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Biomedical subjects

K Abe

Publications and source records attributed to K Abe.

At least 811 records · Page 45Linked to original sources
PubMed1998

[Spontaneous resolution of pulmonary cryptococcosis--report of 2 cases].

We encountered two patients with pulmonary cryptococcosis that resolved spontaneously without antifungal treatment. A 59-year-old man (patient 1) and 37-year-old man (patient 2) were admitted to our hospital for the examination of abnormal shadows on their chest x-ray films. Transbronchial lung biopsies were performed, and cryptococci were detected in both patient's lung tissues. Latex aggultination tests for cryptococcal antigen were positive (1:16 and 1:4, respectively). The size of the shadows reduced spontaneously and the titers of the cryptococcal antigen in sera decreased within three months although no antifungal therapy was performed. Bronchoalveolar lavage fluid (BALF) was obtained from each patient and examined. In patient 1, the lymphocyte to CD 4/8 ratio was high in the BALF obtained on admission and the lymphocyte count was low; however, the CD 4/8 ratio was still high in a BALF sample obtained 3 months after discharge. In patient 2, the findings of the BALF analysis on admission were almost normal. The analysis of BALF may contribute to the immunological conditions to in the patients with pulmonary cryptococcosis.

Adult↗
PubMed1997

Scanning and transmission electron microscopy of Ruffini endings in the periodontal ligament of rat incisors.

The Ruffini organ is an arborized axon ending categorized as a low-threshold stretch receptor. We have previously shown that the lingual periodontal ligament of rat incisors is densely innervated with Ruffini endings. In the present study, fine structures in the surface of the periodontal Ruffini endings and their topographical relationship with the surrounding collagen fibers were observed by a combination of scanning and transmission electron microscopy to analyze the mechanism of the stretch reception. The entire length of the branches of the Ruffini endings, excepting their terminal portions, corresponded well with those depicted by previous investigators in the following points: (1) their cylindrical appearance covered by Schwann cell processes; (2) the presence of numerous axon fingers protruding through gaps in the Schwann sheath and; (3) their isolation from collagen fibers by multilayered basal lamina. On the other hand, tips of the axon branches-together with their Schwann sheaths-became attenuated and projected into tight bundles of collagen, indicating their susceptibility to mechanical deformations of the surrounding tissue. Margins of the axon terminals were conspicuously ruffled with long tongue-like projections of Schwann cells. The Schwann cell tongues twined around collagen bundles in their distal portions, and associated closely with fine axon projections in their proximal portions, suggesting their involvement in the mechanical transmission of stimuli to axon terminals.

Animals↗
PubMed1997

Possible role of P-450 metabolite of arachidonic acid in vasodilator mechanism of angiotensin II type 2 receptor in the isolated microperfused rabbit afferent arteriole.

Although angiotensin II type 2 (AT2) receptor has recently been cloned, its functional role is not well understood. We tested the hypothesis that selective activation of AT2 receptor causes vasodilation in the preglomerular afferent arteriole (Af-Art), a vascular segment that accounts for most of the preglomerular resistance. We microperfused rabbit Af-Arts at 60 mmHg in vitro, and examined the effect of angiotensin II (Ang II; 10(-11)-10(-8) M) on the luminal diameter in the presence or absence of the Ang II type 1 receptor antagonist CV11974 (CV; 10(-8) M). Ang II was added to both the bath and lumen of preconstricted Af-Arts. Ang II further constricted Af-Arts without CV (by 74+/-7% over the preconstricted level at 10(-8) M; P < 0.01, n = 7). In contrast, in the presence of CV, Ang II caused dose-dependent dilation; Ang II at 10(-8) M increased the diameter by 29+/-2% (n = 7, P < 0.01). This dilation was completely abolished by pretreatment with an AT2 receptor antagonist PD123319 (10(-7) M, n = 6), suggesting that activation of AT2 receptor causes vasodilation in Af-Arts. The dilation was unaffected by inhibiting either nitric oxide synthase (n = 7) or cyclooxygenase (n = 7), however, it was abolished by either disrupting the endothelium (n = 10) or inhibiting the cytochrome P-450 pathway, particularly the synthesis of epoxyeicosatrienoic acids (EETs, n = 7). These results suggest that in the Af-Art activation of the AT2 receptor may cause endothelium-dependent vasodilation via a cytochrome P-450 pathway, possibly by EETs.

8,11,14-Eicosatrienoic Acid↗
PubMed1997

CAG repeat length and disease duration in Machado-Joseph disease: a new clinical classification.

To evaluate the clinical characteristics of Machado-Joseph disease (MJD) with reference to CAG repeat length and disease duration, we analyzed neurologic findings in 108 patients from 84 families. The majority of MJD patients presented with an ataxic gait as the initial symptom. Dysarthria and nystagmus were observed from an early stage. Bulging eyes, muscle atrophy and bradykinesia developed later. Patients with a shorter CAG repeat length or later onset had more frequent involvement of proprioceptive sensory deficit. Incidence of abnormal reflexes, tones, and proprioceptive sensation was not associated with disease duration, but with CAG repeat length. Based on these results, we propose a new clinical classification: type A (juvenile type), with hyperreflexia and dystonia, but without a proprioceptive sensory deficit; type C (adult type), with hyporeflexia and a proprioceptive sensory deficit, but without dystonia; and type B (intermediate type), the remaining patients with a mixed presentation.

Adult↗
PubMed1997

Expression of the glial cell line-derived neurotrophic factor gene in rat brain after transient MCA occlusion.

Change of the glial cell line-derived neurotrophic factor (GDNF) gene expression in rat brain was examined after transient middle cerebral artery (MCA) occlusion of adult rats. Northern blot analysis showed that the mRNA began to be induced in the occluded MCA from 1 h of reperfusion with a peak at 3 h, and almost diminished by 1 day of reperfusion. Immunohistochemical analysis with brain sections showed an expression of GDNF-like immunoreactivity in neurons of the cerebral cortex and caudate after 90 min of ischemia in a similar way to the mRNA, but the staining was more disseminated and stronger in the cerebral cortex than the caudate. No glial cell was stained in the brain sections. The present results indicate that the GDNF gene was expressed in an early stage of reperfusion in neuronal cells of the MCA territory, but that the staining property was different between in the cerebral cortex and caudate.

Animals↗
PubMed1997

Primary central nervous system leukemia with a novel chromosomal translocation.

A case of central nervous system (CNS) leukemia with normal bone marrow, associated with a novel chromosomal abnormality, is described. A 58 year-old woman complained of hearing disturbance, severe headache and vomiting, and showed signs of meningeal irritation, as well as papilledema and bilateral dysacusis. Immature atypical cells were found in the cerebrospinal fluid (CSF) with elevated pressure, pleocytosis, increased protein and decreased glucose levels. She was diagnosed as having neoplastic meningitis. In spite of intensive investigations, including bone marrow puncture, malignancies were not found in organs other than intra-cranial site. The symptoms and CSF findings were temporarily improved with chemotherapy and irradiation, but she relapsed into neoplastic meningitis. The anaplastic cells in CSF were positive with CD45 by immunocytochemistry, and were positive by peroxidase staining. Thus, the anaplastic cells were considered to be myelocytic leukemic cells. Chromosomal analysis showed that these leukemic cells had a novel chromosomal abnormality: 46XX, 4q+, 10q-, 16q-. There has been no report of leukemic meningitis without bone marrow abnormalities. It is possible that this peculiar abnormal chromosome is related to the primary infiltration of the central nervous system. With this novel chromosomal abnormality, this case is important for considering the mechanism of primary leukemic meningitis.

Central Nervous System Diseases↗
PubMed1997

Amygdala beta-noradrenergic influence on hippocampal long-term potentiation in vivo.

We have previously shown that hippocampal long-term potentiation (LTP), one form of synaptic plasticity that may underlie learning and memory, is attenuated by blocking neuron activity of the basolateral amygdala (BLA). In the present study we investigated the amygdala noradrenergic or cholinergic contribution to hippocampal LTP formation. When propranolol, a beta-adrenoceptor antagonist, was injected into the BLA 10 min before tetanus, the formation of LTP in the perforant path-dentate granule cell synapses was significantly impaired. Scopolamine, a muscarinic cholinergic receptor antagonist, did not affect the formation of LTP. These results suggest that amygdala beta-noradrenergic activity plays a critical role in modulation of hippocampal LTP.

Adrenergic beta-Antagonists↗
PubMed1997

Analysis of the McLeod syndrome gene in three patients with neuroacanthocytosis.

McLeod syndrome is a rare X-linked disorder involving neurological defects and acanthocytosis. We examined the XK gene in three patients with neuroacanthocytosis, one of whom had cardiomyopathy, and his symptoms were very similar to those of McLeod syndrome. We found two new transversions (C to G at codon 204 and G to C at codon 205) in exon 3 in all those cases. However, the transversion at codon 205 was found in all 70 Japanese normal subjects and four non-Japanese (two Caucasian males, one Chinese female and one Micronesian female) and that at codon 204 was also detected in all 14 normal Japanese males and the four non-Japanese. These findings suggest that they are not the cause of McLeod syndrome, but normal polymorphisms which have not been reported. Moreover, there is a possibility that patients with neuroacanthocytosis similar to McLeod syndrome exist without the XK gene abnormalities.

Acanthocytes↗
PubMed1997

Taste buds have a cyclic nucleotide-activated channel, CNGgust.

Cyclic nucleotide-gated (CNG) channels have been characterized as important factors involved in physiological processes including sensory reception for vision and olfaction. The possibility thus exists that a certain CNG channel functions in gustation as well. In the present study, we carried out reverse transcription-polymerase chain reaction and genomic DNA cloning and characterized a CNG channel (CNGgust) as a cyclic nucleotide-activated species expressed in rat tongue epithelial tissues where taste reception takes place. Several types of 5'-rapid amplification of cDNA ends clones of CNGgust cDNA were obtained with various 5'-terminal sequences. As the CNGgust gene was a single copy, the formation of such CNGgust variants should result from alternative splicing. The encoded protein was homologous to known vertebrate CNG channels with 50-80% similarities in amino acid sequence, and particularly homologous to bovine testis CNG channel and human cone CNG channel with 82% similarities. CNGgust was functional when expressed in human embryonic kidney cells, where it opened upon the addition of cGMP or cAMP. Immunohistochemical analysis using an antibody raised against a CNGgust peptide demonstrated the channel to be localized on the pore side of each taste bud in the circumvallate papillae, with no signal observed for degenerated taste buds after denervation of the glossopharyngeal nerve. All these results, together with the indication that cyclic nucleotides play a role gustatory signaling pathway(s), strongly suggest the involvement of CNGgust in taste signal transduction.

Amino Acid Sequence↗
PubMed1997

Structural requirement for axonal regeneration-promoting effect of polyamines in cultured rat hippocampal neurons.

We have previously found that spermine, spermidine and putrescine promote axonal regeneration following axotomy in cultured rat hippocampal neurons. In the present study, we investigated which part of the polyamine molecule is responsible for the regeneration-promoting effect. Testing the effects of several synthetic analogues revealed that the butanediamine moiety is essential for the activity and the terminal primary amines are necessary for full agonist activity. The structure-activity relationship indicates that the regeneration-promoting effects of polyamines are not associated with NMDA receptors.

Animals↗
PubMed1997

Amelioration of brain edema by topical application of glial cell line-derived neurotrophic factor in reperfused rat brain.

Glial cell line-derived neurotrophic factor (GDNF) was applied topically on the brain surface of reperfused rat brain after 90 min of transient middle cerebral artery occlusion. In contrast to the cases treated with vehicle, a formation of brain edema was greatly reduced at 2 days by the treatment with GDNF. Terminal deoxynucleotidyl transferase-mediated dUTP-biotin in situ nick end labeling (TUNEL) staining was also markedly reduced in the cases with GDNF treatment both at 1 and 2 days of reperfusion. However, amelioration of the induction of immunoreactive 70 kDa heat shock protein was only a minimum by the GDNF treatment. The present results suggest that the treatment with GDNF has a significant effect on ameliorating brain edema formation after transient focal brain ischemia, and the effect is greatly associated with the reduction of TUNEL staining, but minimally with that of stress response of cells.

Animals↗
PubMed1997

In vivo adenovirus-mediated gene transfer and the expression in ischemic and reperfused rat brain.

In an attempt to study whether ischemic brain could express a foreign gene in vivo, a replication-defective adenoviral vector containing the Escherichia coli lacZ gene was directly injected into the ischemic or reperfused cerebral cortex of rat, and temporal and spatial profiles of the exogenous gene expression were compared with that of the control brain. Right middle cerebral artery (MCA) of rat was continuously occluded by an insertion of nylon thread for 2 days, or only transiently occluded for 90 min and then the blood flow was restored for 21 days. The adenoviral vector was administered just after the MCA occlusion or reperfusion in the case of continuous ischemia and reperfusion, respectively. Adenoviral vector was transferred into the continuous ischemic brain, and the lacZ gene was expressed until 2 days of the occlusion in the cerebral cortex of the occluded MCA territory with the number of expressing cells smaller and the staining just weaker than that of the control brain. In contrast, expression of the lacZ gene was not or only minimally observed in the reperfused brain until 2 days. However, the expression dramatically exploded at 7 days of reperfusion at a level similar to that of the control, and the expression diminished by 21 days. A few neurons in the ipsilateral thalamus, hypothalamus, and basal ganglia, and in the contralateral cerebral cortex expressed the lacZ gene at 7 days after reperfusion, a phenomenon similar to the case of the control. The majority of brain cells that expressed the lacZ gene were neurons, and a part (5-10%) were astroglial cells. Traumatic injury and immunological response in the brain were minimal both in the cases of control and ischemia/reperfusion. The present study shows an effective gene transfer and the expression in neural cells of ischemic and reperfused brains in vivo, and suggests a great potential of the gene therapy for ischemic stroke patients in the future.

Adenoviridae↗
PubMed1997

Human amylin mimics amyloid beta protein-induced reactive gliosis and inhibition of cellular redox activity in cultured astrocytes.

We have previously found that Alzheimer's disease amyloid beta protein (A beta) induces reactive gliosis and inhibits cellular redox activity of astrocytes. In the present study, human amylin, an amyloidogenic peptide with primary sequence dissimilar to A beta, mimicked the effects of A beta in cultured astrocytes. However, the non-amyloidogenic rat amylin showed no effect. These results suggest that amyloidogenic property is important for A beta to induce morphological and functional changes of astrocytes.

Amyloid↗
PubMed1997

Expressions of P-selectin- and HSP72-like immunoreactivities in rat brain after transient middle cerebral artery occlusion.

The role of an adhesion molecule such as P-selectin may be important in the pathogenesis of stroke. However, temporal, spatial and cellular profiles of the expression of such a protein have not been fully studied. Change of immunoreactive P-selectin was examined in rat brain after transient middle cerebral artery (MCA) occlusion in comparison with that of 72 kDa heat shock protein (HSP72) which is a well known marker of cell injury. Western blot analyses were performed to ensure the selective detection of immunoreactive P-selectin and HSP72 proteins with each antibody using brain samples before and after ischemia. Temporal, spatial and cellular changes of immunohistochemical expressions of P-selectin and HSP72 were evaluated with rat brain sections at 2 and 8 h, and 1, 3 and 7 days of reperfusion after 1 h of MCA occlusion (MCAO). Hematoxylin-eosin (HE) staining was performed to evaluate brain cell damage at 3 and 7 days of reperfusion. Western blot showed a single band at molecular weights of 140 and 72 kDa for P-selectin and HSP72, respectively, only after ischemia. No significant band was observed without primary antibody. P-selectin-like immunoreactivity was not normally present in rat brain sections. However, it was expressed mainly in the post-capillary venules of the cerebral cortex and caudate in the MCA territory with a peak at 8 h to 1 day. The expression was diminished by 3 days of reperfusion. An immunoreactive HSP72 was scarcely present in the cerebral cortex and caudate of the sham control brain. However, the protein was induced in neurons of the MCA territory. The HSP72 induction was gradually intensified from 8 h with peaks at 1 day in the cortex and at 3 days in the caudate. The immunoreactivity decreased by 7 days. Histopathological study with HE staining showed no evident cell damage at 3 and 7 days of reperfusion. The present results indicate that temporal, spatial and cellular differences were present in the expressions of immunoreactive P-selectin and HSP72 proteins. P-selectin was expressed from an earlier stage of reperfusion in post-capillary venules, and the expression became maximum at the same time both in the cerebral cortex and caudate. In contrast, HSP72 induction began later in neurons and reached maximum at a different time between the cortex and caudate.

Animals↗
PubMed1997

Postischemic expression of P-selectin immunoreactivity in rat brain.

Change of immunoreactive P-selectin was examined in rat brain after transient middle cerebral artery (MCA) occlusion (O) with anti-P-selectin monoclonal antibody using brain samples of sham control and after ischemia. Temporal, spatial, and cellular changes of immunohistochemical expressions of P-selectin were evaluated with rat brain sections at 2 and 8 h, 1, 3, and 7 days of reperfusion after 1 h of MCAO. Western blot showed a single band at molecular weight of 140 kDa for P-selectin after ischemia. P-selectin immunoreactivity was not normally present in rat brain sections. However, it was expressed mainly in the post-capillary venules of the cerebral cortex and caudate in the MCA territory with a peak at 8 h-1 day. The expression was diminished by 3 days of reperfusion. The present results indicate that P-selectin was expressed from an earlier stage of reperfusion in post-capillary venules, and the expression became maximum at the same time both in the cerebral cortex and caudate.

Animals↗