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K Hashimoto

Publications and source records attributed to K Hashimoto.

At least 757 records · Page 42Linked to original sources
PubMed1996

Basic behavior of migratory Schwann cells in peripheral nerve regeneration.

In axonal regeneration after a peripheral nerve injury, Schwann cells migrate from the two nerve ends and at last form a continuous tissue cable across the gap which guides the axons toward the bands of Bungner. However, the behavior of migratory Schwann cells and their possible role are obscure. Using a film model in which the proximal stump of a transected nerve in mice was sandwiched between two thin plastic films, we analyzed neural regeneration in the early phase up to the 6th day after axotomy. Regenerating neurites emerged from the nodes of Ranvier adjacent to the axotomized nerve stump within 3 h after axotomy and extended along the parent nerve onto the film. All of the regenerating neurites on the surface of the film consisted of naked axons for at least 2 days after axotomy. Thereafter, Schwann cells from the proximal nerve migrated along a network of the regenerating axons and then closely attached to the axons, ensheathing them. Some of the Schwann cells advanced ahead of the axonal growth cones and were distributed over regions in which axonal extension was not yet present. As calculated from the time course of regenerating neurites, the velocity of axonal regeneration showed two phases: an initial slow phase (77 mu m/day) up to the 2nd post-operative day followed by a faster phase (283 mu m/day). The first observation of Schwann cells coincided with the onset of the second phase. In addition, the length of regenerating axons on the surface of the film containing many Schwann cells was significantly greater than that on the surface where Schwann cells were not yet present. It meant that migratory Schwann cells stimulated axons to elongate for a longer distance. Furthermore, Schwann cells from a distal stump showed a stronger ability to accelerate the axonal outgrowth than these from a proximal stump.

Animals↗
PubMed1996

Effects of the antihypoxic and neuroprotective drug, lubeluzole, on repolarization phase of canine heart assessed by monophasic action potential recording.

The cardiovascular effects of the antihypoxic and neuroprotective drug, lubeluzole, were investigated using beagle dogs anesthetized with halothane. Endocardial-contact electrode catheter was used for continuous monitoring of monophasic action potential (MAP), which could provide a precise information of repolarization phase. Intravenous administration of an efficacious dose of lubeluzole (0.63 mg/kg, n = 6) slightly decreased both the heart rate and the blood pressure. It did not change PQ interval and QRS width, while it significantly prolonged QT interval, corrected QT (QTc) and the duration of the MAP during the observation period over 60 min. The effects of drug on repolarization phase were late-onset and long-lasting compared with the time course of plasma drug concentrations, which changed as predicted by the two-compartment theory of pharmacokinetics. Additional injection of lubeluzole (2.5 mg/kg, n = 6) showed qualitatively similar changes to those of lower dose, and did not induce the cardiovascular collapse in any dog. Neither afterdepolarization nor ventricular escaped beat was detected during the observation period. The drug concentration in cardiac tissue was correlated linearly with the plasma drug concentration at 60 min after the second drug administration. These results indicate that lubeluzole exerts only minor cardiovascular effects except the prolongation of the repolarization period. The monitoring of plasma drug concentration may be helpful to estimate the steady-state distribution of drug to the heart, but less helpful to predict the QT prolongation. In future clinical trials, care must be taken with patients, especially those at risk to have prolonged repolarization.

Action Potentials↗
PubMed1996

An unusual cervical chordoma: CT and MRI.

We report CT and MRI findings of an unusual cervical chordoma. CT showed only minimal bony destruction with a lobulated prevertebral mass. Sagittal MRI, however, clearly demonstrated a lesion involving the body of C2 extending prevertebrally and into the spinal canal.

Aged↗
PubMed1996

Lactoferrin-mediated protection of the host from murine cytomegalovirus infection by a T-cell-dependent augmentation of natural killer cell activity.

The administration of bovine lactoferrin (LF) with 1 mg/g body weight before the murine cytomegalovirus (MCMV) infection completely protected the BALB/c mice from death due to the infection. In these LF-treated mice, a significant increase in the activity was found in the NK cells but not in the cytolytic T lymphocytes which recognized an MCMV-derived peptide. Moreover, the elimination of the NK cell activity by an injection with anti-asialo GM1 antibody abrogated such augmented resistance, thus supporting the hypothesis that the LF-mediated antiviral effect in vivo is performed through the augmentation of NK cell activity. No such LF-mediated antiviral effect in vivo with the increased NK cell activity was found in athymic nude mice, whereas it was restored completely by the transfer of splenic T cells from LF-treated donors. These findings therefore suggest that T lymphocytes induce both the augmentation of NK cell activity and the resultant antiviral effect in the LF-treated hosts.

3T3 Cells↗
PubMed1996

Heat shock induces HIV-1 replication in chronically infected promyelocyte cell line OM10.1.

A long period of clinical latency before development of symptoms is characteristic of human immunodeficiency virus type 1 (HIV-1) infection. OM10.1, a promyelocyte cell line latently infected with HIV-1, has been developed as a model for studying the mechanism of viral latency and the activation of virus expression. We found that this latently infected cell line with heat shock at 42 degrees C for 2 h resulted in a high level of HIV-1 production without addition of any cytokines. The mechanism of activation was analyzed by using anti-TNF-alpha antibody and various inhibitors. Although the TNF-alpha level in culture supernatants was below the sensitivity of an ELISA assay system, addition of anti-TNF-alpha antibody in culture medium could partially suppress the heat shock induced HIV-1 production. Staurosporine (PKC inhibitor), pentoxifylline (NF-kappa B inhibitor), and Ro5-3335 (HIV-1 Tat inhibitor) also inhibited significantly the heat shock induced virus activation. In particular, staurosporine achieved approximately 90% inhibition of the HIV-1 antigen expression in heat shock-treated OM10.1 at a non-toxic concentration. Although the mechanism of HIV-1 activation with heat shock has not been fully elucidated yet, it is presumed PKC plays an important role in HIV-1 activation. Thus, the present observations will provide a further insight into the pathogenesis of HIV-1 infections.

Alkaloids↗
PubMed1996

Binding and labeling of omega-conotoxin GVIA in crude membranes from subfractionated fractions and various areas of chick brain.

Specific binding and specific labeling of 125I-omega-CgTX were investigated in crude membranes from both subfractionated fractions and various brain areas in chick whole brain. The specific activities of the marker enzymes 2',3'-cyclic nucleotide 3'-phosphorylase, Na/K ATPase and succinic dehydrogenase in the subfractionated fractions were three- to five-fold higher than those in the P2 fraction. However, the amount of specific [125I] omega-CgTX binding in the fractions of synaptosomes and synaptic plasma membranes was only about 1.2-times higher than that in the P2 fraction. The characteristics of specific 125I-omega-CgTX labeling with disuccinimidyl suberate to the 135-kDa band were generally comparable to those of specific [125I] omega-CgTX binding sites. These results suggest that the specific binding sites of [125I] omega-CgTX were not localized the synaptosomes and synaptic plasma membranes fractions, although each fraction was well isolated from the others from which were decided by the strength of specific activity for marker enzymes.

Animals↗
PubMed1996

Paradoxical uptake of F-18 fluorodeoxyglucose by successfully reperfused myocardium during the sub-acute phase in patients with acute myocardial infarction.

The myocardial uptake of F-18 fluorodeoxyglucose (FDG) has been shown to indicate ischemia. To elucidate whether this is applicable to reperfused myocardium in patients with acute myocardial infarction (AMI), Tl-201 SPECT and F-18 FDG PET were performed in 10 patients with successfully recanalized AMI (male myocardial perfusion on the infarct-related area was classified, on the basis of Tl-201 images, into 2 groups (normal and defect) during the sub-acute phase, and into 3 grades (normal, redistribution (RD), and persistent defect) during the chronic phase (1 and 3 months after onset). Regional FDG uptake was calculated as FDG uptake in the region of interest normalized relative to that in a normal area. During the chronic phase, FDG accumulated only in the region of RD, indicating ischemia, but during the sub-acute phase, FDG accumulated mainly in the peri-infarct area. To elucidate whether the reperfused myocardium itself shows signs of accelerated glucose uptake, an experimental study was performed in rats. Glucose uptake in the isolated heart was measured by deoxyglucose and 31P-NMR spectroscopy, and was significantly increased after reperfusion compared with the pre-ischemic level. In conclusion, the enhancement of FDG uptake during the sub-acute phase was observed in successfully reperfused myocardium of patients with acute myocardial infarction. Such augmentation disappeared during the chronic phase. An experimental study in rats indicated that ischemia and reperfusion themselves augment glucose uptake. This mechanism may be responsible for the increase in FDG uptake of reperfused myocardium observed clinically.

Aged↗
PubMed1996

A 4-base pair deletion mutation of Gs alpha gene in a Japanese patient with pseudohypoparathyroidism.

Mutations in the guanine nucleotide binding protein alpha subunit (Gs alpha) have been found in patients with pseudohypoparathyroidism (PHP). We have screened the Gs alpha gene for mutations in a Japanese patient with this disorder and identified a novel 4-base pair deletion in exon 7 in codons 189-190. This deletion causes a frameshift and if synthesis of a truncated form of Gs alpha occurred, it would likely be biologically inactive. The patient was heterozygous for this deletion. The patient's mother and an unaffected brother were tested for the presence of this mutation. His mother had the same mutation, and although her serum calcium and parathyroid hormone levels were within the normal range, she had subcutaneous calcifications. Thus, this mutation appears to be necessary but not sufficient to cause the complete pseudohypoparathyroidism phenotype and thus, other unknown factors, either genetic or acquired, may be necessary for the full syndrome to occur.

Adult↗
PubMed1996

The main HTLV-I-harboring cells in the muscles of viral carriers with polymyositis are not macrophages but CD4+ lymphocytes.

We have analyzed muscle biopsy specimens from polymyositis patients who are also positive for human T cell lymphotropic virus type I (HTLV-I) using both immunohistochemistry for surface antigens of lymphocytes and macrophages and in situ polymerase chain reaction for HTLV-I proviral DNA on the same sections. We found HTLV-I in CD4+ cells but not in macrophages. This finding suggests that most of the HTLV-I-containing CD4+ cells are not macrophages but lymphocytes.

CD4-Positive T-Lymphocytes↗
PubMed1996

Translocation (9;11;22)(p22;q23;q11). A new type of complex variant translocation of t(9;11)(p22;q23) with MLL rearrangement.

We describe a patient with acute monocytic leukemia (M5a, FAB classification) associated with a new type of variant translocation (9;11). Southern blot analysis showed the rearrangement of the MLL (ALL-1/HRX) gene at 11q23. Fluorescence in situ hybridization (FISH) with painting probes of chromosomes 9, 11, and 22 revealed the translocation as t(9;11;22) (p22;q23;q11). This is more evidence that the production of chimeric mRNA following the translocation of the LTG9 (MLLT3/AF9) gene at 9p22 to 11q is a critical event in this leukemia subtype.

Adult↗
PubMed1996

Translocation (3;14)(q27;q11): a new variant translocation in a patient with non-Hodgkin's lymphoma of B-cell type with BCL6 rearrangement.

We report a 65-year-old woman with non-Hodgkin's lymphoma (NHL) carrying a t(3;14)(q27;q11) and BCL6 rearrangement in the affected cells. She had generalized lymphadenopathy and the bone marrow was infiltrated by lymphoma cells at presentation. Histological diagnosis was "malignant lymphoma, diffuse, large cell" type according to an International Working Formulation. Chromosome analysis revealed a t(3;14)(q27;q11), which is a new variant translocation of t(3;14) (q27;q32). Southern blot analysis showed rearrangement of BCL6, JH, and TCR beta but not of TCR delta. Cosmid probe of BCL6 hybridized to 14q11 and 3q27 by fluorescence in situ hybridization (FISH). Although the band 14q11 is a locus of T-cell receptor alpha- and delta-chains (TCR alpha/delta), lymphoma cells expressed B-cell, IgGk phenotype. The findings suggest that a novel proto-oncogene in the vicinity of TCR alpha/delta is involved in this translocation.

Aged↗
PubMed1996

2-Glycineamide-5-chlorophenyl 2-pyrryl ketone, a non-benzodiazepin Tat antagonist, is effective against acute and chronic HIV-1 infections in vitro.

In the search for effective Tat-dependent transcription inhibitors using a screening assay system that has recently been developed, 2-glycineamide-5-chlorophenyl 2-pyrryl ketone (GCPK) has proved to be a potent and selective inhibitor of human immunodeficiency virus type 1 (HIV-1) replication in vitro. This compound was inhibitory to HIV-1 replication in both acutely and chronically infected cells. The 50% effective concentration (EC50) of GCPK in acutely infected MOLT-4 and CEM cells was 0.62 and 0.13 microgram/ml, respectively. These values were similar to those of the known Tat-dependent transcription inhibitors Ro5-3335 and Ro24-7429. Like these inhibitors, GCPK could inhibit HIV-1 replication in MOLT-4/IIIB (MOLT-4 cells chronically infected with HIV-1) and tumor necrosis factor-alpha-(TNF-alpha)-induced viral activation in OM10.1 cells (a HL-60 clone latently infected with HIV-1). GCPK is distinct from Ro5-3335 and Ro24-7429 in that this novel Tat-dependent transcription inhibitor has no benzodiazepin ring.

Anti-HIV Agents↗
PubMed1996

Failure to detect paramyxovirus RNA in the skin of connective tissue disease.

Etiology of connective tissue disease is unknown. The association of infectious agents has been suspected serologically, ultrastructurally and recently by means of molecular biological techniques. We extracted RNA from lesions of 25 discoid lupus erythematosus, 9 systemic LE, and 3 systemic sclerosis biopsies, and reverse transcription-polymerase chain reaction was performed for all paramyxoviruses known to infect human beings. None of the samples yielded positive signal for any of the viruses. The existence of paramyxovirus in the skin of connective tissue disease is very unlikely.

Base Sequence↗
PubMed1996

Differential localization of TGF-beta-precursor isotypes in psoriatic human skin.

Transforming growth factor-beta (TGF-beta) can act as a multi-functional regulator of both cell growth and differentiation. Three isoforms of TGF-betas, namely TGF-beta 1 TGF-beta 2 and TGF-beta 3, have been identified in human tissues. Previously we reported the expression of TGF-beta isoforms in normal human skin. However little is known about the role of TGF-beta isoforms in the pathogenesis of psoriasis. Using the TGF-beta precursor-specific antibodies to strengthen the specificity, we studied the immunohistochemical distribution of TGF-betas 1-3 in psoriatic skin. TGF-beta 2, which was found in the intercellular space of all the layers of the epidermis in normal human skin, was decreased in the psoriatic epidermis. The intensity of immunoreactivity has the tendency to decrease in the lower epidermis rather than in the upper epidermis of the transitional lesion. In contrast, TGF-beta 3 was present in the subepidermal area of the psoriatic skin as in the normal human skin. TGF-beta 1 was observed in neither epidermis nor dermis in both normal and psoriatic skin. Since TGF-beta is a potent growth inhibitor for human keratinocytes, the decrease of TGF-beta 2 in the epidermis of psoriatic skin may contribute to epidermal hyperplasia, a hallmark of psoriasis.

Humans↗
PubMed1996

A new non-random chromosomal translocation t(3;6)(q27;p21.3) associated with BCL6 rearrangement in two patients with non-Hodgkin's lymphoma.

We describe two cases of non-Hodgkin's lymphoma associated with t(3;6)(q27;p21.3) and BCL6 rearrangement. The first case was in a 78-year old woman, whose performance status (PS) was 1, the serum lactate dehydrogenase (LDH) level was elevated, and the Ann Arbor stage was IIIA with no extra nodal lymphomatous site. The pathological diagnosis from a biopsy of the inguinal lymph node was 'malignant lymphoma (ML), follicular, small cleaved' according to the Working Formulation. Complete remission was achieved. Although she had relapse in 1992, remission was obtained again. The second case was in a 62-year old man, whose PS was 1, the serum LDH was normal, and Ann Arbor stage was IVA with the involvement of the small intestine. Histological diagnosis of the cervical lymph node was 'ML, diffuse, large cell'. Complete remission was obtained without relapse. The 3q27 translocations, found in 20-30% of non-Hodgkin's lymphoma, are unique in having multiple chromosomal translocation partners. Chromosome band 6p21.3 is one of these partner sites that may be the site of a novel gene. The two cases presented here show that this translocation is a non-random chromosomal change involving 3q27 and BCL6. Since t(3;6) was the sole karyotypic abnormality in one case, this translocation may play a role in lymphomagenesis.

Aged↗