Biomedical subjects

R Tanaka

Publications and source records attributed to R Tanaka.

At least 271 records · Page 15Linked to original sources

PubMed1997

Serotyping of Cryptococcus neoformans strains isolated from clinical specimens in Thailand and their susceptibility to various antifungal agents.

One hundred and thirty-nine strains of Cryptococcus neoformans were isolated in Thailand from clinical specimens including 97 AIDS patients: 67 from Northern, 48 from Central, 17 from Northeastern and 7 from Southern regional hospitals. Six out of the 139 strains were serotype B and the remaining 133 were A. There was no correlation between serotypes and regional distribution. To our knowledge, this is the first report of serotyping studies on C. neoformans in Thailand. Studies on random amplified polymorphic DNA (RAPD) analysis showed that this method is useful for the differentiation of C. neoformans var. gattii (serotypes B and C) and C. neoformans var. neoformans (serotypes A and D). They also indicated that Thai isolates of C. neoformans var. gattii (serotype B) were a homogeneous group on the basis of their genotypes. Antifungal susceptibility tests using 5 antifungal agents including amphotericin B, fluconazole, flucytosine, itraconazole and micronazole against 50 selected strains of C. neoformans showed that they were sensitive to all of the antifungal agents tested except for one strain that was resistant to flucytosine.

AIDS-Related Opportunistic Infections↗

PubMed1997

Thrombopoietin alone stimulates the early proliferation and survival of human erythroid, myeloid and multipotential progenitors in serum-free culture.

We examined the effects of recombinant human thrombopoietin (TPO, c-Mpl ligand) on the proliferation and differentiation of human haemopoietic progenitors other than megakaryocytic progenitors using serum-free cultures. TPO alone supported the generation of not only megakaryocytic (MK) but also blast cell (blast) colonies from cord blood CD34+ cells. Delayed addition of a cytokine cocktail (cytokines; interleukin (IL)-3, IL-6, stem cell factor, erythropoietin, granulocyte-macrophage colony-stimulating factor, and TPO) to cultures with TPO alone on day 7 induced various colonies including granulocyte-macrophage (GM) colonies, erythroid bursts (E), granulocyte-erythrocyte-macrophage-megakaryocyte (GEMM) colonies. Replating experiments of blast colonies supported by TPO alone for culture with cytokines revealed that approximately 60% of the blast colonies contained various haemopoietic progenitors. Single cell cultures of clone-sorted CD34+ cells indicated that TPO supported the early proliferation and/or survival of both primitive and committed haemopoietic progenitors. In serum-free suspension cultures, TPO alone significantly stimulated the production of progenitors for MK, GM, E and GEMM colonies as well as long-term culture-initiating cells. These effects were completely abrogated by anti-TPO antibody. These results suggest that TPO is an important cytokine in the early proliferation of human primitive as well as committed haemopoietic progenitors, and in the ex vivo manipulation of human haemopoietic progenitors.

Antigens, CD34↗

PubMed1997

Thrombopoietin-independent effect of interferon-gamma on the proliferation of human megakaryocyte progenitors.

Flow cytometric study revealed that almost all CD34+ cells in human umbilical cord blood expressed interferon-gamma receptor (IFN-gammaR). To clarify the precise functional roles of IFN-gammaR in human CD34+ cells, we examined the effect of IFN-gamma alone and in combination with various cytokines on the growth of haemopoietic progenitor cells in CD34+ cells using a serum-free clonal culture. Surprisingly, IFN-gamma alone supported only megakaryocyte (MK) colonies in a dose-dependent manner with a plateau level at 1000 U/ml of IFN-gamma. IFN-gamma at 1000 U/ml induced 10 +/- 1.2 MK colonies from 1 x 10(3) CD34+ cells, whereas thrombopoietin (TPO), interleukin (IL)-3, stem cell factor (SCF) or IL-6 alone induced 22 +/- 4.0, 22 +/- 4.2, 4 +/- 0.6 and 0 MK colonies, respectively. The addition of anti-IFN-gamma monoclonal antibody (mAb) to the IFN-gamma culture completely abrogated MK colony formation, whereas the mAb had no effect on TPO-dependent production of MK colonies. In contrast, although anti-TPO polyclonal Ab almost completely blocked TPO-dependent MK colony formation, it failed to inhibit the generation of MK colonies induced by IFN-gamma, suggesting that the observed effect of IFN-gamma on the proliferation of human MK progenitor cells is independent of TPO. The addition of IFN-gamma to culture with TPO or SCF significantly augmented the development of MK colonies, whereas it did not affect IL-3-dependent MK colony formation. Additionally, IFN-gamma induced the increase of DNA content of cultured glycoprotein IIb/IIIa-positive megakaryocytes. These results suggest that IFN-gamma may have regulatory roles in human megakaryocytopoiesis.

Antibodies, Monoclonal↗

PubMed1997

B7-1(CD80)-transfected human glioma cells and interleukin-12 directly stimulate allogeneic CD8+ T cells.

To obtain more effective cytotoxic T lymphocytes (CTLs), we examined the effect of B7 costimulation and interleukin-12 (IL-12) on the induction of allogeneic CTLs. Peripheral blood lymphocytes (PBLs) or positively selected human CD8+ T cells (purity > 99%) from healthy donors were used as effector cells, and B7-1-transfected or nontransfected U251 human glioma cells (U251-B7 or U251-Vec.) were used as stimulator cells. In mixed lymphocyte culture (MLC) with PBLs and U251 cells, nonspecific natural killer (NK) activity was raised by addition of IL-12, and the effect of B7 costimulation was not observed. However, in MLC with CD8+ T cells, efficient proliferation, generation of CTLs, and cytokine production were induced by MLC with U251-B7 in the presence of IL-12. Efficient generation of CTLs was not induced by either MLC with U251-B7 alone or the addition of IL-12 alone. Our results indicate that a combination of B7-1 costimulation and IL-12 is effective for inducing generation of CTLs, and that the CD8+ T cells can be differentiated into CTLs without the help of CD4+ T cells or antigen-presenting cells or both.

B7-1 Antigen↗

PubMed1997

Detection of delayed cerebral vasospasm, after rupture of intracranial aneurysms, by magnetic resonance angiography.

OBJECTIVE: The goal of this study was to assess the value of magnetic resonance angiography (MRA), compared with conventional angiography, in the diagnosis and follow-up monitoring of delayed cerebral vasospasm after subarachnoid hemorrhage resulting from rupture of intracranial aneurysms. METHODS: For 32 patients undergoing examination by both MRA and conventional angiography during the period of risk for vasospasm, on the same day, the frequency and severity of and sequential changes in vasospasm were evaluated. The three-dimensional time-of-flight method was used. MRA was performed three times, i.e., before, during, and after the period of risk for vasospasm. Conventional angiography was performed twice, i.e., at admission and during the period of risk for vasospasm. Vasospasm was assessed at 22 regions of the cerebral arteries, including the bilateral anterior cerebral (A1, A2, and A3 segments), middle cerebral (M1, M2, and M3 segments), internal carotid (C1 and C2 segments), posterior cerebral (P1 and P2 segments), and posterior communicating arteries. RESULTS: Seven patients were excluded because of poor MRA images. Twenty-two of 25 patients (125 arteries) showed vasospasm in conventional angiograms. Nineteen of the 22 patients also showed vasospasm in MRA images; however, 57 arteries (45.6%) were diagnosed as showing vasospasm by MRA, and 59 (47.2%) could not be evaluated because of artifacts. For the remaining three patients (nine arteries, 7.2%), vasospasm could not be detected by MRA. Sequential changes in vasospasm could be well evaluated by MRA. CONCLUSION: MRA could be useful for management of cerebral vasospasm, although it cannot become a practical alternative to conventional angiography.

Adult↗

PubMed1997

Mass effect caused by clinically unruptured cerebral arteriovenous malformations.

OBJECTIVE: It is generally considered that mass effect caused by arteriovenous malformations (AVMs) is evidence of ruptures. In the present study, the incidence of mass effect in clinically unruptured AVMs was evaluated, and the underlying causative factors and pathophysiological mechanisms were studied. METHODS: Twenty-seven patients with clinically unruptured supratentorial pial AVMs were examined. The majority were suffering from epilepsy, and frontal lobe involvement was revealed in approximately half of the patients. Angiographic studies, computed tomographic scans, and magnetic resonance images were obtained for all patients. Twenty-one patients underwent removal of AVMs. In 10 of the surgically treated patients, intraoperative vascular pressure measurements were obtained before removal of the AVMs. RESULTS: Mass effect was detected in 12 (44%) of the 27 patients. Cortical sulci obliteration (eight patients) and lateral ventricle displacement (seven patients) were frequently noted. The volume of AVMs was significantly larger in patients with mass effect than in those without mass effect (P < 0.001). Large dilated venous sacs or ectatic veins were observed to be associated with mass effect (P < 0.001). In only one patient was gross displacement related to a surrounding massive brain edema. Draining vein pressure in patients with mass effect was significantly elevated as compared to the average value in patients without mass effect (22 +/- 5 versus 12 +/- 3 mm Hg) (P < 0.01). CONCLUSION: The present study suggests that mass effect is not infrequent in clinically unruptured AVMs. Furthermore, multiple causative factors were detected, including the large size of AVMs, marked draining vein dilatation, and brain edema around the AVMs. Findings also indicated that a pathophysiologically high pressure in the venous drainage system may contribute to mass effect.

Adolescent↗

PubMed1997

Productive and lytic infection of human CD4+ type 1 helper T cells with macrophage-tropic human immunodeficiency virus type 1.

It is generally recognized that macrophage-tropic human immunodeficiency virus type 1 (HIV-1) is the predominant population during the acute and asymptomatic phases of HIV-1 infection. Here, we compared the proliferation and syncytium-inducing activities of different HIV-1 strains in primary CD4+ T cells expressing various helper T (Th)-type cytokine profiles. The macrophage-tropic HIV-1 strains HIV-1JR-CSF, HIV-1NFN-SX, and HIV-1SF162 could proliferate vigorously and generate syncytia in primary CD4+ T cells irrespective of their Th subtype, in contrast to the T-cell-line-tropic HIV-1 strains HIV-1NL4-3 and HIV-1IIIB, which favored non-type 1 Th conditions. These results indicate that macrophage-tropic HIV-1 may be more invasive and virulent, since it kills more CD4+ Th1 cells than T-cell-line-tropic HIV-1 during the early stages of HIV-1 infection, when the Th1 immune response is dominant.

Giant Cells↗

PubMed1997

Mutational analysis of human immunodeficiency virus type 1 (HIV-1) accessory genes: requirement of a site in the nef gene for HIV-1 replication in activated CD4+ T cells in vitro and in vivo.

Human immunodeficiency virus type 1 (HIV-1) accessory genes including nef, vif, and vpr are important factors that determine the replication and pathogenesis of HIV-1. The state of activation is also important for the replication of HIV-1. We evaluated the properties of nef-, vif-, and vpr-minus macrophage-tropic HIV-1(JR) CSF in primary CD4+ Th1- or Th2-like cell cultures which had been activated through CD3 molecules in the presence of interleukin-2 (IL-2) and IL-12 (Th1-like culture) or IL-4 (Th2-like culture), respectively. In activated Th1- or Th2-like cultures, replication of nef-minus HIV-1(JR-CSF) was markedly lower than that of wild-type HIV-1. Subsequent analysis by site-directed mutagenesis showed that (i) the presence of an acidic amino acid-rich domain (amino acid residues 72 to 75) in the Nef protein was critical for the enhancement of viral DNA synthesis, resulting in increased virus growth rate, and (ii) prolines that form part of Src homology 3 binding domain were not essential for viral replication. We also confirmed the importance of sites by using an HIV-1-infected animal model, the hu-PBL-SCID mouse system, representing HIV-1 replication and pathogenesis in activated CD4+ T cells in vivo. These results indicate that Nef accelerates viral replication in activated CD4+ T cells.

Amino Acid Sequence↗

PubMed1997

Primary human immunodeficiency virus type 1 viremia and central nervous system invasion in a novel hu-PBL-immunodeficient mouse strain.

We established four new mouse strains with defective T and B cells as well as defects in innate immunological reactions using an NK cell depletion antibody and showed that all mutant mouse strains efficiently received human peripheral blood leukocyte (PBL) engraftment (hu-PBL-scid mice). Higher levels of human immunodeficiency virus type 1 (HIV-1) replication were observed in these new hu-PBL-scid mice than in conventional hu-PBL-C.B-17-scid mice. In one particular strain, hu-PBL-NOD-scid mice, high levels of HIV-1 viremia (more than 10(6) 50% infectious doses per ml) were detected after infection with HIV-1. The plasma viral load was about 100 to 1,000 times higher than that observed in other hu-PBL-scid mice infected with HIV-1. Although high-level viremia did not correlate with the total amount of HIV-1 RNA in cells from infected mice, high levels of free virions were detected only in hu-PBL-NOD-scid mice. HIV-1 viremia induced systemic HIV-1 infection involving the liver, lungs, and brain. PCR in situ hybridization confirmed that HIV-1-infected cells invaded the brain tissue of the hu-PBL-NOD-scid mice. Our results suggest that the genetic background, including innate immunity, is critical in the development of primary HIV-1 viremia and subsequent central nervous system invasion with HIV-1. The hu-PBL-NOD-scid mouse represents a useful model for the study of the pathogenesis of HIV-1 in vivo, especially brain involvement, and therapy of primary HIV-1 viremia.

Animals↗

PubMed1997

Early administration of Bifidobacterium breve to preterm infants: randomised controlled trial.

AIM: To investigate the colonisation with Bifidobacterium breve of the bowels of very low birthweight (VLBW) infants. METHODS: The adverse effects of B breve were examined in 66 VLBW infants (preliminary study). A prospective randomised clinical study of 91 VLBW infants was also completed and these infants were followed up for three years. Precise viable bacterial counts of serial stool specimens were examined for the first eight weeks after birth in 10 infants. The colonisation rates of administered bacteria were examined using immunohistochemical staining of stool specimens with a B breve specific monoclonal antibody. RESULTS: In the preliminary study there were no side effects attributable to the bacteria. Immunohistochemical staining of stool specimens showed that the colonisation rates of the administered bacteria were 73% at 2 weeks of age, but only 12% in the control group. Early administration of B breve significantly decreased aspirated air volume from the stomach and improved weight gain. CONCLUSIONS: B breve can colonise the immature bowel very effectively and is associated with fewer abnormal abdominal signs and better weight gain in VLBW infants, probably as a result of stabilisation of their intestinal flora and accelerated feeding schedules.

Bifidobacterium↗

PubMed1997

Fruiting-inducing activity and antifungal properties of lipid components in members of Annelida.

Fruiting-inducing activity and antifungal properties of lipid components in the phylum Annelida were examined. Some amphoteric cerebrosides carrying a phosphocholine group showed fruiting-inducing activity on Schizophyllum commune, and one of them possessed activity comparable to that of Sch II, the most potent substance known. Furthermore, alkyl lysophosphatidylcholines were found to have an inhibitory effect on the growth of phytopathogenic fungi, Alternaria kikuchiana and Phomopsis mali. The relationship between structure and biological activities is discussed.

Alternaria↗

PubMed1997

Tryptase inhibitors: a novel class of anti-inflammatory drugs.

Tryptase, a serine protease released from mast cell secretory granules, is found at elevated levels in pathophysiologic conditions associated with allergic inflammation. The in vitro and in vivo biological activities of tryptase strongly suggest that tryptase influences lung function, inflammation, matrix degradation, and tissue remodelling. The pathophysiologic role for tryptase in diseases of airway inflammation such as asthma has been confirmed from studies using the selective tryptase inhibitor APC 366 in the allergic sheep model. APC 366 inhibited the allergen-induced early and late airway responses, blocked postchallenge airway hyperresponsiveness, and reduced airway inflammation. A pilot clinical trial with mild to moderate asthmatics also showed that APC 366 protected against allergen-induced early and late responses and reduced airway hyperresponsiveness. Current data provide compelling evidence that tryptase plays a fundamental role in allergic inflammation, and selective tryptase inhibitors may represent a novel class of anti-inflammatory therapeutics for treating asthma and other mast cell-mediated diseases.

Journal Article↗

PubMed1997

Induction of a sister-chromatid exchange by nitrogen oxides and its prevention by SOD.

Observations were made on the increase in the frequency of sister-chromatid exchanges (SCEs) induced by a nitric oxide (NO) releaser (NOR4) and NaNO2 in Chinese hamster lung cells (CHL/IU). During these observations, NaNO3 did not have any effect on SCE induction. NOR4- and NaNO2- induced SCE frequencies decreased due to treatment with bovine serum (10%), bovine serum albumin (BSA, 0.1%, 1.0%), oxyhemoglobin (Hb, 10 microM), and superoxide dismutase (SOD, 250 U/ml), but not with glutathione (oxidized and reduced forms), cysteine, cystine and catalase. NO2- concentrations decreased with Hb, but not with any other agent, indicating that NO and/or NO2- have a strong binding reaction with Hb. The mechanism for a decrease in genotoxicity due to SOD is still unclear. However, it would appear that S-nitrosothiols in the cells can be stabilized by SOD in consideration of the S-nitrosothiols stabilizing effect of SOD reported by Kowaluk et al. (1990). In the presence of NO and superoxide anions, genotoxicity seemed to be decreased by catalase and SOD, since the former decreases the superoxide anion-induced SCE frequency, and the latter, the NO-induced frequency.

Animals↗

PubMed1997

Infrequent mutation of Waf1/p21 gene, a CDK inhibitor gene, in brain tumors.

Possible mutations of the Waf1/p21 gene, a cyclin-dependent kinase (CDK) inhibitor gene, were investigated in biopsy specimens of 28 brain tumors using polymerase chain reaction (PCR)-single strand conformation polymorphism and nucleotide sequence analysis. There were 15 astrocytic tumors, six medulloblastomas, five pineal parenchymal tumors, and two neuroblastomas. A mutation was detected in exon 2, which comprises 90% of the cording region including the CDK inhibitory domain, in only two samples. A missense mutation was detected at codon 33 in rare PCR clones from an astrocytic tumor and a silent mutation was detected at codon 35 in a medulloblastoma. Therefore, mutation of the Waf1/ p21 gene is infrequent in these brain tumors. Examination of deoxyribonucleic acid (DNA) from normal subjects and paired DNA of brain tumor patients observed a polymorphism at codon 31, which encodes either Ser (AGC) or Arg (AGA).

Adolescent↗

PubMed1997

Effect of acquired tolerance to ischemia on focal infarction in gerbils.

The protective effect of prior ischemia on focal cerebral infarction produced by permanent middle cerebral artery (MCA) occlusion was studied in a gerbil model. Forebrain ischemia for 2 and 5 minutes at an interval of 48 hours was used as the prior ischemic insult. Forty-eight hours after the second forebrain ischemia, the MCA was occluded. Progression of ischemic change caused by the MCA occlusion was delayed in the early ischemic period in animals with prior ischemia, as compared to animals without prior ischemia. The mean infarct volume 24 hours after the MCA occlusion was the same in animals with and without prior ischemia. Ischemic tolerance was acquired in this model, but had no effect on the extent of infarction caused by permanent ischemia.

Animals↗

PubMed1997

Short-latency somatosensory evoked potentials in patients with brain stem tumor: study of N20 and N18 potentials.

Short-latency somatosensory evoked potentials (SSEPs) elicited by median nerve stimulation were studied in 17 patients with brain stem tumor. A total of 35 SSEP records were obtained and classified into five groups: 13 in Group I, central conduction time (CCT) < 7.56 msec (within the normal limits); eight in Group II, CCT > or = 7.56 msec; nine in Group III, N20 potential was abolished; four in Group IV, N20 and N18 potentials were abolished; and one in Group V, N20, N18, and P14 potentials were abolished. These SSEP groups were correlated with the size and location of the brain stem tumor on magnetic resonance images. N20 potentials were unchanged in latency in patients with small localized gadolinium (Gd)-enhanced lesions. In contrast, the N20 potentials were abolished in patients with tumors extending to the dorsal pons and the upper medulla oblongata. The extent of nonenhanced low-intensity lesion did not correlate with the changes of the N20 potentials. The degree of the impairment of the N20 potentials reflected the severity of the clinical symptoms. The N20 potential can evaluate brain stem dysfunction caused by brain stem tumor. The N18 potentials were abolished in four patients, in whom the tumor extension (one Gd-enhanced lesion, three low-intensity lesions) involved not only the pons but also the medulla oblongata. Therefore, the N18 potentials are probably generated from the medulla oblongata.

Adolescent↗

PubMed1997

Hemifacial spasm resulting from facial nerve compression near the internal acoustic meatus--case report.

A 61-year-old female presented with a rare case of hemifacial spasm (HFS) resulting from facial nerve compression near the internal acoustic meatus. She underwent a first surgery for microvascular decompression at the root entry zone of the facial nerve, but this did not achieve resolution of the HFS. During the second surgery, the meatal loop of the anterior inferior cerebellar artery (AICA) was found to be the offending artery near the internal acoustic meatus. When the AICA was dissected and separated from the facial nerve, abnormal muscle responses of the mentalis muscle due to electrical stimulation of the zygomatic branch of the facial nerve were abolished. Following surgery the patient was completely free of the HFS.

Decompression, Surgical↗

PubMed1997

Histological interaction of cultured endothelial cells and endovascular embolic materials coated with extracellular matrix.

This study was undertaken to evaluate the histological reaction of cultured endothelial cells to endovascular embolic materials in vitro. Endothelial cells were isolated and cultured from a canine carotid artery. Embolic materials (platinum microcoils, polyvinyl alcohol particles, silicon balloons, or silk threads), either in their normal state or after having been coated with type 1 collagen, fibronectin, or laminin, were placed on endothelial cells and cocultured for 6, 12, and 24 hours and 2, 3, 7, 14, and 21 days. The cocultures were investigated histologically using a scanning electron microscope. Endothelial cells were not found on any uncoated embolic materials, even at 21 days. On the materials coated with fibronectin or laminin, endothelial cells began to proliferate in 7 days, covering the materials extensively in 14 days. On the other hand, endothelial cells began to proliferate on the collagen-coated materials in 3 days, covering them extensively in 7 days and reaching confluence with a cobblestone pattern in 21 days. The densities of endothelial cells on collagen-coated materials were much higher than those observed on the materials coated with other extracellular matrices. Future advantages of the clinical use of collagen-coated embolic materials in interventional treatment are discussed.

Animals↗