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Biomedical subjects

L Weiss

Publications and source records attributed to L Weiss.

At least 361 records · Page 20Linked to original sources
PubMed1986

An enzymatic method for calibration of serum lipase assays.

An enzymatic method for the calibration of a turbidimetric lipase assay is described, based on measurement of free fatty acids liberated by the action of lipase. The substrate of the turbidimetric assay is a colipase-containing triolein emulsion. For determination of the free fatty acids a commercial test kit including acyl-CoA synthetase, acyl-CoA oxidase, and peroxidase is used. Intra- and interassay imprecision (CV) is about 5% at above-normal lipase activities, about 10% at normal values. Temperature coefficients are 1.24 and 1.45, respectively, for measurements at 30 and 37 degrees C vs 25 degrees C.

Animals↗
PubMed1985

The effects of single versus triple intravenous injections of B16 melanoma cells on the development of pulmonary tumors in mice.

During natural metastasis, cancer cells are released continuously into the bloodstream and arrested in target organs; the process is repetitive rather than a single event. In this communication, the effect of preceding on successive "pulses" of cancer cells is discussed in relation to the arrest, retention and tumor formation of B16 melanoma cells in the lungs of mice receiving 3 separate tail-vein injections at 2-hr intervals. When animals received the same total number of cells in either 1 or 3 injections, no significant differences were detected in the initial arrest and subsequent retention in the lungs. However, 15 days after injection, mice which had received 3 pulses of cancer cells were found to have fewer pulmonary tumors than those which had received a single pulse of cells. The results show that interactions between 2 successive waves of B16 melanoma cells and their host did not affect the initial arrest and "short-term" retention of a third wave of radiolabelled cells. However, the "longer-term" experiments on tumor formation show that preceding pulses of cancer cells resulted in the lungs becoming more hostile to a succeeding pulse than was the case in appropriate controls. The results indicate that the relative metastatic capacities of cancer cells arrested in microvascular beds during hematogenous metastasis could well be diminished by antecedent interactions of this type.

Animals↗
PubMed1985

Bone lining cells and hematopoiesis: an electron microscopic study of canine bone marrow.

Hematopoietic bone marrow in the dog is enclosed by a nearly complete and rather complex layer of endosteum, consisting of a diverse group of cells collectively called bone lining cells (BLC). Cell types comprising BLC include osteoblasts and osteoclasts, and other cell types, among which are elongated, flat cells with a spindle-shaped nucleus, and small cytoplasmic vesicles. The composition and thickness of the layer of BLC varies along the perimeter of the marrow. The layer may be simple or stratified. Occasionally a zone of tightly packed regularly arranged collagenous fibers lies between the bone lining cells and bone. Hematopoiesis, particularly neutrophilic, often occurs in the bone marrow next to the BLC. Cytoplasmic processes of BLC occasionally extend into the hematopoietic spaces and stromal cells in the hematopoietic compartment may extend processes to the layer of BLC. Occasionally cells of the BLC are similar in appearance to stromal cells within the marrow. Our observations together with the experimental findings of others (that fibroblastic stromal cells contribute to the hematopoietic inductive microenvironment, that hematopoietic stem cells are concentrated subosteally, that cells responsible for regeneration of the marrow stroma are derived from the endosteal layer, and that high concentrations of hematopoietic colony-stimulating factors are produced there) indicate that the hematopoietic capacities of bone marrow may be regulated by BLC.

Animals↗
PubMed1985

Equine bone marrow: a quantitative analysis of erythroid maturation.

The equine bone marrow responds to blood loss by increased erythropoiesis, only releasing reticulocytes into the peripheral circulation in severe chronic anemia. We have used morphometric analysis based on electron microscopy of the equine marrow to examine the maturation and release of reticulocytes. Developing red cells in the bone marrows of normal and chronically anemic horses were divided into four stages: early, intermediate, late-stage erythroblasts, and reticulocytes. Morphometric analysis of each stage included volume density of mitochondria per micron3 of cytoplasm, surface area of the outer mitochondrial membrane per unit volume of mitochondria, and the number of ribosomes per unit volume of cytoplasm (total, clustered, single). Matched t tests between normal and anemic animals showed significant differences (P less than or equal to .001) for volume density of mitochondria and numbers of ribosomes only at the reticulocyte stage. The large reticulocyte produced and released in chronic anemia may be best explained by a skipped mitotic division.

Anemia↗
PubMed1985

Mouse monoclonal antibodies to the human C3b receptor.

Mouse monoclonal antibodies were raised against the human C3b receptor (CR1) molecule that had been purified from solubilized erythrocytes membranes. Four hybridomas were selected, cloned and expanded because their supernatants reacted strongly with insolubilized CR1 by ELISA and intensely stained B-dependent areas of the spleen and glomerular podocytes by indirect immunofluorescence. The four monoclonal antibodies, named J3D3, J8B10, J3B11 and J7C2, were IgG1 immunoglobulins. J3D3 immunoprecipitated two protein bands of apparent mol. wts 200,000 and 220,000 from 125I-surface-labeled human erythrocytes, which correspond to the two major allotypic forms of CR1. By indirect immunofluorescence, monoclonal antibodies stained polymorphonuclear leucocytes (PMN), most peripheral blood B-cells and a small subset of peripheral blood T-cells. J3D3 bound to CR1 on erythrocytes, PMN and lymphocytes with an affinity of 1-3 X 10(9) M-1 and recognized 170-1330 antigenic CR1 sites with an average of 740 sites/erythrocyte in 100 healthy individuals, approx. 50,000 sites/PMN and 15,000 sites/lymphocyte. There was a bimodal distribution of CR1 numbers on erythrocyte in the normal population. The four monoclonal antibodies similarly inhibited CR1-mediated decay of preformed cell-bound alternative- and classical-pathway C3 convertase sites. Two antibodies, J3D3 and J3B11, inhibited C3b-dependent rosette formation with lymphocytes, although much less efficiently than F(ab')2 polyclonal anti-CR1 antibody. Differences that were observed in the relative capacity of the antibodies to inhibit some of the functions of CR1 and in their ability to compete for binding of 125I-J3D3 to CR1 on erythrocytes, suggested that they are directed against different epitopes on CR1. Monoclonal antibodies provide useful means to assess and analyze the biological and immunoregulatory functions of the C3b receptor.

Animals↗
PubMed1985

Quantitative determination of human IgG antibodies to the peptide subunit determinant of peptidoglycan by an enzyme-linked immunosorbent assay.

An enzyme-linked immunosorbent assay (ELISA) was developed for the quantitative measurement of IgG antibodies to the immunodominant R-D-Ala-D-Ala-OH determinant of peptidoglycan. Synthetic peptides R-D-Ala-D-Ala-OH, revealing structural analogy with the C-terminal sequence of the antigenic determinant H-L-Ala-D-Glu(L-Lys-D-Ala-D-Ala-OH)-NH2 of peptidoglycan, were coupled covalently to albumin via their amino groups. The resulting peptidyl proteins were employed as an antigen in an ELISA for the specific detection of human IgG antibodies against the C-terminal R-D-Ala-D-Ala-OH moiety of H-L-Ala-D-Glu(L-Lys-D-Ala-D-Ala-OH)-NH2. Antigenic specificity was proved by comparing the high binding to albumin-(D-Ala-D-Ala-D-Ala-OH)9 with a lack of binding to albumin-(L-Ala-L-Ala-L-Ala-OH)13 and by appropriate inhibition studies of the ELISA. IgG, totally free from IgA and IgM, was isolated from reference serum 004, and the particular specificity was entirely found in this fraction. Quantification of the ELISA was effected by affinity chromatography. Isolated IgG was applied to an affinity column of Sepharose-[albumin-(D-Ala-D-Ala-D-Ala-OH)9]n, unbound IgG was eluted with phosphate-buffered saline and specific IgG against the C-terminal R-D-Ala-D-Ala-OH moiety of H-L-Ala-D-Glu(L-Lys-D-Ala-D-Ala-OH)-NH2 was eluted with 6 M guanidinium chloride.

Binding, Competitive↗
PubMed1985

Effects of noradrenaline on interstitial fluid pressure in induced rat mammary tumours.

Interstitial fluid pressure was measured by the wick-in-needle technique in DMBA-induced rat mammary tumours during resting conditions and during noradrenaline infusion. The rate of infusion was chosen to increase the systemic blood pressure by 30-40 mmHg, known to result in a markedly increased vascular resistance of these tumours. During resting conditions tumour interstitial fluid pressure was 10.3 +/- 1.3 mmHg (n = 13) but fell to 7.0 +/- 1.1 mmHg (n = 13) during noradrenaline infusion. The results suggests that noradrenaline is likely to affect the pre-capillary resistance vessels of the tumour vascular bed. This result, together with earlier perfusion studies, indicates that noradrenaline is unsuitable for increasing tumour cell perfusion as an adjunctive in radiation and cytotoxic drug therapy.

Animals↗
PubMed1985

Resistance to mycobacteria in mice treated with fractionated total lymphoid irradiation (TLI) and in mice reconstituted with allogenic bone marrow cells following radiotherapy.

The increased clinical use of total lymphoid irradiation (TLI) as an immunosuppressive adjunct in transplantation suggested the need for determining the effects of TLI on the in vivo susceptibility of animals to infections controlled by cell-mediated immunity. TLI-treated, TLI-treated and splenectomized, and chimeric mice prepared with TLI were inoculated in the hind foot pad with Mycobacterium marinum or Mycobacterium leprae. Although M. marinum organisms multiplied in greater numbers in the TLI mice, ultimately they were destroyed as effectively in TLI mice as in the non-irradiated control mice. M. leprae multiplied at the same rate and to the same maximum in TLI mice as in controls. Mice previously challenged with M. marinum in one hind foot pad, and challenged subsequently with the same organism in the opposite hind foot pad, showed a solid immunity against this reinfection. It appears that upon recovery from the immediate effects of radiotherapy TLI-treated mice are able to mount an effective immune response to experimental infection with M. marinum and M. leprae.

Animals↗
PubMed1985

The hemodynamic destruction of intravascular cancer cells in relation to myocardial metastasis.

A variety of observations in humans and experimental animals indicate that large numbers of circulating cancer cells are killed in the microvasculature. It is suggested that this occurs when friction or adhesion between individual cancer cells and capillary walls results in an increase of tension in the cancer cell peripheries above a critical level because of (blood) pressure differentials between their free ends. Hemodynamic and anatomic data relating to the myocardial circulation and deformability measurements on four types of rat cancer cells have been reported previously by others. Novel calculations based on these data suggest that the increased tension at the peripheries of cancer cells passing through the myocardial capillaries will exceed the critical levels for rupture. Analysis of autopsy data for solid tumors reveals a low (less than 3%) incidence of myocardial metastases in the absence of lung metastases and a higher (15%) incidence in their presence. One explanation for these observations is that, in the absence of lung metastases, relatively few of the cancer cells enter the coronary arteries from primary tumors with systemic venous drainage because many are retained or destroyed in transit through the pulmonary vasculature, and most of those delivered to the myocardium then suffer hemodynamic destruction. In the presence of pulmonary metastases, large numbers of viable cancer cells are liberated directly into the pulmonary venules and subsequently are delivered to the myocardium without prior exposure to the arterial side of the microcirculation. The combined effects of increased delivery and the protective effects of arrested cells on those preceding them in files along the capillaries account for the higher incidence of myocardial metastases. It is proposed that hemodynamic destruction of circulating cancer cells may be an important underlying cause of metastatic inefficiency, together with other cytocidal mechanisms.

Biophysical Phenomena↗
PubMed1985

An approach to the therapy of metastases from cancer of the upper rectum: a working hypothesis.

Previously reported analyses of autopsy data gathered from patients dying from the sequelae of adenocarcinomas of the upper rectum revealed a step-wise sequence in the development of distant metastases. First, dissemination via the portal vein led to secondary hepatic metastases. Cancer cells from these liver metastases (not the primary cancer) disseminated via the inferior vena cava to generate tertiary pulmonary metastases. Cancer cells from the lung metastases (not the primary or secondary cancers) then disseminated via the arterial route to give rise to metastases in other organs. We propose a protocol for the treatment of patients with upper rectal carcinomas, based on the expectation that, at different times after diagnosis, some patients will have no distant metastases, metastases in the liver only, or in the liver and lungs only. The protocol for therapy is based on currently available liposome technology, by means of which high doses of drugs can be targeted to the liver and lungs containing the metastases, yet distinct from the metastases. It is argued that selective local delivery of this type would increase the dose of cytotoxic agent delivered, thereby increasing the chances of overcoming the relative drug-resistance of the metastatic cancer cells and, at the same time, reduce the risk of nonspecific toxicity. Liver and lung-selective liposomes could, when necessary, be delivered at the same time, in the same systemic venous infusion.

Adenocarcinoma↗
PubMed1985

Changes in hematopoietic stem cells in bone marrow of mice with Plasmodium berghei malaria.

An impaired erythropoietic response to anemia has been noted in human patients with malaria and in rodents experimentally infected with Plasmodium berghei. We have attempted to characterize the erythropoietic response in mice with a fatal P berghei infection, with particular emphasis on changes in marrow hematopoietic stem cells. Mice infected with P berghei had dramatic decreases in bone marrow cellularity, erythroblasts, BFU-E, and CFU-E as early as 24 hours postinfection and before there was any change in hematocrit. With development of anemia, marrows became erythropoietic with some expansion of the CFU-E compartment, but the BFU-E pool remained depleted and reticulocyte response was inadequate. There was no significant change in CFU-S from marrows of malaria-infected mice one day after infection. The lethality of malaria infection may take three weeks to be revealed, but it may be determined within hours of the infection by the irreparable changes in marrow erythroid stem cells.

Animals↗
PubMed1985

Vascular resistance characteristics of 7,12-dimethylbenz(a)anthracene-induced rat mammary tumors and normal tissues as studied in vitro.

Vascular perfusion characteristics have been studied in dimethylbenz(a)anthracene-induced rat mammary neoplasia and compared with those of skin, skeletal muscle, salivary gland, kidney, spleen, uterus, and brain by means of an artificial perfusion technique. Perfusion of tissues and organs was measured by the microsphere tracer technique. This procedure makes possible a detailed hemodynamic analysis of several tissues under controlled conditions, in this study maximum vascular relaxation, without confounding endogenous vasoregulation. The maximal perfusion capacity, i.e., during smooth muscle relaxation, of tumors and various tissues was related to perfusion pressure at three levels by means of three differently labeled microspheres. Tumors, especially large ones, have a low maximum perfusion capacity, i.e., high vascular resistance, compared to most other tissues. For the tumors, a relatively high perfusion pressure is required to open up the otherwise collapsed vascular network.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1985

Mechanically induced trauma suffered by cancer cells in passing through pores in polycarbonate membranes.

As mechanically induced trauma to cancer cells passing through the micro-circulation may well modify their metastatic behavior, we have categorized the damage done to cultured L1210 and Ehrlich ascites tumor cells passing through 5-12 micron pores in polycarbonate membranes, as a simple, albeit limited in vitro mechanical model. It was shown that in passing through membrane pores, impaired cell reproductive integrity and 3H-thymidine incorporation were the first detected signs of trauma, followed by impaired protein synthesis (14C-labelled amino acid incorporation) and finally, impaired plasma membrane integrity (loss of trypan blue exclusion). This, together with consideration of whole cell and nuclear diameters, suggests that damage may be the consequence of traumatic spatial dissociation between components of the cell periphery, the cytoskeleton and nucleus. Following a single filtration and return to culture, there was a progressive decline in cell numbers up to 96 h. After this, the survivors remained in a 'dormant' steady state for a further 5-6 days, and only then began to divide. The induction of a 'dormant' state in cancer cells by mechanical trauma, analogous to that inflicted in the passage through the microvasculature, is as interesting as it is unexpected.

Animals↗