11A (gamma 2) are described and appear to have similar binding specificities. They bind, in immunofluorescence, with greater than 95% of infant thymocytes, staining both cortical and medullary cells, 65-80% of blood lymphocytes and selectively stain the T cell-dependent paracortical areas of tonsil. A small proportion (9-12%) of bone marrow lymphocytes stain, but this population excludes the terminal transferase-positive cells. Both the gamma 1 and gamma 2 antibodies stain the surface membrane Ig-negative lymphocytes in blood and tonsil and are to block sheep E rosette formation (to normal or leukemic T cells). In contrast, other monoclonal anti-T reagents tested (OKT1, OKT3, OKT4, OKT6, OKT8, OKT9, OKT10) did not block E rosette formation. E rosette formation and OKT11 bindings are coincident on T-ALL cell lines and both are trypsin-sensitive. In a series of 145 leukemias and 26 leukemic cell lines investigated, only leukemias with a T cell phenotype including E rosette positivity were reactive with OKT11 and OKT11A. OKT11A binds to a polypeptide of approximately 50 000 molecular weight on thymic lymphocytes. This structure may carry the recognition site for sheep erythrocytes. These antibodies provide additional useful markers for T cell analysis and are of potential therapeutic value.
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The precise localization of human complement C3b receptors in human kidneys was investigated by means of indirect immunoperoxidase staining of frozen kidney sections with the monoclonal antibody C3RT05, which is specific for human C3b receptors. Transmission electron microscopy indicated that C3b receptors are located on the entire cell membrane of the visceral epithelial cells of the glomeruli.
This paper describes an immunoperoxidase technique for labelling cryostat tissue sections which is routinely used in the authors' laboratories both in the initial screening of hybridoma culture supernatants, and also during the subsequent cloning and growth of antibody-secreting cell lines. The technique can readily be performed on 100 samples in less than 3 h and is free of non-specific background labelling. The staining pattern of a monoclonal antibody on a single tissue section allows semiquantitative assessment of its reactivity against a wide variety of tissue constituents and is thus inherently much more informative than conventional screening techniques (such as binding assays) which yield only a single numerical value for each test performed. In consequence it is often possible to identify the probable specificity of a new monoclonal antibody at the primary screening stage. A further important advantage of immunohistological screening is that it detects antigens on cells or other tissue structures which do not readily enter suspension and also antibodies against nuclear and cytoplasmic antigens. Examples of monoclonal antibodies analysed by immunohistological screening include antibodies against C3b receptor, HLA-DR, factor VIII-related antigen, human syncytiotrophoblast, dendritic reticulum cells and a proliferation-associated cell surface glycoprotein.
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