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Biomedical subjects

H Konno

Publications and source records attributed to H Konno.

At least 163 records · Page 9Linked to original sources
PubMed1991

Advanced gastric cancer associated with acute myelocytic leukemia--report of a case.

A case of advanced gastric cancer associated with acute myelocytic leukemia (AML) is reported. Synchronous double malignancies of gastric cancer and AML are very rare. Combination chemotherapy (BHAC-DMP) was used as the method for induction and consolidation therapy for AML and a complete remission was obtained. However, it failed to show any therapeutic effect on the gastric cancer. A radical subtotal gastrectomy was performed with lymphadenectomy. During the postoperative course, both respiratory failure and severe thrombocytopenia progressed. Fortunately, the patient responded well to mechanical ventilation and the administration of heparin. She was discharged on day 52 after surgery, and no sign of recurrence of either gastric cancer or AML has been observed over the one-year period following the gastrectomy. In principle, in order to achieve a good prognosis, a radical resection should be carried out for gastric cancer associated with AML. However, chemotherapy for AML might make the patient vulnerable to surgical stress, although we could not demonstrate any concrete evidence which could prove the impairment of host immunity in this case. It is, therefore, possible that not only the relapse of AML but also the impairment of host immunity may cause some other difficulties during the post-gastrectomy course.

Aged↗
PubMed1991

Reoxygenation injury following anoxic perfusion preferentially impairs bile acid-independent bile flow.

We perfused isolated rat livers with Krebs-Ringer buffer, with no recirculation. Bile flow virtually stopped during 30 min of anoxia and resumed following reoxygenation to reach a plateau of 44% of the control level. When taurodehydrocholic acid (TDHC, 50 nmol/min/g liver) was administered during reoxygenation, bile flow increased three-fold (16.1 +/- 1.3 to 45.3 +/- 6.3 microliters/g liver). The increase in bile output with TDHC was 27.8 microliters/g liver, which was 89% of the control output. Bile acid output during this period was 1.4 mumol/g liver, which was 93% of the control level. Addition of allopurinol (50 nmol/min/g liver) without TDHC increased bile flow significantly (16.1 +/- 1.3 to 21.3 +/- 1.2 microliters/g liver), but the change was not significant when allopurinol and TDHC were given. The addition of allopurinol also reduced the cumulative release of lactate dehydrogenase from the liver during the reoxygenation period, but had no effect on hepatic adenosine triphosphate levels. Our data suggest that the bile acid-independent bile flow is sensitive to reoxygenation injury following anoxia whereas bile acid output and bile acid-dependent bile flow are resistant.

Adenosine Triphosphate↗
PubMed1990

Intraneuronal laminin-like immunoreactivity in the human central nervous system.

Because laminin possesses potent neurotrophic activity, laminin-like immunoreactivity was investigated in formalin-fixed human brains, using affinity-purified anti-human placental laminin rabbit serum. Distinct laminin-like immunoreactivity was observed in neuronal soma of certain nuclear groups, and a 180-kDa band was noted in an immunoblot study of the supernatant of brain homogenate. These observations imply that many but not all central neurons have laminin-like immunoreactive molecules. Their functional role, however, remains to be clarified.

Autopsy↗
PubMed1990

Targeting of adoptively transferred experimental allergic encephalitis lesion at the sites of wallerian degeneration.

To clarify the implication of the major histocompatibility complex class II (Ia) antigen induction in microglia following Wallerian degeneration in the central nervous system (CNS), experimental allergic encephalitis (EAE) was adoptively transferred to Lewis rats in which Ia antigens had been induced in microglia at the sites of Wallerian degeneration. In addition to randomly distributed typical EAE lesions, the recipient rats developed distinct inflammatory lesions in accord with the distribution of Ia-positive microglia; i.e., in the ipsilateral thalamus after cortical cryoinjury, and in the ipsilateral optic nerve, the contralateral optic tract and superior colliculus after unilateral eye ball enucleation. Thus, the EAE locus may be targeted by this approach. The inflammatory response was inducible by transfer of myelin basic protein-stimulated lymphocytes but not by transfer of phytohemagglutinin-stimulated or non-stimulated lymphocytes. When examined using monoclonal antibody surface markers; OX-6 for Ia antigen, W3/13 for pan T lymphocyte and OX-8 for cytotoxic/suppresser T lymphocyte, the types of lymphocytes in these lesions did not differ from those in ordinary EAE lesions in the spinal cord. The potential role of non-immunologically induced Ia-positive cell clusters that serve as a target for autoimmune CNS diseases was discussed.

Animals↗
PubMed1990

Cytotropism of Theiler's murine encephalomyelitis viruses in oligodendrocyte-enriched cultures.

The cytotropism of two strains, GDVII and DA, of Theiler's murine encephalomyelitis viruses (TMEV) was studied in the oligodendrocyte-enriched murine neural cell cultures. Both GDVII and DA caused cytopathic effects in the neural cell cultures, and double immunostaining for galactocerebroside (Gal-Cer), a marker molecule for oligodendrocyte, and viral antigens disclosed a dual expression of Gal-Cer and viral antigens in over 80% of cells in both cultures 24 h after infection with either GDVII or DA. The kinetics of cell-free and cell-associated infectivity were not significantly different between two cultures. These in vitro observations suggest that neither replication in oligodendrocyte nor cell-associated infectivity is a sole factor in discriminating those two subgroups of TMEV with regard to the demyelinating activity, and that virus cell binding may play an important role in virus persistence and TMEV-induced demyelination.

Animals↗
PubMed1990

The antitumor effects of adriamycin entrapped in liposomes on lymph node metastases.

Adriamycin (ADM) entrapped in liposomes (Lip-ADM) was prepared and its therapeutic effects studied using the mouse leukemia cell line, P388, which metastasized to axillary lymph nodes after inoculation into the foot pads of CDF1 mice. Lip-ADM injections (7.5 mg/kg) were given into the foot pad at two-day intervals. Two series of experiments were performed; one in which Lip-ADM was administered on days 1,3 and 5 following tumor inoculation, and the other in which it was administered on days 5 and 7. Both Lip-ADM injection regimens significantly inhibited metastases to the lymph nodes as compared with mice given injection of saline solution. Furthermore, the therapeutic effects of three Lip-ADM injections were significantly greater than the effects of free ADM. Histological examinations of lymph nodes revealed that three injections of Lip-ADM completely eliminated tumor cells, whereas viable tumor cells were still observed in the lymph nodes after treatment with free ADM. The results of this study suggest that Lip-ADM is useful for the treatment of lymph nodes metastases and that the local injection of Lip-ADM, through such means as endoscopy, would be recommended as a clinical mode of application.

Animals↗
PubMed1989

Ia-expressing microglial cells in experimental allergic encephalomyelitis in rats.

Monoclonal antibodies (MRC OX-6 and OX-17) recognized three types of cells expressing Ia antigen during the course of acute experimental allergic encephalomyelitis (EAE) in rats. In earlier stages of the disease, in animals with or without paralysis, Ia antigens were mostly localized to subarachnoidal and perivascular lymphocytic and histiocytic cell infiltrates, possibly serving as antigen-presenting cells. On the other hand, in convalescent rats, Ia antigens were expressed in a large number of cells with dendritic processes heavily populating the spinal gray matter. The appearance of these Ia-expressing cells in the convalescent stage coincided with the development of degenerating axon terminals in the spinal gray matter. These Ia-expressing cells possessed morphological features characteristic of microglia and were positive for ML-1 lectin but did not express glial fibrillary acidic protein. Immune electron microscopy disclosed the presence of Ia reaction products in the Golgi apparatus, endoplasmic reticulum and plasma membrane of these cells with dendritic processes, indicating active synthesis of Ia molecules in microglia. In addition, Ia antigens were localized to the cells with ultrastructural features of macrophages. Thus, Ia-expressing cells in EAE seems to play dual roles: the induction of immunological reactions during earlier stages and the participation in reparative processes during convalescence.

Animals↗
PubMed1989

Astrocytic pathology of methionine sulfoximine-induced encephalopathy.

To investigate the roles imposed on astrocytes for glutamate metabolism, a specific inhibitor of glutamine synthetase (GS), methionine sulfoximine (MSO), was repeatedly administered to rats and histopathological changes were correlated with glycogen accumulation and the immunocytochemistry of GS and glial fibrillary acidic protein (GFAP). Prolonged MSO-loading (every 12 h up to three times, 100-150 mg/kg body weight) brought about the appearance of astrocytes with swollen, watery nuclei reminiscent of Alzheimer II glia chiefly in the neocortex, hippocampus and lateral thalamus after 24 h. Concomitantly, profound accumulation of glycogen ensued in the superficial three layers of the neocortex, hippocampus and pyriform cortex. GS immunoreactivity appeared enhanced in the cortex, hippocampus and lateral thalamus with parallel increase in GFAP immunoreactivity after prolonged treatment. Oligodendrocytes in the diencephalon and brain stem also normally contained GS immunoreactivity. Some animals developed necrotic lesions in the dorsolateral neocortex. The area of glycogen accumulation coincided with the known distribution of N-methyl D-aspartate (NMDA) glutamate receptors and, thus, GS may play important roles in NMDA receptor-mediated glutamate metabolism. The Alzheimer II type changes, however, did not correlate with NMDA-receptor distribution. These results indicate certain regionalizations in the roles of astrocytes and oligodendrocytes in glutamate and ammonia metabolisms.

Ammonia↗
PubMed1989

Forebrain ischemia induced by temporary bilateral common carotid occlusion in normotensive rats.

Ischemic brain lesions were induced in adult Wistar and Fischer rats by temporary occlusion of the bilateral common carotid artery. The severity of ischemic lesions depended on the duration of carotid occlusion. While 2 h occlusion resulted in 15 deaths among 40 rats and the development of ischemic lesions in 16 of 25 asymptomatic survivors, none died after 0.5 h occlusion and yet 13 of 30 apparently asymptomatic rats had ischemic lesions when examined on day 7. Histological examination combined with immunohistochemistry of autologous albumin for assessing the integrity of the blood-brain barrier (BBB) revealed two distinct lesions: (1) ischemic neural damage with extensive tissue permeation of serum albumin, (2) death of individual neurons sparing other neural elements in the absence of the BBB breakdown. Ischemic neural damage with BBB breakdown was common in animals dying within 48 h after reflow. The lesions without BBB breakdown, on the other hand, were found solely in asymptomatic animals in which groups of severely degenerated neurons were preferentially located in the CA 1 region of the hippocampus, the caudoputamen and deeper layers of the neocortex. The sequential measurements of regional cerebral blood flow (rCBF) in the bilateral hippocampus by the hydrogen clearance method disclosed a steady decrease in rCBF after the occlusion, 51% of the pre-occlusion state at 10 min, 35% at 25 min and 32% at 40 min. The simplicity of procedure could make this model suitable for the study of the pathogenesis of ischemic neuronal damage in a critically low perfusion state.

Animals↗
PubMed1989

Neurotoxic activity in HTLV-I carrier lymphocyte culture.

A close association between human T-lymphotropic virus type I (HTLV-I) infection and a group of chronic myelopathies of unknown etiology has recently been established and the name "HTLV-I associated myelopathy" (HAM) has been coined. Although the mechanism of neural tissue damage in HAM remains virtually unknown, several lines of evidence suggest the involvement of a soluble factor(s) including cytokines and viral proteins in the disease process. In this study, we examined cytopathic effects of the supernatants from 6 HTLV-I carrier human T lymphocyte cell lines on 4 human and one murine neuroblastoma cell lines, and 2 human glioma cell lines. Among 6 lymphocyte cell culture supernatants, only 1 from MT-2 cell culture repeatedly exerted cytopathic effects on human neuroblastoma cells, particularly on IMR-32 cells: marked retraction of neurites leading to cellular clumping. This activity was neither abolished by treatment of the medium at 80 degrees C for 30 min or by UV-irradiation, nor was it neutralized by anti-HTLV-I antibodies. The MT-2 supernatant also induced mild cytopathic changes in 2 other human neuroblastoma cell lines and 2 human glioma cell lines. This activity was abolished by treatment of the medium at 80 degrees C for 30 min but not at 56 degrees C for 30 min. Myelinated murine cerebellum explants and other cell lines showed no morphological changes when incubated with the MT-2 supernatant. In addition, the growth of THP-1 cells, a monocyte/macrophage lineage cell line, was remarkably suppressed when maintained in the MT-2 conditioned medium, accompanied by enhancement of phagocytic activity. The THP-1 conditioned medium, on the other hand, suppressed tumor necrosis factor (TNF) activity detected in the MT-2 culture. These observations suggest that HTLV-I induced cytokines may directly act on neural cells, but their action appears to be regulated by the intricate interactions of lymphocytic and monocytic cells.

Animals↗
PubMed1989

Wallerian degeneration induces Ia-antigen expression in the rat brain.

Strong expression of class II major histocompatibility (MHC II, Ia) antigens was observed in areas of Wallerian degeneration following either a cryoinjury to the cerebral and cerebellar cortex or unilateral eye enucleation in adult Wistar and Lewis rats. The Wallerian degeneration was disclosed by the Fink-Heimer method but not by routine histological examination. The Ia antigens were localized exclusively to the cells labeled with OX-42 antibody and mistletoe-1 lectin (ML-1) and possessing the morphological identity of microglia. Development of Ia-expressing microglia at the sites of Wallerian degeneration was accompanied by neither tissue permeation of serum components as assessed by immunohistochemistry for autologous albumin nor tissue migration of hematogenous inflammatory cells.

Animals↗
PubMed1989

[Importance of the conjugated antibody for the induction of selective effect of adriamycin conjugated with anti AFP monoclonal antibody and entrapped in liposomes against AFP producing tumors].

We investigated experimentally the effect of adriamycin (ADM) conjugated with anti alpha-fetoprotein (AFP) monoclonal antibodies and entrapped in liposomes (Lip-ADM = AbAFP) in vitro or in vivo. In the present study, we examined the importance of the conjugated antibody for the induction of selective therapeutic effect of Lip-ADM = AbAFP against AFP producing tumors. As the target tumors, AFP producing human hepatoma strain, Li-7, and AFP non-producing human breast cancer strain, MX-1 maintained in BALB/c nu/nu male mice were used. In order to evaluate the importance of the conjugated antibody, we prepared also ADM conjugated with normal mouse IgG, and entrapped in liposomes Lip-ADM = NIgG, of which therapeutic effects were compared with that of Lip-ADM = AbAFP. Judging from the tumor growth curve and the tumor weight, the therapeutic effect of Lip-ADM = AbAFP was greater against Li-7 than that of Lip-ADM = NIgG. On the other hand, both conjugates showed similar effects against MX-1. As the results it is suggested that the antibody which recognizes the antigen expressed on the target tumor cells can solely increase the therapeutic effect of ADM entrapped in liposomes (Lip-ADM) and that the main factors which contribute to the efficient therapeutic effect of the conjugate were the sensitibility to ADM, the affinity of the tumor cells to liposomes and the superiority of the conjugated antibody.

Animals↗
PubMed1989

[Antitumor effect of IL-2 entrapped in liposomes on rat hepatoma, AH-66].

The human recombinant interleukin 2 (IL-2) was entrapped in liposomes, and the therapeutic effects of the liposomes containing IL-2 (Lip-IL-2) were experimentally studied using the rat hepatoma strain, AH-66, maintained in donryu rats and challenged subcutaneously in the inguinal region. The peri-tumor injections of Lip-IL-2 (15 X 10(4)/kg units for the IL-2 dose) significantly inhibited the tumor growth as determined from the relative mean tumor weight, although no therapeutic effects were observed when the unentrapped IL-2 or liposomes containing saline was administered rats in the same way as the injections of Lip-IL-2. They also prolonged the survival time of rats. The studies of serum IL-2 values after i.v. or s.c. injections of Lip-IL-2 revealed that IL-2 was released gradually from the liposomes containing IL-2 into the circulation. As the result of the tumor tissue staining of the immunoperoxidase 18 hrs after the peri-tumor injection of IL-2, it was shown that a number of macrophages infiltrated into the tumor tissue and degenerated tumor cells were observed adjacent to those macrophages. It is suggested that Lip-IL-2 is useful as an antineoplastic agent in the immunotherapy and that the therapeutic effects of Lip-IL-2 would be related to both the slow release of IL-2 and the cytotoxicity on the tumor cells mediated by the macrophages.

Animals↗
PubMed1989

[Hemorrhagic gastric ulcer associated with consumption coagulopathy in the dissecting aortic aneurysm--a case report].

A case of the hemorrhagic gastric ulcer and post-operative stomal ulcer associated with the consumption coagulopathy in the dissecting aortic aneurysm is presented. A 68 year old man, who had diagnosed as having the dissecting aortic aneurysm (DeBakey III) in 1985 and had been attending to our hospital as an outpatient since then, was admitted to our hospital because of the hemorrhagic gastric ulcer on July 3rd, 1987. Although the wide resection of stomach was performed after the admission, the hemorrhagic stomal ulcer was developed 4 weeks after the operation. The administration of heparin in addition to antacids to improve the consumption coagulopathy, having been caused by thrombus formation in the aneurysm, was effective in control of the hemorrhage and also making the stomal ulcer scarred. It is suggested that ischemia of the stomach mucosa, which seemed to have been induced by the dissecting aortic aneurysm, was responsible for the development of the ulcers in this case and the hemorrhage from them was caused mainly by the consumption coagulopathy derived from thrombus formation in the aneurysm.

Aged↗
PubMed1988

Intraneuronal laminin-like molecule in the central nervous system: demonstration of its unique differential distribution.

Laminin, an extracellular matrix glycoprotein rich in basement membrane, is a multifunctional molecule of approximately 1000 kDa and is known to possess a potent neurotrophic activity. Laminin-like immunoreactivity (LLI) was for the first time demonstrated in mouse and rat CNS neurons by a sensitive immunohistochemical technique. Transblotting of SDS-PAGE of the supernatant of the mouse and rat brain homogenate identified distinct 180 kDa and weak 380 kDa bands immunoreactive to anti-laminin and these molecules differed from authentic laminin subunits. The intraneuronal distribution of LLI disclosed two distinct patterns; LLI-1 (diffuse perikaryal stain) and LLI-2 (coarse granular stain). By immunoelectron microscopy, LLI was localized to the ERs in LLI-1 neurons, whereas it appeared to be confined to lysosomes in LLI-2 neurons. LLI-1 neurons were found predominantly in hippocampal pyramidal, granule and neocortical layers 1-3, 6 neurons, in most of the striatal and thalamic neurons, and Purkinje cells. The majority of neurons in neocortical layers 4-5, medial septal and Meynert neurons, somatic motor neurons, and neurons of the deep cerebellar nuclei were classified as LLI-2 cells. No LLI was found in hypothalamic mammillary, habenular and vagal dorsal motor neurons (LLI-3). These observations may indicate intraneuronal production of laminin-related molecules in central neurons. We speculate that the laminin-related molecules (neurolaminin) play important roles in trophic or servo mechanisms in the CNS.

Brain↗