[A case of primary gastric T-cell malignant lymphoma].
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Aged↗
Biomedical subjects
A Horiuchi
Publications and source records attributed to A Horiuchi.
[Immunoblastic lymphadenopathy-like T cell lymphoma associated with erythroid hypoplasia and thrombocytopenia].
A 71-year-old female patient was admitted with generalized lymphadenopathy, anemia and thrombocytopenia. On admission a peripheral blood examination showed a red blood cell (RBC) count of 1.95 x 10(6)/microliter, hemoglobin (Hb) 5.0 g/dl, platelet count (Plt) 2.2 x 10(4)/microliter and no reticulocytes. A bone marrow aspiration specimen was hypocellular with a nuclear cell count 1.0 x 10(4)/microliter, erythroblasts less than 0.3% and no megakaryocytes. Serum examination showed polyclonal hypergammaglobulinemia and the results of the direct/indirect Coombs test indicated the existence of auto-antibodies. as immunoblastic lymphadenopathy-like T cell lymphoma was diagnosed based on the lymph node biopsy specimen. Cyclophosphamide, doxorubicin and etoposide obtained improvement of lymphadenopathy, hypergamma globulinemia, hypoplastic bone marrow and thrombocytopenia. On the other hand, the anemia did not improve and the ratio of erythroblasts in total bone marrow cells was remainde 0.5%. The detailed mechanism of this hypoplastic anemia is still unknown, however, our results imply some
Aged↗
Autoimmune chronic pancreatitis simulating pancreatic lymphoma.
A 51-yr-old man, who presented with diabetes mellitus, abdominal pain, inguinal lymphadenopathy, and diffuse enlargement of the whole pancreas on ultrasonography, was at first thought to have pancreatic lymphoma. Chemotherapy including steroid was carried out successfully, although the definitive diagnosis of lymphoma was not made. However, on follow-up, we realized that both laboratory findings, such as hyperglobulinemia and autoantibody-positive results, and radiographic features in this case were very similar to those of a case of autoimmune pancreatitis recently reported by Yoshida et al. (Dig Dis Sci 1995;40:1561-8). When the disease recurred, therefore, treatment with steroid alone was performed with an excellent result. We report a case of autoimmune pancreatitis simulating primary pancreatic lymphoma.
Autoimmune Diseases↗
[Age-related changes in morphological studies in rat and human kidney].
There have been many reports on changes in renal morphology with aging. In this study, morphological comparisons were made on the influence of aging in humans and rats. Kidneys were obtained from 63 autopsies (except those from cases of tumor, severe cicatrization, and cysts 10 mm or more in diameter) performed on humans aged from 0 to 92 years, including 7 cases with a past history of hypertension; the findings were compared with those from 201 Wistar male rats aged three to 115 weeks. First, changes in renal weight and renal cortex width were investigated. Next, changes in renal morphology were examined by microscopy. Finally, after performing alcian-blue-PAS staining, the ratio of the intima/outer diameter (I/OD ratio) of renal blood vessel was measured under a microscope with an image analyzer, and the results compared. A decrease in renal weight was observed in humans from about 50 years of age, but there was no decrease in weight with aging among rats. While significant thickening in the vascular intima was observed with aging in humans, there was no such thickening among rats. Furthermore, the presence of hypertension caused renal cortex width to be significantly decreased in humans (p < 0.04). Findings of sclerogenous changes of the glomeruli, infiltration of chronic inflammatory cells and fibrosis in the stroma, and tubular casts were observed with aging in both humans and rats. In conclusion, arteriosclerosis apparently develops with aging in humans, suggesting that arteriosclerosis greatly influences the reduction of human renal weight.
Adolescent↗
[Renal disorders in patients with immunoproliferative disorder].
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Animals↗
Plasma (1-->3)-beta-D-glucan measurement in diagnosis of invasive deep mycosis and fungal febrile episodes.
(1-->3)-beta-D-glucan is a characteristic fungal cell-wall constituent. To assess the clinical usefulness of this glucan in screening for invasive fungal infection or fungal febrile episodes, we measured the plasma concentration at the time of routine blood culture in 202 febrile episodes by means of factor G, a horseshoe-crab coagulation enzyme that is extremely sensitive to this polysaccharide. With a plasma cut-off value of 20 pg/mL, 37 of 41 episodes of definite fungal infections (confirmed at necropsy or by microbiology) had positive results (sensitivity 90%). All of 59 episodes of non-fungal infections, tumour fever, or collagen diseases had concentrations below the cut-off value (specificity 100%). Of 102 episodes of fever of unknown origin, 26 had plasma glucan concentrations of more than 20 pg/mL. With those 102 cases taken as non-fungal infections, the positive predictive value of the test was estimated as 59% (37/63), the negative predictive value as 97% (135/139), and the efficiency as 85% (172/202). The positive predictive value should improve if there were a sensitive gold standard that could discriminate fungal from non-fungal infections. Causative fungi included candida, aspergillus, cryptococcus, and trichosporon. Determination of plasma (1-->3)-beta-D-glucan with factor G is a highly sensitive and specific test for invasive deep mycosis and fungal febrile episodes, and will substantially benefit immunocompromised patients.
Adolescent↗
Membrane-associated lymphotoxin-expressing lymphokine-activated killer cells up-regulate intercellular adhesion molecule-1 expression on target tumor cells in vitro.
Human lymphokine-activated killer (LAK) cells cultured with interleukin-2 express membrane-associated lymphotoxin (mLT) on the cell surface. mLT-lacking (mLT-) LAK cells, which are generated by culturing without IL-2 for 24 hr, fully retained natural killer (NK) and LAK activity. However, they partially lost their killing activity against various tumor cells when compared to mLT-expressing (mLT+) LAK cells. An anti-LT but not anti-tumor necrosis factor (TNF) antibody somewhat suppressed the killing activity of mLT+ LAK cells against these tumor cells. However, an anti-LT antibody did not alter NK or LAK activity of mLT+ LAK cells. Anti-CD18 (beta chain of LFA-1) and anti-CD54 (ICAM-1) monoclonal antibodies, by inhibiting LAK cell binding to targets, suppressed the killing activity of mLT+ LAK cells. During the process in the cytotoxic assay, mLT+ but not mLT- LAK cells up-regulated ICAM-1 expression on target tumor cells, the effect of which was marginally inhibited by anti-TNF and anti-IFN-gamma but not by anti-LT antibodies. The up-regulation of ICAM-1 expression elicited by LAK cells on target tumor cells was not simply caused by diffused soluble factors but required membrane contact of LAK and target cells. Paraformaldehyde-fixed mLT+ but not mLT- LAK cells up-regulated ICAM-1 expression on target cells. These findings indicate that mLT+ but not mLT- LAK cells up-regulate ICAM-1 expression on target tumor cells via undetermined membrane factor(s), and this effect appears to be at least partially responsible for the higher killing activity of mLT+ LAK cells than that of those lacking mLT in vitro.
Antibodies↗
Clonal origin of Philadelphia chromosome negative cells with trisomy 8 appearing during the course of alpha-interferon therapy for Ph positive chronic myelocytic leukemia.
The transient appearance of a Philadelphia chromosome (Ph) negative clone with trisomy 8 was found in the bone marrow cells from a patient with Ph positive CML during the course of alpha-interferon (IFN) therapy. To determine whether this clone was derived from a Ph positive clone or from some other cell lineage, we performed molecular cytogenetic studies on bone marrow cells from the patient by fluorescence in situ hybridization (FISH). No fusion of BCR-ABL could be detected in cells with trisomy 8, clearly indicating that the Ph negative trisomy 8 clone was not derived from the Ph positive CML population.
Adult↗
Nafamostat enhances IBMX and secretin-stimulated water and bicarbonate secretion in the isolated, blood-perfused dog pancreas.
1. The effect of nafamostat mesilate, a synthetic protease inhibitor, on pancreatic exocrine secretion was investigated in isolated, blood-perfused dog pancreas. 2. Intra-arterial injections of nafamostat (2-10 mumol) dose-dependently enhanced water and bicarbonate secretion stimulated by 3-isobutyl-1-methylxanthine (IBMX) or secretin, although nafamostat alone did not affect the basal secretion. 3. In the nafamostat-enhanced pancreatic juice, bicarbonate concentrations were increased dose-dependently as compared with the control, while protein concentrations were not significantly changed. 4. These results indicate that nafamostat enhances IBMX and secretin-stimulated water and bicarbonate secretion, which may be mediated through cAMP activation.
1-Methyl-3-isobutylxanthine↗
Prediction of histopathologic features and proliferative activity of uterine leiomyoma by magnetic resonance imaging prior to GnRH analogue therapy: correlation between T2-weighted images and effect of GnRH analogue.
To predict the histological features and proliferative activity of leiomyomas and to evaluate the effect of GnRH analogues (GnRHa) by MR images, the correlation between MR images and histopathologic findings was studied on 137 leiomyomatous nodules from 79 patients. The correlation among cellularity, proliferative activity and MR images was studied on sections of 42 leiomyomatous, nodules stained with hematoxylin-eosin and immunohistochemistry for proliferating cell nuclear antigen. The utility of MR imaging in assessing response to therapy with a GnRHa (buserelin 900 micrograms/day, intranasal for 16 weeks) was studied on 62 leiomyomatous nodules from 29 patients. On T2-weighted MR images, we encountered five major images. According to the increase of signal intensity relative to that of the myometrium and/or the endometrium, the images were classified as Type 1, Type 2, Type 3, Type 4, and Type 5. Histopathologically, the majority of Type 1, Type 2 and Type 3 images had features of typical leiomyoma. Almost all cellular leiomyomas and bizarre leiomyomas had Type 4 images. Variable degenerative features were observed in the nodules with Type 5 images. According to the increase of signal intensity, leiomyomas had a tendency to show a high degree of both cellularity and proliferative activity. Moreover, the reduction rate of leiomyomatous nodules after GnRHa therapy correlated with the tumor signal intensity on T2-weighted images before therapy. The reduction rate was the lowest in Type 1 images (20.9%) and the highest in Type 4 images (50.7%). These results suggest that increased the signal intensity on T2-weighted MR images correlates with the cellularity and proliferative activity of leiomyomas, and with tumor response to GnRHa treatment. MR imaging enables quantitative monitoring of GnRHa therapy in patients with leiomyomatous nodules, and allows us to predict the histopathology, cellularity, proliferative activity, and shrinkage rate of nodules before GnRHa treatment.
Adult↗
D-1 dopamine receptors mediate dopamine-induced pancreatic exocrine secretion in anesthetized dogs.
Characterization of dopamine (DA) receptor subtypes was examined on the canine exocrine pancreas using selective DA receptor agonists and antagonists in anesthetized dogs. Each drug was injected i.a. in a single bolus fashion. Graded doses of DA (0.01-3 mumol) produced dose-dependent increases in the secretory rate of pancreatic juice, with a maximum effect at approximately 1 mumol. SCH23390 (3-30 nmol), a selective D-1 DA receptor antagonist, caused a progressive parallel shift to the right in the dose-response curve for DA-induced pancreatic secretion without changes in the maximal response. However, domperidone (3 mumol), a selective D-2 DA receptor antagonist, did not antagonize the DA-induced pancreatic exocrine secretion. A Schild analysis of the data indicates that the inhibitory constant value for SCH23390 to inhibit DA-stimulated secretion was 6.9 nmol. In addition, the stimulatory effects of SKF38393 (0.1-10 mumol) and YM435 (0.3-30 nmol), selective D-1 DA receptor agonists, and LY171555 (1-10 mumol), a selective D-2 DA receptor agonist, on pancreatic secretion were demonstrated. The rank order of agonist potency was YM435 > DA > SKF38393 >> LY171555. These results suggest that DA-induced pancreatic exocrine secretion is mediated by activation of D-1 DA receptors.
2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
[Measures for infection in multiple myeloma].
A peculiarity of infection, as a complication of multiple myeloma in hematopoietic malignancies, is discussed. The Hanshin Study Group of Hematopoietic Disorders and Infection treated 3346 cases of bacterial infection during the past 13 years. Myeloma patients showed a low rate of 3.0% as compared with 28.2% of acute myelogenous leukemia patients. In patients with long term administration of antibiotics or bone marrow suppression, it is necessary to watch for fungus infection. Recently, new combination chemotherapy (DMVM-IFN alpha) is widely used in Japan. A high complete remission rate has been achieved by this regimen, but the incidence of infection tends to increase. Measures for infection in multiple myeloma should therefore be similar to that acute leukemia.
Bacterial Infections↗
Improvement of ELISA sensitivity by allogeneric adsorption of polyclonal antibodies--a technical note for non-experts.
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Animals↗
The elevation of plasma soluble tumor necrosis factor receptor levels by TNF induction therapy for patients with malignancy.
Soluble tumor necrosis factor receptor (sTNF-R) is known to inhibit patient immunity via specific binding with the TNF molecule. To examine the possible involvement of sTNF-R in cancer immunotherapy, the plasma levels of sTNF-R of both 55 kDa and 75 kDa origins were estimated when TNF was induced in patients with malignancy using both a polysaccharide preparation (Lentinan) and a streptococcal preparation (OK-432). The pretreatment plasma levels of the 55 kDa and 75 kDa sTNF-R were 1.04 +/- 0.53 and 1.06 +/- 0.34 ng/ml (mean +/- SE), respectively. The plasma levels of TNF were undetectable before treatment. The plasma sTNF-R levels peaked 2 h after the administration of OK-432 and followed the same pattern as the TNF levels in plasma. Both TNF and sTNF-R nearly returned to pretreatment levels at 16 h after the induction of TNF. The peak plasma levels of the 55 kDa and 75 kDa sTNF-R were 2.46 +/- 0.95 and 3.03 +/- 0.88 ng/ml, respectively, but they did not correlate with the plasma TNF levels. When peripheral white blood cells were cultured with the addition of lipopolysaccharide in vitro, an elevation of the 72 kDa sTNF-R was detected. Thus, the plasma source of this soluble receptor can at least be partly attributed to the white blood cells. However, the 55 kDa sTNF-R showed little increase in the cultures, and its source remains unknown. We should therefore be aware of the elevation of plasma sTNF-R levels by the induction therapy of TNF for patients with malignancies because of the immunosuppressive effect of sTNF-R.
Adult↗
Possible involvement of protein kinase C activation in down-regulation of CD3 antigen on adult T cell leukaemia cells.
The role of protein kinase C (PKC) system on CD3 expression on adult T-cell leukaemia (ATL) was examined. The down-regulation of CD3 on ATL cells is reportedly induced by CD3 down-regulating factor (CD3DF) contained in serum and culture supernatants of leukaemia cells from acute type ATL patients. After we cultured normal PBMC with a PKC inhibitor, H-7, CD3DF activity for PBMC was reduced significantly. Culture with H-7 of HTLV-1 transformed T cells, ATL-2 cells whose CD3 expression had been decreased, led to enhancement of CD3 expression in a time-dependent manner. These findings suggest that CD3DF may play an important role as a PKC system activator, resulting in CD3 down-regulation.
1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
Role of membrane-associated lymphotoxin (mLT) in the killing activity of lymphokine-activated killer (LAK) cells towards various tumour cell lines.
Human lymphokine-activated killer (LAK) cells developed by an incubation of peripheral mononuclear cells with IL-2 express the membrane-associated lymphotoxin (LT)-related molecule (mLT). By a further cultivation of mLT expressing (mLT-positive) LAK cells for 24 h without IL-2, mLT disappears (mLT-negative LAK cells). Cytotoxicities of various tumour cell lines by either mLT-positive or -negative LAK cells were compared. Eight out of 12 tumour cell lines, less susceptible to mLT-negative LAK cells than mLT-positive LAK cells, were categorized as group A. Two tumour cells (K562 and Molt-4) had the same susceptibility to both kinds of LAK cells. The others (Daudi and Jurkat) had less susceptibilities only when they were assessed at E:T ratios of less than 5. The four tumour cell lines in the latter two cases, containing K562, Molt-4, Daudi and Jurkat cells, were categorized as group B. The cytotoxicities of group A tumour cells, but not group B tumour cells, by LAK cells were significantly suppressed by the presence of anti-LT antibody. Group A tumour cells had higher LT-binding ability (2.82-16.44 fmol/10(6) cells) than group B tumour cells (less than 1.46 fmol/10(6) cells). Both mLT-positive and -negative LAK cells had similar perforin activities and tumour cell-binding capacities. These results suggest that the mLT-mediated killing mechanism is involved in tumour cell killing by LAK cells. Further, various tumour cell lines can be classified into two large groups according to their susceptibilities to the mLT-mediated killing by LAK cells.
Animals↗
Anti-cytokine nature of natural human immunoglobulin: one possible mechanism of the clinical effect of intravenous immunoglobulin therapy.
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Autoantibodies↗
Down-regulation of CD3 antigen on adult T cell leukemia cells.
The immunological abnormality of T lymphocytes in patients with adult T cell leukemia (ATL) is characterized by the abnormal enhanced expression of the 55 kDa chain of the receptor for interleukin 2 (IL-2R/p55) (Tac), and down-regulation of CD3 antigen. Using serum and culture supernatants of leukemic cells from ATL patients (Group A) whose CD3 expression was down-regulated and those whose CD3 was not low (Group B), the possible mechanism of CD3 down-regulation on ATL cells was investigated. When PBMC from normal individuals were cultured with sera from ATL patients for 24 hrs, CD3 expression revealed by means of fluorescent intensity (MFI) was down-regulated by sera from ATL patients in Group A (MFI: Pt.1 = 51.6 +/- 4.5, Pt.2 = 48.0 +/- 6.9, Control = 96.5 +/- 6.6), not by sera from patients in Group B (MFI: Pt.3 = 105.5 +/- 7.9, Pt.4 = 102.5 +/- 8.3, Control = 96.5 +/- 6.6). When normal PBMC were cultured with supernatants of leukemic cells from ATL patients in Group A, the same CD3 down-regulating activity was also detected (MFI: Pt.1 = 78.0 +/- 10.2, Pt.2 = 70.6 +/- 8.7, Control = 94.0 +/- 6.6). By using gel-chromatography, the fractionated supernatants from ATL patients in Group A decreased CD3 expression of normal PBMC significantly (MFI: Pt.1 = 22.9 +/- 5.8, Pt.2 = 28.8 +/- 7.4, Control = 92.1 +/- 9.6).(ABSTRACT TRUNCATED AT 250 WORDS)
Acute Disease↗