Detection of immediate hypersensitivity in rabbits by direct basophil degranulation.

The direct in vitro antigen-induced degranulation of rabbit basophils based on a simplified one-step method for the staining of these cells is reported. Degranulation was assessed by counting the number of basophils before and after exposure to antigen at 37 degrees C in the presence of Ca++. The degranulation was IgE-mediated, as shown by its passive transfer to nonimmunized rabbits by IgE-containing serum; also, the reaction was dependent on the presence of Ca++ ions and normal cell metabolism. The technique allowed the detection of serum factors capable of blocking the degranulation. It provided a means for following IgE sensitization at the cellular level, which is a better index of immediate hypersensitivity than the presence of circulating specific IgE.     

Lymphocytotoxic definition of combined ABH and Lewis antigens and their transfer from Sera to lymphocytes

Analysis of lymphocytotoxic reactions with peripheral blood lymphocytes from 74 donors, typed for ABO, secretor, and Lewis phenotypes, identified clusters of reactions distinguishing six antigens resulting from the interactions of Lewis, secretor, and ABO systems: Lea, Leb, ALed, BLed, ALeb, and BLeb. In these experiments, Led on O lymphocytes and Lec were not detected as expected from the experience of other authors with A antigen, B and Leb were detected only on the lymphocytes of ABH secretors, demonstrating that all the ABH antigens of lymphocytes are controlled by the secretor system as are the ABH antigens in external secretions. The ABH and Lewis antigens identified on lymphocytes could be transferred in vitro to lymphocytes, cultured for 2 to 7 days at 37 degrees C in the serum of donors of selected ABO, Lewis, and secretor phenotypes, confirming that ABH and Lewis antigens are not synthesized by lymphocytes but are acquired from circulation as are the Lewis antigens on erythrocytes. As expected, the HLA antigens of lymphocytes were not modified after culture.     

Translocation 1;7 in preleukemic states

A translocation t(1;7) interpreted as t(1;7)(p11;p11) was first reported by Scheres et al. in eight patients with various hematologic disorders. The karyotype of the abnormal cells was trisomic for 1q and monosomic for 7q. Those investigators reported having found four other cases in the literature. We report herein studies of two patients with the same t(1;7).     

Effect of a memory retrieval task on recall of verbal material obtained after awakening from sleep.

After 66 awakenings from sleep without spontaneous recall of verbal material in the report, the subjects were submitted to a memory retrieval task concerning this kind of material. In 39.3% of the awakenings we found either syntactic, semantic or generic material (the latter never appeared in spontaneous recall); differences are found between fast sleep and slow wave sleep concerning semantic and generic material. The results are discussed in relation to the problem of retrieval and of hypothetical coding and verbal material assessments.     

Chronic myelogenous leukemia with a Philadelphia chromosome resulting from a complex translocation (2; 9; 22), following an undifferentiated acute leukemia

This case report concerns a patient with acute leukemia considered at diagnosis to be undifferentiated. Unfortunately, because of the failure of the culture, a cytogenetic evaluation was not possible at that stage. A full remission was induced, but 17 months after the onset of the disease the patient developed chronic myelogenous leukemia. The karyotypes prepared at that time and during the follow-up revealed the presence of a Philadelphia chromosome (Ph1) in all examined cells. This Ph1 resulted from a complex translocation involving chromosomes No. 2, 9, and 22.     

Cytogenetic studies on Burkitt's lymphoma cell lines

Cytogenetic findings on 15 new cell lines established from endemic and nonendemic Burkitt's lymphoma are reported. Specific translocations t(8;14) and t(8;22) were found, respectively, in 13 and in 2 of the cell lines. Particular attention has been paid to the additional chromosome abnormalities found in 10 of the 15 cell lines. These anomalies involve the long arm chromosome No. 1 with a relatively high frequency. These additional chromosome anomalies argue in favor of the concept of the existence of primary and secondary chromosome abnormalities in malignancies.     

Adenocarcinoma of the gallbladder: chromosome abnormalities in a genetic form of cancer

Chromosome studies on gallbladder adenocarcinoma in a Papago Indian woman were performed. These studies revealed a high degree of aneuploidy including multiple instances of missing chromosomes, extra chromosomes, and chromosome rearrangements. Double minute chromosomes and homogeneous staining regions on chromosomes were present in the cancer cells. To our knowledge this is the first report on the cytogenetic analysis of a gallbladder cancer. Chromosome studies on gallbladder cancers will be of unusual interest because of the relatively high frequency of this rare genetic form of cancer in American Indians.     

Bone marrow graft of a Fanconi's anemia patient. Cytogenetic study

Lymphocyte chromosome studies before and after allogenic graft of a Fanconi's anemia (FA) patient showed that chromosome breakage disappeared following grafting. The fact that this condition was maintained up to 36 months after grafting demonstrates that the defect responsible for chromosome breakage lies in the FA cell itself.     

Immunoblastic lymphoma following Hodgkin's disease: a case report with translocation t(8;14) in tumoral cells and sporadic t(7;14) in peripheral lymphocytes

A non-Hodgkin's lymphoma was observed in a patient who had been treated for Hodgkin's disease (HD). The initial treatment consisted of radiotherapy alone, but following three subsequent relapses, both chemotherapy and radiotherapy were administered several times. Twenty years later, the biopsy of an isolated cervical lymph node revealed a non-Hodgkin's lymphoma. The histologic subtype was immunoblastic. Cytogenetic studies of the tumoral cells revealed a t(8;14)(q24;q32) translocation. At the same time, multiple chromosomal rearrangements were observed in peripheral blood lymphocytes, especially t(7;14)(q35;q12), which was noted in 6 of 53 mitoses. This anomaly, frequently observed in patients with ataxia telangiectasia or severe immunodeficiency, has not previously been described in such circumstances.     

Immunodeficiency diseases and expression of HLA antigens

The role of HLA antigens in lymphocyte differentiation is strongly suggested by the existence of a recently identified immunodeficiency associated with, and probably resulting from, the lack of expression of HLA-A, B, and C antigens as well as /gB₂ microglobulin on various cells of hematopoietic origin. This “bare lymphocyte syndrome” has been described in a family where the transmission appeared to be autosomal recessive, and the responsible gene was not borne by the sixth chromosome.Another infant with a severe combined immunodeficiency disease has been treated with fetal liver and thymus transplants (FLTT). A persisting chimerism has been documented: T cells derived from the donor and B cells from the host. Despite complete HLA-A, B, and DR mismatch, T and B cells did cooperate resulting in significant antibody production, and defense against viral infection has been normal. Such an observation may suggest that “allogeneic restriction” of T-cell effector functions can be circumvented.     

Bronchial response to inhaled prostaglandin F2α in patients with common or aspirin-sensitive asthma

The effect of aerosolized prostaglandin F₂α (PGF₂α) on specific airway resistance (SRaw) has been measured in patients with common (n = 10) or aspirin-sensitive asthma (n = 5). In all subjects PGF₂α caused a dose-related increase in SRaw, but considerable individual differences in sensitivity were observed. The patients with aspirin intolerance did not differ from regular asthmatics in terms of their response to PGF₂α. Two types of reactions to PGF₂α could be distinguished from their time-course: immediate and short-lasting (3 cases) or delayed and long-lasting (12 cases). Inhalation of a β-adrenergic drug rapidly and completely reversed the effect of PGF₂α, suggesting that the increase in SRaw was due to bronchospasm. In 7 subjects the inhalation of an anticholinergic drug (SCH 1000) prior to PGF₂α inhibited to a large extent the effect of the latter, suggesting that the cholinergic system played an important role in the bronchial response to PGF₂α. In 9 subjects no correlation was found between the bronchial sensitivity to carbachol and PGF₂α.     

Renin storage and cell differentiation in juxtaglomerular cell tumors: an immunohistochemical and ultrastructural study of three cases

Three renin-secreting juxtaglomerular cell tumors were studied by ultrastructural and immunocytochemical methods. Both active and inactive renins were identified in tumor extracts. By immunofluorescence and the peroxidase-antiperoxidase (PAP) method with antirenin antiserum, immunolabeling was intracytoplasmic and irregularly distributed throughout the tumor tissue. Electron microscopic examination revealed various types of secretory granules, including atypical giant crystalloid protogranules in one case, and the postembedding PAP procedure showed labeling of all types of granules. Acid phosphatase staining was observed within secretory granules and autophagic vacuoles. The process of renin storage and release is discussed. The presence in one case of a neural component and a distal tubular structure supports the view of a hamartomatous lesion.     

Translocation involving chromosome 22 in Ewing's Sarcoma. A cytogenetic study of four fresh tumors

Ewing's sarcoma was described in 1921 by James Ewing as a diffuse endothelioma of bone and, for some time, was believed to be an undifferenciated type of Parker's sarcoma. At present, these two entities are thought to be distinct, the macroscopic and microscopic aspects of Ewing's sarcoma being very characteristic, although the exact cell type of this tumor remains unknown. This has lead many workers to study this sarcoma in order to recognize its origin.We thought it of interest to carry out cytogenetic investigations of our cases of Ewing's sarcoma, since very few chromosomal data on this malignancy exist in the literature [1–3].     

Cytogenetic studies on African Burkitt's lymphoma cell lines: t(8;14), t(2;8) and t(8;22) translocations

Cytogenetic studies on ten African Epstein-Barr virus (EBV) positive Burkitt's lymphoma (BL) cell lines were performed. The usual translocation t(8;14) (q24;q32) was found in five of them, a deletion del(8) (q24→qter) in another one, while four variants were observed, two of these having a t(2;8) (p12;q24) translocation and two a t(8;22) (q24;q11) translocation. Other chromosome abnormalities were seen in seven of the cell lines, but these varied from one cell line to another. Thus, variant translocations, such as we describe here, are found in endemic BL cases. Two of these variants are identical to those previously identified in BL from nonendemic areas. The common chromosome abnormality of these BL cell lines was a rearrangement of the 8q24 band. The role of this constant cytogenetic change remains to be elucidated.     

Glomerular matrix proteins in nodular glomerulosclerosis in association with light chain deposition disease and diabetes mellitus

The diagnosis of light chain deposition nephropathy is based on the immunohistochemical demonstration of monoclonal light chain deposits within connective tissue matrix and on the presence at the ultrastructural level of electron-dense granular deposits along glomerular and tubular basement membranes. A nodular glomerulopathy characterized by amorphous periodic acid-Schiff-positive and argyrophilic widened mesangium and nodules is described in three patients with light chain deposition nephropathy. Light microscopic examination did not allow discrimination between the glomerular changes found in these specimens and the nodular glomerulosclerosis described in four patients with well-documented diabetes mellitus. Electron microscopic examination revealed microtubular fibrils 10 to 12 nm thick in mesangial areas in both groups. Such microfibrils could be glycoproteins. Immunofluorescence localization of matrix proteins, by staining with affinity-purified antibodies to types I, III, IV, and V (A, B) collagens, fibronectin, laminin, and heparan sulfate-containing proteoglycans, showed similar distributions in the two conditions. The mechanism of this abnormal accumulation of mesangial and glomerular basement membrane matrix proteins in two different conditions remains unknown.     

t(15;17) in a promyelocytic form of chronic myeloid leukemia blastic crisis

Two simultaneous translocations, t(15;17) and t(9;22), have been observed in a chronic myelogenous leukemia patient with acute promyelocytic blastic crisis. After remission obtention only karyotypes with t(9;22) were present. The occurrence of the two translocations in the same cell argues in favor of the specificity of t(15;17) versus acute promyelocytic differentiation.     

Cytogenetic studies on acute nonlymphocytic leukemias following polycythemia vera

Chromosome studies were performed on 15 patients suffering from acute nonlymphocytic leukemia (ANLL) and in one patient in a preleukemic state following polycythemia vera (PV). Clonal chromosome abnormalities that were present in all cases were clearly nonrandom and involved chromosomes #1, #5, #7, #8, #9, #11, and #21. A subdivision of ANLL into two categories occurring in the course of PV is proposed from the clinical, hematologic, and cytogenetic data: one resembling de novo ANLL with rapid initial evolution, easy classification into one group of the FAB nomenclature, and simple chromosome abnormalities; the other resembling induced leukemia, often with more progressive initial evolution, difficulty or impossibility of classification into one group of the FAB nomenclature, and complex chromosome abnormalities. The consequences for the commitment level of progenitor cell from which the leukemic clones originate are discussed.     

Nitrogen mustard-induced chromosome breakage: A tool for Fanconi's anemia diagnosis

Chromosome studies were performed on phytohemagglutinin-stimulated lymphocytes from 9 Fanconi's anemia (FA) patients, 6 of their parents, 7 controls, 2 children with aplastic anemia of unknown etiology, and one child with Zinsser-Cole-Engman syndrome. The addition of low doses (0.0085 μg/ml) of nitrogen mustard to cultures dramatically increased the chromosome breakage level in FA, the increase evaluated from means of chromosome anomalies per cell was highly significant (p < 0.001). On the other hand, the means of chromosome anomalies per cell increased greatly only at higher dilutions in all non-FA subjects. The high susceptibility of FA cells to chromosome breakage by nitrogen mustard may be of use as a diagnostic test and might be useful for prenatal detection of the disease.     

Malignant and reactive erythroblasts in erythroleukemia (M6)

A cytogenetic and cytological study of 16 cases of erythroleukemia (M6) is reported. No chromosomal abnormalities were observed in 10 cases. Abnormalities were present in the other 6 cases, of which 4 were complex abnormalities. It was not possible to establish any correlation between the occurrence of morphologic abnormalities of the erythroid and megakaryocyte-platelet series and the presence of cytogenetic defects. Studies of mitoses by cytologic and cytogenetic methods concurrently performed in some cases suggest that two types of erythroleukemia can be distinguished: (1) cases with chromosomal abnormalities and a persistence of erythroblast mitoses in vitro (which suggests that the erythroblasts belong to the leukemic clone) and (2) cases with no chromosome abnormality and a disappearance of erythroblast mitoses after culture, suggesting that the erythroblasts are not members of the leukemic clone.