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Biomedical subjects

A Horiuchi

Publications and source records attributed to A Horiuchi.

At least 109 records · Page 6Linked to original sources
PubMed1994

Change of serum alpha-1 microglobulin and beta-2 microglobulin following allogeneic bone marrow transplantation.

By serially measuring serum levels of alpha-1 microglobulin and beta-2 microglobulin following allogeneic bone marrow transplantation (BMT), we tried to define their relationship to renal dysfunction, acute graft-versus-host disease (GVHD) and infection as complications of the transplantation. The study involved a total of 25 patients with leukemia, myelodysplastic syndrome and aplastic anemia who received BMT in this department; one patient received re-transplantation, thus bringing the total number of transplants to 26. Twenty-four patients received BMT from HLA-identical siblings while two others received BMT from unrelated donors. Alpha-1 microglobulin was within normal limits in all patients before BMT; among various complications such as nephrotoxicity, acute GVHD and infection which took place after transplantation, a raised alpha-1 microglobulin level was found only in nephrotoxicity; however, the increase was not significant compared with the pre-transplantation level. The pre-transplantation beta-2 microglobulin level was higher than normal in some patients; it was significantly increased in all of the above complications compared with the pretransplantation level (1.57 +/- 0.57 mg/l). A significant correlation was found between the serum creatinine level and the beta-2 microglobulin level (r = 0.849) in patients with renal dysfunction. In some patients, however, the beta-2 microglobulin level increased earlier than the serum creatinine level, and this finding was considered useful for the early diagnosis of renal dysfunction following allogeneic BMT.

Adolescent↗
PubMed1994

[Clinical efficacy of arbekacin on MRSA infections with hematopoietic disorders. The Hanshin Study Group of Hematopoietic Disorders and Infections].

Arbekacin (ABK) was administered to 17 patients with MRSA infections that complicated underlying hematopoietic disorders, and the efficacy and safety were evaluated. The underlying diseases included acute myelocytic leukemia (8 cases), acute lymphocytic leukemia (1) myelodysplastic syndrome (3), chronic myelocytic leukemia (1), non-Hodgkin's lymphoma (2), Hodgkin's disease (1) and adult T cell leukemia (1). The infections consisted of septicemia (5 cases), pneumonia (4), upper respiratory tract infections (6) and urinary tract infections (2). ABK was administered by i.v. drip infusion in daily doses of 150-200 mg, given in two divided dosages. The therapeutic efficacies were: excellent in 2 (2 septicemias), good in 7 (1 septicemia, 4 upper respiratory infections, 2 urinary tract infections), fair in 2 (septicemia and pneumonia) and poor in 6 (1 septicemia, 3 pneumonias, 2 upper respiratory infections). As a side effect, reversible renal dysfunction was detected in four cases. Causative bacteria were isolated from six cases. They were all coagulase type II and MIC's of ABK were from 0.25 microgram/ml to 4.0 micrograms/ml. Arbekacin therapy was found to be effective even in patients with hematopoietic disorders accompanied by MRSA infections.

Adolescent↗
PubMed1994

[Co-operative study of all-trans retinoic acid as a differentiation induction therapy of acute promyelocytic leukemia].

Efficacy and safety of tretinoin (all-trans retinoic acid, ATRA, Ro01-5488) for refractory and relapsed acute promyelocytic leukemia were studied by multi-institutional study in Japan. 22 out of 27 (81.5%) patients with previously untreated who were intolerable to chemotherapy, relapsed and refractory were achieved CR. And 4 out of 11 (36.4%) in relapsed patients who received ATRA remission induction therapy previously responded. Side effects, such as dryness of the lip and skin, headache, increase of triglyceride, beta-lipoprotein and lactate dehydrogenase, were observed in 36 of 41 eligible patients (87.8%) but these were well tolerated. In addition to these, hyperleukocytosis in 4 cases and retinoic acid syndrome in 3 cases were observed. However, all patients were prescribed tretinoin again by adequate management.

Administration, Oral↗
PubMed1994

Expression of mRNAs encoding ARPP-16/19, ARPP-21, and DARPP-32 in human brain tissue.

In this study we have isolated and sequenced human cDNAs for the phosphoproteins DARPP-32, ARPP-21, and ARPP-16/19, and have compared these sequences to previously characterized bovine and rat cDNAs. In situ hybridization and Northern blot analysis with the human cDNA probes were used to study the expression of mRNAs encoding ARPP-16/19, ARPP-21, and DARPP-32 in human postmortem brain tissue. In situ hybridization was performed using horizontal whole hemisphere sections. Five representative levels of the brain ranging from 71 mm to 104 mm ventral to vertex were examined. All three probes showed distinct hybridization patterns in the caudate nucleus, putamen, nucleus accumbens, and the amygdaloid complex. For ARPP-16/19 mRNA, a hybridization signal comparable to the signal in caudate nucleus, putamen, and nucleus accumbens was also detected in the neocortex. ARPP-21 and DARPP-32 mRNA, on the other hand, were present in lower levels in neocortical regions. DARPP-32 mRNA was abundant in the cerebellar cortex at the level of the Purkinje cell layer. High levels of ARPP-16/19 and ARPP-21 mRNA were also found in the cerebellar cortex, where they were confined to deeper layers. The present result demonstrate that mRNAs for the three phosphoproteins are expressed in overlapping, but also distinct, areas of the human brain that in many cases coincide with previously described distribution of the dopamine D1 receptor.

Aged↗
PubMed1993

Effects of KRN2391, a novel vasodilator, on pancreatic exocrine secretion in anesthetized dogs.

The effects of KRN2391, a newly synthesized vasodilator, on pancreatic exocrine secretion in anesthetized dogs were compared with those of Ki3315, pinacidil and nitroprusside. Graded doses of KRN2391 (0.03-3 mumol/kg) and nitroprusside (0.003-0.3 mumol/kg) injected i.a. produced dose-dependent increases in the secretion of pancreatic juice, with a high concentration of protein and low concentration of bicarbonate, but Ki3315 or pinacidil did not (up to 10 mumol/kg). KRN2391 and nitroprusside increased the cyclic GMP levels in pancreatic tissue together with the increase in pancreatic secretion. Methylene blue decreased pancreatic secretion and cyclic GMP levels stimulated by KRN2391 and nitroprusside, but glibenclamide did not. KRN2391, Ki3315, pinacidil and nitroprusside caused vasodilator actions. These results suggest that KRN2391 has direct secretory properties on pancreatic exocrine glands of the dog and its nitro moiety has an important role in the stimulation of pancreatic secretion, but the K+ channel opening action or increasing of blood flow rate does not participate in the secretion.

Animals↗
PubMed1993

Dual actions of glucagon: direct stimulation and indirect inhibition of dog pancreatic secretion.

The secretory actions of glucagon on the exocrine pancreas were examined using two kinds of canine preparations. In the isolated and blood-perfused dog pancreas with venous drainage, i.a. injection of glucagon did not inhibit secretin/cholecystokinin-octapeptide (CCK-8)-stimulated pancreatic secretion, but instead dose dependently enhanced both basal and stimulated pancreatic secretion. Glucagon-induced increase of pancreatic secretion was potentiated by 3-isobutyl-1-methylxanthine. In contrast, i.v. bolus injection of glucagon (3 and 10 nmol/kg) first augmented transiently then suppressed secretin/CCK-8-stimulated pancreatic secretion while simultaneously increasing circulating plasma somatostatin immunoreactivity from 14.2 to 214 fmol/ml in anesthetized intact dogs. The inhibition of secretin/CCK-8-stimulated pancreatic secretion and elevation of plasma somatostatin immunoreactivity induced by glucagon were comparable with those due to somatostatin-14. Thus, these results indicate that glucagon stimulates pancreatic secretion directly; the inhibitory action of glucagon is indirect and appears to be related to a rise in the circulating level of somatostatin immunoreactivity.

1-Methyl-3-isobutylxanthine↗
PubMed1993

Operative stress potentiates the inductivity of membrane associated lymphotoxin (mLT) on lymphokine activated killer (LAK) cells in vitro.

Membrane-associated lymphotoxin (mLT) is induced in human peripheral blood mononuclear cells when cultured with interleukin 2, in the form of lymphokine-activated killer (LAK) cells. The inductivity of mLT is thought to be dependent upon the differentiation potential of LAK cell precursors, being T cells and natural killer cells. In this study, we investigated the inductivity of mLT on LAK cells from surgical patients. The preoperative values of mLT inductivity were found to be generally higher in malignant than benign cases, and the postoperative time course of mLT inductivity showed a transient decrease immediately after the operation followed by gradual increase over 2 weeks. Moreover, patients with an intraoperative bleeding volume of more than 1,000 ml showed a delay in the postoperative increase of mLT inductivity. These data suggest that operative stress potentiates the inductivity of mLT on LAK cells; however, excess stress may cause a delay in the restoration of mLT inductivity.

Adult↗
PubMed1993

Natural human IgG inhibits the production of tumor necrosis factor-alpha and interleukin-1 alpha through the Fc portion.

The overproduction of cytokines such as the tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 alpha (IL-1 alpha) may cause further deterioration in the already critical condition of patients with shock, sepsis, and acute inflammation. The effectiveness of infusion therapy of natural human IgG to such patients is suggested to depend partly upon the inhibition of the productivity of these cytokines. In this study, we investigated the modulation effects of IgG and its fragments on the production of TNF-alpha and IL-1 alpha, on human peripheral blood mononuclear cells (PBMC). The production of TNF-alpha and IL-1 alpha was found to be dose-dependently inhibited by IgG when stimulated by lipopolysaccharide (LPS), phytohemagglutinin (PHA), concanavalin A (Con A), and interleukin-2 (IL-2). However, no inhibition was seen when stimulated by phorbormyristate acetate (PMA). The F(ab')2 fragment showed enhancing effects on cytokine production by LPS, while the Fc fragment showed not as much inhibitory effect as whole intact IgG. IgG showed no direct cytotoxic effect on PBMC. These data suggest that natural human IgG inhibits TNF-alpha and IL-1 alpha production by PBMC through the Fc portion. The results of this study led us to conclude that whole intact IgG may be the best form of therapeutic delivery.

Cells, Cultured↗
PubMed1993

Membrane-associated lymphotoxin expression and functional analysis of lymphokine-activated killer cells derived from tumor-infiltrating lymphocytes.

The expression of a membrane-associated lymphotoxin molecule (mLT) on lymphokine-activated killer (LAK) cells obtained from 18 patients with malignant tumors and its role in the tumor cell killing mechanisms were investigated. LAK cells from tumor-infiltrating lymphocytes (TIL-LAK cells) were mainly composed of CD3-positive cells, whereas LAK cells from peripheral blood lymphocytes (PBL-LAK cells) were mainly composed of CD16- and CD56-positive cells. However, mLT was found to be expressed on TIL-LAK cells as well as PBL-LAK cells. The degree of mLT expression correlated with the killing activity of LAK cells towards L929 cells (r = 0.806, P < 0.01, n = 15), but not with that towards Daudi or K562 cells. Although the degree of mLT expression correlated with the amount of secreted lymphotoxin (LT) in the supernatant of LAK cell culture, the secreted LT itself could not account for the tumor cell killing activity of LAK cells. Polyclonal rabbit anti-LT antibody partially inhibited the killing activities of LAK cells towards L929 cells and this inhibition was found in the combination of autologous tumor cells and PBL-LAK cells. These findings suggest the possibility that the mLT-related cytotoxicity is involved in the tumor cell killing mechanisms of TIL-LAK cells as well as PBL-LAK cells.

Adult↗
PubMed1993

CD3 down-regulating factor in sera and culture supernatants of leukaemic cells from patients with adult T cell leukaemia.

Immunological abnormality of T lymphocytes in patients with adult T cell leukemia (ATL) is characterized by abnormal expression of the 55 kD chain of the receptor for interleukin 2 (IL-2R/p55) (Tac), and the down-regulation of CD3 expression. Using serum and culture supernatants of leukaemic cells from ATL patients (Group A) whose CD3 expression was down-regulated and those (Group B) whose CD3 was not low, the possible mechanism of CD3 down-regulation on ATL cells was discussed. When PBMC from normal individuals were cultured with sera from ATL patients for 24 h, CD3 expression revealed by mean 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 leukaemic cells from ATL patients in Group A, this 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 = 22.9 +/- 5.8, Pt 2 = 28.8 +/- 7.4, control = 92.1 +/- 9.6). This CD3 down-regulating activity in fractionated supernatant was not inhibited by any lymphokine antibodies, anti-IL-1 alpha antibody (Ab), anti-IL-1B Ab, anti-IL-2 Ab, anti-IL-3 Ab, anti-IL-4 Ab, anti-IL-6 Ab, anti-TNF-alpha Ab and anti-IFN-gamma Ab. Any known cytokines (IL-1, IL-2, IL-3, IL-4, IL-6, TNF-alpha and IFN-gamma) could not modulate CD3 expression of normal PBMC. These findings suggested that there are novel factor(s) with CD3 down-regulating activity in the serum and culture supernatant of ATL patient and those factor(s) are involved in progression of ATL.

Adult↗
PubMed1993

Abnormal expression of intercellular adhesion molecule-1 on peripheral blood mononuclear cells from patients with systemic lupus erythematosus.

The expression of intercellular adhesion molecule-1 (ICAM-1) on peripheral blood mononuclear cells (PBMC) from patients with systemic lupus erythematosus was observed by flow cytometry. ICAM-1 expression on PBMC was increased in the patients with active disease, and was increased especially on CD5- or CD19+ lymphocytes and monocytes. Furthermore, when B cells were fractionated by Percoll-density gradients, ICAM-1 was more expressed on the low- and the intermediate-density B cells, which are thought to contain activated B cells, than on the high-density B cells, which are thought to contain resting B cells. This might be due to the polyclonal B-cell activation occurring in vivo. Together with the function of B cells and monocytes as antigen presenting cells, this enhanced expression of ICAM-1 on these cells might be associated with the mechanism to maintain the pathophysiology of this disease.

Adolescent↗
PubMed1993

D1A dopamine receptor stimulation inhibits Na+/K(+)-ATPase activity through protein kinase A.

We stably expressed the rat D1A dopamine receptor in mouse fibroblast LTK- cells and obtained specific ligand binding and functional activity characteristic of the D1A dopamine receptor coupled to stimulation of adenylyl cyclase. In the transfected cells, the selective D1 agonist fenoldopam caused a concentration-dependent inhibition of Na+/K(+)-ATPase activity, achieving maximum inhibition of approximately 30%. The latter was abolished by the selective D1 antagonist (+)-SCH 23390 and by the specific protein kinase A inhibitor protein kinase inhibitor-(6-22) amide. In the nontransfected cells, fenoldopam did not affect Na+/K(+)-ATPase activity. 8-Chlorophenylthio-cAMP inhibited Na+/K(+)-ATPase activity in both transfected and nontransfected cells; this effect was blocked by protein kinase inhibitor-(6-22). These results indicate that the inhibition of Na+/K(+)-ATPase activity induced by agonist occupancy of D1A receptors is mediated by protein kinase A.

Adenylyl Cyclases↗
PubMed1993

[Unrelated match bone marrow transplantation for severe aplastic anemia].

The results of unrelated bone marrow transplantation (BMT) is poor because of the rejection of bone marrow graft and graft versus host disease (GVHD). However, the rate of rejection has been reported to be decreased by intensive immuno-suppressive preconditioning regimens combined with total body irradiation (TBI). We report a case of an 18-year-old male with severe aplastic anemia who received a matched BMT from an unrelated donor. The pre-conditioning regimen included cyclophosphamide (50mg/kg) for 4 days, total lymphoid irradiation (TLI: 6Gy) and TBI (5Gy). GVHD (grade 1), hemorrhage cystitis and varicella occurred after BMT but were cured. His performance status is now 100% on the Karnofsky score at 10 months after BMT.

Adolescent↗
PubMed1993

[Detection of minimal residual clone after sex-mismatched bone marrow transplantation by fluorescent in situ hybridization].

In our previous paper we reported that fluorescent in situ hybridization (FISH) using DYZ1 and DXZ1 was a highly reproducible technique and cellular chimerism consisting of cells of male and female origins could be detected in the order of 0.1%. In the present study FISH was applied to detect minimal residual clones (MRC) in 10 patients with a variety of leukemias who received sex-mismatched bone marrow transplantation (BMT). In 9 patients who had no signs of recurrence, serial FISHs performed on each patient revealed the presence of 0.1 to 3.2% recipient residual clone. On the other hand, in the remaining one patient 10.6% and 16.9% of MRC were found by FISH performed 6 and 10 months after BMT. Immediately thereafter, this patient was diagnosed as in relapse by bone marrow examination.

Adolescent↗
PubMed1993

[Complications and management of hematopoietic malignancy therapy].

Infection and refractoriness to platelet transfusion, as complications in hematopoietic malignancy therapy, were investigated. The Hanshin Study Group of Hematopoietic Disorders and Infection treated with 3,346 cases of bacterial infection (7.8% sepsis, 71% sepsis suspected, 13.7% respiratory infection) during the past 13 years. A total of 688 strains were detected as causative organisms, 59.2% being gram-negative bacilli and 40.3% gram-positive bacteria. Comparison of the detection rates obtained 10 years ago and those obtained in the last three years showed a decrease from 73.8% to 46.8% for gram-negative bacilli and an increase from 25.1% to 53.2% for gram-positive bacteria. Twenty-eight antibiotics administered singly and nine combinations of two drugs administered concomitantly were assessed. Efficacy rates were 43.9% to 67.2% for single-drug administration and 35.2% to 64.2% for concomitant administration. Notably, some combinations were less effective than single-drug administration. Of 153 cases of fungal infection seen in the last three years, 80% were caused by the genus Candida. Two antifungal drugs were used, with efficacy rates ranging from 45.5% to 70.0%. In 150 patients undergoing frequent transfusion, anti-HLA alloantibody was measured. The positive rate was 32.9%. In 76 subjects receiving leukocyte-depleted platelet transfusion using a polyester filter, a decreased alloantibody positive rate of 17.1% was obtained.

Adolescent↗
PubMed1992

Species and sex differences of aflatoxin B1-induced glutathione S-transferase placental form in single hepatocytes.

Species and sex differences of aflatoxin B1 (AFB1)-induced glutathione S-transferase placental form (GST-P) positive single hepatocytes have been investigated 48 h after an intraperitoneal injection of AFB1 to young male and female Fischer rats (2 mg AFB1/kg body wt) and male Syrian golden hamsters (6 mg AFB1/kg body wt). The presence of GST-P positive hepatocytes was examined by the immunohistochemical method. Male rats formed three times as many AFB1-induced GST-P positive hepatocytes as females. Pretreatment of both male and female rats with an inhibitor of GSH synthesis, buthionine sulfoximine (BSO) (4 mmol/kg body wt), 2 h and 4 h before AFB1 injection increased AFB1-induced GST-P positive hepatocytes by about 120% above the controls. Male hamsters formed several-fold less AFB1-induced GST-P positive hepatocytes than male rats. Pretreatment with BSO did not increase AFB1-induced GST-P positive hepatocytes in hamsters even though it produced an increase in hepatic necrosis. It appears that GSH and GSH S-transferases play an important role in modulating hepatic AFB1-DNA binding and AFB1-induced GST-P positive hepatocytes in rats and hamsters.

Aflatoxin B1↗
PubMed1992

Correlation between killing activity towards the murine L929 cell line and expression of membrane-associated lymphotoxin-related molecule of human lymphokine-activated killer cells.

Human lymphokine-activated killer (LAK) cells expressed a membrane-associated lymphotoxin-related molecule (mLT) which was detected by flow cytometric analysis with anti-lymphotoxin antibody. Upon removal of exogenous interleukin-2 from LAK cell culture medium and another 24 h cultivation, the expression of mLT was decreased. Corresponding to the decrease of mLT expression, the killing activity of LAK cells towards L929 cells was remarkably reduced and killing of MIA PaCa-2 and U937 cells was moderately reduced, whereas killing of Daudi and K562 cells was fully restored. The supernatant of mLT-expressing LAK cells had no cytotoxic activity towards L929 cells in the absence of actinomycin D. Moreover, not only the killing of L929 cells but also that of human tumor cell lines (MIA PaCa-2, U937) by mLT-expressing LAK cells was partially inhibited in the presence of anti-lymphotoxin antibody. These results suggest an involvement of mLT in the killing of some tumor target cells by LAK cells.

Animals↗