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Biomedical subjects

B Ly

Publications and source records attributed to B Ly.

16 recordsLinked to original sources
PubMed1979

Why do crystalline precipitates in plasma cells always coalesce with parallel light and dark lines strictly end-to-end and side-to-side?

During transmission electron microscopy of plasma cells from two patients with plasma cell proliferative disorders, we observed a large number of small crystals, most of which showed a striation with alternating light and dark parallel lines. Ultraphotos strongly suggested that smaller crystals often coalesced to larger ones. The coalescence occurred in such a way that the parallel lines of the respective smaller crystals always met each other end-to-end and hardly ever end-to-side. A similar pattern can be seen on previously published ultraphotos from other patients with plasma cell proliferative disorders and intracellular crystals, although not commented upon by the respective authors. The parallel lines of the smaller crystals certainly must correspond to defined structures of the crystal. The stability of a certain configuration is therefore in all likelihood due to electrical potentials created by the crystal structure.

Crystallization↗
PubMed1979

Characterization of peripheral blood, spleen and bone marrow cells from a patient with hairy cell leukaemia.

The peripheral blood cells, spleen cells and bone marrow cells from a patient with hairy cell leukaemia were studied by means of several immunological methods and by phase contrast and electron microscopy. Both by light and electron microscopy the cells had the morphology of hairy cells. 60 % of all the peripheral blood cells, and 80 % of the spleen cells had membrane-bound IgGk immunoglobulin. 60 % of the peripheral blood lymphocytes and 90 % of the spleen cells were positive for Ia-antigens, and 80 % of the peripheral blood, and 70 % of the spleen cells had receptors for complement factor C3. The percentages of cells with receptor for the Fc part of IgC and receptors for sheep red blood cells (SRBC) were low both in peripheral blood and in spleen. Reduced numbers of peroxidase positive cells and cytotoxic plaque-forming cells were also observed as well as reduced lymphocyte responses after stimulation of peripheral blood lymphocytes with PHA, PWM, ConA, PPD and allogeneic cells. A normal antibody-dependent cell cytotoxicity (ADCC) and PHA-induced cytotoxicity was observed for the peripheral blood lymphocytes of the patients. Our results suggest that the hairy cells in our patient are derived from B lymphocytes and have a monoclonal origin.

Aged↗
PubMed1978

A prospective study of streptokinase and heparin in the treatment of deep vein thrombosis.

In a prospective trial, 42 medical patients with a history of deep vein thrombosis of less than five days were allocated at random to treatment with streptokinase or heparin. Only patients with extensive thromboses were included. Streptokinase was given in a loading dose of 250 000 IU and a maintenance dose of 100 000 IU/hour for 4 days as a mean. Heparin was given in a loading dose of 15 000 IU and a maintenance dose of 20 000-50 000 IU/day. The therapeutic results were evaluated by phlebography. Significant thrombolysis occurred in 71.4% of 21 patients treated with streptokinase and in 23.8% of the 21 heparin-treated patients. Using the chi2-test for overall association, this difference was statistically highly significant (p = 0.002). Three patients in each treatment group experienced major bleeding, two in each group requiring blood transfusions. Minor bleeding and slight rise in temperature were encountered more often in the streptokinase than in the heparin group. It is concluded that patients with acute deep vein thrombosis with proximal extension of the thrombus beyond the calf veins should be offered a therapeutic trial with streptokinase.

Acute Disease↗
PubMed1978

A controlled clinical trial of streptokinase and heparin in the treatment of major pulmonary embolism.

Treatment with streptokinase or heparin was allocated randomly to 20 patients with major pulmonary embolism verified by angiography. In addition, 4 patients treated with streptokinase and 1 patient treated with heparin were included in the trial prior to the start of treatment. Streptokinase of heparin was given for 72 hours and pulmonary angiography was repeated. The angiographic evidence of thrombolysis was significantly greater (p less than 0.01) in the 14 patients treated with streptokinase than in the 11 treated with heparin. In the heparin group, 1 patient died from massive embolism 15 hours after the start of treatment. In another patient who died 4 weeks later from cerebral glibolastoma, persistent massive embolism contributed to the fatal outcome. In the streptokinase group, 1 patient with a metastatic pulmonary carcinoma died 3 weeks after the start of treatment from gangrene of both legs following thrombotic occlusion of the inferior vena cava. Bleeding was more common after treatment with streptokinase than with heparin, but was not a serious problem in any patient. It is concluded that patients with life-threatening pulmonary embolism should be offered the benefits of streptokinase.

Adult↗
PubMed1978

A syndrome of factor VII deficiency and abnormal platelet release reaction.

A 15-year-old girl with severe factor VII deficiency and chronic arthropathy showed an excessively prolonged bleeding time. Further studies demonstrated low platelet adhesiveness and abnormal platelet aggregation with ADP, collagen and epinephrine. Release of 14C-serotonin was deficient after aggregation with ADP and epinephrine, but was normal with thrombin. Transfusion of plasma or prothrombin complex concentrate resulted in a partial or complete correction of the bleeding time, respectively, but had no effect on in vitro platelet function tests. Both parents and the only sister had factor VII activities of 42%-72% and factor VII antigen levels of 45%-66% of normal and may thus be heterozygotes with respect to factor VII deficiency. All three had normal bleeding times in spite of abnormal in vitro platelet functions. The observations are interpreted to mean that in this family with factor VII deficiency and abnormal platelet release reaction the platelet abnormality as such was not sufficiently severe to prolong the bleeding time unless the factor VII activity was also very low.

Adenosine Diphosphate↗
PubMed1978

Acute eosinophilo-myelomonocytic leukaemia, one of the 'in between leukaemias'.

A patient is reported to have an in between type of acute myeloid leukaemia, namely acute eosinophilomyelomonocytic leukaemia. The blasts in the peripheral blood showed a definite transition towards immature monocytes. The bone marrow contained 65% blasts and 13% eosinophil promyelocytes. The large number of immature eosinophils in the bone marrow strongly support the view that they were part of the leukaemic process and not merely a reactive eosinophilia.

Acute Disease↗
PubMed1978

Acute myelogenous leukaemia occurring at the same time in husband and wife.

Acute myelogenous leukaemia was diagnosed within a 1 week's interval in a married couple without consanguinity. The husband had acute myelomonocytic leukaemia whereas the wife had acute myelogenous leukaemia of the classical type. Neither the histories nor findings contributed to an understanding of leukaemogenesis. The calculated risk that a husband and wife should develop acute myelogenous leukaemia within the same year is approximately 1:400 millions.

Adult↗
PubMed1977

Light green crystals in May-Grünwald and Giemsa-stained bone marrow macrophages in patients with myeloid leukaemia.

A patient in a terminal stage of myelomocytic leukaemia had a number of elongated crystals in many bone marrow macrophages. The crystals were up to 20 micron long, showed a characteristic light green colour with May-Grünwald & Giemsa, but did not stain with Sudan Black B or PAS. Electron microscopy showed that many of the crystals had a rhomboid form, but failed to show periodicity with the magnification used. A search was made for similar light green crystalline inclusions in patients with different types of leukaemia. Identical inclusions were found in 2 out of 5 other cases of myelomonocytic leukaemia, and in 3 out of 5 cases of chronic myeloid leukaemia. In contrast, such inclusions were not found in any of 6 patients with acute lymphoblastic leukaemia, nor in 4 patients with chronic lymphocytic leukaemia.

Bone Marrow↗
PubMed1977

An inhibitor of activated factor XIII, inhibiting fibrin cross-linking but not incorporation of amine into casein.

An inhibitor of fibrin cross-linking was studied. The inhibitor was quantitatively separated together with the IgG fraction of plasma, but attempts to neutralize the purified inhibitor by commercial anti-IgG sera gave inconstant results, possibly due to anti-factor XIII activity demonstrable in these sera. The inhibitor prevented cross-linking by activated factor XIII, even when tested on preformed fibrin, but was inactive when assayed by the use of a synthetic substrate (monodansylcadaverine). Since, the inhibitor remained in the supernatant after defibrination, and was thus not associated with clottable proteins, the present findings suggest inhibition of activated f. XIII and not blockade of cross-linking sites on fibrinogen.

Amines↗
PubMed1977

A study of the variable heavy chain (VH) region of membrane-bound Ig on human chronic leukemic lymphocytes.

Lymphocytes from 20 patients with chronic lymphocytic leukemia (CLL) were studied for membrane staining by direct immunofluorescence by employing anti-F(ab')2, anti-VHI, anti-VHII, anti-VHIII subgroup-specific antisera, as well as light chain-specific antisera. Some lymphocyte preparations were also studied in indirect immunofluorescence with an antiserum raised against a fragment (VH) corresponding to the variable region of the heavy chain of a human IgG3 myeloma protein (Kup). Lymphocytes from each CLL patient demonstrated a restriction of VH subgroups expressed on the cell membrane; six were restricted to the VHI subgroup, seven to VHII, and seven to the VHIII subgroup. This restriction gave further evidence for monoclonality of the membrane-bound Ig and the leukemic cell proliferation. Antiserum to the VH fragment stained closely similar percentages of CLL lymphocytes to that obtained with anti-F(ab')2 antiserum. Furthermore, double staining revealed that the same cells were stained with anti-VH antiserum as were stained with anti-F(ab')2 antiserum, i.e., only the B lymphocytes.

Adult↗