bluuebunny/crossref_metadata_2025_split huggingface dataset:
A Factor in Lungs of Anaphylactically Shocked Guinea Pigs Which Can Induce Eosinophilia in Normal Animals
Authors: SAMTER MAX , KOFOED MARTHA A. , PIEPER WILLIAM 
Published: October 2019

Abstract
1 . Absolute eosinophil counts of normal guinea pigs were obtained before, and twenty-four hours after, intraperitoneal implantation of lung slices from normal and sensitized guinea pigs, and of lung and other tissues—intestines, uterus, gall bladder, liver, and skin—from guinea pigs which died in anaphylactic shock. Changes in the number of circulating eosinophils of normal recipients were also determined after transfer of lung obtained from the same sensitized donor animal before and after reinjection of the specific antigen, and of lungs from shocked animals incubated at 56 C. for 40 minutes.
2. Transfer of lung tissue from normal and sensitized (but not reinjected) guinea pigs into the peritoneal cavity of normal animals produces a significant, but limited, increase in the number of circulating eosinophils of the recipients.
3. Transfer of lung tissue of guinea pigs which died in anaphylactic shock into the peritoneal cavity of normal recipients produces a marked transitory eosinophilia.
4. Removal and transfer of one lung of sensitized guinea pigs, compared with transfer of the other lung after reinjection of the specific antigen demonstrates that the eosinotactic factor develops immediately after anaphylactic shock.
5. Transfer of intestines, uterus, gall bladder, and liver (compared with lung) of shocked guinea pigs into the peritoneal cavity of normal animals produces a small, but significant, transitory increase in the number of circulating eosinophils in the recipient; transfer of skin in a limited number of experiments appears to depress the peripheral eosinophil count of the recipients.
6. Transfer of lung tissue from shocked donors incubated at 58 C. for 40 minutes produces a less marked eosinophilia in normal recipients than transfer of lung tissue kept at room temperature for the same period.
The Finding of the L. E. (Lupus Erythematosus) Cells in Smears of Untreated, Freshly Drawn Peripheral Blood
Authors: CHOMET BERNHARD , KIRSHEN MARTIN M. , SCHAEFER GERSHON , MUDRIK POLA 
Published: October 2019

Abstract
A case of lupus erythematosus is reported in which L.E. cells were found in the smears of freshly drawn peripheral blood.
Studies on the Mechanical Fragility of Erythrocytes
Authors: GOLDBLOOM RICHARD B. , FISCHER ENID , REINHOLD JOHN , HSIA DAVID YI-YUNG 
Published: October 2019

Abstract
1. The mechanical fragilities of incubated and nonincubated erythrocytes of normal newborn infants, children and adults have been determined through the use of a simplified rotator.
2. The mean mechanical fragility of nonincubated erythrocytes was 7.1 per cent for newborns, 4.0 per cent for children and adults; the mean mechanical fragility of incubated erythrocytes was 13.4 per cent for newborns, 10.5 per cent for children and 10.8 per cent for adults.
3. The possible relationship of increased mechanical fragility of erythrocytes in the newborn to increased hemolysis in the neonatal period is suggested.
4. Possible causes of variation in the determination of mechanical fragility of incubated erythrocytes are discussed.
Antifibrinolytic Activity in Plasma after Exposure to Cold and after Chymotrypsin Administration
Authors: JENSEN H. , CHAMOVITZ DAVID L. , VOLKRINGER EVELYN , GRAY ELIZABETH , GOSNEY JAMES E. , KOCHOLATY WALTER 
Published: October 2019

Abstract
Exposure of rats and of human subjects to cold was associated with an elevation of the antifibrinolytic activity of blood. Administration of chymotrypsin to rats and rabbits caused a decrease in the antifibrinolytic activity of blood The possible significance of these and earlier observations on the fibrinolysis antifibrinolysis system in blood is discussed.
The Adrenal Cortex and Hemolysis
Authors: FELDMAN J. D. , RACHMILEWITZ M. , STEIN O. , STEIN Y. 
Published: October 2019

Abstract
The intravenous administration of phenylhydrazine caused a significantly greater destruction of red cells in adrenalectomized rats than in controls. Cortisone given to adrenalectomized rats prevented this increased destruction and maintained red cells at a level comparable to controls. ACTH almost completely prevented phenylhydrazine anemia in intact rats and the red cell level was significantly higher than that in intact rats which did not receive ACTH.
Electron Microscopic Studies of the Action of Thrombin on Blood Platelets
Authors: DE ROBERTIS E. , PASEYRO P. , REISSIG MAGDALENA 
Published: October 2019

Abstract
The action of thrombin on blood platelets has been studied under the electron microscope. In control experiments with preparations treated with normal plasma or Tyrode fluid, the normal structure of platelets in their different forms of extension and flattening on the film has been observed.
Thrombin (Parke-Davis Co.) in concentrations of 25 and 50 units per ml. has a lytic effect on platelets. The number of platelets affected by this treatment increases in the period of 5 to 30 minutes.
Disintegration proceeds in the hyalomere from the periphery to the center with the formation of long fibrillar processes constituted by microvesicles. These processes resemble myelin figures. The granulomere turns into an amorphous dense body which also undergoes lysis. The final residue of disintegration is constituted by microvesicular material and dense amorphous bodies.
The purified bovine thrombin of Seegers has exactly the same action. The lytic effect is observed with concentrations of thrombin as low as 2.5 units per ml. The number of platelets undergoing disintegration increases proportionally to the logarithm of the thrombin concentration. The probable role of thrombin and the lysis of platelets in normal blood clotting is discussed.
Hemophilia-like Disease Following Pregnancy
Authors: FRICK PAUL G. 
Published: October 2019

Abstract
1. A hemophilia-like disease acquired during the first pregnancy of a young woman, is described.
2. The clotting abnormality was caused by a circulating anticoagulant which, in all probability, inhibited the antihemophilic globulin.
3. The anticoagulant was demonstrated in the patient's second child during his first two and one-half months of life.
4. The transplacental transfer of the anticoagulant and the analogy of this condition to hemophilia (resistant to therapy) following iso-immunization against antihemophilic globulin, strongly suggest that an immunologic mechanism accounts for the development of this abnormality.
5. The patient recovered eighteen months after her second delivery and sixteen months after x-ray sterilization. The possible relation between endocrine factors and recovery is discussed.
Maintenance of high levels of pluripotent hematopoietic stem cells in vitro: effect of stromal cells and c-kit
Authors: Wineman JP , Nishikawa S , Muller-Sieburg CE 
Published: October 2019

Abstract
We show here that mouse pluripotent hematopoietic stem cells can be maintained in vitro on stroma for at least 3 weeks at levels close to those found in bone marrow. The extent of stem cell maintenance is affected by the nature of the stromal cells. The stromal cell line S17 supported stem cells significantly better than heterogeneous, primary stromal layers or the stromal cell line Strofl-1. Stem cells cultured on S17 repopulated all hematopoietic lineages in marrow-ablated hosts for at least 10 months, indicating that this culture system maintained primitive stem cells with extensive proliferative capacity. Furthermore, we demonstrate that, while pluripotent stem cells express c-kit, this receptor appears to play only a minor role in stem cell maintenance in vitro. The addition of an antibody that blocks the interaction of c-kit with its ligand essentially abrogated myelopoiesis in cultures. However, the level of stem cells in antibody-treated cultures was similar to that found in untreated cultures. Thus, it seems likely that the maintenance of primitive stem cells in vitro depends on yet unidentified stromal cell-derived factor(s).
Establishment and characterization of a new granulocyte-macrophage colony-stimulating factor-dependent and interleukin-3-dependent human acute myeloid leukemia cell line (GF-D8)
Authors: Rambaldi A , Bettoni S , Tosi S , Giudici G , Schiro R , Borleri GM , Abbate M , Chiaffarino F , Colotta F , Barbui T 
Published: October 2019

Abstract
A novel factor-dependent human myeloid leukemia cell line (GF-D8) was established from the peripheral blood of an 82-year-old man suffering from acute myeloblastic leukemia (AML). By morphology, cytochemical staining, and analysis of surface antigens, GF-D8 cells are myeloblasts of immature progenitor origin. The consensus karyotype is 45, XY, -5, 7q-, inv(7) (q31.2q36), 8q+, +8q+, 11q+, 12p-, -15, -17, + marker. The long-term survival and proliferation of GF-D8 cells is dependent on the presence of either granulocyte-macrophage colony-stimulating factor (GM- CSF) or interleukin-3 (IL-3). Weak colony growth was observed after exposure of GF-D8 cells to stem cell factor (SCF) but not after exposure to granulocyte-CSF (G-CSF), macrophage-CSF (M-CSF), IL-1 beta, IL-2, IL-5, or tumor necrosis factor-alpha (TNF-alpha). GM-CSF- and IL- 3-induced proliferation is dose dependent, with significant growth observed at concentrations as low as 0.1 ng/mL, but the combination of both factors has no synergistic effect. A significant proliferation is induced by GM-CSF and IL-3 even in serum-deprived cultures, although with a slightly decreased efficiency. GF-D8 cells were shown to express specific messenger RNAs for the alpha chains of the GM-CSF and IL-3 receptors as well as for the beta chain, common to both receptors. Interestingly, despite the absence of biologic response to G-CSF, specific transcripts for the G-CSF receptor gene were similarly identified by reverse polymerase chain reaction analysis. GF-D8 cells represent a useful tool for studying chromosome abnormalities of human AML as well as the regulation of myeloid proliferation and differentiation in vitro.
Molecular rearrangements on chromosome 11q23 predominate in infant acute lymphoblastic leukemia and are associated with specific biologic variables and poor outcome
Authors: Chen CS , Sorensen PH , Domer PH , Reaman GH , Korsmeyer SJ , Heerema NA , Hammond GD , Kersey JH 
Published: October 2019

Abstract
Acute lymphoblastic leukemia (ALL) in infants generally shows distinctive biologic features and has a poor prognosis. Cytogenetic studies indicate that many infant leukemias have chromosome 11q23 translocations. Because of these findings and the distinct clinical features of infant leukemia, we investigated 30 cases of infant ALL for molecular defects of 11q23. Fourteen cases had cytogenetic abnormalities of 11q23, and all of them showed 11q23 rearrangements at the molecular level. An additional seven cases also had 11q23 molecular rearrangements, including one with normal cytogenetic analysis. Molecular abnormalities of 11q23 were significantly correlated with adverse prognostic factors, including age under 6 months, hyperleukocytosis, CD10- phenotype, and early treatment failure. Molecular analysis identified a group of infants with germline 11q23 that had a very good treatment outcome with a projected event-free survival of 80% at median follow-up of 46 months compared to 15% in infants with rearranged 11q23 (P < .001). These findings suggest that a high proportion (70%) of infants with ALL have 11q23 rearrangements and that these rearrangements are not always detectable by cytogenetic analysis. The presence of germline 11q23 DNA may identify a subgroup of infant ALL patients with a good outcome using current therapy and a different etiology for their ALL.
Immunoglobulin levels and monoclonal gammopathies in children after bone marrow transplantation
Authors: Gerritsen EJ , van Tol MJ , Lankester AC , van der Weijden-Ragas CP , Jol-van der Zijde CM , Oudeman-Gruber NJ , Radl J , Vossen JM 
Published: October 2019

Abstract
Bone marrow graft recipients suffer profound immunodeficiency during at least 3 months after transplantation. B-cell reconstitution following allogeneic bone marrow transplantation (BMT) in children was studied longitudinally by quantification of Ig (sub)class levels in serum and by investigation of numbers and characteristics of homogeneous Ig components (H-Ig); ie, monoclonal gammopathies (MG). For the latter purpose, a sensitive immunoblotting technique capable of detecting H-Ig of a concentration as low as 0.5 microgram/mL was used. Sera of 40 children grafted for a variety of diseases were investigated and followed up for 5 years. It was found that Ig (sub)classes reached normal levels from 3 months after BMT onward. The sequential increase of the different Ig isotypes was in accordance with that seen in normal ontogeny. This was especially clear following BMT for severe congenital immunodeficiency. H-Ig appeared from as early as 6 weeks after BMT in increasing numbers, beginning within IgM, IgG3, and IgG1, and afterward within other isotypes. After an initial increase of serum Ig levels, “overshooting” occurred accompanied by high frequency of H-Ig. H-Ig were still present at 5 years after BMT, when Ig levels normalized. Our data indicate that B-cell reconstitution after allogeneic BMT recapitulates normal ontogeny but in a clonally dysregulated fashion; that is, with overexpression of some clones and underexpression of others.
Involvement of the high-affinity receptor for IgG (Fc gamma RI; CD64) in enhanced tumor cell cytotoxicity of neutrophils during granulocyte colony-stimulating factor therapy
Authors: Valerius T , Repp R , de Wit TP , Berthold S , Platzer E , Kalden JR , Gramatzki M , van de Winkel JG 
Published: October 2019

Abstract
Three different classes of Fc receptors for IgG (Fc gamma R) are currently distinguished in humans, of which polymorphonuclear phagocytes (PMN) normally express both low-affinity receptor classes-- Fc gamma RII (CD32) and Fc gamma RIII (CD16). During therapy with granulocyte colony-stimulating factor (G-CSF), neutrophils from patients with various malignancies and different hematologic disorders were found to additionally express high levels of the receptor with high affinity for IgG (Fc gamma RI; CD64). For these patients, the relative fluorescence intensity (rFI) for Fc gamma RI was 5.3 (range, 1.7 to 10.3; n = 19), compared with 1.0 (range, 1.0 to 1.1; n = 8) for healthy donors. The expression of Fc gamma RI during G-CSF therapy could be confirmed by using a panel of six CD64-specific antibodies, and by showing mRNA for Fc gamma RI. So far, three genes for Fc gamma RI have been identified, encoding four distinct transcription products. By reverse transcriptase-polymerase chain reaction technology, transcripts for both membrane-associated isoforms (hFc gamma RIa and hFc gamma RIb2) could be detected. The functional activity of Fc gamma RI on PMN during G-CSF therapy was shown by measuring binding of monomeric human IgG and antibody-dependent cellular cytotoxicity (ADCC). Thus, Fc gamma RI-positive neutrophils displayed enhanced ADCC activity to glioma (A1207), squamous cell (A431), and ovarian (SK-ov3) carcinoma cell lines. The involvement of Fc gamma RI in this increased cytotoxic activity was shown by blocking Fc gamma receptors with monoclonal antibodies, and by using F(ab')2 x F(ab')2-bispecific antibodies with specificities against tumor-related antigens and Fc gamma RI, resulting in solely Fc gamma RI-mediated cytotoxicity. Therapeutically, this additional Fc receptor on PMN may increase the efficacy of experimental antibody therapy.
Predictability of the t(1;19)(q23;p13) from surface antigen phenotype: implications for screening cases of childhood acute lymphoblastic leukemia for molecular analysis: a Pediatric Oncology Group study
Authors: Borowitz MJ , Hunger SP , Carroll AJ , Shuster JJ , Pullen DJ , Steuber CP , Cleary ML 
Published: October 2019

Abstract
The t(1;19)(q23;p13) translocation occurs in approximately 5% of B- precursor acute lymphoblastic leukemias (ALLs) occurring in children. Its presence has been associated with a poor prognosis, which may be overcome with more intensive therapy. Although leukemic cells from cases of t(1;19)-ALL frequently express cytoplasmic mu heavy chains, their complete antigenic profile remains undefined. Among 697 consecutive cases of B-precursor ALL with complete phenotypic studies using a panel of monoclonal antibodies, 22 cases were found to carry the t(1;19). Twenty of 22 cases had an identical, complex phenotype characterized by homogeneous expression of CD19, CD10, and CD9; complete absence of CD34; and at least partial absence of CD20. Overall, this phenotype was seen in only 8.0% (56 of 697) of childhood B-precursor ALL. One of the two remaining t(1;19)-carrying cases conformed to this phenotype, but was lacking data for CD9. The other case differed by virtue of expression of CD34 and was also hyperdiploid with 55 chromosomes. Molecular studies showed E2A-PBX1 abnormalities in all examined cases (12 of 12) with the t(1;19), including the case lacking CD9 data. In contrast, no E2A-PBX1 abnormalities were detected in the sole t(1;19)-ALL with CD34 expression. Seventeen cases with the characteristic phenotype and uninformative cytogenetics were also molecularly analyzed and 5 of 17 (including 4 of 8 with unsatisfactory cytogenetics and 1 of 9 with a normal karyotype) contained E2A gene rearrangements and E2A-PBX1 fusion mRNAs. Our results show that all cases of t(1;19)-ALL with concomitant E2A-PBX1 fusion invariably express a characteristic but uncommon profile of surface antigens. These observations suggest that selective molecular analysis of a small subset of patients (those with uninformative cytogenetics and the characteristic phenotype) can identify a significant number of additional cases of ALL with E2A-PBX1 fusion that might benefit from more intensive therapy.
The interleukin-2 receptor: a target for monoclonal antibody treatment of human T-cell lymphotrophic virus I-induced adult T-cell leukemia
Authors: Waldmann TA , White JD , Goldman CK , Top L , Grant A , Bamford R , Roessler E , Horak ID , Zaknoen S , Kasten-Sportes C 
Published: October 2019

Abstract
Adult T-cell leukemia (ATL) is a malignancy of mature lymphocytes caused by the retrovirus human T-cell lymphotrophic virus-I (HTLV-I). It is an aggressive leukemia with an overall mortality rate of 50% within 5 months; no conventional chemotherapy regimen appears successful in inducing long-term disease-free survival in ATL patients. However, ATL cells constitutively express high-affinity interleukin-2 receptors (IL-2Rs) identified by the anti-Tac monoclonal antibody, whereas normal resting cells do not. To exploit this difference in receptor expression, we administered anti-Tac intravenously (IV) to 19 patients with ATL. In general the patients did not suffer untoward reactions, and in 18 of 19 cases did not have a reduction in normal formed elements of the blood. Seven patients developed remissions that were mixed (1 patient), partial (4 patients), or complete (2 patients), with partial and complete remissions lasting from 9 weeks to more than 3 years as assessed by routine hematologic tests, immunofluorescence analysis, and molecular genetic analysis of T-cell receptor gene rearrangements and of HTLV-I proviral integration. Furthermore, remission was associated with a return to normal serum calcium levels and an improvement of liver function tests. Remission was also associated in some cases with an amelioration of the profound immunodeficiency state that characterizes ATL. Thus the use of a monoclonal antibody that blocks the interaction of IL-2 with its receptor expressed on ATL cells provides a rational approach for treatment of this aggressive malignancy.
Clinical course of human T-lymphotropic virus type I carriers with molecularly detectable monoclonal proliferation of T lymphocytes: defining a low- and high-risk population
Authors: Ikeda S , Momita S , Kinoshita K , Kamihira S , Moriuchi Y , Tsukasaki K , Ito M , Kanda T , Moriuchi R , Nakamura T 
Published: October 2019

Abstract
To characterize the prodromal phase of adult T-cell leukemia (ATL), a prospective follow-up study was conducted on 50 carriers in a putative pre-ATL state. This state was defined by the presence of molecularly- detectable monoclonal proliferation of human T-lymphotropic virus type I (HTLV-I)-infected T lymphocytes, and the absence of clinical symptoms of leukemia. The median observation time was 50 months. The pre-ATL subjects were divided into two groups according to initial white blood cell (WBC) counts: group A, those with a normal WBC count (9,000/microL) (n = 30), and group B, those with an increased WBC count (9,000 to 15,000) (n = 20). Comparisons were made between the two groups and with a group of 25 patients with chronic ATL (group C) who had WBC counts of more than 15,000. Significant differences in survival rate were found between groups A and B (10-year survival 65.7%) and group C (32.8%) (P < .01), and between group A (10-year survival 90.0%) and group B (52.1%) (P < .05). The incidence of transformation to overt ATL was 10% (3 of 30) in group A and 50% (10 of 20) in group B (P < .01). In six transformed cases (one in A and five in B) we found exactly the same integration sites in pre-ATL and overt ATL phases, confirming the multistep leukemogenesis hypothesized for this disease. However, the pre-ATL subjects could be divided into two distinct prognostic groups based on the initial WBC count; those with good and those with poor prognosis. Although the 10% transformation rate (2.5% annually) in group A seemed to be extremely high compared with that in the general population of HTLV-I carriers (around 0.06% to 0.4% annually), the majority of group A subjects and some in group B showed stable clinical courses without transformation. Further, development of ATL was not observed in four group A subjects with HTLV-I-associated myelopathy (HAM), which is rarely associated with ATL. We propose to call this group of rather benign HTLV-I carriers “HTLV-I carriers with monoclonal proliferation of T lymphocytes (HCMPT).” Thus far we have been unable to identify reliable parameters other than WBC counts that prospectively distinguish HCMPT from the true pre-ATL state, in which there is a high probability of developing ATL. Further clinical and biologic approaches should elucidate the natural history of the HTLV-I carrier state and early events in ATL leukemogenesis.
Growth of human myeloid leukemias in the human marrow environment of SCID-hu mice
Authors: Namikawa R , Ueda R , Kyoizumi S 
Published: October 2019

Abstract
It has been shown previously that multilineage human hematopoiesis is maintained within human fetal bone marrow (BM) fragments implanted into severe combined immunodeficient (SCID) mice. We describe here an application of this animal model, the SCID-hu mouse, to the study of human myeloid leukemias. BM cells from 8 patients with various types of myeloid leukemias were injected directly into human bone grafts in the SCID-hu mouse. Cells from 7 patients grew in the human marrow without spreading to the mouse marrow. Cells from 6 of these patients were successfully transferred in vivo to secondary SCID-hu recipients. The surface phenotype and the cytologic features of the leukemia cells were conserved during passage in vivo. Thus, human myeloid leukemia cells could be reproducibly propagated in the human marrow environment in SCID-hu mice. The differentiation of promyelocytic leukemia cells in the SCID-hu mice was induced by all-trans retinoic acid, suggesting that the biologic features of the leukemia cells were maintained as well. Finally, evidence for a leukemic progenitor cell population in one case of acute myelogenous leukemia was provided with this system. This model may provide a useful tool for studying the biology of human myeloid leukemia as well as for evaluating new therapeutic modalities for myeloid leukemias.