bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cytomegalovirus DNA in the sera of patients with cytomegalovirus pneumonia
Authors: Ishigaki Seishi , Takeda Mitsuaki , Kura Toshiro , Ban Noriyoshi , Saitoh Tadanori , Sakamaki Sumio , Watanabe Naoki , Kohgo Yutaka , Niitsu Yoshiro 
Published: March 2008

Summary We attempted to detect cytomegalovirus DNA (CMV‐DNA) in the sera of four leukaemia patients who underwent an allogeneic bone marrow transplant (BMT), in six leukaemia patients who suffered from pneumonia and in 16 healthy subjects, using the polymerase chain reaction (PCR). Three of the four BMT patients subsequently developed CMV pneumonia. In two cases, CMV‐DNA was detected in the sera at about the time the pneumonia occurred, and the amount of DNA increased with disease progression. The serum of the third patient became positive for CMV‐DNA before he developed pneumonia. The fourth patient did not develop CMV pneumonia, but his urine became persistently positive for CMV‐DNA soon after the BMT, whereas the serum was negative. A relationship was found between the occurrence of pneumonia and the serum level of CMV‐DNA. CMV‐DNA was also detected in three of six pneumonia patients whose anti‐CMV IgM antibodies were elevated in the circulation. Sera from the 16 normal subjects were negative for CMV‐DNA, regardless of their being seropositive or seronegative for CMV.While it had been previously thought that CMV did not exist in serum, we detected CMV‐DNA in serum by PCR in the active disease stage. Our results suggest that PCR would be useful for the early diagnosis of CMV pneumonia and in monitoring its course.
Sensitivity of erythroid progenitor colonies to erythropoietin in azidothymidine treated immunodeficient mice
Authors: Chow Fung‐Phing Rose , Sutton Patricia A. , Hamburger Anne W. 
Published: March 2008

SummaryThe anaemia induced by 3′‐azido‐3′dideoxythymidine (AZT) is poorly understood. We have used a murine model of AIDS, infection of female C57BL/6 mice with LP‐ BM5 murine leukaemia (MuLV) virus, to determine if AZT‐ induced anaemia is due, in part, to decreased responsiveness of erythropoietic precursors (BFU‐e) to erythropoietin (EPO). Mice in the early stage of LP‐BM5 MuLV disease were given AZT in their drinking water at 1·0 and 2·5 mg/ml. AZT produced anaemia in both groups, in a dose‐dependent fashion. Despite the anaemia, the number of splenic and bone marrow BFU‐e in AZT treated mice increased up to five‐fold over levels observed in infected untreated animals after 15 d of treatment. Colony formation by splenic and bone marrow BFUe was stimulated at lower concentrations of EPO in mice receiving AZT for 15 d than for infected, untreated mice. By day 30, sensitivity of both splenic and bone marrow BFU‐e of treated animals returned to that observed from cells of infected untreated animals. The mean plasma levels of EPO observed in AZT treated mice were appropriate for the degree of anaemia observed when compared with phenylhydrazine (PHZ) treated mice. The numbers of BFU‐e and the percent‐ age of bone marrow erythroblasts observed were comparable in AZT and PHZ treated mice with similar degrees of anaemia. However, reticulocytosis was inappropriate for the degree of anaemia observed in AZT treated infected mice. AZT‐induced peripheral anaemia in the face of increased numbers of BFU‐e and increased levels of plasma EPO suggest a lesion in terminal differentiation.
Absence of phosphatidylinositol (PI)‐linked proteins in a very early human multipotential haematopoietic marrow cell
Authors: Huang Andrew T. , Panella Timothy J. , Mold Nelda G. , Rosse Wendell F. 
Published: March 2008

SummaryA very early human haematopoietic progenitor cell population which was negative for the major histocompatibility class II antigen (HLA‐DR) and positive for the CD34 (MY10) antigen was separated into two subsets according to the expression of decay‐accelerating factor (DAF) on the cell surface. Using immunoadherence, cell cycle analysis, and cell culture, we determined that there is a DAF− multipotential cell and a more differentiated DAF+ lineage specific progenitor cell existing in human bone marrow. The DAF+ subset was highly enriched for CFU‐GEMM, while the DAF+ subset contained only BFU‐E and CFU‐GM. The DAF− subset was approximately 0·03% and the DAF+ subset approximately 0·0·08% of the original bone marrow population. MIRL (membrane‐inhibitory of reactive lysis), another Pl‐linked protein, was not expressed on the DAF− population but was expressed on the DAF+ cells. These observations indicate that PI‐linked proteins are absent from the multipotential stem cell but are present on an early lineage specific cell. The absence of expression of PI‐linked proteins can be used to further isolate and characterize a very early multipotential haematopoietic progenitor cell population.
The effects of interferon‐α on the proliferation of CML progenitor cells in vitro are not related to the precise position of the M‐BCR breakpoint
Authors: Dowding C. , Guo A‐P. , Maisin D. , Gordon M. Y. , Goldman J. M. 
Published: March 2008

SummaryWe investigated the effects of brief (2 h) and continuous exposure to recombinant interferon‐α2a (rIFN‐α) on the proliferation of primitive (blast colony‐forming cells, Bl‐CFC) and committed myeloid progenitor cells (BFU‐E and GM‐CFC) derived from blood and bone marrow of patients with chronic myeloid leukaemia (CML) and normal subjects. In all three clonogenic assays, rIFN‐α suppressed colony formation in a dose‐dependent manner. No differences were detected in the proliferation of CML or normal Bl‐CFC and GM‐CFC exposed to rIFN‐α. Erythroid colony formation by normal, but not by CML BFU‐E, was inhibited by relatively low concentrations (100 U/ml) of rIFN‐α. However, in patients whose blood or marrow contained a mixture of Philadelphia chromosome (Ph)‐positive and Ph‐negative BFU‐E, cytogenetic analysis of individual erythroid colonies showed no differential inhibition by rIFN‐α. We found no difference in the sensitivity to rIFN‐α of GM‐CFC from patients whose leukaemic cells expressed BCR/ABL mRNA with the b2a2 junction and that of GM‐CFC from patients with the b3a2 mRNA. We conclude that (1) rIFN‐α does not have a significant leukaemia‐specific effect on the progenitor cells detected in these assays, and (2) the sensitivity of CML GM‐CFC to rIFN‐α is independent of the type of BCR/ABL message present in the cells. The clinical efficacy of rIFN‐α could be due to selective toxicity to cells not assayed in this study, to effects on accessory cells or to alterations induced in progenitor cell/stromal cell interactions.
Correlation of serological, quantitative and cell‐mediated functional assays of maternal alloantibodies with the severity of haemolytic disease of the newborn
Authors: Hadley A. G. , Kumpel B. M. , Leader K. A. , Poole G. D. , Fraser I. D. 
Published: March 2008

SummarySerum samples containing IgG red blood cell (RBC) antibodies were collected without reference to clinical information from 131 pregnant alloimmunized women. Anti‐D and anti‐K were present in sera from 75 and 20 patients respectively. Antibody titres were determined by indirect antiglobulin test (IAGT), anti‐D levels were measured by AutoAnalyzer, RBC‐binding IgG was quantified using an enzyme‐linked immunosorbent assay (SOL‐ELISA), and functional activities were measured using the monocyte chemiluminescence (CL) test, antibody‐dependent monocytemediated and K cell‐mediated cytotoxicity (ADCC) assays, and rosette formation with U937 cells.Details of clinical outcomes were obtained retrospectively from 104 pregnancies. Forty‐one babies were ‘antigen‐negative’, and of the remainder, four required top‐up transfusions, 12 required exchange transfusions, three received intrauterine transfusions, and two died in utero. A comparison of test results with severity of haemolytic disease of the newborn (HDN) showed that, provided sera tested were collected within 8 weeks of the expected delivery date, the CL test and the monocyte‐mediated ADCC assay differentiated those D‐positive babies which required exchange transfusions from those unaffected or only mildly affected. The usefulness of results from the AutoAnalyzer and IAGT in predicting disease severity was compromised by the wide range of results from mothers of unaffected babies. This variability was less apparent in the SOL‐ELISA which predicted severe HDN with greater precision. Results from the U937 rosette assay and the K cell‐mediated ADCC assay failed to correlate with disease severity.
Primary human acute myeloblastic leukaemia: an analysis of in vitro granulocytic maturation following stimulation with retinoic acid and G‐CSF
Authors: Colombat Ph. , Santini V. , Krefft Delwel J. , Bredmond J. L. , Löwenberg B. 
Published: March 2008

Acute myeloid leukaemia (AML) is characterized by the inability of myeloid cells to reach terminal maturation. We examined to what degree granulocytic maturation could be achieved by stimulating AML blast cells in an in vitro serum‐free system with a combination of granulocyte‐colony stimulating factor (G‐CSF) and all‐trans‐retinoic acid (RA). Specimens from 41 AML patients were cultured for 7 d and then examined for cytochemistry (myeloperoxidase, Sudan Black, napthyl‐ASD‐chloracetate esterase, periodic acid Schiff) and nitroblue tetrazolium reduction. The expression of CD11a, CD11b. CD11c, CD15, CD18, CD10, CD24 and B13‐3 membrane antigens was also evaluated. Morphological and cytochemical studies were also performed after AML colony culture and culture of normal bone marrow cells (NBM). The comparative analysis of the panel of parameters was indicative of granulocytic maturation although to different degrees.The cells from 25/41 cases showed morphologic maturation (May‐Grünwald‐Giemsa). A positive correlation was evident between morphological maturation and CD11b expression (11/22 patients) as well as that of CD11c and CD15 (6 patients). Napthyl ASD chloroacetate esterase and PAS stainings also correlated with morphology (in 10/22 and 10/24 patients respectively). Nevertheless, the pattern of granulocytic maturation was remarkably variable among the 41 cases examined. The cells from only a few patients acquired the full spectrum of granulocytic markers. The comparison with normal bone marrow blasts indicates that serum‐free culture conditions can, per se, limit granulocytic maturation, but it also confirms the intrinsic inability of AML cells to attain complete maturation in response to two potent granulocytic inducers.
A cathepsin‐like cysteine proteinase proaggregating activity in thrombotic thrombocytopenic purpura
Authors: Falanga A. , Consonni R. , Ruggenenti P. , Barbui T. 
Published: March 2008

The platelet aggregating activity (PAA) of serum and plasma from thrombotic thrombocytopenic purpura (TTP, eight patients) and haemolytic uraemic syndrome (HUS, three patients) was investigated, Sample‐induced aggregation of washed platelets and the parallel 3H‐serotonin release were studied both in the presence and the absence of purified von Willebrand factor (vWF) or defibrinated cryoprecipitate, according to Kelton et al (1987). All the samples but two were positive in the test, vWF being indispensable for aggregation in all but two of the active cases. Samples from five patients during remission were ineffective under the same conditions, as were 14 controls from healthy donors.An inhibition study using four cysteine proteinase inhibitors (1 mM iodoacetamide, 0·5 mM E‐64, 0·1 mM antipain and 0·1 mM leupeptin) and two serine proteinase inhibitors (200 U/ml aprotinin and 0·2 U/ml hirudin) confirmed that TTP/HUS's PAA behaved enzymatically as a cysteine proteinase, as described (Murphy et al, 1987a). These results were confirmed on a protein preparation obtained from pooled plasmas after AI(OH)3 adsorption, ammonium sulphate precipitation, binding to and elution from a p‐(chloromercuri)benzoate (PCMB) affinity resin.To further characterize this activity we investigated whether it was a calcium‐dependent neutral protease or a lysosomal cathepsin by testing the sensitivity to a series of peptidyl diazomethyl ketones, synthetic inhibitors specifically designed for cysteine proteinases. We confirm here the presence of a circulating platelet aggregating cysteine proteinase in TTP/HUS and provide evidence for the first time that this activity behaves like a lysosomal cathepsin.
Colony‐cluster ratio and cluster number in cultures of circulating myeloid progenitors as indicators of high‐risk myelodysplasia
Authors: Tennant G. B. , Bowen D. T. , Jacobs A. 
Published: March 2008

SummaryCirculating myeloid progenitors were assayed in 172 normal subjects and 147 patients with myelodysplastic syndrome (MDS). Patients whose cultures had colony/cluster ratios (CCR) < 0·3 had significantly shorter survival periods than comparable patients with CCR > 0·3. A second prognostic indicator, which complemented CCR, was identified in patients with < 5% blasts. Median survival was significantly reduced in patients with > 15 clusters/ml blood despite colony and cluster numbers being predominantly within the normal range. Characteristic differences were found in three FAB groups large enough to allow statistical analysis. Survival amongst patients with refractory anaemia with excess of blasts (RAEB) was related to CCR and was independent of cluster number. Amongst sideroblastic patients (SA) survival related only to cluster number. Refractory anaemia (RA) patients included individuals in both high‐risk groups with only three patients out of 64 showing both features. Amongst all the MDS patients, those with CCR > 0·3 and < 15 clusters/ml blood formed a low‐risk group (n= 60) with a relatively good prognosis of whom 85% survived the study period (median duration 938 d) including 94% of those in this group with < 5% marrow blast cells.
Primary thrombocythaemia in pregnancy
Authors: Beard J. , Hillmen P. , Anderson C. C. , Lewis S. M. , Pearson T. C. 
Published: March 2008

SummaryNine pregnancies in six patients with primary thrombocythaemia are reported. Eight pregnancies resulted in the delivery of normal infants. One pregnancy ended in spontaneous abortion at 7 weeks gestation. One pregnancy was complicated by superficial thrombophlebitis and a postpartum haemorrhage. We suggest that pregnancy in patients with primary thrombocythaemia can have a favourable outcome, but requires close monitoring. Administration of aspirin during pregnancy may be of benefit.
A comparison of sickle cell syndromes in Northern Greece
Authors: Christakis J. , Vavatsi N. , Hassapopoulou H. , Angeloudi M. , Papadopoulou M. , Loukopoulos D. , Morris J. s. , Serjeant B. E. , Serjeant G. R. 
Published: March 2008

SummaryHaematological and clinical characteristics have been examined in 30 patients with homozygous sickle cell (SS) disease, 28 with sickle cell‐beta° thalassaemia, and 21 with sickle cell‐beta+ thalassaemia. The latter could be divided into three groups on their molecular basis and HbA levels, four subjects with an IVS‐2 nt 745 mutation having 34% HbA (designated Sbeta+ thalassaemia type I), 14 subjects with an IVS‐1 nt 110 mutation having 8–15% HbA (designated Sbeta+ thalassaemia type 11). and three subjects with an IVS–1 nt 6 mutation having 20–25% HbA (designated Sbeta+ thalassaemia type III). Comparisons were conducted between SS disease, Sbeta° thalassaemia, and Sbeta+ thalassaemia type II. Compared to SS disease, both thalassaemia syndromes had higher HbAr levels and red cell counts and lower mean cell haemoglobin content (MCHC), mean cell volume (MCV) and MCH, and Sbeta° thalassaemia had higher HbF and reticulocyte counts. Compared to Sbeta° thalassaemia. Sbeta+ thalassaemia had a higher haemoglobin and MCHC. Clinically, persistence of splenomegaly was more common in Sbeta° and Sbeta+ thalassaemia type II compared to SS disease. Few significant differences occurred between SS disease, Sbeta° and Sbeta+ thalassaemia type II in Northern Greece suggesting that the 8–15% HbA in the latter condition was insufficient to modify the clinical course.
PCR analysis of HIV‐1 sequences and differential immunological features in seronegative and seropositive haemophiliacs
Authors: Chelucci C. , Hassan H. J. , Gringeri A. , Macioce G. , Mariani G. , Santagostino E. , Testa U. , Vulcano F. , Mannucci P. M. , Peschle C. 
Published: March 2008

We have compared the immunological features of two matched groups of seronegative and seropositive haemophilia A individuals. Both groups were exposed from 1981 to 1985 to comparable amounts and batches of FVIII concentrates not subjected to virus inactivation procedures, and had therefore a 100% probability of receiving HIV‐contaminated material. The presence of proviral HIV‐1 sequences was evaluated by PCR in the DNA from peripheral blood lymphocytes and/or monocytes. After hybridization with specific probes, DNA from all seropositive haemophiliacs revealed HIV sequences; no HIV sequences were observed from the DNA of seronegative patients, even after two rounds of amplification, thus suggesting that these patients were not affected by a latent HIV infection.Seronegative/PCR‐ and seropositive/PCR+ patients showed a normal and reduced number of CD4+ lymphocytes, and a slight and marked increase of CD8+ cells respectively. Activated T cells expressing the HLA‐DR antigen were elevated in both groups. Interestingly, a significant reduction of circulating CD56+/CD3‐ NK lymphocytes was observed only in seropositive haemophiliacs, whereas NK lymphocytes with CD56+/CD3+ phenotype were within normal levels in both groups. In seropositive patients no correlation was found between the number of CD4+ and CD56+/CD3‐ lymphocytes. The marked reduction of CD56+/CD3‐ lymphocytes observed in seropositive haemophiliacs in addition to the CD4+ cell depletion may represent a key pathogenetic factor which facilitates the onset and/or the progression of HIV‐1 infection in haemophiliacs, and is related to the capacity of HIV to infect NK cells.
A prospective study to determine the safety of omitting the antiglobulin crossmatch from pretransfusion testing
Authors: Heddle Nancy M. , O'Hoski Pamela , Singer Joel , McBride John A. , Ali Mahmoud A. M. , Kelton John G. 
Published: March 2008

Transfusion medicine laboratories routinely perform a series of pretransfusion serological tests including: ABO grouping, Rh typing, and investigation of the recipient's serum to detect antibodies against blood group antigens (antibody screen). As a final check, most laboratories also perform a crossmatch in which the recipient's serum is incubated with the donor's red cells followed by the addition of an antiglobulin reagent (antiglobulin crossmatch). The need for the antiglobulin crossmatch when the antibody screen is negative has been questioned because there are few antibodies that are detected by this test. Such antibodies are usually directed against low incidence antigens that are not expressed on the screening cells and in many cases the clinical importance of these antibodies is uncertain. For these reasons, we performed a prospective study in which patients requiring red cell transfusion had a group and screen performed. If the antibody screen was negative the antiglobulin crossmatch was omitted. Following the transfusion of the blood, the antiglobulin crossmatch was performed to look for any potential incompatibility. All patients were monitored both serologically and clinically.Over the 2‐year interval of the study 9128 patients were entered. There were 8936 patients (97·9%) with a negative antibody screen and 26·9% (2404 patients) were transfused a total of 10899 red cell concentrates. The antiglobulin crossmatch performed after the transfusion indicated that 168 red cell concentrates (1·5%) would have been incompatible if the antiglobulin crossmatch had been performed pretransfusion. These 168 red cell concentrates were transfused to 119 patients during 130 transfusion episodes (defined as all transfusions administered within 24 h). Of the 130 transfusion episodes, 79·2% (103/130) were false positive laboratory results. There were 27 transfusion episodes where the antiglobulin crossmatch on blood transfused was positive due to an IgG antibody. Even though these transfused red cell concentrates were designated incompatible by the antiglobulin crossmatch, none of the patients receiving this blood had clinical or serological evidence of haemolysis. We concluded that the antiglobulin phase of the crossmatch can be omitted from pretransfusion testing without putting patients at risk.
Serum erythropoietin in the diagnosis of polycythaemia and after phlebotomy treatment
Authors: Birgegård Gunnar , Wide Leif 
Published: March 2008

Serum erythropoietin (S‐Epo) was measured with a radiommunoassay method in 36 patients with polycythaemia vera, 17 patients with secondary polycythaemia and 14 patients with relative polycythaemia. The diagnoses were made without the aid of the S‐Epo values. It was found that S‐Epo was below the reference range in 34/36 patients with polycythaemia vera (mean 2·1 ± 1·0 U/1), elevated in all cases of secondary polycythaemia (mean 121·7 ± 242 U/l) and normal in all but one of the cases with relative polycythaemia (mean 7·0 ± 2·5 U/l). Previous studies of S‐Epo levels in the differential diagnosis of polycythaemia have shown significant differences between the means of the groups but a considerable overlap. After phlebotomy treatment to normal haematocrit levels, the S‐Epo levels remained subnormal in most of the polycythaemia vera patients even after 18 months at a haematocrit around 45%. Two patients who had been kept at normal haematocrit for 6 and 7 years both had subnormal S‐Epo.We conclude that with an Epo assay method of high sensitivity and specificity it is possible to differentiate between different forms of polycythaemia with a high degree of certainty, even between patients with relative polycythaemia and polycythaemia vera patients.The reason why S‐Epo remains low in spite of a normal haematocrit in treated polycythaemia vera patients is not known.