[Anatomy of cerebrospinal fluid system and blood-brain barrier].
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Blood-Brain Barrier↗
Biomedical subjects
T Amano
Publications and source records attributed to T Amano.
Molecular switch of F0F1-ATP synthase, G-protein, and other ATP-driven enzymes.
Exchange-out of amide tritium from labeled gamma-subunit of alpha 3 beta 3 gamma complex of F0F1-ATP synthase was not accelerated by ATP, suggesting that hemagglutinin-type transition of coiled-coil structure did not occur in gamma-subunit. Local topology of nucleotide binding site and "switch II" region of G-protein alpha resemble those of F1-beta subunit and other proteins which catalyze ATP-triggered reactions. Probably, binding of nucleotide to F0F1-ATP synthase induces conformational change of the switch II-like region with transforming beta subunit structure from "open" to "close" for and this transformation results in loss of hydrogen bonds with gamma subunit, thus enabling the gamma subunit to move.
Adenosine Triphosphate↗
Analysis of roles of natural killer cells in defense against Plasmodium chabaudi in mice.
Mice that have recovered from a primary infection with Plasmodium chabaudi have been shown to resist a secondary infection. In the present study the authors investigated how natural killer (NK) cells were involved in this resistance. Spleen cells from P. chabaudiprimed C57BL/6 mice could transfer protection against P. chabaudi infection into naive syngeneic mice, but spleen cells from unprimed mice could not. T-enriched cells purified from primed spleen cells could also transfer such protection. Transfer of NK cells from primed spleen cells failed to protect against challenge infection. However, depletion of NK cells in host mice by injection of an anti-NK1.1 monoclonal antibody resulted in higher mortality relative to controls. The possible protective roles of NK cells in P. chabaudi infection are discussed.
Animals↗
Case report: bladder leiomyoma--pre-operative diagnosis by transrectal ultrasonography guided needle biopsy.
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Adult↗
Cross-reactive idiotypes on rabbit anti-SEA antibodies stimulate anti-idiotype spleen and lymph node cell responses of mice infected with Schistosoma mansoni.
Antibodies to Schistosoma mansoni soluble egg antigens (SEA) generated in outbred rabbits from two different sources were used to study cross-reactive idiotype/anti-idiotype (Id/anti-Id) interactions in S. mansoni-infected mice in two different locations. Immunoaffinity purified rabbit polyclonal anti-SEA antibody preparations (RabId) were predominantly Ig by SDS-PAGE and demonstrated anti-SEA activity by ELISA and Western blot. RabId prepared from three separate rabbits and used at 40 micrograms/ml in vitro stimulated lymphocyte proliferative responses of spleen cells from mice with eight week infections (Mean +/- SEM [E-C]) of 3869 +/- 764, 18594 +/- 3046 and 8962 +/- 1734 cpm. Spleen cells from uninfected mice exposed to the same RabId preparations in vitro had respective [E-C] values of 206 +/- 144, 494 +/- 154 and 363 +/- 180. Lymph node cells from mice infected for 8 weeks demonstrated [E-C] of 123 +/- 400, 5073 +/- 828 and 2361 +/- 656 upon exposure to these 3 RabId preparations. Lymph node cells from uninfected mice had [E-C] of 220 +/- 76, 194 +/- 82 and 143 +/- 72 when exposed to these RabId. Maximum in vitro proliferative response to Ig from unimmunized rabbits was 761 +/- 400 by spleen cells from mice with eight week infections. These data indicate the presence of cross-reactive Id on rabbit anti-SEA antibodies from different rabbits that can stimulate in vitro lymphoproliferative responses of spleen or lymph node cells from S. mansoni-infected mice.
Animals↗
Requirement of CD80 and CD86 molecules for antigen presentation by eosinophils.
The authors analysed the antigen-presenting ability of eosinophils purified from peritoneal exudate cells of interleukin-5 (IL-5) transgenic mice. The granulocyte-macrophage colony-stimulating factor (GM-CSF)-treated eosinophils induced proliferative responses of primed lymph node T cells and thymus T cells to staphylococcal enterotoxin B (SEB), while untreated eosinophils induced little or no response. GM-CSF-treated eosinophils also induced proliferation of ovalbumin (OVA)-primed lymph node T cells to OVA. Although untreated eosinophils expressed no MHC class II molecule on the surface the eosinophils could be induced to express major histocompatibility complex (MHC) class II molecules when treated with GM-CSF. In the present study, anti-I-Ak monoclonal antibodies (MoAbs) strongly inhibited proliferation of thymus T cells and proliferation of OVA-primed lymph node T cells in response to OVA, but weakly inhibited proliferation of primed T cells in response to SEB. Furthermore, CD80 (B7-1) and CD86 (B7-2) were expressed on the surfaces of untreated eosinophils. The expression of those two molecules on the eosinophils was increased by incubation with GM-CSF. Moreover, anti-CD80 or anti-CD86 MoAbs blocked proliferative responses of primed lymph node T cells and thymus T cells to SEB, and also blocked responses of primed lymph node T cells to OVA. Thus, CD80 and CD86 play an important role in stimulation of T cells by eosinophils.
Animals↗
Bronchiolitis obliterans organizing pneumonia associated with systemic lupus erythematosus with antiphospholipid antibody.
Bronchiolitis obliterans organizing pneumonia (BOOP) is a pathologic entity characterized by the formation of fibrous tissue plugs within terminal bronchioles and alveolar ducts. Although BOOP has been associated with several connective tissue disorders, there are rare reports of BOOP in patients with systemic lupus erythematosus (SLE). We present a patient with SLE accompanying antiphospholipid antibody who developed recurrent respiratory symptoms and radiographic abnormalities. The diagnosis of BOOP was confirmed by transbronchial lung biopsy. This case suggests that not only SLE, but also the presence of antiphospholipid antibody, may be associated with the development of BOOP.
Adult↗
[A case report of concomitant UFT-E and CDDP against lung epidermoid carcinoma].
A 52-year-old male with the chief complaint of hemo-sputum was diagnosed after detailed examination as epidermoid carcinoma in the right upper lobe bronchus through the bifurcation. Thoracotomy revealed infiltration of carcinoma into the right main pulmonary artery and the superior vena cava, which could not be excised. Subsequent postoperative radiotherapy (69 Gy) showed NC. Then concomitant administration of UFT-E and a low dose of CDDP was started on an outpatient basis. After the third course of treatment (six weeks per course), a significant reduction was noted in the size of the carcinoma. Bronchoscopy revealed CR with the elimination of carcinoma to mere traces. Besides the myelosuppression seen at the end of the second course of treatment, which resulted in a two-week hospitalization for blood transfusion, no adverse effect prevented the patient from continuing the outpatient treatment courses and from returning to work. We consider that the treatment was very successful not only for its effectiveness in reducing the carcinoma but also for the high QOL achieved.
Administration, Oral↗
[A case of posttraumatic spinal pseudomeningocele which caused spinal cord compression 20 years after injury].
We reported an extremely rare case of posttraumatic spinal pseudomeningocele which caused spinal cord compression 20 years after getting injury, and demonstrated that sequelae of an injury may occur many years after the original wound. A 39-year-old man, who got left cervical root avulsion due to a traffic accident when he was 17 years old, began to complain of progressive muscle atrophy and weakness of left lower extremity 1 year ago. Myelography demonstrated pseudomeningocele at left C6-C8 level, and MRI and CT myelography revealed that the pseudomeningocele extends through the intervertebral foramen and compresses the spinal cord to the right side in the spinal canal. Bilateral functional compression of spinal cord dorsal and lateral column was also verified with SEP and MEP electrophysiologically.
Accidents, Traffic↗
Point mutation of the p53 gene is an infrequent event in untreated prostate cancer.
The p53 gene is known to be one of the frequently altered tumor suppressor genes, involved in the oncogenesis of a wide spectrum of human malignant tumors. We investigated mutational events of the p53 gene in 18 clinically untreated prostate cancers. Direct sequencing analysis demonstrated that 1 of 18 cases harbored point mutation in the highly conserved transcript region. The case showed CAT at codon 273 instead of wild-type CGT, substituting the encoded amino acid form histidine to arginine. The case had previously revealed homozygous loci on 17p, including the p53 locus, by restriction fragment length polymorphism analysis. The other 17 cases harbored neither mutation nor small deletion. It is concluded that point mutation of the p53 gene is a infrequent event in the oncogenesis of untreated prostate cancer.
Base Sequence↗
-Clinical features of 10 cases of tuberculous meningitis--with special reference to patient's delay and doctor's delay.
We retrospectively evaluated the clinical findings of 10 cases of tuberculous meningitis who had been admitted to our department from 1987 to 1994. Four patients were male and six were female. All of them were Japanese, and their age ranged from 17 to 74 years old. Regarding the patient's delay, nine patients visited a doctor in 1 to 20 days after the onset of headache, and one patient visited a doctor in 14 days after the onset of general malaise. It is suggested that the patient's delay could not be longer than 3 weeks because of progressively worsening symptoms of tuberculous meningitis such as severe headache and fever. The time interval between the first contact of the patient to a doctor and the commencement of antituberculous therapy (doctor's delay), ranged from 14 to 66 days. When the diagnosis of meningitis was obtained based on the findings of the cerebrospinal fluid (CSF), focal neurological signs including psychological symptoms, cranial nerve palsies and seizure were noted besides meningeal signs or the disturbance of consciousness in 4 patients. The CSF revealed an increase in cell counts with mononuclear cell dominance in 9 patients, but the findings typical for tuberculous meningitis such as increase in total protein content and a decrease in glucose concentration were obtained in only 5 patients. Mycobacterium tuberculosis had not been detected in all cases when the antituberculous chemotherapy was started. Later, it was found to be positive in the CSF sample from only three patients by culture or polymerase chain reaction (PCR) method. When the antituberculous therapy was completed, meningitis was cured without remaining any symptom or sign in all patients. All patients had no active pulmonary tuberculosis when the meningitis was diagnosed, and only one of them had sequels of lung tuberculosis. Four patients had the past history of tuberculosis, and 1 had the familial history of pulmonary tuberculosis. At the first contact to a doctor, seven patients were diagnosed as having common cold or headache related with fever because of the lack of typical signs of meningitis. Similarly three other patients were initially diagnosed as having meningitis due to viral infection or unknown etiology. In summary, it was difficult to obtain the solid diagnosis of tuberculous meningitis at the initial stage of this disease, since the symptoms and signs at its onset often similar to those of common cold or non-specific headache. Therefore, when we see the patients with subacute onset of headache and fever followed by the meningeal signs, tuberculous meningitis should always be included in the list of diseases requiring differential diagnosis. In addition, when tuberculous meningitis is suspected, the antituberculous therapy should be started without any delay.
Adolescent↗
Diabetes insipidus with Behçet's disease.
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Adult↗
[A case of tuberculous meningitis associated with facial nerve paralysis and MRI findings of brain stem lesion].
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Aged↗
Age-related changes in cellular localization and enzymatic activities of cathepsins B, L and D in the rat trigeminal ganglion neuron.
Altered localization and cellular level of three distinct lysosomal proteinases, cathepsins B (CB), L (CL), and D (CD), with aging were investigated in the rat trigeminal ganglion (TG) by immunohistochemical and quantitative analyses. At the light microscopic level, the intracytoplasmic distribution of these three enzymes was found to change with aging: These lysosomal proteinases in the TG of young rats (2-3 months of age) were widely and evenly distributed throughout the cytoplasm as coarse intracytoplasmic granules, whereas they were localized at focal cytoplasmic sites of the TG neurons of aged rats (28-31 months of age) as coarse aggregates. A similar distribution was observed with a major lysosomal membrane sialoglycoprotein having an apparent molecular mass of 107 kDa (LGP107). The cellular distribution of the three cathepsins as well as LGP107 in the TG neurons of aged rats corresponded well with that of autofluorescent lipofuscin. At the electron microscopic level, the age-related redistribution of these cathepsins in the TG neurons was found to be due to their great accumulation in autolysosomes localized at the focal perinuclear sites. The cellular levels of CB and CL determined by activity measurement in the TG of the young rats were 1.8 and 1.7 times as much as those of the aged rats respectively. In contrast, no significant difference was observed between the CD activities in the two age groups. These results strongly suggest that age related changes in localization and cellular level of CB, CL, and CD in TG neurons are closely linked with the increased formation of autolysosomes and lipofuscins, which is the most ubiquitous age-related cytological alteration.
Aging↗
A common topology of proteins catalyzing ATP-triggered reactions.
A protein fold, six parallel beta strands surrounding the central alpha helix, is likely to be a common structure in protein families known to have a typical set of nucleotide binding consensus sequence motifs A and B and to catalyze ATP-triggered reactions. According to this ATP-triggered protein fold, the conserved Glu (or Asp), which acts as a general base to activate a water molecule for an in-line attack of the gamma-phosphate, is at the exit of the second beta strand. The fifth beta strand may be involved in propagation of conformational change triggered by ATP hydrolysis.
Adenosine Triphosphate↗
Analysis of an initial step of T cell adhesion to endothelial monolayers under flow conditions.
We analyzed an initial step of T cell adhesion to endothelial cells under flow conditions. An initial step in T cell-endothelial cell interactions was characterized either by a rolling phase, or by an immediate arrest without rolling. Anti-E- and P-selectin Abs inhibited T cell rolling on endothelial cells under flow conditions. The rolling velocity of T cells on endothelial cells increased after treatment of endothelial cells with anti-E- or P-selectin Abs. Also, rolling of T cells was observed on E-selectin-transfected CHO cells but not on ICAM-1-transfected CHO cells. Thus, rolling of T cells under flow condition was dependent on E-selectin as well as P-selectin expressed on endothelial cells. In contrast, neither anti-E- nor P-selectin Abs inhibited the immediate arrest of T cells on endothelial cells significantly and anti-ICAM-1 Abs also failed to inhibit the immediate arrest of T cells. Therefore, other adhesion molecules may play an important role in the immediate arrest of T cells under flow conditions. The number of CD45RA- T cells rolling on E-selectin-transfected CHO cells was much higher than that of CD45RA+ T cells.
Animals↗
Increased expression of cathepsins E and D in reactive microglial cells associated with spongiform degeneration in the brain stem of senescence-accelerated mouse.
Senescence-accelerated mouse (SAM) P8 and P10 exhibit a spongy degeneration, especially in the brain stem, and a brain atrophy mainly in the frontal portion of the cerebral cortex, respectively, with advancing age. In an attempt to clarify the role of two distinct intracellular aspartic proteinases, cathepsins E (CE) and D (CD), in these age-related pathological changes, accumulation and localization of these enzymes were investigated in the brain stem and the cerebral cortex of SAMP8 and P10 and in the senescence-resistant control SAMR1 with four different age groups (1 week and 2, 6, and 12 months). In the brain stem of SAMP8, a marked spongy degeneration was observed at more than 2 months of age. The same degree of spongy degeneration was also observed in the brain stem of age-matched SAMP10 but not SAMR1. The nonlysosomal enzyme CE was barely detectable in the brain stem of all three strains at 1 week of age, but it was markedly accumulated in the brain stem of SAMP8 and P10 at 2 months of age. The lysosomal enzyme CD was found in relatively high concentration in the brain stem of all three strains at 1 week of age. At 2 months of age, CD contents were significantly increased in the brain stem of SAMP8 and P10 compared with those of age-matched SAMR1. At the light-microscopic level, increased immunoreactivities for CE in the brain stem of 2-month-old SAMP8 and P10 were found in reactive microglial cells clustered at the spongy areas but not in microglial cells with resting or ramified morphology and astrocytes. The increased immunoreactivity for CD was observed mainly in reactive astrocytes and partially in reactive microglial cells. Immunoblotting analyses revealed that CE in the brain stem of 2-month-old SAMP10 consisted of only the mature form of 42 kDa, whereas CD in this tissue is composed of mainly the mature form of 44 kDa and partially its degradation products. On the other hand, there was a marked brain atrophy mainly in the frontal portion of the cerebral cortex of 6-month-old SAMP10 but not in age-matched SAMP8 or SAMR1. Although CE was not detectable even in the atrophied cortical area of SAMP10, CD contents in the cerebral cortex slightly increased with senescence in all three strains.(ABSTRACT TRUNCATED AT 400 WORDS)
Age Factors↗
Prednisolone excitation of medial vestibular nucleus neurons in cats.
An electrophysiological study was performed to determine whether prednisolone hydrochloride directly influenced neuronal activities of the medial vestibular nucleus (MVN) in alpha-chloralose-anesthetized cats. Single neuronal activities of MVN were recorded extracellularly with a glass-insulated silver wire microelectrode attached along a seven-barreled micropipette. Each barrel was filled with prednisolone, glutamate, glutamic acid diethylester (GDEE) or CoCl2. Except for prednisolone, which was administered both intravenously and microiontophoretically, other chemicals were applied microiontophoretically to the immediate vicinity of the target neurons. These MVN neurons were classified as type I and II neurons according to their responses to horizontal and sinusoidal rotations. Intravenous prednisolone (up to 5 mg/kg) enhanced spontaneous and rotation-induced neuronal firings of both type I and II neurons in a dose-dependent manner. In a similar tendency, microiontophoretically applied prednisolone (50-200 nA) dose-dependently increased spontaneous and rotation-induced firings of both type I and II neurons. Microiontophoretic GDEE, a non-selective glutamate receptor antagonist, inhibited glutamate- and rotation-induced neuronal discharges without affecting prednisolone-induced increases in neuronal responses of MVN. In addition, iontophoretically applied CoCl2, a Ca2+ channel blocker, did not affect prednisolone-, glutamate- and rotation-induced neuronal findings of MVN. These results suggest that prednisolone induces excitation of type I and II neurons, probably by acting directly on the membrane of MVN neurons. Thus, glucocorticoids such as prednisolone may be effective for the treatment of vertigo resulting from hypofunction of vestibular nucleus neurons.
Animals↗