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Biomedical subjects

E Klein

Publications and source records attributed to E Klein.

At least 541 records · Page 30Linked to original sources
PubMed1977

The management of pericardial effusion in cancer patients.

The relatively little attention given in the literature to the problem of pericardial effusion in patients with cancer reflects the general attitude that if this complication is disclosed, the future of the patient is sealed, and therapy will not change his outcome. We challenge this pessimistic approach, and describe here our experience with seven patients with solid tumors, in whom pericardial effusion was diagnosed; one of them is described in detail. We advocate an active and sometimes even an aggressive therapy, which should always be related to the degree of the hemodynamic impairment. If instant relief is indicated, pericardiocentesis should be done; pericardiectomy is the treatment of choice if the fluid reaccumulates rapidly. After overcoming the urgent problem, the underlying disease and the local pericardial condition should be treated; and in our opinion, a combined approach, such as systemic or local chemotherapy, or both, with or without precordial irradiation, will lead to the optimal result.

Adult↗
PubMed1977

The volume of isoflow and increase in maximal flow at 50 percent of forced vital capacity during helium-oxygen breathing as tests of small airway dysfunction.

The purpose of this report is to review the role of helium in the early detection of obstructive pulmonary disease. The underlying physiologic mechanisms of the volume of isoflow (the volume at which flow was the same with the subject breathing air and breathing a mixture of 80 percent helium and 20 percent oxygen) and increases in maximal flow at 50 percent of vital capacity (Vmax50) after breathing helium are reviewed. These tests are able to detect physiologic abnormalities in asymptomatic subjects when the results of other tests are normal; and following cessation of smoking, abnormal results may be reversible. The volume of isoflow is increased when maximal flow is reduced because of loss of elastic recoil or increase in upstream resistance. The increase in Vmax50 after breathing helium appears to be relatively specific for the caliber of the small airways, being uninfluenced by loss of elastic recoil; it can further help to localize the major site of obstruction to either small or large airways. At present, random screening for early unsuspected disease is not warranted, and these tests remain an investigative tool.

Evaluation Studies as Topic↗
PubMed1977

Sensitization of rat T cells to syngeneic tumor cultures by cocultivation in diffusion chambers.

Total population and T cell enriched fractions of rat spleen were cultivated in diffusion chambers implanted intraperitoneally to mice and rats. 10-16% of the input cells were recovered after 5 days. When the chambers were carried in the xenogeneic environment activation occurred as indicated by blastogenesis and non-discriminative cytotoxicity. Specific activation of the T population was induced by mixed lymphocyte-tumor culture in chambers implanted in rats. The presence of tumor cells induced blastogenesis, elevation of the proportion of Fc receptor positive cells and generated cytotoxic cells to the sensitizer tumor. The precursor of cytotoxic cells did not have Fc or C3 receptors since nylon wool colum passed fractions depleted from these cells by elimination of EA- or EAC-rosettes were also activated.

Animals↗
PubMed1977

Rejectability of virus-induced tumors and nonrejectability of spontaneous tumors: a lesson in contrasts.

In contrast to the excellent surveillance against tumors induced by the ubiquitous viruses in their natural host species, spontaneous tumors developing naturally, without experimental interference, evoke little or no rejection reaction. This may be viewed in relation to the natural history of tumors. In most cases, tumors evolve in several steps, with a successful of clonal variants following each other, characterized by increasing independence of host regulations (including immune restrictions). This process is commonly designated as tumor progression. In all probability, selection for nonrejectability is part of this process. Selection of the host for rejecting capacity is unlikely to play any major role, since the overwhelming majority of the naturally occurring tumors arise after the host has passed the peak of its reproductive period. The nonrejectability of spontaneous tumors may be overcome by target-cell modification, e.g., by chemical coupling, somatic cell hybridization, or viral xenogenization. Furthermore, genetic analysis of the F1 resistance effect in relation to seemingly nonrejectable tumors may reveal the existence of specific immune-response (Ir) genes that can influence the recognition of tumor-associated membrane changes by the host immune system.

Animals↗
PubMed1977

Preoperative intermittent positive pressure respiration as preparation for emergency valvular surgery for pulmonary edema.

Immediate emergency surgery is the accepted treatment of intractable pulmonary edema due to valvular heart disease. The presence of severe tissue hypoxia, acidosis, low cardiac output state and renal insufficiency results in a high operative risk. Delay of operation by several hours may prove advantageous in that it permits improvements of the patient's condition by means of intermittent positive pressure respiration with correction of acidosis and at the same time allows for treatment of the cardiac failure. Three illustrative cases are presented, all successfully managed by preoperative treatment in an intensive care unit. The pathophysiological basis of this therapeutic approach is discussed.

Adolescent↗
PubMed1977

Group-specific human granulocyte antigens on a chronic myelogenous leukemia cell line with a Philadelphia chromosome marker.

Group-specific human granulocyte antigens are serologically detectable with granulocytotoxic-positive human alloantisera on a cell line, K562, of chronic myelogenous leukemia origin which bears a Philadelphia chromosomal marker. The same cell line lacks serologically detectable HLA, B2 microglobulin, and B-lymphocyte antigens. Granulocyte antigens are important cell markers for cell lines of suspected myeloid lineage.

Antigens↗
PubMed1977

Fc receptors on human blood B lymphocytes.

The frequency of Fc-receptor positive B lymphocytes in human blood was investigated. Under the conditions used heat-aggregated gammaglobulin binding and EA(ox)-rosette formation labelled the same lymphocyte populations. Using various techniques, double marking and cell separations the proportion of Fc-receptor positive cells within the surface Ig carrying population was estimated to be between 11-8 and 36-2%. The proportion of SIg carrying cells within the population forming EA-rosettes was between 11 and 26-4%. This represents extreme values due to known technical circumstances.

B-Lymphocytes↗
PubMed1977

Enhancement of granulocyte phagocytosis by products of PPD stimulated human lymphocytes.

The effect of supernatant fluids from cultures of stimulated human lymphocytes on the phagocytic activity of human neutrophilic granulocytes was investigated. It was found that lymphocytes of tuberculin (PPD) positive donors after in vitro stimulation with PPD produced factors that significantly increased granulocyte phagocytosis of latex particles.

Granulocytes↗
PubMed1976

Properties of the K562 cell line, derived from a patient with chronic myeloid leukemia.

The K562 cell line derived from a CML patient in blast crisis was examined for properties of B and T lymphocytes and cell lines. K562 lacks the B markers of immunoglobulins, Epstein-Barr virus (EBV) genome and associated nuclear antigen, and receptors for EBV. A low proportion of cells from rosettes with sheep erythrocytes, the frequency of which is considerably increased after neuraminidase treatment. Unlike B lines but like T lines, K562 cells are lysed rapidly by C'/Fc receptor-positive human blood leukocytes and do not stimulate MLC reactions. On the other hand, K562 lacks T antigen, high radiosensitivity and sensitivity to growth inhibition by thymidine. The cells do not contain N-APase, an enzyme found in all lines derived from lymphoid cells and in lymphoproliferative diseases. By scanning electron microscopy, K562 cells were seen to be rounded and relatively smooth, with small numbers of short microvilli resembling undifferentiated leukemic cells. A few cells had narrow ridge-like profiles and small ruffles similar to granulocytic leukemic cells. K562 is strongly positive for immunoglobuln Fc receptors and pinocytosis, but does not phagocytose or mediate antibody-dependent phagocytosis or cytolysis. Among histochemical stains, K562 is positive for esterase, lipid, and acid phosphatase. There seems to be no doubt that K562 is not a B cell line. While it has some T cell properties, these are not exclusive. Some of its characteristics indicate that it is probably not lymphoid. Due to its low level of differentiation, its nature cannot be stated with certainty. On the basis of the possible presence of the cellular marker of chronic myeloid leukemia, the Ph chromosome, it may be regarded as belonging to the granulocytic series of cells.

Alkaline Phosphatase↗
PubMed1976

Search for anti-tumor response in a bone tumor patient with a long clinical history.

Immunological studies are presented on a patient with a long clinical history suggesting the existence of a tumor-specific immune response. His tumor, first considered benign, progressed to a highly malignant osteosarcoma. Cell-mediated immune reactivity against biopsy cells and against tumor extract was detected in vitro by the autologous tumor stimulation test (ATS) and in vivo by the skin test. In one ATS-test with tumor extract, blastogenesis of T-cells was demonstrated. The amount of Ig(s) in consecutive biopsies increased. Biopsies taken in the later period of the disease stimulated only after trypsin treatment. This stimulation was inhibited by autologous serum or acid eluate of the biopsy. The inhibitory factor in the serum was not intact immunoglobin. Blood lymphocytes did not show a discriminatory or disease-related cytotoxicity, either directly or after co-cultivation with the tumor material. Lymphocytes isolated from one biopsy were non-reactive in both the ATS and the cytotoxicity test.

BCG Vaccine↗
PubMed1976

Interaction of antibody and cell surface localized antigen.

The changes occurring in the expression of a membrane-associated antigen following binding of specific antibodies and the fate of the bound antibodies were investigated. Daudi cells, carrying membrane 7S IgM molecules, were coated with radio-labelled anti-IgM antibodies and incubated under culture conditions at 37degrees C. Within 10 h, more than 80% of the cellbound radioactivity was shed from the cells into the culture medium. Concomitantly, IgM molecules were lost, as the cells had a diminished ability to bind a new aliquot of antibody. This phenomenon occurred also when the antibody was used at a low concentration, i.e. did not saturate the cell-surface antigens. The precipitability of the antibody released from the cells with 10% TCA and 40% saturated ammonium sulphate was lower than that of native antibody, indicating some degradation. Also, shed antibody could rebind to fresh Daudi cells less efficiently than native antibody. The presence of immune complexes in the culture supernatants was indicated by the following results: (1) some of the shed radioactivity could bind to IgM-negative but Fc receptor-bearing cells; and (2) immune precipitates of sheep anti-IgM shed from 3H-leucine labelled Daudi cells and of rabbit anti-sheep IgG antibodies contained 3H activity.

Antigen-Antibody Reactions↗
PubMed1976

Tumor-bound immunoglobulins. I. Further analysis of the characteristics of binding of immunoglobulins to in vivo-grown tumor cells.

Immunoglobulin (Ig) "coating" on different in vivo growing mouse tumors was investigated using several approaches. Radioiodine-labelled purified protein A from Staphylococcus aureus, a specific reagent for Fc of IgG, and/or iodinated purified antibodies against mouse immunoglobulins, were fixed by various in vivo-grown mouse tumor cells, but not by the corresponding in vitro-cultivated tumor cells. Removal of host macrophages from the in vivo tumor-cell preparations did not affect the fixation of anti-mouse Ig reagents by the tumor cells. After an initial lag period in vivo, the intensity of the Ig coating of tumor cells increased with time after tumor inoculation. Conversely, the detectable coating decreased rapidly as a function of time after ascites tumor cells were explanted in vitro at 37 degrees C. Iodoacetamide did partially block this 37 degree C in vitro-induced "uncoating process". Surface-bound Ig could also be released from in vivo-coated tumor cells treated at low pH in vitro. Analysis of the behavior of tumor-bound Ig indicated a composite pattern. At the membrane level, uncoating was best shown with in vitro incubation favorable to cellular metabolism; however IgG was detected equally well in the supernatants of the cells, whether they were incubated at 37 degrees C or at 4 degrees C, and so far has failed to display antibody activity towards uncoated tumor cells. This was in contrast to the case of IgG released from ascites tumor cells cultured at low pH in vitro: such eluted Ig, when neutralized, could rebind to the "same" uncoated tumor cells. Under favorable metabolic conditions, the fate of tumor-bound Ig might be one of internalization and/or of degradation.

Animals↗
PubMed1976

[Intracellular endobiosis as a basic factor in acquired immunity in man (author's transl)].

An attempt is made to explain the significance of intracellular endobiosis for the human acquisition of immunity against cyclic infections diseases. It is pointed out that, taking into account the temporally limited reduplication of an immune-potent cell clone, a species-specific induction of immunity against infections and other diseases is sustained for a sufficiently long period of time only by a microorganism which is still living.

Antibody-Producing Cells↗