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Biomedical subjects

K Kojima

Publications and source records attributed to K Kojima.

At least 235 records · Page 13Linked to original sources
PubMed1998

Bone marrow uptake of thallium-201 before and after therapy in multiple myeloma.

We describe a patient with multiple myeloma who was found to have diffuse bone marrow uptake of 201Tl. Magnetic resonance (MR) imaging of the lumbar spine demonstrated abnormal low signal intensity on T1-weighted images and abnormal high signal intensity on T2-weighted images. The bone marrow consisted of 68% plasma cells, and the serum immunoglobulin (Ig)G concentration was 7900 mg/dL. After receiving chemotherapy, the percentage of plasma cells and serum IgG concentration declined and there was a decrease in the bone marrow uptake of 201Tl. However, the MR abnormalities in the lumbar spine showed no change after chemotherapy. This patient illustrates a limitation of the use of MR imaging for evaluation of disease state in patients with multiple myeloma, and demonstrates the potential usefulness of 201Tl imaging in these patients.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1998

[A combination chemotherapy with cytarabine ocfosfate, low dose etoposide, and G-CSF for the treatment of high risk MDS (RAEB, RAEBt)--a pilot study].

We evaluated a combination chemotherapy with cytarabine ocfosfate (SPAC), low dose etoposide and G-CSF for the treatment of high-risk MDS (RAEB, RAEBt). Seven patients with high-risk MDS were treated with a daily combination, 200 mg/day SPAC p.o., 50 mg/day etoposide p.o. and 75 micrograms/day G-CSF s.c. One patient achieved complete response, 2 achieved good response and one patient minor response. Although all of the patients developed severe marrow hypoplasia after chemotherapy, the nonhematologic adverse effects were mild enough to be tolerated. This combination chemotherapy should be useful in the clinical management of patients with high-risk MDS.

Aged↗
PubMed1998

[Portal hypertensive gastropathy and colopathy].

Gastrointestinal bleeding in patients with portal hypertension is usually secondary to esophageal varices, but massive bleeding from gastric mucosal lesions and colonic mucosal lesions including colorectal varices, have been variably described. These lesions are called portal hypertensive gastropathy and colopathy. The incidence and profile of portal hypertensive gastropathy (PHG) has been frequently reported during the last decade, and many studies showed that development of PHG is influenced by coexisting esophageal varices, absence of major portal systemic shunts, severity of liver disease and sclerotherapy and is directly correlated with portal venous pressure. Although hyperdynamic congestion seems to be the underlying mechanisms for the development of PHG, results of gastric mucosal blood flow in patients with PHG is controversial. The treatment can be currently recommended to prevent bleeding, is oral administration of propranolol which decreased portal venous pressure. The clinical feature and profile of portal hypertensive colopathy is classified two groups, which are named colorectal varices and colonic mucosal lesions including vascular spider, dilated fine branching vessels. Although colorectal varices are usually seen at rectum and sigmoid colon, colonic mucosal lesions are seen all part of colon. Significant relationship between colorectal varices and liver disease has been reported and colorectal varices is highly appeared in patients with extrahepatic portal obstruction. Such patients are revealed arteriovenous communications at angiogram. In general, colonic resection or transanal ligation should be the first option for treatment of bleeding colonic varices and colonic mucosal lesions. Transendoscopic sclerotherapy may be an alternate choice.

Colonic Diseases↗
PubMed1998

Bronchial wall schwannoma removed by sleeve resection of the right stem bronchus without lung resection.

A 28-year-old man presented with a bronchial wall schwannoma occurring in the right main to the intermediate bronchus. The tumor was resected en-bloc with the stem bronchi without pulmonary resection. Airway reconstruction consisted of an end-to-end anastomosis of the intermedius bronchus to the right main bronchus, and an end-to-side anastomosis of the right upper lobe bronchus to the lateral wall of the trachea. Postoperative course was uneventful. Bronchoplastic procedure with preservation of the lung parenchyma seems to be the technique of choice for benign tumors occurring intramurally in the stem bronchus.

Adult↗
PubMed1998

Bile acids inhibit tumour necrosis factor alpha-induced interleukin-8 production in human colon epithelial cells.

To clarify the regulatory mechanism of the production of various inflammatory mediators by intestinal epithelial cells, the effect of bile acids (tauroursodeoxycholate, TUDC; taurochenodeoxycholate, TCDC; and taurocholate, TC) on the cytokine-induced production of interleukin (IL)-8 in a human colon epithelial cell line (HT-29) was examined. HT-29 cells were incubated for 24 h in a culture medium containing tumour necrosis factor alpha (TNF alpha; 1 ng/mL) and/or interleukin (IL)-1beta (1 ng/mL) in the presence or absence of bile acids. The IL-8 concentration in the medium was measured by an enzyme-linked immunosorbent assay. The binding assay of TNF alpha was performed using [125I]-TNF alpha (100 pmol/L). Interleukin-8 production during incubation with TNF alpha was markedly reduced in the presence of 0.5 and 1 mmol/LTUDC, 0.5 and 1 mmol/LTCDC and 0.5 and 1 mmol/LTC, by 56, 85, 86, 91, 37 and 70%, respectively. The IL-8 production during incubation with IL-1beta was not significantly reduced in the presence of these bile acids. The specific binding of TNF alpha to cells was inhibited 33, 47, and 14% by 1 mmol/LTUDC, TCDC and TC, respectively. These findings suggest that bile acids inhibit TNF alpha-induced IL-8 production by the colonic cells. The suppression may be partly due to inhibition of TNF alpha binding to the cells by bile acids.

Bile Acids and Salts↗
PubMed1997

The carbohydrate moiety of factor V modulates inactivation by activated protein C.

An important risk factor for thrombosis is the polymorphism R506Q in factor V that causes resistance of factor Va to proteolytic inactivation by activated protein C (APC). To study the potential influence of the carbohydrate moieties of factor Va on its inactivation by APC, factor V was subjected to mild deglycosylation (neuraminidase plus N-glycanase) under nondenaturing conditions. The APC resistance ratio values (ratio of activated partial thromboplastin time [APTT] clotting times with and without APC) of the treated factor V were increased (2.4 to 3.4) as measured in APTT assays. O-glycanase treatment of factor V did not change the APC resistance ratio. The procoagulant activity of factor V as well as its activation by thrombin was not affected by mild deglycosylation. Treatment of factor V with neuraminidase and N-glycanase mainly altered the electrophoretic mobility of the factor Va heavy chain, whereas treatment with O-glycanase changed the mobility of the connecting region. This suggests that the removal of the N-linked carbohydrates from the heavy chain of factor Va, which is the substrate for APC, is responsible for the increase in susceptibility to inactivation by APC. Thus, variability in carbohydrate could account for some of the known variability in APC resistance ratios, including the presence of borderline or low APC resistance ratios among patients who lack the R506Q mutation.

Amidohydrolases↗
PubMed1997

Modulation of cell surface lectin receptors on K562 human erythroleukemia cells induced by transfection with annexin IV cDNA.

Annexin IV was found to be highly expressed in various human adenocarcinoma cell lines, but not in an erythroleukemia cell line, K562. We investigated the effects of transfection of human annexin IV cDNA into K562 cells on cell surface lectin receptors. cDNA transfectants were found to be more sensitive to cytotoxic lectins such as Ricinus communis agglutinin and wheat germ agglutinin than mock transfectants. The results of flow cytometric analyses with various lectins showed that the transfectants expressed more sugar chains which bind to Ulex europaeus agglutinin I and Maackia amurensis mitogen than mock transfectants. These results suggest that transfection of annexin IV cDNA increases the expression of alpha-2,3-sialylated and/or fucosylated sugar chains on the surface.

Annexin A4↗
PubMed1997

Induction of experimental autoimmune encephalomyelitis by CD4+ T cells specific for an astrocyte protein, S100 beta.

S100 beta protein is a calcium binding protein that is not only expressed by astrocytes in the CNS, but also in many other tissues including the eye, thymus, spleen and lymph nodes. Despite this tissue distribution, which was expected to induce a firm state of self-tolerance to S100 beta, the Lewis rat mounts a strong T cell response to this autoantigen. The pathogenicity of this T cell response was demonstrated by the adoptive transfer of S100 beta-specific T cells which induced an inflammatory response in the CNS and eye of naive syngeneic recipients. The distribution of lesions in this novel model of EAE resembles that seen in some patients with MS, suggesting that the initial autoimmune insult in MS may be directed against a non-myelin antigen co-expressed in the CNS and extra-neural tissues.

Adoptive Transfer↗
PubMed1997

Perforation of acalculous cholecystitis associated with localized atherosclerosis: report of a case.

We describe herein the unusual case of a 68-year-old Japanese man who underwent laparotomy for an acute abdomen caused by diffuse peritonitis, which revealed perforation of the gallbladder without any stones. A cholecystectomy was subsequently carried out, and histological examination showed marked atherosclerosis of the gallbladder associated with acute inflammatory changes. It is most likely that circulatory disturbance of the gallbladder wall due to the atherosclerosis played an important role in the events leading to perforation. Acute acalculous cholecystitis is an uncommon condition which is extremely difficult to diagnose preoperatively. The clinicopathological features of this patient are of particular interest and importance in terms of pathogenesis as well as treatment.

Acute Disease↗
PubMed1997

Localization of ectopic parathyroid glands using technetium-99m sestamibi imaging: comparison with magnetic resonance and computed tomographic imaging.

The aim of the study was to compare the accuracy of technetium-99m sestamibi imaging for localization of ectopic parathyroid glands in patients with hyperparathyroidism with that of magnetic resonance (MR) and computed tomographic (CT) imaging. Eleven patients with primary (n=3) or secondary (n=8) hyperparathyroidism were studied with 99mTc sestamibi parathyroid imaging CT and MR imaging. Images of the neck were acquired at 10 min and 2-3 after tracer injection. The three patients with primary hyperparathyroidism and five patients with secondary hyperparathyroidism underwent parathyroidectomy. The ectopic glands were confirmed by histopathological examination of the resected specimens. In respect of 20 parathyroid glands in the eight patients explored surgically, the sensitivity and specificity of sestamibi imaging were 70% (14/20) and 88%, respectively, those of CT, 40% (8/20) and 88%, and those of MR imaging, 60% (12/20) and 88%. Of these patients, three had parathyroid adenomas while five had hyperplasia (17 glands). Sestamibi imaging localized eight ectopic parathyroid glands, which were surgically confirmed (six were located in the thymus and two in the mediastinum). In one patient explored surgically, the ectopic gland was located outside the field of the MR coil. Although the remaining three cases of secondary hyperparathyroidism were not confirmed surgically, these patients demonstrated sestamibi uptake in five parathyroid glands, including three ectopic glands. MR images demonstrated abnormal parathyroid glands in the same regions as sestamibi imaging. Our data indicate that 99mTc-sestamibi imaging should be used initially to localize the ectopic parathyroid glands in patients with hyperparathyroidism for anatomical guidance prior to MR or CT imaging.

Choristoma↗
PubMed1997

Cyclosporine A inhibits interleukin-8 production in a human colon epithelial cell line (HT-29).

Intestinal epithelial cells produce various inflammatory mediators. However, the way in which immunosuppressive agents influence the production of these mediators by intestinal epithelial cells is not understood. The effects of cyclosporine A (CsA), tacrolimus (FK506), and dexamethasone (DEX) on cytokine-induced production of interleukin (IL)-8 in a human colonic cancer cell line (HT-29) were examined. HT-29 cells were stimulated with either IL-1 beta or tumor necrosis factor alpha (TNF alpha) together with CsA, FK506, or DEX. The presence of IL-8 protein was detected by enzyme-linked immunosorbent assay, and the expression of IL-8 messenger RNA (mRNA) by reversetranscription polymerase chain reaction. CsA (1, 5, and 10ng/ml) significantly reduced IL-1 beta-induced IL-8 production (by 32%, 41%, and 48%, respectively), and reduced TNF alpha-induced IL-8 production (by 21%, 42%, and 50%, respectively). FK506 or DEX had no effect on IL-1 beta- or TNF alpha-induced IL-8 production. The expression of IL-8 mRNA was also inhibited by CsA. These findings suggest that CsA may influence the production of inflammatory mediators in colonic cells in a different manner from FK506 and DEX.

Cell Count↗
PubMed1997

Glomerular handling of immune complex in the acute phase of active in situ immune complex glomerulonephritis employing cationized ferritin in rats. Ultrastructural localization of immune complex, complements and inflammatory cells.

The ultrastructural localization of immune complex (IC) and inflammatory mediator systems in the glomerulus was investigated in active in situ IC glomerulonephritis employing cationized ferritin in rats. Glomerulonephritis was induced by unilateral renal perfusion of cationized ferritin as antigen (Ag) in preimmunized rats, and anti-ferritin antibody (Ab), C3 and the rat C5b-9 complex were localized by means of immunogold electron microscopy. Ag-Ab complexes were initially formed subendothelially, associated with C3, and attracted platelets, polymorphonuclear leucocytes (PMN) and monocytes. Then Ag-Ab complexes, without C3, passed across the glomerular basement membrane to re-aggregate subepithelially accompanied by C3 deposition after 1 day. Ag-Ab complexes without C3 accumulated in the inter-podocyte space within 1 day and were seen in the epithelial cells at 6 h. C5b-9 complexes were found in subepithelial immune deposits and in membrane vesicles of the epithelial cells, but only in very small amounts in subendothelial immune deposits. Accumulated platelets, PMN, and monocyte were in direct contact with endothelial cells or subendothelial IC. PMN and monocytes contained Ag, Ab and C3 in intracytoplasmic vacuoles. Ag-Ab complexes were also found in the mesangial matrix adjacent to the subendothelial region after 2 h and increased slightly in number, with expansion of the mesangial area thereafter. Most ICs formed in the subendothelial space rapidly formed lattices of a size that activated C3 and were then translocated to the subepithelial space. The potential ability of C3 to solubilize ICs in the subendothelial region may be important in this process. Endocytosis of subendothelial ICs by PMN and/or monocytes and the movement of ICs to the mesangial matrix may also contribute to the removal of IC from the subendothelial space.

Acute-Phase Reaction↗
PubMed1997

TNF-alpha receptor fusion protein prevents experimental auto-immune encephalomyelitis and demyelination in Lewis rats: an overview.

To explore the therapeutic use of TNF-alpha inhibitors in human inflammatory demyelinating diseases we examined the effect of a recombinant TNFRp55 protein constructed by fusing TNFRp55 extracellular domain cDNA to a human IgG1 heavy gene fragment containing the hinge and constant domains CH2 and CH3 (TNFRp55-IgG1) in diverse experimental model systems representing inflammation and inflammatory demyelination of encephalitogenic T cells in vivo. In EAE actively induced by immunization of Lewis rats with MBP, a single dose of TNFRp55-IgG1 protected the recipient animals from clinical signs. Interestingly, the treatment neither prevented the formation CNS infiltrations, nor did it alter the cellular composition of the infiltrates. In EAE transferred by MBP specific activated T line cells, a model of inflammatory (not demyelinating) brain disease, the inhibitor's therapeutic effect on clinical disease was also striking achieving almost complete protection even after repeated transfers of encephalitogenic T cells. Finally, the recombinant inhibitor was also protective in Lewis rats with demyelinating experimental autoimmune panencephalitis produced by combined transfer of panencephalitogenic T cells and demyelinating monoclonal antibody specific for MOG. In this system, the T cells are of low encephalitogenic activity, but open the blood-brain barrier for the demyelinating immunoglobulins. The fusion protein treatment, however, prevented the formation of inflammatory lesions and demyelination. The strong therapeutic effect of the recombinant chimeric TNF-alpha inhibitor in three models of myelin specific autoimmunity raises hopes as to TNF-alpha directed therapy of human diseases like MS.

Animals↗
PubMed1997

Immunohistochemical study of tumour angiogenesis in oral squamous cell carcinoma.

To assess the clinical significance of angiogenesis in oral squamous cell carcinoma (SCC), we examined vessel density immunohistochemically in 44 primary oral SCCs using the JC-70A antibody which reacts specifically with vascular endothelial cells. In addition, the expression of vascular endothelial growth factor (VEGF) and its receptors, KDR, Flt-1 and Flt-4 in oral SCCs was examined in relation to the vessel density and lymph node metastasis. There was no association of vessel density with tumour site, T-category (tumour size), degree of differentiation or cervical lymph node metastasis, except that the vessel density of carcinomas with a well-defined tumour-stromal boundary was higher than that of diffusely invasive carcinomas. The intensity of VEGF expression correlated with lymph node metastasis (P < 0.01), but not with vessel density. The expression of KDR and Flt-1 did not correlate with vessel density and lymph node metastasis. However, the vessel density in Flt-4-positive carcinomas was higher than that in Flt-4-negative carcinomas (P < 0.05), and expression of Flt-4 most significantly correlated with lymph node metastasis (P < 0.001). These results suggest that the expression of VEGF or Flt-4 rather than vessel density may be a predictor of lymph node metastasis in oral SCC.

Carcinoma, Squamous Cell↗
PubMed1997

A novel ALL-L3 cell line, BALM-16, lacking expression of immunoglobulin chains derived from a patient with hypercalcemia.

A human acute lymphoblastic leukemia (ALL) cell line, BALM-16, was established from the peripheral blood specimen of a patient with B cell ALL L3 type (ALL-L3) in relapse. As with the original leukemia cells, the established line was negative for both cell surface and cytoplasmic immunoglobulin (Ig) chains. Absence of Ig expression was confirmed by Western blotting. Southern blot analysis demonstrated homozygous deletion of the C kappa gene, germ line configuration of the C lambda and rearrangement of IgJH genes. Cytogenetic analysis of both leukemic bone marrow and BALM-16 cells showed the t(8;22)(q24;q11) abnormality which is specifically associated with ALL-L3 and Burkitt lymphoma. The patient's serum showed hypercalcemia, prompting further investigation of the established cell lines which showed parathyroid hormone-related peptide (PTHrP) mRNA detected by reverse-transcriptase polymerase chain reaction. However, PTHrP production was not detected in the culture supernatant. The established cell line, BALM-16, could provide a useful material for analyzing the lack of Ig expression and of clarifying the pathogenesis of this type of B cell malignancy.

Adult↗
PubMed1997

Common clonal origin of lymphocytes and plasma cells in splenic lymphoma with villous lymphocytes.

In two-thirds of patients with splenic lymphoma with villous lymphocytes (SLVL) a small amount of M-protein can be detected in association with the presence of plasma cells in the peripheral blood (PB) and/or bone marrow (BM). However, it is not known whether lymphoma cells and plasma cells originate from the same clone. In this report we describe a case of SLVL which was characterized by the presence of marked monoclonal gammopathy (IgG-kappa 90 g/l) and increased plasma cells in the BM. In an attempt to elucidate the origin of lymphoma cells and plasma cells, we performed morphological, cytogenetic and molecular studies on PB mononuclear cells (PBMNC) without plasma cells and BMMNC containing 10% plasma cells from this patient. Immunofluorescence showed that lymphoma cells and plasma cells were positive for cytoplasmic gamma heavy and kappa light chains. Well-developed endoplasmic reticulum was observed in the cytoplasmic organelles of PBMNC using an electron microscope. The mean IgG concentration in the 3 d supernatant cultures of PBMNC was 374 +/- 24 microg/l. More than 50% PBMNC differentiated into plasmacytoid cells in 6 d of liquid culture with IL-3 and IL-6. Analysis by two-colour FISH revealed that karyotypic abnormalities of monosomy X and trisomy 17 existed simultaneously in both lymphoma cells and plasma cells. JH gene rearranged bands from PBMNC and BMMNC by Southern blot hybridization were identical, whereas DNAs from PBMNC failed to hybridize with the Cmu probe. These observations strongly suggest that lymphoma cells and plasma cells originate from the same clone, and that plasma cells, as well as lymphoma cells, which have undergone class switch recombination, could produce IgG type M-protein in this case.

Aged↗