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Biomedical subjects

H Takami

Publications and source records attributed to H Takami.

At least 235 records · Page 13Linked to original sources

Carcinoembryonic antigen and nonspecific cross-reacting antigen in medullary carcinoma of the thyroid.

Carcinoembryonic antigen (CEA) and nonspecific cross-reacting antigen (NCA) were studied immunohistochemically in formalin-fixed, paraffin-embedded tissues of 73 cases of medullary carcinoma of the thyroid (MTC) using 2 polyclonal antibodies (CEA antisera cross-reactive with or without NCA), 3 monoclonal antibodies recognizing epitopes only on CEA, and one monoclonal antibody against NCA. The staining patterns of the 5 antibodies against CEA in MTCs were not different, and they reacted with 86.3% of all cases. With regard to the effects of fixatives on the staining patterns, samples fixed with formalin or 4% paraformaldehyde demonstrated CEA immunoreactivity in both the cell membrane and cytoplasm. In Bouin-fixed tissue, the immunoreactivity was predominant on the cell membrane, whereas cytoplasmic positivity predominated in alcohol-fixed specimens. Thus the difference in fixatives used in previous studies does not appear to be a major reason for the difference in the reported incidence of CEA-positive MTCs. It is concluded that CEA is still a useful tumor marker for MTC and that it is detectable only in thyroid tumors originating from C cells, as seen in our series. The epitope defined by monoclonal antibody F106-88, present only on NCA, was found in 42.5% of all cases (49.2% of CEA-positive MTCs). The NCA immunoreactivity was located in the tumor cell cytoplasm as globular aggregates, which were also labeled for CEA.

Antigens, Differentiation, Myelomonocytic↗

Analysis of clinical factors for survival after left and biventricular bypass using centrifugal pump following open heart surgery in infants and adults.

A total of eight patients, including three infants, received left or biventricular assist using centrifugal pump (CFP) following open heart surgery. Three infants, aged 9-11 months and with complex cardiac lesions, were supported by left heart bypass (LHB) using pediatric type CFP for 63 h, 64 h, and 13 days. All were weaned from LHB, but long-term survival was not obtained, mainly due to complications. In five adult patients, LHB alone was used in three, and biventricular support in two for 33-240 h with three survivals. The factors related to unsuccessful recovery were delayed start of support and multiorgan failure.

Adult↗

Potassium-39 nuclear magnetic resonance observation of intracellular potassium without chemical shift reagents during metabolic inhibition in the isolated perfused rat heart.

The intracellular potassium content of perfused rat heart was measured by potassium-39 nuclear magnetic resonance (NMR) spectroscopy at 33 degrees C with an inversion recovery technique based on the fact that the spin-lattice relaxation time (T1) of the intracellular potassium (8.3 msec at 8.45 T) is much faster than that of the extracellular potassium (68 msec). Intracellular potassium decreased to 60.2 +/- 4.3% of the control level (mean +/- SEM, n = 6) at 40 minutes from the start of metabolic inhibition (2 mM cyanide, 0 mM glucose). Removal of cyanide restored intracellular potassium to 94.2 +/- 3.9% at 30 minutes from the restart of oxidative metabolism. The cumulative potassium loss was determined from the flow rate and potassium concentration of the coronary effluent, which reached 139 +/- 12 mumol/g dry wt during 40 minutes of metabolic inhibition. This value was calculated as 41.8% of intracellular potassium in the control heart and agreed with the decrement of intracellular potassium measured by NMR. During the metabolic inhibition and recovery period, a linear correlation was observed between the changes in 39K NMR-observed intracellular potassium and the cumulative potassium loss. The present results evaluate the inversion recovery technique as a method to successfully monitor the myocardial intracellular potassium.

Animals↗

[Macrothrombocytopenia with deafness, nephritis, cataract, short small intestine, and double ureter].

A 23 year old female, born in 1957, was diagnosed as having idiopathic thrombocytopenic purpura at the age of 3 and treated with prednisolone during her childhood with no response. On her regular check-up in 1978, facial edema and proteinuria suggested renal disease. The family history was negative for bleeding diathesis or renal disease. Close examination revealed the following: WBC 4,200/microliters without leukocyte inclusions, RBC 3.42 x 10(6)/microliters, Hb 11.7 g/dl. PT 10.6 sec, APTT 28.9 sec. Platelet count 4,500/microliters by HEMATRAK 360, and 40 x 10(3)/microliters measured by microscopic method. Giant platelets were noted on peripheral blood smear with an average diameter of 6.1 microns. Bleeding time (Duke) was 12.0 min. Number of megakaryocytes was increased although platelet production was remarkably decreased. Results of platelet aggregation and retention tests were normal. Platelet life span (T1/2) was 2.3 days. Sensory neural hearing loss, congenital cataract, double ureter and short small intestine were also found. Chromosome analysis showed 46XX. She underwent splenectomy resulting in increase of the platelet count to 226 x 10(3)/microliters. The increased platelet count, however, gradually decreased to the initial count in 2 years although the bleeding tendency was improved. In 1987, renal function deteriorated, causing intractable hypertension. The serum creatinine was 4.8 mg/dl. The following year she developed cerebral bleeding and died 4 days after the episode. The serum creatinine was 8.6 mg/dl.

Adult↗

[Bleeding time and volume in vitro by THROMBOSTAT].

We tested an in vitro system simulating bleeding time reported by Kratzer et al. Primary hemostasis was studied perfusing an artificial vessel with citrated blood under a constant pressure of 40 mmHg, measuring the blood volume perfused (bleeding volume) and the time until blood flow stopped (bleeding time). The artificial vessel consists of a glass capillary simulating arteriole and a filter covered with collagen type I to provide a surface for the adhesion of platelets. The bleeding volume (mean +/- SD microliters) was 317.7 +/- 93.8 in controls (n = 19), 487.3 +/- 242.1 in idiopathic thrombocytopenic purpura (n = 9), 666.8 +/- 224.1 in aplastic anemia and paroxysmal nocturnal hemoglobinuria (n = 4), greater than 820 in von Willebrand's disease (n = 3), 231.0 +/- 74.5 in hemophilia A (n = 3), 499.0 +/- 269.4 in liver cirrhosis (n = 6), and 457.7 +/- 229.0 in myeloproliferative disorders (n = 11). When citrated blood was applied to this system after incubation with monoclonal antibodies (MoAb) to von Willebrand factor or platelet membrane glycoprotein Ib (GPIb), bleeding volume was significantly increased while no effects were observed after incubation with MoAb to GPIIb/IIIa, factor VIII: CAg and factor XIIIa. These data suggest that in vitro model of primary hemostasis could be used for not only diagnosing bleeding disorders although 'time' is not reliable, but also investigating the mechanisms of hemostasis.

Antibodies, Monoclonal↗

[Reoperation of tetralogy of Fallot long after correction with aortic homograft: a case report].

Late results in the surgery for congenital heart disease repaired with external conduit have not yet been fully elucidated. We experienced a reoperation of tetralogy of Fallot (TF) that was previously repaired with an aortic homograft pretreated with beta-propiolactone for the reconstruction of right ventricular outflow tract. Ten years after correction of TF, right ventricular failure developed due to the regurgitation of tricuspid valve. At reoperation tricuspid annuloplasty was performed, and the valve of aortic homograft was also replaced with xenograft because of its uncertain durability. However, the resected valve had pliability with least degenerative change macroscopically. The postoperative course was smooth. The case was a rare one of late reoperation of TF due to the tricuspid valve regurgitation, and the case also indicated unexpected long durability of the valve cusp of the aortic homograft.

Adult↗

[Measurement of plasma calcitonin gene-related peptide (CGRP) level in patients with thyroid disease].

To elucidate the pathophysiology of CGRP in patients with medullary thyroid carcinoma (MTC), we measured the plasma CGRP level in patients with thyroid disease employing RIA. The plasma CGRP level (normal level 12.7 pg/ml) was elevated in all five preoperative patients with MTC, ranging from 128 pg/ml to 2010 pg/ml, and in ten of 17 postoperative patients who indicated possible recurrence. On the other hand, CGRP levels showed low frequencies of elevation in 96 patients with other thyroid tumors (anaplastic carcinoma, malignant lymphoma, follicular adenoma and adenomatous goiter), subacute thyroiditis, chronic thyroiditis and Graves' disease. Provocation test (calcium gluconate plus pentagastrin) in 12 MTC patients showed that, although the CGRP level fluctuated in parallel with the calcitonin level, the elevation rate (maximum level after administration/basal level) of CGRP was lower than that of calcitonin. Particularly, the rate of elevation of CGRP in three virulent and advanced patients with poorly differentiated MTC was below 2.0, while that in nine patients with well-differentiated MTC ranged from 2.8 to 23.3. These results suggest that CGRP may be a humoral marker of MTC and is possibly related to the degree of malignancy.

Calcitonin Gene-Related Peptide↗

Evaluation of prostacyclin analogue OP-41483 as an adjunct to crystalloid cardioplegia in infants and children.

A chemically stable prostacyclin analogue (PGI2-A, carbacyclin, OP-41483) was evaluated as an adjunct to potassium cardioplegia in infants (n = 13) and children (n = 32), in whom the current potassium cardioplegia may be limited in its effects. PGI2-A was added in a dose of 300 micrograms/L to the potassium cardioplegic solution. Postoperatively, peak levels of the myocardial-specific isoenzyme of creatine kinase (MB-CK) were compared for the PGI2 group and a control group (n = 65). In patients 1 year of age or older (n = 32 and 49 for the PGI2 and control groups, respectively), the MB-CK level was significantly lower in the PGI2 group only when compared between the subgroups with an aortic cross-clamp time of 120 minutes or more (n = 9 and 10; MB-CK level, 35.2 +/- 15.6 vs 68.3 +/- 32.4 IU/L;p less than 0.05). In patients less than 1 year of age, in whom aortic cross-clamp times were generally less than 120 minutes, the MB-CK level was also lower in the PGI2-A group than in the control group (n = 13 and 16; MB-CK level, 33.6 +/- 14.3 vs 61.6 +/- 36.3 IU/L;p less than 0.05). Infants less than 6 months of age (n = 18) underwent ultrastructural assessment of left ventricular myocardial biopsy specimens, and the PGI2-A group showed better results in mitochondrial and intracellular edema scores. This clinical trial showed beneficial effects of PGI2-A used with crystalloid potassium cardioplegia in infants and children.

Adolescent↗

Factor XIII is not involved in human platelet-collagen interaction.

A role of factor XIII (FXIII) on the interaction of human platelets with collagen was investigated using either formaldehyde fixed-washed platelets (FWP) or nonfixed platelets. The adhesion of FWP to bovine type I collagen was measured by using either an aggregometer or a collagen immobilized glass beads column. The interaction of non-fixed human platelets with collagen was measured with in vitro bleeding time (Thrombostat-4,000), which was performed by passing citrated whole blood through the filter covered with rat type I collagen under the constant shear stress. FWP adhesion to the collagen immobilized column (1,300 micrograms collagen) was not changed by the addition of commercial FXIII preparation (Fibrogammin); the adhesion was 42.7% in the presence of 1% human serum albumin, 42-43% in the presence of 1-2 U/ml of FXIII. The addition of rabbit antibody to FXIII to normal FWP did not change the degree of adhesion; 42.3% (1:100 anti-FXIII) and 46.1% (normal rabbit serum). Furthermore, platelets from the patient with congenital FXIII deficiency normally aggregated by bovine collagen and the adhesion of the patient FWP to the collagen was similar to that of normal FWP. Prolongation of partial thromboplastin time and the changes of thromboelastograph of normal plasma were observed after mixing with the collagen, and factor VIII, FXIII and von Willebrand factor were adsorbed by the collagen. The amount of FXIII in normal human plasma bound to collagen was 17, 23 and 54% at the concentration of the collagen 250, 500 and 1,000 micrograms/ml, respectively. The binding of plasma ristocetin cofactor was not different between normal control and the patient with FXIII deficiency. These data suggest that FXIII is not involved in human platelet interaction with the type I collagen, while FXIII in normal human plasma binds to the collagen.

Bleeding Time↗

[The influence of theophylline on polyamine metabolism and colonic carcinogenesis induced by 1.2-dimethylhydrazine in mice].

The administration of theophylline (120 mg/kg.day, 14 wk) to the drinking water of female BALB/c mice after treatment with 1,2-dimethylhydrazine (DMH) (30 mg/kg.sc, 1/wk, 14 wk) resulted in both an increase in number of colon carcinoma and increases in ornithine decarboxylase (ODC) activities and polyamine (PA) levels in colon tissue. This increase in number of colon carcinoma was about 3-fold to mice receiving same amount of DMH and drinking water without theophylline. ODC activities (pmoles 14CO2/hr/mg prot, mean +/- SD) in colon tissue were 122 +/- 10.6 (n = 6) in DMH with theophylline group, 28.3 +/- 2.13 (n = 8) in DMH alone group, 21.3 +/- 1.67 (n = 6) in control group respectively. Putrescine and spermidine levels (nmoles/g, mean +/- SD) were 31.0 +/- 10.5, 527 +/- 86.6 (n = 11) in DMH with theophylline group, 24.0 +/- 11.4, 464 +/- 129 (n = 11) in control group respectively. Thus with marked increase of ODC activities and slight increase of PA levels, theophylline has shown to significantly enhance the promoting phase of carcinogenic process with DMH.

Animals↗

[Acute myelomonocytic leukemia with inv (16) (p13 q22) disappeared abnormal karyotype during complete remission].

A 21-year-old man was admitted to our hospital because of anorexia and general malaise in July, 1988. On admission, the white blood cell count of 18,600/microliters with 72% leukemic cells. The bone marrow aspirate showed 76.8% immature monocytes, 10% mature and immature eosinophils. Leukemic cells were 66.6% myeloperoxidase positive cells, and 20.6% naphthylbutyrate esterase positive cells. The lysozyme activity in urine was high. Cytogenetic analysis revealed the presence of 46 XY inv (16) (p13 q22). Under the diagnosis of acute myelomonocytic leukemia with eosinophilia (M4Eo) associated with inv (16) (p13 q22), one course of DCMP induction therapy was performed. After complete remission, the bone marrow aspirate showed disappearance of inv (16) (p13 q22), and associated with decreased residual leukemic cells.

Adult↗

[Diagnosis and treatment of the precancer state in hereditary medullary thyroid carcinoma].

We attempted to elucidate the diagnosis and treatment in 11 patients with hereditary medullary thyroid carcinoma which were inherited as autosomal dominant traits. The oncogens are thought to be supported by the two-mutational event theory; the C cell hyperplasia, the first step, is the expression of the genetic mutation, which requires a subsequent somatic mutation to transform the initially mutated cell into a cancer cell. The C-cell hyperplasia was thought to be precancer state. The definitive diagnosis was established by measurement of calcitonin and CEA levels in sera. In patients with normal levels of calcitonin and CEA, the provocative test (Ca-gluconate plus pentagastrin) was useful such as in pt. no. 11,K.N.). The principle of surgery is total thyroidectomy because of multicentric occurrence in both lobes. Two patients (pt nos. 10, 11) with normal postoperative levels of provocative test underwent total thyroidectomy.

Adult↗

[Radioimmunoassay of plasma calcitonin gene-related peptide (CGRP) levels in patients with endocrine tumor].

For the purpose of determining the significance of CGRP for endocrine tumors, we attempted to establish CGRP radioimmunoassay (RIA) system and to measure plasma CGRP levels in patients with endocrine tumor. One ml of plasma (EDTA-2K + aprotinin 500.KIE/ml) was applied to Sep-Pak C 18 column, and was eluted by 90% MeOH plus 0.1% TFA. The eluted samples were used for RIA. RIA was performed by two day-one day system (delayed assay). B/F separation was made by two Ab-PEG method. Cross-reactivity of antisera was 0.0025% and below 0.0001% against PTH and calcitonin in human, respectively. The standard curve of CGRP showed a dose response curve. Results of dilution and reproduction tests were excellent. Normal range of serum CGRP was 6.7 +/- 3.0 pg/ml (M +/- SD) and the cut-off level was determined to be 12.7 pg/ml. Plasma CGRP showed 128,323 and 2,010 pg/ml in three preoperative patients with medullary thyroid carcinoma, indicating extremely high levels. On the other hand, plasma CGRP levels increased in 2/7, 2/4, 2/5, and 0/3 in patients with parathyroid adenoma, benign insulinoma, carcinoid and pheochromocytoma, respectively. Correlation between CGRP level and calcitonin levels was significant (r = 0.789) in only 16 patients with medullary thyroid carcinoma. This study suggests that our CGRP RIA system was satisfactory for clinical use and measurement of CGRP may be potentially useful for clearing the pathophysiology of neuroendocrine tumors, although CGRP level was raised in patients with medullary thyroid carcinoma.

Biomarkers, Tumor↗