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S Berliner

Publications and source records attributed to S Berliner.

At least 91 records · Page 5Linked to original sources
PubMed1991

Possible role for a plasma factor in the induction and/or maintenance of the state of leukocyte adhesiveness/aggregation in the peripheral blood. A study of mothers and their newborns.

The adhesive property of white blood cells is essential for a normal immune response. We examined the state of leukocyte adhesiveness/aggregation (LAA) in the peripheral blood of 31 mothers and their newborns by means of a direct slide test and found it to differ significantly, the respective per cents of aggregated leukocytes found in the peripheral blood being 15 +/- 6.4 and 5 +/- 3.3 (mean +/- SD). However, the particle concentration of white blood cells in the peripheral blood did not differ significantly (14.2 +/- 4.4 and 13.6 +/- x 10(9) l-1). By incubating a mother's plasma with her newborn's whole blood we could induce a significant (p less than 0.0001) increment in the state of LAA. We conclude that deficiency of a plasma factor that does not cross the placenta is responsible for the low LAA in the newborn's peripheral blood.

Cell Adhesion↗
PubMed1991

Heterotypic leukocyte aggregation in the peripheral blood of patients with leukemia, inflammation and stress.

This study deals with the question of whether the aggregates of leukocytes in the peripheral blood are homo- or heterotypic. One hundred-fifty individuals with leukemia, inflammation, and physical and mental stress, were examined. It was found that the various cell populations of the peripheral blood are represented in the aggregates and that aggregates are generally heterotypic. Normal and malignant leukocytes were noted in aggregates of patients with leukemia, suggesting that adhesive mechanisms are similar for both normal and malignant leukocytes. This was also supported in two animal models, one with leukocytosis of normal cells and the other with leukocytosis of leukemic cells, in which the state of leukocyte adhesiveness/aggregation in the peripheral blood correlated with tissue leukostasis. The possibility exists that "non specific stickers", present in the peripheral blood, promote interactions between the white blood cells, normal and malignant, and between these cells and the endothelium.

Adolescent↗
PubMed1990

State of leukocyte adhesiveness/aggregation in the peripheral blood of pemphigus and psoriatic patients.

The purpose of this study was to assess the role of leukocyte adherence in the pathogenesis of the psoriatic lesion. Use was made of the fact that psoriasis and pemphigus differ considerably as to the presence of leukocytes in the respective lesions: abundance in psoriasis, and absence in pemphigus. The state of leukocyte adhesiveness/aggregation (LAA) was determined in the peripheral blood of 56 patients with psoriasis and 31 patients with pemphigus. Both classes of patients were subdivided into two categories according to the severity of the disease. It was found that in both diseases elevated values of LAA were obtained in the severe cases, whereas the mild cases did not differ significantly from normal controls. Thus, in psoriasis mean LAA values of 9.5% +/- 8% were recorded in the severe patients and 5.5% +/- 4.2% in the mild cases (p = 0.01), while in pemphigus the values were 15% +/- 9.6% and 6.6% +/- 3.7% respectively (p = 0.03). It is concluded that LAA per se does not play a primary role in causing the psoriatic lesion.

Cell Adhesion↗
PubMed1990

The state of leukocyte adhesiveness/aggregation in the peripheral blood of patients with respiratory tract infections.

The state of leukocyte adhesiveness/aggregation (LAA) in the peripheral blood has been employed as a marker of inflammation. In the present study we examined patients with varying intensities of inflammation caused by respiratory tract infections to further investigate the reliability of the state of LAA for the detection and assessment of the severity of disease activity. The study includes 140 controls, 46 patients with upper respiratory tract infection, 30 with bronchitis, 27 with suspicion of pulmonary infiltrate, and 39 with small and 18 with large pulmonary infiltrate. Assessment was based on assuming an increasing severity of inflammation from the 1st to the 6th diagnostic category and by making use of discriminant analysis. It was found that the state of LAA proved to be the best variable to classify the patients into their diagnostic category (F to enter 27), followed by erythrocyte sedimentation rate at the 1st h (F to enter 20.8) and total white blood cell count (F to enter 8.3). These studies were followed by animal experimentation. A highly significant correlation (p = 0.005) was found between the state of LAA in the peripheral blood and the degree of pulmonary leukostasis in a model of endotoxemia in rabbits. These results suggest that the state of LAA is not an epiphenomenon and represents the tendency of the white blood cells to stick to the endothelium which facilitates their migration into the tissues.

Adolescent↗
PubMed1990

Acute coronary events following cisplatin-based chemotherapy.

Six patients with no previous signs or symptoms suggestive of coronary artery disease developed acute coronary ischemia/infarction shortly after cis-diamine-dichloroplatinum II (cisplatin) -based chemotherapy. In two patients this was the sole chemotherapeutic agent used. One patient underwent coronary angiography which disclosed no pathology, but following which, while on a calcium channel blocking agent regimen, he had an uneventful course of chemotherapy with cisplatin. Documentation of cisplatin-related vascular events is important in view of the growing number of patients who undergo cisplatin-based chemotherapy.

Aged↗
PubMed1989

Visualization of vascular platelet aggregation by plastic embedding and light microscopy.

Previous studies have indicated that platelets play a role in inflammation and microvascular damage but routine histologic preparations do not permit clear visualization of the platelets in tissues. Plastic embedding was used in this study to demonstrate platelet aggregates in the pulmonary vasculature of mice exposed to complement activation. The degree of platelet aggregation in the excised lungs was graded semiquantitatively in a total of 75 mice. Control Balb/c mice had a mean aggregation score of 0.16 while mice which received 0.3 ml zymosan-activated plasma (ZAP) intravenously (iv) had a score of 2.2. Injection of 0.3 or 0.4 ml of ZAP to which epsilon-aminocaproic acid was added prior to incubation with zymosan resulted in a score of 2.6 or 4.7 respectively. Balb/c (C5 sufficient) and AKR/J (C5 deficient) mice injected iv with 1 mg zymosan had scores of 2.9 and 3.2, respectively. Cobra venom factor (CVF) injected iv to Balb/c mice induced a dose-dependent aggregation. Taken together, these results confirm that complement activation products can mediate intrapulmonary platelet aggregation and they also demonstrate the suitability of plastic embedding for visualization of intravascular platelet aggregates under light microscopy.

Animals↗
PubMed1988

Generation and characterization of peptide-specific antibodies that inhibit von Willebrand factor binding to glycoprotein IIb-IIIa without interacting with other adhesive molecules. Selectivity is conferred by Pro1743 and other amino acid residues adjacent to the sequence Arg1744-Gly1745-Asp1746.

We have generated antibodies against a synthetic peptide corresponding to the sequence of human von Willebrand factor (vWF) between residues Glu1737-Ser1750 which includes the Arg-Gly-Asp sequence common to several adhesive molecules. Two anti-peptide antibodies, one polyclonal, and one monoclonal reacted with native vWF and inhibited its binding to platelet glycoprotein (GP) IIb-IIIa, but showed negligible cross-reactivity with fibrinogen, fibronectin, and vitronectin, three other molecules that contain the sequence Arg-Gly-Asp and bind to platelets. The structural bases for the specificity of the two antibodies were evaluated by testing the ability of peptides homologous to the parent sequence, but with single amino acid substitutions, to neutralize the binding of the two antibodies to vWF. The substitution of Pro1743, the residue immediately adjacent to the Arg-Gly-Asp sequence on the amino-terminal side, with Phe resulted in a peptide that failed to interact with either antibody. Thus, Pro1743 is important for maintaining a peptide conformation recognized by two antibodies specific for the GP IIb-IIIa-binding domain of vWF. Other residues important for optimal peptide reactivity with the polyclonal antibody were Ser1742, Arg1744, and Gly1745, whereas Gly1741, Gly1745, and Asp1746, but not Arg1744, were important for reactivity with the monoclonal antibody. The epitopes of both antibodies, therefore, included at least 2 of the residues in the sequence Arg-Gly-Asp considered the common cell-binding site of adhesive molecules that interact with GP IIb-IIIa. Nevertheless, both antibodies reacted only with vWF. These studies demonstrate that peptide-specific antibodies, unlike the promiscuous GP IIb-IIIa receptor, can recognize distinctive structural characteristics of the cell-binding domain of adhesive molecules imposed by residues adjacent to the sequence Arg-Gly-Asp.

Amino Acid Sequence↗
PubMed1988

Instability of leukocyte aggregation: lack of evidence for leukoembolization during various states of inflammation.

This study centers on the question of whether the phenomenon of leukocyte aggregation, which is typical to inflammatory conditions, is pathogenic per se. We examined patients and laboratory animals in whom the presence of aggregated leukocytes in the peripheral blood was documented by direct visualization and where, despite the presence of aggregated leukocytes, neither the patients nor the laboratory animals showed clinical or pathological evidence for leukoembolization. Our in vitro findings about the reversibility of the phenomenon of leukocyte aggregation help to explain the above-mentioned observations as well as the well-known daily clinical experience that, despite complement activation and other aggregatory stimuli, there is no clinical or pathological evidence for leukoembolization.

Aged↗
PubMed1988

Evaluation of disease activity in rheumatic patients by leucocyte adhesiveness/aggregation.

Previous work has shown that leucocyte adhesiveness/aggregation (LAA), as measured by the leukergy test, correlates well with disease severity in rheumatic patients. As LAA is probably a manifestation of the acute phase reaction various components of the acute phase reaction were measured in order to identify the best marker of disease activity. In addition to LAA, the following variables were measured in 79 patients with various rheumatic diseases and in 10 controls: white blood cell and platelet counts, erythrocyte sedimentation rate, haptoglobin, fibrinogen, C reactive protein, albumin, globulin, caeruloplasmin, alpha 1, alpha 2, beta, and gamma globulin, and haemoglobin concentrations. Patients were graded according to the state of their disease as mild, moderate, or severe. The extent of leucocyte adhesiveness/aggregation in peripheral blood proved to be the best laboratory variable for the grading of disease activity. Correct grading was obtained in 63% of the patients by means of the LAA, compared with 48% with C reactive protein, 41% with caeruloplasmin, 40% with haptoglobin, and 32% with haemoglobin. It is suggested that LAA of the peripheral blood during inflammation may be used as a reliable marker of disease severity.

Adolescent↗
PubMed1988

Synergism between zymosan-activated serum and heparin in the induction of polymorphonuclear leukocyte aggregation.

During the course of extracorporeal circulation, leukocyte aggregation is known to occur in some patients. This is attributed to complement activation and release of the chemotactic factor C5a. We investigated the effect of heparin on in vitro complement induced aggregation of polymorphonuclear leukocytes (PMNAGG), since most patients undergo heparinization during the extracorporeal circulation. Our results indicate that sub-aggregating concentrations of zymosan-activated serum (ZAS) enhance heparin-induced PMNAGG and that sub-aggregating amounts of heparin increase the aggregation induced by ZAS. Heat inactivation of the serum prior to zymosan activation abrogated the aggregating activity of the ZAS. Furthermore, the combined ZAS and heparin-induced PMNAGG was partially inhibited by specific antibodies to C5a but not to C3a. Therefore, we suggest that heparin and C5a may have a synergistic effect on the aggregation of polymorphonuclear leukocytes. These data might be relevant to situations in which patients are subjected to extracorporeal circulation.

Cell Aggregation↗
PubMed1987

Possible role of fibrinogen in the aggregation of white blood cells.

In order to verify whether leukocyte aggregation correlated with aggregation of other cellular elements during inflammation, we examined the state of leukocyte adhesiveness/aggregation (LAA) in the peripheral blood and red cell aggregation. Correlation was found to be significant as was the correlation between LAA and fibrinogen, and with the fibrin/fibrinogen degradation products concentration during various inflammatory states. In vitro leukocyte aggregation was decreased when the cells were suspended in autologous heat defibrinogenated plasma as compared to cells suspended in autologous native plasma. Heat aggregated fibrinogen but not native fibrinogen caused leukocyte aggregation in vitro. Finally, Arvin defibrinogenation in rabbits reduced the state of LAA in endotoxinemic rabbits. Integrating all this information, we assume that fibrinogen participates not only in the aggregation phenomena of red cells and platelets, but also in those of leukocytes.

Animals↗
PubMed1987

Aggregation of white cells and C-reactive protein: relation between these two indices in acute phase reaction.

The association between aggregates of leucocytes in blood drawn from patients with various inflammatory conditions and the serum concentration of C-reactive protein (CRP) was examined: serum concentration of CRP might contribute to the development of cellular aggregations. A total of 213 patients with various inflammatory or necrotic conditions were examined (including 31 women with normal pregnancy and 59 controls). A significant correlation between the degree of leucocyte aggregation and CRP concentration was noted in patients with bacterial infections and in a group of patients with various inflammatory conditions. In contrast, there was no correlation between the extent of leucocyte aggregation and CRP concentrations in patients with viral infections, malignancies, or pregnancy. The presence or absence of aggregated leucocytes can help in differentiating between the respective bacterial or viral infections. The serum concentrations of CRP were increased in both types of infection, although when a quantitative CRP assay was used, considerably higher concentrations were detected in bacterial diseases.

Acute-Phase Reaction↗
PubMed1987

The phenomenon of leukergy: induction and detection of leukocyte aggregation in whole human blood.

Leukocyte aggregation is involved in the generation of vascular damage during various inflammatory conditions. So far, in vitro leukocyte aggregation has been studied by mixing patients' plasma or serum with leukocytes of a normal donor in a platelet aggregometer. We evaluated the leukergy phenomenon, that is, the occurrence of aggregated leukocytes in peripheral blood of patients with inflammatory disorders, as an alternative tool to the former method. Leukocyte aggregation could be induced by zymosan-activated plasma, phorbol myristate acetate, and formyl-methionyl-leucyl-phenylalanine, as well as by the calcium ionophore A23187 in vitro in whole human blood. This aggregation was blocked by various lipoxygenase and cyclooxygenase pathway inhibitors. Leukergy was diagnosed in peripheral blood of patients with inflammatory disorders and was generally not associated with elevated concentrations of immune complexes, lactoferrin, C3a des Arg, or C5a des Arg. To the best of our knowledge, this is the first report on leukocyte aggregation studies performed in whole blood. Such study permits evaluation of the aggregation phenomena of leukocytes in their natural milieu. Furthermore, it is possible with this method to obtain direct visualization of leukocytic aggregates in the peripheral blood of patients. The significance of our results and their possible implications are discussed in light of the pertinent literature.

Adult↗
PubMed1986

Leukocytosis in non hematological malignancies--a possible tumor-associated marker.

Leukocytosis (WBC counts 10,000/mm3) was detected in 77 out of 252 patients (30%) with ten different types of nonhematological malignancy (NHM) at the time of diagnosis. A full search including serological and bacteriological screening was performed to exclude other possible causes of leukocytosis. Among the different tumors, carcinomas of the lung and colorectum were the most prevalently associated with leukocytosis. Absolute monocytosis was found in 25% of the patients and absolute eosinophilia in only 4.8%. The leukocytosis was attributed mainly to an increase in the mature polymorphonuclears, suggesting a release mechanism of WBC from storage pools by factors secreted or induced by the tumor. Neither the age nor the sex of the patients affected the incidence or magnitude of leukocytosis. However, the presence of metastases was associated with a significantly higher incidence of leukocytosis (p less than 0.05). The associated leukocytosis may be regarded as a poor prognostic sign, and was associated with a significantly (p less than 0.007) shorter survival time. In contrast, absolute lymphocytosis may have a positive effect on the survival time (p = 0.01). Tumor-associated leukocytosis may be an additional tumor-associated marker, of value in assessing and monitoring patients with NHMs.

Female↗
PubMed1986

The leukergy test in patients with ischemic heart disease.

In search of a simple method for potential evaluation of leukocyte aggregation in states of infarction, we compared the leukergy test, which consists of leukocyte aggregation visualized in a peripheral blood test, to the neutrophil aggregation activity (NAA) test, which consists of in vitro aggregation of neutrophils from normal donors by a patient's plasma. Seventy-five patients participated in the study; 20 with ischemic heart disease and no infarction, 41 with relatively small myocardial infarctions, and 14 with large myocardial infarctions, the respective values of leukergy being 6.9 +/- 3.2, 10.8 +/- 4.6, and 20.5 +/- 14%. On the other hand, neutrophil aggregation activity was the same in a group of 10 patients without myocardial infarction and 10 with myocardial infarction. In these two groups, which showed no difference in the NAA test, the respective leukergy values were 4 +/- 1.5 and 21.7 +/- 10.6%. Thus leukergy correlates better with the clinical picture than does the NAA test.

Aged↗
PubMed1985

The leukergy test in rheumatic diseases. New implications for an old test.

In order to assess the value of the leukergy test in which leukocytes aggregate in citrated whole blood, we examined 65 patients with various rheumatic conditions. In addition, plasma samples from 40 patients were examined for neutrophil aggregation activity in vitro. Results of the leukergy test were found to be in very good correlation with disease activity (P = 0.0001), whereas no increased neutrophil aggregation activity was found in the 40 plasma samples examined. The value of the leukergy test in assessing patients with rheumatic disease and its theoretical etiopathogenic role in these diseases are discussed.

Adult↗