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Biomedical subjects

T Koike

Publications and source records attributed to T Koike.

At least 469 records · Page 26Linked to original sources
PubMed1994

beta 2-Glycoprotein I reactivity of monoclonal anticardiolipin antibodies from patients with the antiphospholipid syndrome.

OBJECTIVE: To elucidate the specificity of anticardiolipin antibodies (aCL) from patients with the antiphospholipid syndrome (APS) to various phospholipids (PLs), DNA, and beta 2-glycoprotein I (beta 2-GPI). METHODS: Five monoclonal aCL were established from peripheral blood lymphocytes of 3 patients with the APS. The reactivity of monoclonal aCL with various PLs, with DNA, and with beta 2-GPI was examined by enzyme-linked immunosorbent assay (ELISA). RESULTS: All of the monoclonal aCL bound to anionic PLs, only in the presence of beta 2-GPI. Neither monoclonal aCL nor beta 2-GPI bound to DNA. Monoclonal aCL bound to solid-phase beta 2-GPI on polystyrene ELISA plates that had carboxyl groups on their surface, but did not react with solid-phase beta 2-GPI on ordinary polystyrene plates. A mixture of beta 2-GPI and CL inhibited the binding of monoclonal aCL to beta 2-GPI, but CL or beta 2-GPI alone did not. CONCLUSION: Monoclonal aCL may recognize a cryptic epitope, which appears as a result of beta 2-GPI binding to anionic PLs or to polystyrene with carboxyl groups.

Adult↗
PubMed1994

Induction of apoptosis by a dominant negative H-RAS mutant (116Y) in K562 cells.

Recent extensive work on apoptosis has begun to reveal its molecular mechanisms. Several genes that regulate apoptosis have been identified. Among them, the BCL2 gene is considered to be an important gene that inhibits apoptosis. However, there must be other genes, yet to be identified, which suppress apoptosis. It has been suggested that the activation of RAS function by BCR-ABL fusion protein in chronic myelogenous leukemia may be an important mechanism in the BCR-ABL mediated transformation. Therefore, in this study we have investigated whether the suppression of endogenous H-RAS function inhibits the BCR-ABL mediated transforming activity in a K562 human chronic myelogenous leukemia cell line. The induced expression of a dominant negative v-H-RAS mutant (116Y) in K562 cells has resulted in cell death. The morphological characteristics and the detection of fragmented DNA by gel electrophoresis in the dead cells have revealed that this cell death is apoptosis. These results directly indicate that the RAS gene as well as the BCL2 gene has an ability to suppress apoptosis.

Apoptosis↗
PubMed1994

Cerebral haemodynamic changes after endovascular treatment of arteriovenous malformations: evaluation by single-photon emission CT.

Cerebral haemodynamic changes in 17 patients with cerebral arteriovenous malformations (AVMs), who showed hypoperfusion on single-photon emission computed tomography (SPECT) before endovascular treatment, were studied after embolization. Nine of them had non-haemorrhagic clinical manifestations and the other eight had a history of intracranial haemorrhage. Obliteration of AVMs was nearly total in six patients and partial in eleven. New low density lesions on X-ray computed tomography (CT) developed in 3 of 6 patients after nearly total obliteration and one of 11 patients after partial obliteration. The first SPECT after embolization showed diminished hypoperfusion in 11 of 13 patients without new low density lesions and one of 4 patients with new low density lesions. Diminution of hypoperfusion was seen even in two patients who underwent SPECT study immediately after the embolization. Cerebral circulation was improved in five of eight patients with low density lesions before embolization and in nine of eleven patients after partial obliteration. Hypoperfused state in the haemorrhagic group tended to remain unchanged compared with that in the non-haemorrhagic group. The hypoperfused area was expanded after embolization in three patients with new cerebral infarction. It is important for improvement of cerebral circulation to reduce the shunt flow without causing new infarction due to the embolization itself. In one of two patients who had a hyperperfused area surrounding the AVM after embolization, an unexpected and abnormal degree of brain swelling and haemorrhage occurred at the end of the surgery 20 days after the embolization. In the other patient, total extirpation was successfully performed after confirming disappearance of hyperperfusion in the follow-up SPECT.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1994

Vasoactive intestinal peptide suppresses neuronal cell death induced by nerve growth factor deprivation in rat sympathetic ganglion cells in vitro.

Neuropeptides were examined for their effects on the survival of cultured rat superior cervical ganglion cells after acute deprivation of nerve growth factor (NGF). Vasoactive intestinal peptide (VIP, 3 microM) delayed the neuronal death about 6 h alone. The phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (0.2 mM) greatly potentiated its effect, reducing EC50 from 2.5 microM to 8 nM. The neuronal death was completely suppressed under this condition. On the other hand, substance P (1-100 microM) or enkephalin (1-100 microM) alone did not modify the death, whereas the latter (100 microM) enhanced the survival-promoting effect of membrane depolarization with elevated K+. These results suggest strongly that neuropeptides regulate the NGF-independent survival of sympathetic neurons through a cAMP-dependent mechanism.

1-Methyl-3-isobutylxanthine↗
PubMed1994

Prevention of insulitis and diabetes in beta 2-microglobulin-deficient non-obese diabetic mice.

beta 2-Microglobulin (beta 2m)-deficient non-obese diabetic (NOD) mice were established by crossing beta 2m-deficient 129/Sv mice with NOD mice, and used to examine the possible involvement of MHC class I molecules and CD8+ T cells in the development of insulitis and diabetes. In these mice, MHC class I molecules were not expressed, resulting in no generation of CD8+ T cells. None of eight lines of beta 2m-deficient NOD mice (-/-) established developed overt diabetes by 32 weeks, while control littermates (+/+) became diabetic by 22 weeks. histological studies showed no significant lymphocyte infiltration of the islets (insulitis score: 0.03 +/- 0.03) in any of the beta 2m-deficient NOD mice (-/-) compared with littermate NOD mice (+/+) with overt insulitis (1.42 +/- 0.28). These findings support the notion that the expression of MHC class I molecules and/or CD8+ T cells plays an essential role in the infiltration of CD4+ T cells in islets as well as the development of diabetes in NOD mice.

Animals↗
PubMed1994

Recombinant human interleukin-4 inhibits the production of granulocyte-macrophage colony stimulating factor by blood mononuclear cells.

The effect of recombinant human (rh) interleukin-4 (rIL-4) on human blood BFU-E was investigated using two populations of cells: platelet-depleted low-density mononuclear cells (FH,Pl- cells), as unpurified cells, and highly purified BFU-E. When FH,Pl- cells were cultured with rh-erythropoietin (rEp), rIL-4 inhibited BFU-E growth in a dose-dependent manner. However, the addition of rIL-4 did not affect rh-interleukin-3 (rIL-3) supported BFU-E growth. Limiting dilution analysis (LDA) of FH,Pl- cells showed that rIL-4 suppressed endogenous production of burst-promoting activity (BPA) by accessory cells. Highly purified BFU-E were used as target cells to measure BPA in the conditioned medium (CM) that was prepared by FH,Pl- cells. When 100 purified BFU-E were cultured in 0.5 ml clots with 20% (vol/vol) of the CM, the number of BFU-E colonies was increased by the CM. The increase was significantly reduced by the addition of the CM prepared in the presence of rIL-4, but anti-IL-4 blocked the effect of rIL-4. The concentration of IL-3 and granulocyte-macrophage colony-stimulating factor (GM-CSF) in CM was determined by an enzyme-linked immunoadsorbent assay (ELISA). The spontaneous production of GM-CSF but not IL-3 was detected, and this was significantly decreased in the presence of rIL-4. Anti-GM-CSF but not anti-IL-3 inhibited CM supported BFU-E growth, indicating that the main BPA in the CM is GM-CSF and that rIL-4 suppresses the spontaneous production of GM-CSF by accessory cells. From these studies, we conclude that rIL-4 has a unique mechanism as a negative regulator on erythropoiesis through the inhibition of BPA production by blood mononuclear accessory cells.

Adult↗
PubMed1994

Serial changes in hemostasis after intracranial surgery.

We performed hemostatic studies on eight patients undergoing clipping of unruptured cerebral aneurysms to assess the influence of intracranial surgery itself on hemostasis. Blood samples were collected from each patient 10 times: before and after the induction of anesthesia and 6, 12, and 24 hours and 2, 3, 5, and 7 days immediately after surgery. The changes and our interpretation of them include the following: 1) the elevation of thrombin antithrombin III complex levels (activation of blood coagulation) was transient and monophasic; 2) the elevation of plasmin alpha 2-antiplasmin complex and D-dimer levels (activation of fibrinolysis) was biphasic, despite the monophasic elevation of tissue plasminogen activator or plasminogen activator inhibitor-1 levels; 3) the elevation of beta-thromboglobulin and platelet-factor-4 levels (activation of platelet) was also biphasic; 4) fibrinogen level and alpha 2-antiplasmin activity increased in the acute phase of the postoperative course (acute phase reaction); 5) the changes in hematocrit appeared to parallel those in various other parameters, especially platelet count, antithrombin III, and plasminogen levels for 1 or 2 days after surgery; 6) fibronectin appeared to be consumed in the acute phase of postoperative course; and 7) general anesthesia did not significantly affect hemostasis. These serial changes seem to be related to the activation of hemostatic systems after intracranial surgery and the subsequent acute phase reaction.

Acute-Phase Reaction↗
PubMed1994

Liver dysfunction in spontaneous intracerebral hemorrhage.

The purpose of this study was to investigate the relationship between mild degrees of liver dysfunction and spontaneous intracerebral hemorrhage (ICH) from the hemostatic standpoint. A detailed study of hemostatic systems was made in 462 patients with ICH. To compare ICH with the other cerebrovascular diseases, data from 120 patients with subarachnoid hemorrhage and 114 others with cerebral infarction were reviewed. At admission, the medical histories of the patients, including information about previous alcohol consumption, was taken, and blood samples were collected to perform the following studies: platelet count, fibrinogen level, prothrombin time, activated partial thromboplastin time, antithrombin III, plasminogen and alpha 2-antiplasmin activity, platelet aggregability, and liver function tests. The incidence of liver dysfunction and alcohol consumption in patients with ICH was significantly (P < 0.05) higher than in patients with subarachnoid hemorrhage and in those with cerebral infarction. Hematoma volume, mortality rate, and past alcohol consumption in patients with ICH significantly increased with worsening severity of liver dysfunction. Although almost all hemostatic parameters became worse with increasing severity of liver dysfunction, they changed within the normal limits. Platelet aggregability and alpha 2-antiplasmin activity in patients with liver dysfunction were remarkably deteriorated beyond normal limits. In conclusion, liver dysfunction associated with alcohol consumption appears to be an important factor in the deterioration of the clinical status of patients with ICH and may be one of the causative factors in the development of ICH. Although mildly impaired hemostatic systems may be partially responsible for these adverse effects of liver dysfunction on ICH, it seems probable that nonhemostatic mechanisms are attributed to the effects.

Adult↗
PubMed1994

Inhibition of human immunodeficiency virus proliferation by macrocyclic polyamines and their metal complexes.

The macrocyclic polyamines, cyclen and cyclam, and their derivatives have been tested for inhibitory activity against the cytopathogenic effect (CPE) of human immunodeficiency virus type 1 strain HTLV-IIIB (HIV-1IIIB) on CD4+ human lymphoblastoma MT-4 cells. Cyclam and its derivatives were complexed with a variety of transition metal ions NiII, ZnII, CuII, FeIII and CoIII. The divalent metal complexes effected lower toxicity and greater anti-HIV-1 activity, while the trivalent metal complexes had no effect on HIV-1-dependent CPE. When dimerized, the anti-HIV activity of monomers was significantly enhanced. A potent inhibition of CPE by biscyclam was transiently observed 4 d after the virus infection, but was not seen at 6 d due to severe toxicity. The toxicity of biscyclam, referred to as delayed toxicity, could be overcome by a metal complexation. The strain specificities of biscyclams were further studied by testing their effects on syncytium formation between HIV-infected and uninfected human acute lymphoblastic leukemia MOLT-4 cells. The 50% inhibitory concentrations of biscyclams against HIV-2GH-1-dependent syncytium formation were less than one hundredth those for the other HIV strains (HIV-1IIIB, HIV-1RF and HIV-1SF-2).

Cations, Divalent↗
PubMed1994

Effect of hypoxia on proliferation of microvascular endothelial cells derived from Mongolian gerbil brain.

This study investigated the effect of hypoxia on the proliferation of microvascular endothelial cells in the brain. Endothelial cells derived from microvessels of Mongolian gerbil brain and control cells (3T3) were incubated for 7 days under various hypoxic and normoxic conditions at 37 degrees C. The proliferation of endothelial cells was inhibited by severe hypoxia, but stimulated by moderate hypoxia. No significant effect of hypoxia on the proliferation of control cells was observed. Endothelial cell-conditioned medium cultured under moderate hypoxia did not affect the growth of endothelial cells. The stimulatory effect of moderate hypoxia on the proliferation of cultured endothelial cells is due to an inherent property of brain endothelial cells.

Animals↗
PubMed1994

Hematoma enlargement in spontaneous intracerebral hemorrhage.

In order to evaluate the incidence and risk factors of hematoma enlargement in spontaneous intracerebral hemorrhage (ICH), 419 cases of ICH were reviewed. The first computerized tomography (CT) scan was performed within 24 hours of onset and the second within 24 hours of admission; a blood sample was taken for laboratory examination within 1 hour of admission. In 60 patients (14.3%) the second CT scan showed an enlarged hematoma. The incidence of enlargement significantly decreased with time (p < 0.05) and significantly increased with the severity of liver dysfunction and the volume of the hematoma on the first CT scan. Patients with an irregularly shaped hematoma had a higher risk of hematoma growth than those with a round hematoma. In addition, patients with hematoma enlargement were more likely to have coagulation abnormalities (low platelet counts and low levels of fibrinogen, alpha 2-antiplasmin activity and platelet aggregation). Moreover, hematoma growth was associated with a poor clinical outcome. It is concluded that patients admitted to a hospital within 6 hours of onset of ICH, especially those admitted within 2 hours, and patients with liver dysfunction or irregularly shaped large hematomas should be closely observed for at least 6 hours after onset in preparation for emergency surgery, since the risk of hematoma growth in these circumstances is high.

Adult↗
PubMed1994

[Development of a three-dimensional impedance meter and its clinical applicability to diagnosing middle ear diseases].

An impedance meter (IM) is well known to be a valuable apparatus for the diagnosis of secretory otitis media (SOM). However, it is insufficient for the diagnosis of ossicular chain disorders, because the probe tone is limited to one or two frequencies. Therefore, we developed a new IM, with sweeping functions for both frequency and pressure which can display measurement results in a three-dimensional format. In this study, the middle ear dynamic characteristics of normal subjects and patients were measured, and the effects of various kinds of middle ear diseases on these dynamic characteristics were examined. The measurement results of the patients with ossicular chain separation, ossicular chain fixation, SOM, tympanic membrane perforation and tympanic membrane atelectasis showed their own distinctive patterns, and were also clearly different from those of normal subjects. Therefore, it is concluded that this apparatus has a high degree of clinical applicability to the diagnosis of these diseases.

Acoustic Impedance Tests↗
PubMed1994

[The effect of aging on middle ear dynamic characteristics].

The effect of aging on middle ear function has not been investigated thoroughly, as there is no simple measuring apparatus except for the conventional impedance meter (IM). However, the reliability of the IM is insufficient, because the stimulus frequency is fixed and the information provided by the IM is minimal. We have developed a sweep frequency middle ear analyzer (MEA), which provides much more information on middle ear dynamic characteristics than a conventional IM, and have obtained various measurements with this device. In this paper, middle ear dynamic characteristics of 187 normal subjects (309 ears) ranging from a 4-year-old child to an elderly person, 79 years old, were measured with the MEA in the middle ear resonance frequency region where dynamic characteristics can be seen clearly, and the effect of aging on middle ear dynamic characteristics was examined. The main results obtained were as follows: Middle ear mobilities tend to increase up to the twenties, then decrease up to the forties. Subsequently, a clear difference between those of males and females is observed. The middle ear mobilities of males decrease gradually with an increase in age. In contrast, although the standard deviation values are large, those for females tend to rise with increasing age.

Adolescent↗
PubMed1994

A time course study for optimal harvest of peripheral blood progenitor cells by granulocyte colony-stimulating factor in healthy volunteers.

In a search for the optimal method to harvest peripheral blood progenitor cells (PBPC) without myeloablative chemotherapy, we administered recombinant human granulocyte colony-stimulating factor (G-CSF) to adult, healthy volunteers and investigated the mobilization rate of the PBPC. The consecutive subcutaneous administration of G-CSF in a dose of 2 micrograms/kg/d for 5 days significantly increased colony-forming units-granulocyte/macrophage (CFU-GM) up to 2340 +/- 980 per mL whole blood with a 30 +/- 21-fold mobilization of PBPC, range 11- to 76-fold. Burst-forming units-erythroid (BFU-E) and mixed erythroid progenitors (CFU-Mix) were also increased, and the mobilization rate was 8.4 +/- 4.5-fold and 7.6 +/- 4.7-fold, respectively. A time course study of PBPC after final G-CSF injection was done for 0 to 30 hours on days 1, 3, and 5. After a single administration of G-CSF (day 1), there was no increment of PBPC during the subsequent 30 hours, but the white blood cell count (WBC) markedly increased. Three days after the injection of G-CSF, no increase of CFU-GM was seen during the first 2 hours, then a significant, time-dependent increase occurred for up to 30 hours. Five days after the injection of G-CSF, there was no increase of CFU-GM during the first 2 hours, and the significant increase at 24 hours was maintained for up to 30 hours. BFU-E and CFU-Mix showed the same pattern of expansion as seen with CFU-GM. Thus, subcutaneous administration of 2 micrograms/kg/d G-CSF for 5 days will lead to a successful PBPC harvest for transplantation, and the most suitable period for this is 24 to 30 hours after the final G-CSF administration.

Adult↗
PubMed1994

Transitional changes in immunophenotypic subpopulations of human peripheral blood CD34+ cells expanded in vitro.

We determined the appropriate incubation period to expand human peripheral blood (PB) CD34+ cells for clinical application and the role of recombinant human (rh) interleukin-3 (rhIL-3) in the expansion and differentiation of these cells. The cells were purified up to 40 +/- 16% and transitional changes in immunophenotypic subpopulations in suspension culture were examined following stimulation with three different combinations of rh colony-stimulating factors (rhCSFs): 1) rhIL-3 alone, 2) rhIL-6, rhSCF, rhG-CSF, plus rhGM-CSF, and 3) the four CSFs plus rhIL-3. With all three CSF combinations, the total cells increased continuously after day 5 until day 14, and a combination of the five CSFs always gave rise to the highest number of total cells. Immunophenotypic analysis of the expanded cells showed that with all three CSF combinations CD34+ cells reached a maximal rate on day 5 and then decreased in an inverse correlation between the logarithm of CD34 positive rate and the duration of suspension culture. The maximum expansion of CD34+ cells and PB progenitor cells (PBPC) with rhIL-3 alone, the four CSFs, or the five CSFs was observed on day 5, 10, or 7, respectively. The combination of the five CSFs was identified as the most potent stimulus for expansion of PBPC and CD34+ cells, as it increased non-erythroid PBPC 89 +/- 69-fold, with a range of 24 to 204-fold on day 7. However, differences in the expansion rate of these cells on days 5, 7, and 10 were not statistically significant. The majority of purified CD34+ cells coexpressed CD38 (91 +/- 3%) but were negative for CD33 (85 +/- 4%), and one-half coexpressed CD13. With all three combinations of CSFs, the mature CD34+ cells that coexpressed CD38, CD33, or CD13 expanded in parallel with the total CD34+ cells, while an increase in relatively immature CD34+ cells, which do not express CD38, CD33, or CD13, was only statistically significant with the five CSFs. Thus, rhIL-3 played a critical role when combined with the four CSFs by increasing both mature and immature CD34+ cells.

Adult↗
PubMed1994

[Chronic cold agglutinin disease accompanied with an increase of CD20+/CD5+ cells; a case report].

A 61-year-old male complained of acrocyanosis and dark urine when exposing to cold temperatures. This had continued for several years. His physical examinations showed neither lymphadenopathy nor hepatosplenomegaly. Laboratory findings were as follows; RBC 305 x 10(4)/microliters, Hb 10.3 g/dl, reticulocytes 4.32%, platelets 27.3 x 10(4)/microliters, WBC 7,400/microliters with 50% lymphocytes, and a high cold agglutinin titer (2,048-fold) with anti-I specificity. Bone marrow smear preparations showed erythroid hyperplasia and increase of lymphocytes (52%). Immunophenotypic analysis showed an increase of CD20+/B-lymphocytes in peripheral blood (32.6%) and in bone marrow, and 94% of these cells co-expressed CD5. Most B-lymphocytes expressed surface IgM-lambda, suggesting a monoclonal proliferation of B-lymphocytes. At this point we diagnosed cold agglutinin disease (CAD) because there was no evidence of lymphoma, and the absolute number of peripheral blood lymphocytes was lower than the criteria of chronic lymphocytic leukemia (CLL) proposed by the International Workshop (1989). However, there still remains the possibility of the transitional form between "idiopathic" CAD and B-CLL or lymphoma.

Anemia, Hemolytic, Autoimmune↗