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Biomedical subjects

A Shibata

Publications and source records attributed to A Shibata.

At least 307 records · Page 17Linked to original sources
PubMed1992

In vitro study of erythropoiesis in patients with aplastic anemia and myelodysplastic syndromes: a possible tool for prospective determination of the clinical effectiveness of growth factors.

Effects of recombinant human erythropoietin (rhEpo) and the combination of recombinant human interleukin-3 (rhIL-3) or recombinant human granulocyte-macrophage colony-stimulating factor (rhGM-CSF) with rhEpo on erythroid colony formation were examined in vitro in 13 patients with aplastic anemia and 16 with myelodysplastic syndromes (MDS). The methylcellulose cultures of marrow cells from normals and the patients yielded no erythroid colonies in the absence of rhEpo. In normals, CFU-E and BFU-E colony formation was significantly increased by adding either rhIL-3 or rhGM-CSF with rhEpo, compared with rhEpo alone, and rhIL-3 was more potent than rhGM-CSF to form colony-forming units and burst-forming units of erythroid (CFU-E) (BFU-E) colonies. By adding rhIL-3 with rhEpo, CFU-E colony formation was increased in half of patients with RA, compared with rhEpo alone, and by rhGM-CSF, in one third. Approximately one third or one fourth of the patients with MDS showed increased BFU-E colonies when rhIL-3 or rhGM-CSF were added to rhEpo. Cultures containing rhIL-3 or rhGM-CSF with rhEpo yielded larger numbers of BFU-E colonies in half of the patients with nonsevere aplastic anemia than those containing rhEpo alone. These observations suggest that the combination of these growth factors, especially rhIL-3 with rhEpo, is applicable to the treatment of anemia in some patients with aplastic anemia and MDS.

Adolescent↗
PubMed1992

[Clinical assessment of serum myosin light chain I in patients with dilated cardiomyopathy].

Serum cardiac myosin light chain I (LCI) levels were quantitated using a radioimmunoassay kit in patients suspected of dilated cardiomyopathy (DCM). In this study, 55 patients were evaluated between 1986 and 1991. They were composed of 40 males and 15 females, and their age was 27-75 years (51 +/- 11 years). The patients with renal dysfunction were excluded due to their serum creatinine levels (greater than 2.0 mg/dl). 1) After cardiac catheterization, endomyocardial biopsy and echocardiography, 44 patients were diagnosed as DCM, 2 as ischemic heart disease, 2 as chronic myocarditis, 1 as restrictive cardiomyopathy, 1 as dilated hypertrophic cardiomyopathy, 1 as cardiac amyloidosis, 2 as myopathy, 1 as polymyositis and 1 as hypothyroidism. 2) Only two patients with DCM had elevated LCI. Besides, two patients with myopathy or hypothyroidism had elevated LCI. 3) In the follow-up, one patient died suddenly 6 months later and another showed normal value of LCI four years later. 4) LCI elevation in DCM was not related to either the severity of heart failure or cardiac function and it showed no finding of 201Tl myocardial defect or elevated CPK. 5) The mechanism for elevated LCI in myopathy is related to a cross-reaction with myosin light chain in the skeletal muscle. In hypothyroidism, it may be related to decreased clearance of normal LCI concentration or increased myosin light chain from damaged skeletal muscle. In conclusion, it is evident that the measurement of LCI is not helpful in clinical assessment of patients with DCM, but may be useful in detection of secondary cardiomyopathy.

Adult↗
PubMed1992

Stress platelets in normal individuals and patients with idiopathic thrombocytopenic purpura.

To test the hypothesis that stress platelets (SPs) described by Tong et al. in rats may be a parameter of young platelets in humans, we examined and characterized SPs in normal individuals and in patients with idiopathic thrombocytopenic purpura (ITP). Our results indicated that SPs comprise about 1.2% of the circulating platelets in normal individuals and 2.6% in ITP patients. The configuration of SPs as well as of various irregular forms of circulating platelets was found to be supported by synergism of both the platelet microfilaments and microtubules. SPs showed some segmentation, the degree of which was similar in normal individuals and ITP patients, and they underwent further segmentation during in vitro incubation, mainly promoted by microtubules, so that they sometimes appeared like discoid platelets in a chain. These observations suggest a new mode of production of discoid platelets in the circulation. Thus, identification and enumeration of SPs may be useful for evaluating thrombocytopoiesis in humans.

Adult↗
PubMed1992

[PI metabolism and Ca mobilization in patients with platelet dysfunction].

The effect of STA2, thrombin and NaF on PI metabolism and Ca mobilization was investigated in patients with three kinds of platelet dysfunction, one each with platelet cyclo-oxygenase deficiency (A), defective aggregation to A23187 (B) and defective aggregation to STA2 (C). These responses were normal in patient (A), suggesting cyclooxygenase activity did not affect PI metabolism and Ca mobilization. PI metabolism was also normal in (B), although Ca mobilization in response to A23187 was delayed and that in response to thrombin was defective in the presence of extracellular Ca2+. This suggests that the patient's platelets have a defective IP3-induced Ca mobilization pathway. STA2 selectively failed to induce IP3 formation and Ca mobilization in (C), although 3H-labelled thromboxane ligand (3H-U46619) bound to the patient's platelets normally. It was suggested that the patient's platelets have a defect in postreceptor signal transduction, especially thromboxane receptor-mediated PLC activation pathway.

Blood Coagulation Disorders↗
PubMed1992

[Hemostatic control in platelet dysfunction and abnormality by DDAVP].

DDAVP infusion shortens the bleeding time in patients with some types of platelet dysfunction and may be useful for hemostatic control. In order to clarify the mechanism of DDAVP to correct or bypass the release defect, we examined the effect in 17 patients with prolonged bleeding time, i.e., 11 with various kinds of platelet dysfunction, 4 with idiopathic thrombocytopenic purpura (ITP), 1 with chronic myelocytic leukemia (CML), and in an aspirin-ingested volunteer. DDAVP shortened the bleeding time in 9 patients with platelet dysfunctions, one with ITP, and the one aspirin ingested volunteer. No improvement was found in the aggregability and the retention rates, and no signs of activation occurred in the platelet shape. The RCof was elevated in all of the patients after the infusion. Our data suggests that DDAVP improves the hemostasis through primary aggregation and release of dense bodies, and not directly through an increase of RCof.

Bleeding Time↗
PubMed1992

[Natural interferon-alpha induced cytogenetic complete remission in a patient with chronic myelocytic leukemia, diagnosed in early chronic phase with basophilia and normal blood cell counts].

A 57-year-old woman visited to our hospital complaining of paresthesia in the right leg. She had no abnormal physical findings. However, the peripheral blood examination demonstrated 7% basophilia with 8000/microliters WBC count and decreased neutrophil alkaline phosphatase activity (score 37, rate 19%). She was diagnosed as Ph1 chromosome positive CML in early phase by the chromosomal analysis of bone marrow cells. She received subcutaneous injection of natural interferon-alpha at a dosage of 600 x 10(4) IU daily from March 10, 1987. The dosage and administration interval were gradually reduced and prolonged. Since November 1988, weekly injections of 300 x 10(4) IU has been administered as maintenance therapy. Cytogenetic improvement was seen at 4 months after the start of IFN. Disappearance of Ph1 chromosome positive cells was observed on December 11, 1987. It was suggested that the administration of IFN from the early chronic phase played an important role in the control of the disease.

Basophils↗
PubMed1991

[A case of fibrous dysplasia (McCune Albright syndrome) associated with acromegaly].

We report a case of a 47-year-old woman with McCune-Albright syndrome associated with unusual growth-hormone and prolactin hypersecretion. Acromegaly was suspected on clinical examination, and she was referred to us. She had no history of precocious puberty or pathological fracture. She was 154cm tall, weighing 62kg with so-called acromegalic facies. There were two lumps, one of which was on her right lateral forehead. The other on the right lower extremity seemed to be due to a bone deformity. Some brown pigmented macules with irregular borders were present on her lips and oral mucosa. Endocrine examination revealed elevated basal levels of plasma GH (54ng/ml) and PRL (36.2ng/ml), which paradoxically increased after injection of TRH. Plasma levels of these hormones did not change after LHRH test, and plasma GH level increased after GHRH test. A skull X-ray film showed a double floor of the sella turcia and hyperostotic formation of the right sphenoid bone. MRI and CT showed a tumor shadow in the right sella turcica. Bone roentogenography of the right fibula and tibia showed a large centrally expanding lesion with a ground-glass or cystic appearance and a thin cortex. The left fibula showed a similar lesion. We recognized similar findings in other bones which also showed abnormal accumulation in a radionuclide bone scan with 99mTc. On the basis of physical, endocrinological and roentogenographical examination, we diagnosed her as displaying McCune-Albright syndrome. We operated on her by transsphenoidal surgery and confirmed a functioning chromophobe adenoma which was removed during surgery. She has been free of GH and PRL hypersecretion since then. The pathology of the sphenoidal sinus affected with fibrous bone was in accordance with the findings of fibrous dysplasia. McCune-Albright syndrome (MCAS) is known as a syndrome characterized by polyostotic fibrous dysplasia and cutaneous pigmentation and multiple endocrinopathy. Its etiology is unknown. This syndrome with acromegaly is rare, and although 26 cases have been described in literature, pathological examinations have been undertaken in only three cases. This case was very rare and valuable because, by operating on her by the transsphenoidal route in spite of the sphenoidal sinus being affected with fibrous bone, we were able to confirm a chromophobe adenoma secreting both GH and PRL. We recognized that acromegaly with MCAS was endocrinologically, morphologically and immunohistologically the same as acromegaly without MCAS. Therefore, we concluded that acromegaly with MCAS is much the same as acromegaly without MCAS.

Acromegaly↗
PubMed1991

GM-CSF-mediated impairment of liver to synthesize albumin, cholinesterase, and cholesterol.

Serum albumin, cholinesterase, and cholesterol were measured in ten patients with aplastic anemia and eight with myelodysplastic syndrome who received the administration of recombinant human GM-CSF. Serum albumin, cholinesterase, and cholesterol were significantly lowered by the administration of GM-CSF and recovered after the cessation of GM-CSF. These data suggest that GM-CSF impairs the biosynthesis of liver cells and that cholesterol-lowering activity of GM-CSF, which is previously reported, is due to the impairment of liver biosynthesis by GM-CSF.

Anemia, Aplastic↗
PubMed1991

Plasmin generation and fibrin(ogen)olysis following desmopressin infusion.

Desmopressin acetate (DDAVP) is known to stimulate the release of tissue-type plasminogen activator (t-PA) from endothelial cells, but it is unclear whether the increased t-PA actually elicits the plasmin generation and fibrin(ogen)olysis in the circulating blood. We measured plasma levels of plasmin-alpha 2-plasmin inhibitor complex, fibrinogen degradation products (FgDP) and fibrin degradation products (FbDP) following desmopressin infusion in 19 patients with bleeding disorders or thrombophilia. Administration of desmopressin (0.3-0.4 microgram/kg) produced a 4.0-fold increase in plasmin-alpha 2-plasmin inhibitor complex at 30 min, whereas neither FgDP nor FbDP was elevated significantly. These findings indicate that desmopressin infusion provokes the generation of plasmin in vivo, but most of the plasmin generated is complexed to alpha 2-plasmin inhibitor and does not degradate fibrin or fibrinogen.

Antifibrinolytic Agents↗
PubMed1991

Circulating thrombomodulin in thrombotic thrombocytopenic purpura.

Endothelial 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 less than 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 tissue-type 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.

Adult↗