bluuebunny/crossref_metadata_2025_split huggingface dataset:
Case report: Interleukin‐6 positive follicular hyperplasia in the lymph node of a patient with rheumatoid arthritis
Authors: Numata Yukiko , Matsuura Yasushi , Onishi Saburo , Yamamoto Yasutake , Ohno Fumitoshi , Tagoh Hiromi , Yoshizaki Kazuyuki , Fujimoto Shigeyoshi , Yamamoto Hiroshi 
Published: February 2007

AbstractWe examined interleukin‐6 production in the hyperplastic lymph node of a 77‐year‐old male rheumatoid arthritis patient with lymphadenopathy. The interleukin‐6 production of the lymph node was observed by both immunohistological staining and in vitro culture. The results suggest that interleukin‐6 plays a significant pathogenic role in the etiology of the lymphadenopathy seen in many rheumatoid arthritis patients.
Novel effect of cyclicization of the Arg‐Gly‐Asp‐containing peptide on vitronectin binding to platelets
Authors: Mohri Hiroshi , Hashimoto Yoshimi , Ohba Masataka , Kumagai Hiromichi , Ohkubo Takao 
Published: February 2007

AbstractVitronectin is one of the glycoproteins that mediate cell adhesion and spreading of a variety of cells through the RGD(S) sequence. Vitronectin is demonstrated to bind to glycoprotein IIb‐IIIa and play a role in platelet aggregation. Synthetic peptides containing the RGD(S) sequence can inhibit vitronectin binding to platelets, but the affinity of these peptides is less than 1/100th that of native vitronectin. The present study thus examined the ability of modified RGD(S)‐containing peptide to inhibit vitronectin binding to thrombin‐stimulated platelets. The cyclicization of GRGDSPA peptide was done by the linkage of NH2‐terminal glycin and the COOH‐terminal alanin. The circular dichroism spectrum of cyclic GRGDSPA peptide only showed negative minimum at approximately 220 nm, but those of other linear peptides such as GRGDSPA and GRGESPA had no effect. This result indicated that only the cyclic GRGDSPA peptide retained some conformational structure to restrict its flexibility. Inhibition experiments revealed that the affinities of the ligands for the receptor decreased in the order of vitronectin = fibronectin = fibrinogen = von Willebrand factor (vWF) > cyclic GRGDSPA peptide > GRGDSPA peptide. GRGESPA peptide had no effect. These results demonstrate that the conformational structure of the RGD(S) sequence plays the important role for the affinity of vitronectin binding to activated platelets and the increased affinity of the modified peptide is a prerequisite for the potential antithrombotic use.
The effect of rhGM‐CSF on the proliferation of osteogenic sarcoma cells
Authors: Baker W. Jeffrey , Hargis Jeffrey B. , Danesi Romano , La Rocca Renato V. 
Published: February 2007

AbstractRecombinant human granulocyte–macrophage colony‐stimulating factor (rhGM‐CSF) promotes the growth of a variety of hematopoietic and nonhematopoietic cells, both benign and malignant. There is now evidence that osteoblast‐like cells produce GM‐CSF and their growth is stimulated by this cytokine in vitro. We have studied the effect of rhGM‐CSF on DNA synthesis and cell proliferation in the human osteogenic sarcoma cell lines U‐20S, G‐292, MG‐63, and HOS. RhGM‐CSF stimulated a dose‐dependent increase in radioactive thymidine incorporation in each of the four cell lines in the presence of serum‐free media, and in two cell lines (HOS and U‐20S) in the presence of fetal bovine serum (FBS). In addition, rhGM‐CSF produced significant increases in cell proliferation in two cell lines (MG‐63 and U‐20S) in the presence of 2% FBS. These results suggest that GM‐CSF may have an important role in the biology of human osteogenic sarcoma cells. The clinical implications of these findings merit further investigation.
Evaluation of continuous infusion low‐dose 5‐azacytidine in the treatment of myelodysplastic syndromes
Authors: Chitambar Christopher R. , Libnoch Joseph A. , Matthaeus William G. , Ash Robert C. , Ritch Paul S. , Anderson Tom 
Published: February 2007

AbstractThe treatment of myelodysplastic syndromes (MDS) is both difficult and controversial. In the current study, we evaluated the efficacy of low‐dose 5‐azacytidine in the treatment of this disorder. Fifteen patients with MDS were entered on study to be treated with 5‐azacytidine by continuous intravenous infusion for 14 days. Doses of the drug ranged from 10 mg/m2/day to 35 mg/m2/day, with most patients receiving 16.5 mg/m2/day. In two patients, the drug was stopped early in the course of treatment because of thrombocytopenia. Thirteen patients completed therapy according to protocol. Three of 13 patients demonstrated a partial response to therapy. Of these three patients, one had an increase in platelet and absolute neutrophil counts, while the other two no longer required support with red cell transfusions. The drug was well tolerated and significant myelosuppression did not occur in most patients. Low‐dose 5‐azacytidine appears to have activity in the treatment of primary MDS and future studies should consider evaluation of this drug in combination with hematopoietic growth factors.
Anaplastic large cell Ki‐1 lymphoma involving bone marrow: Marrow findings and association with reactive hemophagocytosis
Authors: Wong K. F. , Chan J. K. C. , Ng C. S. , Chu Y. C. , Lam P. W. Y. , Yuen H. L. 
Published: February 2007

AbstractThis report describes the bone marrow findings in four patients whose marrow was involved by anaplastic large‐cell Ki‐1 lymphoma, an uncommon event in this type of lymphoma. In the marrow aspirate smears, the involvement was subtle, and was in the form of isolated large cells with irregular nuclear configuration, coarse chromatin, prominent nucleoli, and basophilic cytoplasm which might be vacuolated. One case showed paradoxically massive involvement in the trephine biopsy taken from the same site as the marrow aspirate. Reactive histiocytic proliferation with hemophagocytosis was also present. Since marrow aspirate or biopsy may be the first pathologic specimen examined in patients having anaplastic large‐cell Ki‐1 Iymphoma, it is important to be able to recognize the small population of neoplastic cells, which should lead to prompt treatment or further investigations as deemed necessary.
Splenic function in persons with sickle cell trait at moderately high altitude
Authors: Nuss Rachelle , Feyerabend Angela J. , Lear James L. , Lane Peter A. 
Published: February 2007

AbstractWe investigated the possibility that persons with sickle cell trait who reside chronically at moderately high altitude might develop impaired splenic reticuloendothelial function. Seventeen healthy young black men with sickle trait who had lived at ⩾ 1,609 m for ⩾ 10 years participated in the study along with 25 matched control subjects with normal hemoglobin. Splenic function was assessed by radionuclide liver‐spleen scanning and by red cell pit counts. No evidence of impaired splenic function was found in the sickle trait group. The data suggest that long‐term residence at moderately high altitude does not place persons with sickle cell trait at risk for splenic dysfunction.
Plasma adenosine deaminase2, is a marker for human immunodeficiency virus‐1 seroconversion
Authors: Niedzwicki John G. , Mayer Kenneth H. , Abushanab Elie , Abernethy Darrell R. 
Published: February 2007

AbstractPlasma adenosine deaminase2, (ADA2) has recently been proposed to be a marker for human immunodeficiency virus‐1 (HIV) infection. We measured ADA2, levels in plasma from two groups of white homosexual males at 6‐month intervals for a total of 2.5 years. One group consisted of 6 subjects who seroconverted for HIV, and the other consisted of 8 HIV seropositive patients who progressed from asymptomatic (CDC Groups II/III) to symptomatic (CDC Group IV) disease. Seroconversion was associated with a significant increase in plasma ADA2 which persisted throughout follow‐up of 1.5 years. However, disease progression in HIV seropositive patients was not associated with any significant change in plasma ADA2 In conclusion, ADA2, may represent a unique marker for HIV seroconversion which does not change with later progression to symptomatic disease.
Protein C and S levels in acute leukemia
Authors: Troy Kevin , Essex David , Rand Jacob , Lema Myra , Cuttner Janet 
Published: February 2007

AbstractPatients with acute leukemia undergoing remission induction chemotherapy occasionally develop venous thrombosis despite severe thrombocytopenia and in the absence of disseminated intravascular coagulation. This observation prompted us to study the levels of the naturally occurring anticoagulant proteins C and S prospectively in patient sundergoing remission induction chemotherapy for acute leukemia. Plasma samples from 50 adult patients with acute leukemia (34 AML, 16 ALL) were analyzed for protein C antigen, functional protein C, immunologic total and free protein S as well as levels of C4b binding protein (C4bBP). Plasma levels of immunolgic protein C were significantly lower in patients with active acute myelocytic leukemia (mean = 77.9) than in controls (mean = 123.6) or patients in remission (mean = 132). Functional protein C levels were also significantly lower in AML patients with active disease (mean = 58.5) than controls (mean = 95.5) or patients in remission (mean = 98.5). Patients with acute lymphocytic leukemia (ALL) had normal levels of immunologic and functional protein C. Although total protein S levels were normal in all patients studied, levels of free protein Swere significantly decreased in patients with active AML (mean = 29.3) compared with patients in remission (mean = 42.0) or controls (mean = 42.4). In contrast, patients with ALL, both with active disease and in remission had normal free protein S levels. This decrease in free protein S seen in active AML was not associated with liver disease, white cell count or an increase in C4bBP. These findings provide a possible explanation for the occasional occurrence of venous thrombosis in patients with acute myelocytic leukemia.
CD5 positive immunoregulatory B cells in spleen populations from multiple myeloma patients
Authors: MacKenzie Malcolm R. , Paglieroni Teresa , Caggiano Vincent 
Published: February 2007

AbstractCD19+CD5+ lymphocytes constitute a minority of peripheral blood B cells. In view of the importance of these cells in the pathogenesis of the immunoregulation of myeloma, their incidence in another lymphoid organ was determined. CD5+ B cells were studied in 9 spleens from patients with multiple myeloma and in 10 spleens from normal individuals removed secondary to trauma. The total number of CD19+ B cells were increased in myeloma spleens (44.4% ± 12.6%) as compared to normal spleens (20.4% ± 7.4%). Likewise, the percentage of CD19 cells which co‐expressed CD5 were increased in myeloma (25.3% ± 12.4%) versus normal (4.4% ± 2.3%) spleen. CD5+ B cells isolated from myeloma spleens, but not normal spleens, inhibit production of immunoglobulin in a pokeweed mitogen driven assay. Thus the spleen appears to be an important source of immunoregulatory B cells in multiple myeloma.
Computed tomography for diagnosis of hepatic rupture in primary systemic amyloidosis
Authors: Gastineau Dennis A. , Gertz Morie A. , Rosen Charles B. , Kyle Robert A. 
Published: February 2007

AbstractHepatic rupture in primary systemic amyloidosis is extremely ominous; death occurs in hours to days. We present two cases of hepatic rupture diagnosed ante mortem with computed tomography (CT). Surgical repair was possible in one instance and successfully controlled the bleeding. In the setting of primary amyloidosis, the early use of CT scanning for undiagnosed ascites, hypotension, or rapid organ enlargement may lead to early diagnosis and potential surgical correction.
Retroperitoneal fibrosis accompanying immune thrombocytopenia
Authors: Wallach Paul M. , Flannery Michael T. , Adelman Harold M. , Powsang Julio , Saba Hussein , Altus Philip , Espinoza Luis R. 
Published: February 2007

AbstractRetroperitoneal fibrosis represents an idiopathic systemic fibrosing syndrome which leads to the development of progressive hydronephrosis and azotemia (Stewart and Friberg: Southern Medical Journal 77:1185–1187, 1984; Morad et al.: American Journal of Medicine 82:363–366, 1987). Evidence in the literature supports a hypothesis that retroperitoneal fibrosis represents a systemic autoimmune process (Lichon et al.: Journal of Rheumatology 11:373,374, 1984; Lipman et al.: JAMA 196:204–206, 1966; Littlejohn and Keystone: Journal Rheumatology 8:665–669, 1981; Katz et al.: American Journal of Clinical Pathology 67:436–439, 1977). We report a case of a patient with retroperitoneal fibrosis, immune thrombocytopenia, presence of antinuclear antibody, and direct Coombs positivity which provides further evidence that retroperitoneal fibrosis is an autoimmune process. Progressive obstructive uropathy related to his fibrosis led to bilateral hydronephrosis and significant renal function impairment. Also, he developed marked immune thrombocytopenia. Treatment with prednisone produced a dramatic response in both platelet count and renal function.
Agranlocytosis caused by ticlopindine and its mechanism
Authors: Ono Kazutoshi , Kurohara Kazuhiro , Yoshihara Masahiro , Shimamoto Yoshinori , Yamaguchi Masaya 
Published: February 2007

AbstractA 75‐year‐old female patient with agranulocytosis caused by ticlopidine is reported. She took the drug at 200 mg/day for 30 days to prevent recurrence of cerebral infarction. The leukocyte count at the nadir was 500/μl on the 34th day since she started to take the drug. Complete recovery of her peripheral leukocytes came 12 days after its withdrawal. In this patient, mechanisms of ticlopidine‐caused agranulocytosis were studied. The lymphocyte stimulation test using ticlopidine was negative. In the culture of marrow cells depleted of lymphocytes, ticlopidine directly inhibited the CFU‐C in a dose‐dependent manner. Neither the serum on the day of admission nor the T‐lymphocytes pre‐cultured with ticlopidine had any effect on the CFU‐C. The lymphocyte stimulation test is useless in an attempt to find the causal drug in agranulocytosis if it is caused in a directly toxic manner. Agranulocytosis caused by ticlopidine is rare, but careful follow‐up is necessary in the case of patients on the drug because there are some whose marrow cells are very sensitive to it.
Flow cytometric analysis of anti‐platelet antibodies in patients with chronic idiopathic thrombocytopenic purpura (ITP) using acid‐treated, formalin‐fixed platelets
Authors: Mizumoto Y. , Fujimura Y. , Nishikawa K. , Uchida M. , Fukui H. , Morii T. , Narita N. , Kurata Y. 
Published: February 2007

AbstractAcid treatment of normal washed platelets prepared by albumin density gradient centrifugation followed by formalin fixation effectively eliminates HLA class I antigens from the platelet surface, without altering the immunoreactivity of platelet membrane glycoproteins Ib and IIb/IIIa complex. Using these platelets, flow cytometric analysis was performed on a total of 20 sera from different patients with chronic ITP, and revealed an inverse linear correlation between the platelet count and the mean fluorescence intensity which represents a relative amount of platelet‐bound IgG. These results suggest that acid‐treated, formalin‐fixed platelets can be used as specimens to detect anti‐platelet antibodies to differentiate from those to HLA‐class I antigens.
Hemopoietic inhibition in hairy cell leukemia
Authors: Janckila Anthony J. , Gentile Patrick S. , Yam Lung T. 
Published: February 2007

AbstractLeukopenia, thrombocytopenia, and anemia are important features of hairy cell leukemia (HCL). They are generally considered to be due to hypersplenism and to inadequate production by bone marrow which is heavily infiltrated by the neoplastic hairy cells (HC). However, the cytopenias may also be caused by hemopoietic inhibition by cytokines derived from the mononuclear cells (MNC) of HCL. We studied the MNC of HCL with an in vitro assay for granulocyte‐macrophage progenitors (CFU‐GM) to search for this hemopoietic inhibitor(s) and to determine the cell source and mechanism of its production/release. We found that MNC conditioned media from 7 of 9 HCL cases exerted substantial inhibitory effect (23% to 66%) on normal marrow cells. Peak inhibitory activity was obtained in media conditioned with 106 MNC/ml for 90 minutes to 24 hours. Both HC and lymphocytes could release inhibitor(s) through mutually synergistic cell interactions. HC alone were inactive and lymphocytes alone were only weakly active. Mixtures of conditioned media of HC and of lymphocytes were not synergistic. The lymphocytes responsible for the inhibition were present in preparations depleted of cells bearing the cluster designation 4 antigen (CD4+) and B cells and were most likely the CD8− T‐cells. In one patient so examined, a partial reversal of inhibition was achieved by treating MNC‐CM with antibodies to tumor necrosis factor (TNF)‐alpha suggesting that TNF‐alpha was at least partly involved in the inhibition of CFU‐GM. This mechanism of cytokine release may be operative in vivo to account for the cytopenias in HCL and, if so, could alter the concept of hypersplenism in this disease.
The effect of 1‐hydroxyvitamin D3 for prolongation of leukemic transformation‐free survival in myelodysplastic syndromes
Authors: Motomura Shigeki , Kanamori Heiwa , Ohkubo Takao , Maruta Atsuo , Kodama Fumio 
Published: February 2007

AbstractLeukemic transformation (LT) free survival was studied in 30 patients with myelodysplastic syndromes (MDS). In 15 cases, 4–6 μg/day of 1‐hydroxyvitamin D3 was administered, for a median duration of 17 months (D‐group), other subjects had no therapy (N group). LT free survival of the D group had significant advantage over that of the N group according to the Kaplan—Meier method (P < 0.001). In addition, 7 cases in the N group developed acute leukemia, in contrast to only one in the D group (P < 0.05). These results suggest that oral administration of 1‐hydroxyvitamin D3 prevents the progression of MDS to overt leukemia under the effect of differentiation capacity from blasts to monocytes.
Unexpectedly high toxicity of MACOP‐B in young patients with low grade lymphoma
Authors: Arranz R. , Peréz G. , Steegmann J. L. , Cámara R. , Tomás J. F. , Figuera A. , Vazquez L. , Fernández‐Rañada J. M. 
Published: February 2007

AbstractWe report the results of treatment with MACOP‐B in 11 young patients with low grade lymphoma (LGL). Complete remission was obtained in 4 (57%) and partial remission in 3 (42.8%) of 7 evaluable patients. However, this aggressive chemotherapy has not offered any advantage because of an unacceptably high treatment‐related morbidity and mortality (17%). Serious infection during neutropenia was the most common complication.
Significance of hemostatic molecular markers during disseminated intravascular coagulation in patients with liver cirrhosis treated by endoscopic embolization for esophageal varices
Authors: Koyama Tetsuji , Kakishita Eizo , Nakai Yoshiyuki , Okamoto Eizo 
Published: February 2007

AbstractWe studied the quantitative changes of hemostatic molecular markers with time during the course of disseminated intravascular coagulation (DIC) induced by endoscopic embolization using thrombin for esophageal varices in nine patients with liver cirrhosis. The plasma levels of D–dimer, a product of plasmin degradation of cross‐linked fibrin, and thrombin–antithrombin‐III complex (TAT) were significantly higher in patients before treatment when compared with 60 healthy individuals. The plasma levels of TAT, D‐dimer, and plasmin α2‐plasmin inhibitor complex (PIC) increased significantly 5–15 min after thrombin injection into the varices, earlier than the changes of conventional coagulofibrinolytic factors, reached a maximum level after 180 min, and started to decline after 1 day. Although the plasma PIC level returned to normal after 7 days, both TAT and D‐dimer were still above the pretreatment level.Although there was no change in urokinase‐type plasminogen activator (u‐PA), tissue‐type plasminogen activator (t‐PA) increased significantly after 5 min. The plasma level of plasminogen activator inhibitor type 1 (PAI‐1) showed only a slight elevation after treatment. We propose that the hemostatic molecular markers TAT, D‐dimer, and PIC are suitable for the early diagnosis of DIC after endoscopic embolization using thrombin in patients with liver cirrhosis and that the increase of PAI‐1 is too small for the regulation of fibrinolysis due to t‐PA in DIC occurring in liver cirrhosis.
Circulating thrombomodulin in thrombotic thrombocytopenic purpura
Authors: Takahashi Hoyu , Hanano Masaharu , Wada Ken , Tatewaki Wataru , Niwano Hiroe , Shibata Akira , Tsubouchi Jiro , Nakano Masahiko , Nakamura Tadao 
Published: February 2007

AbstractEndothelial cell injury is thought to be one of the causative factors in thrombotic thrombocytopenic purpura (TTP). A novel index of endothelial injury, plasma thrombomodulin, was measured in 13 patients with acute TTP. The mean plasma concentration of thrombomodulin was elevated in patients with TTP (34.23 ± 19.08 ng/ml) as compared with healthy subjects (16.99 ± 2.63 ng/ml, P <0.001). Eight (61.5%) of 13 patients had high thrombomodulin values. Markedly elevated thrombomodulin levels were observed in TTP patients who had suffered from systemic lupus erythematosus, in whom plasma thrombomodulin was still elevated when they achieved remission. Five of these 13 patients with TTP had normal plasma levels of thrombomodulin. In addition, the plasma thrombomodulin concentrations were correlated well with von Willebrand factor antigen and tissuetype plasminogen activator antigen levels, both of which are released from stimulated or damaged endothelial cells. No difference was found in plasma thrombomodulin levels between patients who achieved remission and who did not. These findings suggest that the magnitude of the endothelial damage in TTP is variable among patients and that plasma thrombomodulin has limited clinical relevance to the severity of TTP.
In vivo efficacy of intravenous gammaglobulins in patients with lupus anticoagulant is not mediated by an anti‐idiotypic mechanism
Authors: Galli Monica , Cortelazzo Sergio , Barbui Tiziano 
Published: February 2007

AbstractThe authors have investigated the presence in commercially available intravenous gammaglobulins (IVlg) of anti‐idiotypic antibodies directed to Lupus Anticoagulant (LA). In vitro incubation of 4 LA plasmas with increasing concentrations of IVlg (from 0 to 39 mg/ml) resulted in a dose‐dependent inhibition of LA activity (the highest inhibitions ranged from 14.0 to 53.4%). Similar results were obtained when patients' plasma was substituted with total IgG (the highest inhibitions ranged from 43.0 to 55.0% and were obtained at IgG:IVIg molar ratios ranging from 1:15 to 1:50). Also the incubation of patients' F(ab's)2 with F(ab')2 from IVIg produced a similar dose‐dependent inhibition of LA activity. These data are suggestive of an in vitro idiotypic‐anti‐idiotypic interaction between LA and IVIg. However, when injected in patients with LA, IVIG do not seem to operate by this mechanism of action. In fact, reduction or disappearance of LA was only observed in 2 out of 4 patients; also the quick reappearance of LA activity was not consistent with the time course of anti‐idiotypic response. Finally, this effect was reached by half the IVIg concentrations necessary to produce an appreciable inhibitory effect on LA activity in vitro. Thus, it is concluded that, even if IVIg contain anti‐idiotypic antibodies reacting with LA, the clinical efficacy of IVIg treatment in patients with these autoantibodies should be attributed to other mechanisms.