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Biomedical subjects

N Kamada

Publications and source records attributed to N Kamada.

At least 235 records · Page 13Linked to original sources
PubMed1992

Loss of heterozygosity at D3S2 locus of short arm of chromosome 3 in chronic myelogenous leukemia.

Loss of heterozygosity (LOH) on the short arm of chromosome 3 was studied in four patients with chronic myelogenous leukemia (CML). The bcr gene rearrangement-negative spleen cells and a B-cell line were used as normal tissue controls. Five probes showing restriction fragment length polymorphisms (RFLP) and a variable number of tandem repeats on chromosome 3 were used. DNA patterns in Southern blotting were compared between normal cells and leukemic cells. One of the four patients had LOH at the D3S2 locus mapped to 3p14.3-3p21.3. The LOH was detected in the blastic phase, but not in the chronic phase. This patient showed normal chromosomes 3 in the blastic phase. These data suggest the possibility of the existence of LOH in CML, occurring as a secondary event in the blastic phase, and which might have been induced by submicroscopic deletion or somatic recombination.

Blotting, Southern↗
PubMed1992

Chromosome abnormalities in adult T-cell leukemia/lymphoma: a karyotype review committee report.

Karyotypes of 107 cases with adult T-cell leukemia/lymphoma (58 male, 49 female; 81 acute or lymphoma type, 26 chronic or smoldering type) were reviewed by a panel of cytogeneticists and were correlated with the subtypes of the disease. Clonal chromosome abnormalities were found in 103 (96%) cases, of which four had hypotetraploidy. Of 184 numerical abnormalities in the remaining 99 cases with near- or pseudodiploidy, trisomies for chromosomes 3 (21% of cases), 7 (10%), and 21 (9%), monosomy for X chromosome (38%) in the female, and loss of a Y chromosome (17%) in the male were more frequent than expected (P less than 0.01). Of 373 structural abnormalities in all the 103 aneuploid cases, translocations involving 14q32 (28%) or 14q11 (14%) and deletion of 6q (23%) were most frequent, followed by deletion of 10p (9%), 3q (8%), 5q, 9q, and 13q (7% each), and 1p and 7p (6% each). The proportion of cases with aneuploid clones (with greater than or less than 46 chromosomes), the average numbers per case of both numerical and structural abnormalities, and marker chromosomes were larger in the aggressive acute or lymphoma type than in the nonaggressive chronic or smoldering type (P less than 0.01). The combination of rearrangement in 14q32 and monosomy X (seven cases) or deletion of 10p (six cases), and that of trisomy 3 and deletion in 6q21 (six cases), occurred only in the acute or lymphoma type and may be associated with the aggressiveness in adult T-cell leukemia/lymphoma.

Adult↗
PubMed1992

Malignant fibrous histiocytoma. A tumor of facultative histiocytes showing mesenchymal differentiation in cultured cell lines.

The histogenesis of malignant fibrous histiocytoma (MFH) is controversial. To elucidate the cellular origin and characteristics of this neoplasm, the authors analyzed cell lines grown from 17 patients (15 soft tissue MFH and 2 bone MFH) by using light and electron microscopy, immunocytochemistry, enzyme cytochemistry, and functional tests for receptors for the Fc portion of immunoglobulin (Fc receptors) and immunophagocytosis. Each culture exhibited a storiform/pleomorphic pattern with mixed cellular populations consisting of spindle cells, polygonal cells, and bizarre giant cells; these morphologic features corresponded to the histologic characteristics of the primary tumors. The cells in each MFH line displayed histiocytic functional markers such as lysosomal enzymes, Fc receptors and immunophagocytosis. However, these cells differed from monocyte-derived macrophages (histiocytes) in immunoreactivity; the MFH cells expressed a mesenchymal antigen (FU3) distributed among perivascular cells and fibroblasts but demonstrated no positive reactions with Leu-M1 (CD15) and Leu-M3 (CD14), which recognize the cells of the monocyte-macrophage lineage. In conclusion, these findings suggest that MFH is not a tumor of true histiocytes but of facultative histiocytes showing mesenchymal differentiation in vitro. Chromosomal analysis performed in one MFH line demonstrated abnormal karyotypes; the modal chromosome number was 58, with 5 marker chromosomes.

Adult↗
PubMed1992

Predictive value of liver tissue flow in assessment of the viability of liver grafts after extended preservation in pigs.

The crucial damage in cold storage of liver allografts is to the hepatic sinusoidal lining (microcirculation). Using different solutions, we studied whether determinations of graft tissue flow were valuable in estimating the viability of liver grafts. Twenty-three pairs of female pigs underwent orthotopic liver transplantation and were assigned to five groups according to the cold preservation time or solutions used: in group I the liver grafts were stored in Euro-Collins solution (EC) for 4 h (n = 3), in group II the grafts were stored in EC for 12 h (n = 5), in group III the donor was pretreated with azathioprine (AZA), 1 mg/kg per day, orally (p.o.) for 3 days before harvesting and the graft was implanted after 12 h cold storage with EC (n = 6), in group IV the graft was stored in modified University of Wisconsin solution (mUW) for 4 h (n = 3), and in group V the graft was stored in mUW for 24 h (n = 6). Liver tissue blood flow (LTBF) was measured, using a laser doppler device, at 60 min after recirculation of the graft. In the case of EC preservation, LTBF (ml/100 g of liver tissue per min) correlated well with 4-day survival: 21.2 +/- 3.0 ml/100 g of tissue per min mean +/- SD, in group I (3/3, 100%); 10.0 +/- 2.8 ml/100 g of tissue per min in group II (0/5, 0%); and 19.1 +/- 3.4 ml/100 g of tissue per min in group III (5/6, 83.3%) (P < 0.05, group II vs I and III). All grafts with LTBF of more than 15 ml/100 g tissue per min functioned well. However, changes in microcirculation of the mUW-stored livers did not correlate with early function of the graft: 23.0 +/- 2.3 ml/100 g of tissue per min in group IV (4-day survival; 3 of 3, 100%) and 23.5 +/- 9.1 ml/100 g of tissue per min in group V (0 of 6, 0%). This was accompanied by graft dehydration during storage and an increased number of erythrocytes in the hepatic sinusoids post-recirculation. We concluded that assessment of liver tissue flow by LDF was very helpful and easy to apply in predicting liver graft failure in the case of preservation with Euro-Collins solution. However, LTBF should be carefully evaluated as a marker of liver graft viability when the liver graft is preserved with mUW.

Animals↗
PubMed1992

A comparison of histadine lactobionate solution with University of Wisconsin solution for rat liver and heart preservation.

We developed a new solution mainly composed of Na-lactobionate and histidine (HL) and compared the effectiveness of this solution with that of University of Wisconsin (UW) solution using orthotopic liver and heterotopic heart transplantation in rats. The new solution has a higher sodium content and a lower potassium content (Na, 90 mEq/l; K, 45 mEq/l) than UW. Hydroxyethyl starch, adenosine, dexamethasone and insulin are not included. Buffering capacity is increased by adding histidine (90 mM/l) together with KH2PO4 (20 mM/l). Rat liver was perserved in either UW or HL solution hypothermically for 24 h and then transplanted orthotopically into the recipient rat. The heart was preserved in either solution for 18 h and transplanted heterotopically into the recipient rat. The 1-week survival rate for rats receiving livers preserved in UW for 24 h at 4 degrees C was 29% (5/17). In contrast, the new solution (HL) gave a 78% (11/14) survival rate (P < 0.01). The 1-week heart graft survival rate, using UW solution was 50% (3/6), following 18-h cold preservation, whereas all hearts (7/7) continued to beat for over a week using new HL solution (P < 0.05). These results demonstrated that the new HL solution, with a substantial buffering capacity, was superior to UW solution in rat liver and heart preservation.

Adenosine↗
PubMed1992

Studies on the participation of different T cell subsets in rat liver allograft rejection. Comparison of liver with heart graft.

In this study, we investigated which subsets of rat T cells (CD8+ vs. CD4+) are involved in the rejection of liver allografts by the in vivo administration of monoclonal antibody (OX-8 or OX-38, and W3/25 MAb) into thymectomized recipient Lewis (RTI(l)) rats prior to DA (RTI(a)) liver transplantation. We also compared the results of allograft survival of liver and heart transplants under the same experimental conditions. In order to deplete either CD8+ T cells or CD4+ T cells from recipient animals, 0.4 ml of OX-8 (ascitic form) or a 0.8 ml cocktail of MAb W3/25 and OX-38 (0.4 ml each) was injected into thymectomized recipient rats, respectively. Untreated Lewis rats consistently rejected donor DA liver grafts between 9 and 11 days (n = 7, 9.8 days +/- 1.1 days). In contrast, anti-CD8 MAb pretreatment extended the survival times of DA liver grafts for up to 40 days (n = 5, 26.8 days +/- 8.4 days). Furthermore, survival of DA liver grafts was significantly prolonged in Lewis rats that had been pretreated with anti-CD4 MAb (n = 7, 35.6 days +/- 17.9 days). Two out of seven recipient animals survived for more than 60 days. For heart transplantation, untreated Lewis rats rejected DA heart grafts between 6 and 8 days after operation (n = 6, 6.5 days +/- 1.2 days). Anti-CD4 MAb treatment prolonged heart graft survival for more than 60 days in all cases (n = 3, > 60 days). However, there was virtually no effect of anti-CD8 MAb treatment on heart graft survival (n = 4, 7.0 days +/- 0.9 days). These results suggested that when whole MHC disparity prevailed between donor and recipient, both subsets of T cells were required for the rejection of liver allografts and that class II reactive T cells predominantly mediated liver graft rejection. Furthermore, CD8+ T cells played a differential role in the rejection of rat liver and heart allograft.

Animals↗
PubMed1992

FK 506 ameliorates normothermic liver ischemia in rats by suppressing production of tumor necrosis factor.

In recent years, there has been growing evidence that tumor necrosis factor-alpha (TNF) plays an important role in the development of hepatic injury after ischemia-reperfusion. We have previously demonstrated that the immunosuppressants, cyclosporine, azathioprine and FK506 (FK), have a protective effect on warm ischemic injury of the rat liver. In the present study, we attempted to elucidate the mechanism for the beneficial effect of FK on liver ischemia, with special reference to the suppression of TNF production. After 60 min and 90 min of warm liver ischemia, the survival rates were significantly improved by FK pretherapy. This was associated with amelioration of hepatic injury, as assessed by histological examinations and determinations of serum AST and lipid peroxide levels in the liver. After 60 min of liver ischemia, TNF was measurable during the reperfusion period in the sera of the control animals, peaking of 6 h after reperfusion (123 +/- 15.8 pg/ml, mean SEM). In contrast, pretreatment with FK significantly suppressed the elevation of serum TNF levels at the same time point (75.8 +/- 13.1 pg/ml, P < 0.05). The present data showed that liver ischemia-reperfusion resulted in TNF production, and that FK could protect the liver from reperfusion injury by suppressing this production of TNF.

Animals↗
PubMed1992

Living related liver transplantation.

Liver transplantation from a brain death donor has not yet been accepted in Japan. The only alternative method at present is transplantation from a living donor. After the first successful living related liver transplantation was performed by Strong in Brisbane, Australia, Japanese hepatic and transplant surgeons also began to perform such operations. As of February 1991, 16 living related liver transplantations had already been performed in Japan, mainly for children with biliary atresia. Five of these patients subsequently died, however, our patient has survived more than 1 year, and she is presently leading a normal school life. The most important issue regarding living related liver transplantation is to ensure the donor's safety. For this purpose, we conducted a preoperative banking of the donor's own blood and plasma. In addition, a selective vascular occlusion was carried out to reduce blood loss during the resection of the liver. Intraoperative color Doppler ultrasonography was introduced for evaluating the circulation of the graft. By using this modality, the following three points were able to be accurately estimated in order to obtain optimal graft perfusion: 1) The most suitable position for the graft to be fixed to the abdominal wall, 2) whether or not the abdominal wall could be closed and 3) the indication for a ligation of the collateral veins to form a porto-systemic shunt. Thanks to these procedures, living related liver transplantations have now become an acceptable transplant method, however, a transplantation from a cadaver that is brain dead but still has a beating heart is still absolutely necessary for adult recipients. Therefore, in the future, both methods should be performed.

Animals↗
PubMed1992

Lack of evidence that a transplanted liver causes acute graft-versus-host disease in rats. A comparison of liver and spleen grafts.

In this study, we used rat transplant models to investigate whether--and, if so, to what extent--transplanted liver had the potential to incite graft-versus-host disease, compared with the disease induced by a spleen graft. Livers from PVG(RT1c) rats were transplanted orthotopically into (DAxPVG)F1 (RT1a/c) rats and vascularized spleen grafts from PVG rats were transplanted heterotopically into (DAxPVG)F1 recipients. The intensity of the GVH disease was assessed by the recipients' morbidity and mortality, recipient-type serum class I (RT1Aa) antigen titer, and histological examination. The recipients of spleen grafts died within 14 and 23 days of transplantation; all animals had lost body weight and showed typical GVH signs, such as ear erythema, diarrhea, and alopecia. However, all the recipients bearing liver grafts survived indefinitely and did not demonstrate weight loss or the typical symptoms associated with GVH disease. The skins, tongues, and intestines of the liver-grafted rats were virtually normal at histological examination, whereas the livers, salivary glands, and skins of spleen-grafted rats were infiltrated by immunoblasts. The recipient-type serum RT1Aa antigen titer increased progressively until death in the spleen graft but not the liver graft recipients. These results provide evidence that suggest that transplanted liver is less likely than transplanted spleen to initiate the GVH disease in rats.

Acute Disease↗
PubMed1992

A high frequency of N-RAS oncogene mutations in multiple myeloma.

Mutation of the RAS oncogene was studied in ten patients with multiple myeloma, and the DNA from nude mouse tumors formed by cells obtained from tumorigenecity assays (in vivo selection assays) in these patients was analyzed by PCR and oligonucleotide hybridization. Mutations of the N-RAS oncogene were identified in two of three patients investigated by in vivo selection assay and in five of ten patients investigated by PCR analysis of DNA from myeloma cells. In the two former patients, mutation of the N-RAS oncogene was observed at the 61st codon. Of the five N-RAS mutant-positive patients investigated by the PCR analysis, one had a mutation at codon 12, two had mutations at codon 13, and two had mutations at codon 61. None of the patients had mutations of the K-RAS oncogene. These results suggest that the frequency of RAS gene mutation in multiple myeloma is higher than in other lymphoid malignancies such as acute lymphocytic leukemia, chronic lymphocytic leukemia, and malignant lymphoma. As the mutation was observed only at the N-RAS oncogene level, it is speculated that N-RAS oncogene activation might play an important role in the progression of multiple myeloma.

Aged↗
PubMed1992

[Apico-aortic conduit repair for the subaortic stenosis in the long-term period after correction of Taussig-Bing malformation].

Apico-abdominal-aortic bypass operation was successfully performed for the left ventricular outflow tract obstruction 17 years after correction of Tausig-Bing malformation. At the age of 14 months old, a 18-year-old patient underwent total correction of Taussig-Bing malformation according to Kawashima's intraventricular re-routing. The right ventricular hemodynamics were normal throughout, however, systolic ejection murmur due to aortic stenosis appeared 3 years after repair. Seventeen years postoperatively, marked aortic valve and subaortic obstruction was detected corresponding with the internal conduit made from the duplicated autopericardial baffle. A composite graft containing 23A-SJM valve was interposed between the left ventricular apex and infrarenal abdominal aorta. After the bypass operation, thickness of the posterior wall of the left ventricle and interventricular septum was significantly reduced and symptoms were remarkably improved. The present paper is concerned with the subaortic stenosis after repair of Taussig-Bing malformation and technique of apico-aortic bypass operation.

Adolescent↗
PubMed1992

[Review: progress of cytogenetics in hematopoietic malignancies].

In 1960, Nowell and Hungerford found, for the first time, a minute chromosome at the metaphase in chronic myelocytic leukemia (CML) cells, which was called Philadelphia chromosome (9; 22 translocation) later. Ph1 chromosome was considered to be specific for the disease and was frequently used as an important marker for the definite diagnosis. In 1970s banding techniques revealed some other specific chromosome abnormalities, like 8; 14, 8; 21, and 15; 17 translocations, for acute leukemias. In 1980s, molecular-biology techniques were applied in the fields of leukemia research. As a result, many break point cluster regions were discovered in relation to the immunoglobulin chain genes and T cell receptor genes (Table 2). In this review, the specificity of chromosome abnormalities as well as genetic changes in types of leukemia is discussed.

Chromosome Aberrations↗
PubMed1992

[Analysis of breakpoints on BCR gene in acute leukemia patients with Ph1 chromosome].

Eight cases with Ph1 positive acute leukemia (7 of acute lymphocytic leukemia: ALL, and one of acute myelocytic leukemia: AML) were studied molecular biologically to identify location of breakpoints on BCR gene in each patient. Six of the 8 patients (5 of ALL and 1 of AML) had rearrangements at bcr (M-BCR) region. Their locations of the breakpoint in M-BCR were similar to those of 59 chronic myelocytic leukemia patients. One of the remaining two patients had gene rearrangements at m-BCR-1 region in BCR intron 1, and the last patient did not have gene rearrangements at any site of m-BCR-1 and IgL C lambda region. Two cases had gene deletion at either 3' or 5' side of the bcr. A patient with bcr rearrangement was also analyzed by PCR method with reverse transcriptase (RT-PCR) and had simultaneous expressions of bcr3-abl and bcr2-abl chimeric mRNAs. These results indicate that Ph1 positive acute leukemia have heterogeneous characteristics in terms of the molecular biology. The molecular analysis will help for classifying the leukemic types and for elucidating the pathogenesis in Ph1 positive acute leukemia.

Acute Disease↗
PubMed1992

Cytogenetic 2; 18 and 18; 22 translocation in chronic lymphocytic leukemia with juxtaposition of bcl-2 and immunoglobulin light chain genes.

The majority of follicular lymphoma cells carry the typical chromosome translocation 14;18, which juxtaposes the bcl-2 gene to the immunoglobulin heavy-chain (IgH) gene. Variant translocations of the bcl-2 gene to the Ig lambda or Ig kappa gene have been found by molecular biological techniques in a significant fraction (approximately 10%) of chronic lymphocytic leukemia (CLL). However, there have been no reports describing the presence of cytogenetic 18;22 and 2;18 translocations in CLL, in spite of extensive karyotypic studies. We present here two cases of CLL, one with cytogenetically detected t(2;18)(p11;q21) and the other with the t(18;22)(q21;q11). The molecular analysis revealed that these translocations juxtaposed the bcl-2 and immunoglobulin light-chain (IgL) genes. The t(18;22) broke the 5' flanking region of the bcl-2 gene and juxtaposed to the immunoglobulin lambda light-chain (Ig lambda) gene in a head-to-head configuration, as in the cases previously described. In the case of the t(2;18), the bcl-2 gene and immunoglobulin kappa light-chain (Ig kappa) gene were juxtaposed in a head-to-tail configuration, which is opposite to that expected from the orientation of the genes on chromosomes. The breakpoint was located within the 5' untranslated region of the bcl-2 gene. The results presented here indicate that the bcl-2/immunoglobulin light-chain (IgL) gene juxtaposition seen in a fraction of CLL is the result of cytogenetically detectable reciprocal chromosome translocations 2;18 and 18;22.

Base Sequence↗