The aim of this study was to analyse the efficacy of 2 second mobilization (MB) protocols in 2 groups of patients who failed to obtain enough peripheral blood progenitor cells (PBPC) in the first MB. In 1 group (8 patients), 10 μg/kg of G-CSF was administered, and in the other group (8 patients), a double dosage (10 μg/kg twice a day) was administered. Both groups of patients received Cyclophosphamide (1.5 g/kg) 10 days before the apheresis. No difference was found among both groups of patients in diagnosis, previous chemotherapy, and time elapsed after the first MB. Administration of higher doses of G-CSF decreased the number of apheresis needed in the second MB to complete 2 × 106/kg of CD34+ cells. It also increased the number of patients who achieved sufficient CD34+, namely, 75% versus 50%.

Effect of dilution of peripheral blood (PB) and umbilical cord blood (UCB) in mononuclear cells (MNC) recuperation, after density gradient separation was studied. Nineteen blood samples (10 PB and 9 UCB) were divided in two fractions, and gradient separation (Lymphoprep d=1.007) was performed in one fraction without, and in the other with 50% PBS dilution. Influence of hematocrit and leukocyte (WBC) count in MNC recovering was analysed. Studcnt-t test was utilized for statistical study. MNC recuperation was not affected by dilution. MNC obtained from diluted and undiluted UCB was higher (p<0.01) than those obtained from PB. Hematocrit and WBC were higher in UCB than in PB (p<0.01). We can conclude that dilution of PB and UCB does not improve the MNC recuperation. The superior MNC recover from UCB, with higher hematocrit and WBC counts, than from PB could be explained if a lesser density of UCB mononuclear cells.

The effect of two concentrations of dimethylsulphoxidc (DMSO) (5 and 10%) in mononuclear cells (MNC) cryopreserved viability and in granulocyte-monocyte colony forming units (GM-CFU) was analysed. Sixty MNC samples were cryopreserved with 10% and 5%DMSO in culture medium with 20% foetal calf serum and stored in liquid nitrogen. Thawing was performed in 40degreesC water bath. Viability was studied by Tripan blue exclusion. In 32 samples GM-CFU cultures were incubated at 37degreesC in 5%CO2 during 14 days. Statistical analysed was performed with the Student t test. Viability was lower in DMSO 10% than before freezing (p<0.001); and DMSO 5% viability was inferior (p<0.001) than DMSO 10%. GM-CFU in DMSO 10% were less than before freezing (p<0.001), but in DMSO 5% CFU-GM were no statistically different from DMSO 10%. We can conclude that DMSO 10% is better than 5% in MNC cryopreservation, although progenitor cells are equally preserved in both DMSO concentrations.

To assess the presence of irregular xenoantibodies against human red blood cells (RBCs) in 6 primate species used in xenotransplantation and other experimental procedures.Serum samples from 109 baboons of 4 different species (olive, chacma, sacred, and Guinea), 38 rhesus macaques, and 30 squirrel monkeys were tested for irregular xenoantibodies using an agglutination test using human RBCs of known phenotype for Rh, Kell, Kidd, Lewis, Lutheran, P1, and Duffy antigens, commercially available as RBC I, II, and III.We found hemagglutination for RBC I in 49%, 22%, 100%, 57%, 32%, and 33% of olive, chacma, sacred, and Guinea baboons, rhesus macaques, and squirrel monkey, respectively. The frequency for RBC II was 49%, 50%, 100%, 57%, 37%, and 33%, respectively, and for RBC III was 56%, 37%, 100%, 79%, 34%, and 33%, respectively. There were differences in frequency depending on the sex of the rhesus macaques; all 3 RBCs tested were higher in the females: 44% vs 0%, P = .008; 48% vs 1%, P = .02, and 44% vs 9.1%, P = .04 for RBC I, II, and III, respectively. There were differences due to age in only olive baboons, and a higher frequency in younger animals compared with juvenile, subadult, and adult animals for all 3 human RBCs.Assessment of irregular antibodies in the presence of primate serum should be taken into account during any experimental xenotransplantation protocol.

Anti-red blood cell (RBC) autoantibodies are the causative agents of autoimmune hemolytic anemia (AIHA), whose estimated incidence is one to three cases per 100,000 per year. The most frequent are immunoglobulin (Ig)G, which are usually directed against epitopes of the Rh system, react at 37 °C, mainly determine extravascular hemolysis, and are responsible for the “warm” forms (WAIHA). IgM are pentameric autoantibodies able to fix complement more efficiently than other isotypes, cause intravascular hemolysis, are directed against the I/i system, have an optimal temperature of reaction at 4 °C, and are responsible for the “cold” forms of autoimmune hemolytic anemia (cold hemoagglutinin disease, CHD). AIHAs can be distinguished as primary (idiopathic) and secondary to other diseases (autoimmune, infections, lymphoproliferative, or neoplastic diseases) and show great clinical heterogeneity, from compensated forms without anemia to fulminating disease. The gold standard for the detection of anti-RBC antibodies is the direct antiglobulin test (DAT) or Coombs test. DAT-tube is the traditional agglutination technique usually performed with broad-spectrum Coombs reagents; the use of monospecific anti-IgG, anti-IgM, and anti-C3 antisera is recommended to define the class of the autoantibody, along with its thermal characteristics. It is worth mentioning a simple test, the spontaneous agglutination of RBCs at 20 °C, a characteristic feature indicating the presence of cold IgM autoantibodies. DAT-tube may give false-negative results due to the small number of RBC-bound IgG molecules below the threshold of the test (estimated 400 molecules per RBC). Moreover, the tube technique with polyspecific (IgG+C) may fail to detect IgA autoantibodies; the use of monospecific antisera against IgA can overcome the DAT negativity. Another cause of DAT-negativity may be the presence of low-affinity autoantibodies, which can be detected by low ionic strength solutions (LISS) or cold washings. More sensitive methods include microcolumn, solid-phase, complement-fixation antibody-consumption test, enzyme-linked and radiolabelled tests, flow-cytometry, mitogen-stimulated-DAT, and the dual direct antiglobulin test. Despite all the above-mentioned tests, 5–10% of AIHA may be DAT negative, and the diagnosis is made after exclusion of other causes of hemolysis and on the basis of the clinical response to therapy.

American Journal of HematologyVolume 57, Issue 2 p. 179-179 Letters and CorrespondenceFree Access Post-chemotherapy Sweet's syndrome in three patients with AML Venancio Conesa, Corresponding Author Venancio Conesa Service of Hematology, Hospital “Virgen, de la Arrixaca,” Murcia, SpainService of Hematology, Hospital “Virgen, de la Arrixaca,” Murcia, SpainSearch for more papers by this authorAlfonso Morales, Alfonso Morales Service of Hematology, Hospital “Virgen, de la Arrixaca,” Murcia, SpainSearch for more papers by this authorMaria J. Majado, Maria J. Majado Service of Hematology, Hospital “Virgen, de la Arrixaca,” Murcia, SpainSearch for more papers by this authorConsuelo Gónzalez, Consuelo Gónzalez Service of Hematology, Hospital “Virgen, de la Arrixaca,” Murcia, SpainSearch for more papers by this authorRicardo Candel, Ricardo Candel Service of Hematology, Hospital “Virgen, de la Arrixaca,” Murcia, SpainSearch for more papers by this author Venancio Conesa, Corresponding Author Venancio Conesa Service of Hematology, Hospital “Virgen, de la Arrixaca,” Murcia, SpainService of Hematology, Hospital “Virgen, de la Arrixaca,” Murcia, SpainSearch for more papers by this authorAlfonso Morales, Alfonso Morales Service of Hematology, Hospital “Virgen, de la Arrixaca,” Murcia, SpainSearch for more papers by this authorMaria J. Majado, Maria J. Majado Service of Hematology, Hospital “Virgen, de la Arrixaca,” Murcia, SpainSearch for more papers by this authorConsuelo Gónzalez, Consuelo Gónzalez Service of Hematology, Hospital “Virgen, de la Arrixaca,” Murcia, SpainSearch for more papers by this authorRicardo Candel, Ricardo Candel Service of Hematology, Hospital “Virgen, de la Arrixaca,” Murcia, SpainSearch for more papers by this author First published: 06 December 1998 https://doi.org/10.1002/(SICI)1096-8652(199802)57:2<179::AID-AJH15>3.0.CO;2-7Citations: 8AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL No abstract is available for this article. References 1 Cohen PR, Talpaz M, Kurzrock R: Malignancy associated Sweet's syndrome: Review of the world literature. J Clin Oncol 6: 1887– 1897, 1988. 2 Torri O, Ruto F, Dierick A, Labeille B, Lok C, Desablens B, Denoeux JP: Dermatose aiguë fébrile neutrophilique (syndrome de Sweet) en période d'agranulocytose thérapeutique au cours d'une leucémie aiguë myéloblastique (LAM). Ann Dermatol Venereol 120: 884– 888, 1993. 3 Fett DL, Gibson LE, Su WPD: Sweet's syndrome: Systemic signs and symptoms and associated disorders. Mayo Clin Proc 70: 234– 240, 1995. Citing Literature Volume57, Issue2February 1998Pages 179-179 ReferencesRelatedInformation

American Journal of HematologyVolume 49, Issue 4 p. 359-360 Letter and Correspondence Long-term complete remission after interferon treatment in a case of multicentric castelman's disease Manuel Tamayo, Manuel Tamayo Servicios de Hematologia, Hospital Virgen de la Arrixaca, Murcia, SpainSearch for more papers by this authorConsuelo Gonzalez, Consuelo Gonzalez Servicios de Hematologia, Hospital Virgen de la Arrixaca, Murcia, SpainSearch for more papers by this authorM. Juliana Majado, M. Juliana Majado Servicios de Hematologia, Hospital Virgen de la Arrixaca, Murcia, SpainSearch for more papers by this authorRicardo Candel, Ricardo Candel Servicios de Hematologia, Hospital Virgen de la Arrixaca, Murcia, SpainSearch for more papers by this authorJose Ramos, Jose Ramos Anatomia Patologica, Hospital Virgen de la Arrixaca, Murcia, SpainSearch for more papers by this author Manuel Tamayo, Manuel Tamayo Servicios de Hematologia, Hospital Virgen de la Arrixaca, Murcia, SpainSearch for more papers by this authorConsuelo Gonzalez, Consuelo Gonzalez Servicios de Hematologia, Hospital Virgen de la Arrixaca, Murcia, SpainSearch for more papers by this authorM. Juliana Majado, M. Juliana Majado Servicios de Hematologia, Hospital Virgen de la Arrixaca, Murcia, SpainSearch for more papers by this authorRicardo Candel, Ricardo Candel Servicios de Hematologia, Hospital Virgen de la Arrixaca, Murcia, SpainSearch for more papers by this authorJose Ramos, Jose Ramos Anatomia Patologica, Hospital Virgen de la Arrixaca, Murcia, SpainSearch for more papers by this author First published: August 1995 https://doi.org/10.1002/ajh.2830490422Citations: 19AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat No abstract is available for this article. References 1 Peterson BA, Frizzera G: Multicentric Castleman's disease. Semin Oncol 20: 636–647, 1993. CASPubMedWeb of Science®Google Scholar 2 Frizzera G, Peterson BA, Bayrd ED, Goldman A: A systemic limphoproliferative disorder with morphologic features of Castleman's disease: clinical findings and clinicopathologic correlation in 15 patients. J Clin Oncol 3: 1202–1216, 1985. 10.1200/JCO.1985.3.9.1202 PubMedWeb of Science®Google Scholar 3 Rossi JF, Fegueux N, Calver B, Godefroy W: Alpha-interferon in angioinmunoblastic lymphadenopathy. Ann Intern Med 109: 512–513, 1988. 10.7326/0003-4819-109-6-512 CASPubMedWeb of Science®Google Scholar 4 Feremans WW, Khodadadi E: Alpha-Interferon therapy in refractory angioimmunoblastic lymphadenopathy. Eu J Haematol 31: 91, 1987. Google Scholar 5 Pavlidis NA, Briassoulis E, Klouvas G, Bai M: Is interferon-a an active agent in Castleman's disease? Ann Oncol 3: 854, 1992. Google Scholar Citing Literature Volume49, Issue4August 1995Pages 359-360 ReferencesRelatedInformation