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Biomedical subjects

S Hirai

Publications and source records attributed to S Hirai.

At least 73 records · Page 4Linked to original sources
PubMed2000

Gamma knife radiosurgery as a primary treatment for prolactinomas.

OBJECT: The purpose of this study was to estimate the efficacy of gamma knife radiosurgery (GKS) in controlling tumor growth and endocrinopathy associated with prolactinomas. METHODS: Between 1993 and 1997, 164 of 469 patients with pituitary adenomas treated by GKS harbored prolactinomas. The dose to the tumor margin ranged from 9 to 35 Gy (mean 31.2 Gy), and the visual pathways were exposed to a dose of less than 10 Gy. The mean tumor diameter was 13.4 mm. The mean follow-up time for 128 cases was 33.2 months (range 6-72 months). Tumor control was observed in all but two patients who underwent surgery 18 and 36 months, respectively, after GKS. Clinical cure was achieved in 67 cases. Clinical improvement was noted with a decrease in the hyperprolactinemia after GKS. Nonetheless, in 31 (29%) of 108 patients who were followed for more than 2 years no improvement in serum prolactin levels was demonstrated, although this could be normalized by bromocriptine administration after treatment. Nine infertile women became pregnant 2 to 13 months after GKS and all gave birth to normal children. There was no visual deterioration related to GKS. Five women experienced premature menopause. In these patients there was subtotal disappearance of the tumor and an empty sella developed. CONCLUSIONS: Gamma knife radiosurgery as a primary treatment for prolactinomas can be safe and effective both for controlling tumor growth and for normalization of prolactin hypersecretion. A higher margin dose (> or = 30 Gy) seemed to be associated with a better clinical outcome. Gamma knife radiosurgery may make prolactinomas more sensitive to the bromocriptine.

Humans↗
PubMed2000

[Malignant mesothelioma presenting as a perineal and pelvic mass--a trial of high dose intra-arterial methotrexate injection and irradiation].

A 50-year-old male with the complaints of lumbago and voiding disturbance was diagnosed to have malignant mesothelioma. Serum CA-125 was found to be elevated. The tumor was stained positive immunohistochemically only for CA-125 and epithelial membrane antigen. Magnetic resonance imaging of the pelvic demonstrated a large mass extending from the right external obturator muscle to the perineum. He was treated by two courses of methotrexate given intra-arterially (2,000 mg) followed by external beam irradiation at a total dose of 60 Gy. Disease progression was not apparent 15 months after treatment.

Antimetabolites, Antineoplastic↗
PubMed2000

[A case of saccular aneurysm of the coronary artery post PTCA].

We experienced a 48-year-old man who was diagnosed as having a saccular aneurym of the coronary artery by CAG after an otherwise uneventful percutaneous transluminal coronary angioplasty (PTCA). At the time of operation, the aneurysm, measured 15 mm, and arose from the 3rd segment of the right coronary artery. Aneurysmal formation after successful PTCA is not rare and is related to the overinflating balloon. It is necessary to evaluate the coronary artery after PTCA by IVUS. There were no symptoms after the operation and he was discharged at 21th postoperative day.

Angioplasty, Balloon, Coronary↗
PubMed2000

Minimally invasive direct coronary artery bypass grafting using the saphenous vein in redo CABG.

We describe a patient who underwent minimally invasive direct coronary artery bypass (MIDCAB), who had previously undergone coronary artery bypass grafting (CABG) through a median sternotomy with a left internal mammary artery (LIMA) graft to the left anterior descending artery (LAD) and a right gastroepiploic artery (GEA) graft to the posterior descending artery. MIDCAB was less invasive and was an effective alternative procedure for the second operation. Because the patient had no LIMA or GEA available for a graft because of prior use, we used a saphenous vein graft (SVG) for bypassing from the left subclavian artery to the coronary artery by MIDCAB via a left minithoracotomy. The left subclavian artery was selected as the proximal anastomotic site because this artery was less diseased and was easier to reach. The SVG-to-coronary artery anastomosis was facilitated by firm adhesion between the epicardium and the pericardium, which reduced the motion of the epicardium itself. These results suggest that the procedure is safe and promising in selected cases of redo CABG.

Cardiopulmonary Bypass↗
PubMed2000

[An investigation of factors associated with failure of extracorporeal shock wave lithotripsy for ureteral calculi].

In this study, we attempted to determine which patients with ureteral calculi are likely to have an unsuccessful outcome for extracorporeal shock wave lithotripsy (ESWL). The records of 388 patients with ureteral calculi treated with ESWL at Ijinkai Takeda General Hospital between January 1997 and December 1998 were retrospectively reviewed. Three hundred seventeen patients had been treated with ESWL alone (single session 156, multiple sessions 161) and 71 with transurethral ureterolithotripsy (TUL) due to failure of ESWL. We compared these two groups by multivariate logistic regression analysis, which revealed that (1) middle and lower ureteral calculi, (2) stones > 8 mm, (3) moderate to severe hydronephrosis and (4) failure of the first session ESWL were factors associated with poor outcome of ESWL. Although each predictive value of these factors was relatively low (29.6-38.6%), the rate of failure of ESWL was 85.0% when patients had all four factors. We therefore recommend an early change in treatment modality to TUL for patients with ureteral calculi when all four risk factors listed above are present.

Adult↗
PubMed2000

Leakage of aquaporin 5 in the tear of dacryoadenitis mice.

PURPOSE: The objective of this study was to investigate whether leakage of aquaporin 5 (AQP5) in tear is associated with damage of lacrimal glands (LGs) in dacryoadenitis models. METHODS: Female MRL/lpr (24-week-old), male NOD/Shi Jci (5-, 8-, and 10-week-old), female NFS/s-TX (10-week-old), and lipopolysaccharide (LPS)-induced dacryoadenitis model mice were used. Tear fluid was collected by a cotton thread. Tear proteins in the thread were dissolved in sodium dodecyl sulfate buffer, and AQP5 proteins were analyzed by the Western blot technique using anti-AQP5 antibody. LGs were prepared for hematoxylin and eosin staining or immunostaining of AQP5. RESULTS: In MRL/lpr, NFS/s-TX, 8- and 10-week-old NOD/Shi Jci mice, AQP5 protein was detected in the tear by Western blot analysis. Inflammatory lymphocyte infiltrations were observed in LGs of these dacryoadenitis model mice. In contrast, AQP5 leakage and damage of LG were not observed in normal mice. In 5-week-old NOD/Shi Jci mice, infiltration was not seen in LG, and AQP5 leakage was not detected in the tear. In LPS-induced dacryoadenitis model mice, either tissue destruction with inflammation in LG or AQP5 leakage in the tear was observed. AQP5 in the tear and tissue inflammation in LGs was not found in control mice. These results indicate that AQP5 is leaked in tears when LGs are damaged by dacryoadenitis. CONCLUSIONS: Leakage of AQP5 in the tear was found to be related to LG damage. This finding suggests that detection of AQP5 in tear is useful for specific diagnosis of LG disorders with tissue destruction.

Animals↗
PubMed2000

[A case of Guillain-Barré syndrome (GBS) following human parvovirus B19 infection].

Human parvovirus B19 (HPV-B19) infection is recently known to produce variable clinical manifestations, but neurological disorder associated with this infection is uncommon. We reported a case of GBS associated with transient lupus-like status following HPV-B19 infection. This is the first report describing an adult case of GBS following HPV-B19 infection. A healthy female, aged 33, developed erythema infectiosum simultaneously with her 5-year-old daughter. On the same day, she noticed leg fatigue, which worsened in the following days. On the day 11th, she became unable to walk. Mild pancytopenia, liver injury, proteinuria, hypocomplementemia, and increased anti-nuclear antibody (ANA) were revealed at a hospital. Polymerase chain reaction detected HPV-B19 DNA in the serum. On the day 17th, she was admitted to our hospital because of moderate generalized weakness and mild sensory disturbance, which were symmetrical and distal-dominant. The deep tendon reflexes were absent. Analysis of cerebrospinal fluid showed albuminocytologic dissociation. Other laboratory data were normal except positive ANA. Enzyme-linked immunosorbent assay (ELISA) showed high titer of the serum IgM antibody to GM1 and GD1b. Serum anti HPV-B19 IgM and IgG tested by ELISA were also positive. She improved gradually after 2 courses of double filtrated plasma pheresis.

Adult↗
PubMed1999

Presenilin 1 suppresses the function of c-Jun homodimers via interaction with QM/Jif-1.

Presenilin 1 (PS1) is the causative gene for an autosomal dominant familial Alzheimer's disease (AD) mapped to chromosome 14. Here we show that QM/Jun-interacting factor (Jif)-1, a negative regulator of c-Jun, is a candidate to mediate the function of PS1 in the cell. We screened for proteins that bind to PS1 from a human embryonic brain cDNA library using the two-hybrid method and isolated one clone encoding the QM/Jif-1 gene. The binding of QM/Jif-1 to full-length PS1 was confirmed in vitro by pull-down assay, and in vivo by immunoprecipitation assays with human samples, including AD brains. Immunoelectronmicroscopic analysis showed that QM/Jif-1 and PS1 are colocalized at the endoplasmic reticulum, and the nuclear matrix in human brain neurons. Chloramphenicol acetyltransferase assays in F9 cells showed that PS1 suppresses transactivation by c-Jun/c-Jun but not by c-Jun/c-Fos heterodimers, consistent with the reported function of QM/Jif-1. By monitoring fluorescent recombinant protein and by gel mobility shift assays, PS1 was shown to accelerate the translocation of QM from the cytoplasm to the nucleus and to thereby suppress the binding of c-Jun homodimer to 12-O-tetradecanoylphorbol-13- acetate (TPA)-responsive element (TRE). PS1 suppressed c-jun-associated apoptosis by retinoic acid in F9 embryonic carcinoma cells, whereas this suppression of apoptosis is attenuated by mutation in PS1. Collectively, the novel function of PS1 via QM/Jif-1 influences c-jun-mediated transcription and apoptosis.

Adult↗
PubMed1999

Cellular co-localization of phosphorylated tau- and NACP/alpha-synuclein-epitopes in lewy bodies in sporadic Parkinson's disease and in dementia with Lewy bodies.

The precursor of the non-Abeta-component of Alzheimer's disease (AD) amyloid (NACP, alpha-synuclein) aggregates into insoluble filaments of Lewy bodies (LBs) in Parkinson's disease (PD) and dementia with LBs (DLB). The microtubule-associated protein tau is an integral component of filaments of neurofibrillary tangles (NFTs). NFTs are occasionally found in brains of PD and DLB; however, the presence of NFTs or tau-epitopes within LB-containing neurons is rare. Double-immunofluorescence study and peroxidase-immunohistochemical study in serial sections, performed to examine the co-localization of tau- and NACP-epitopes in the brainstem of PD and DLB, demonstrated that four different epitopes of tau including phosphorylation-dependent and independent ones were present in a minority of LBs, but more often than previously considered. A tau (tau2)-epitope was localized to filaments in the outer layers of brainstem-type LBs by immunoelectron microscopy. Therefore, we conclude that tau is incorporated into filaments in certain LBs. Extensive investigation has enabled us to classify this co-localization into four types: type 1, LBs with ring-shaped tau-immunoreactivity; type 2, LBs surrounded by NFTs; type 3, NACP- and tau-immunoreactive filamentous and granular masses; and type 4, NACP- and tau-immunoreactive dystrophic neurites. This study raises a new question whether aggregation and hyperphosphorylation of tau in PD and DLB are triggered by the collapse of intraneuronal organization of microtubules due to NACP-filament aggregation in neuronal perikarya and axons.

Aged↗
PubMed1999

Direct interaction of the beta-domain of VHL tumor suppressor protein with the regulatory domain of atypical PKC isotypes.

VHL tumor suppressor protein contains two domains, alpha and beta. The alpha-domain is involved in the formation of a large protein complex suggested to be involved in ubiquitin-mediated protein degradation. However, the role of the beta-domain, which may recognize the target proteins for protein degradation, remains unknown. Here we report that the beta-domain interacts directly with atypical PKC isotypes, PKCzeta and PKClambda. Further, the regulatory domain of aPKC is sufficient for this direct protein-protein interaction. Since aPKC isotypes have been implicated in the regulation of cell growth and apoptosis, these results suggest that aPKC isotypes are potential direct target of the VHL beta-domain.

Amino Acid Sequence↗
PubMed1999

Cloning and characterization of the murine PKC alpha promoter: identification of a retinoic acid response element.

Protein kinase C (PKC) is a family which consists of multiple isoforms whose distinct physiological roles within the cell are unknown. We have previously demonstrated that levels of PKC alpha mRNA, protein, and enzyme activity in B16 melanoma cells can be modulated by retinoic acid. We investigated this regulation by cloning and characterizing the promoter region of the murine PKC alpha gene. A 13 kb mouse genomic fragment containing the 5' flanking region, first exon, and first intron was isolated and sequenced. Two transcription initiation sites were identified at 919 and 925 bp upstream from the translation start site. The promoter region contained a TATA-like box at -93 bp upstream of the transcription start site, but no CAAT box. Promoter activity differed between cell lines and correlated with the levels of PKC alpha expressed in these cell lines. Reporter gene assays showed that the region between -179 and -452 bp likely contains a silencer element(s). The promoter activity of a -179 bp fragment in B16 cells was stimulated twofold by retinoic acid. Within this region (-93 to -65 bp) there is a retinoic acid response element. An oligonucleotide spanning this region specifically bound exogenous RAR-RXR heterodimers and endogenous RAR from B16 nuclear extracts. These results suggest that retinoic acid increases PKC alpha gene expression in B16 cells, at least in part, through direct transcriptional stimulation of its promoter.

Animals↗
PubMed1999

Endovascular treatment of intracranial aneurysms: saccular aneurysms and posttraumatic pseudoaneurysms.

The endovascular treatment of intracranial aneurysms is gaining a definite place in neurosurgery. This is particularly true for treatment using the Guglielmi detachable coil (GDC). "Endovascular treatment or direct surgery?" is a common discussion nowadays. The following papers raise some important issues with respect to this argument. This review also includes several papers that deal with posttraumatic pseudoaneurysms. One of the papers clearly suggests that endovascular treatment could also play an important role in treating pseudoaneurysms.

Journal Article↗
PubMed1999

Dopamine and DOPA cause release of iron from ferritin and lipid peroxidation of liposomes.

We investigated dopamine (DA)- and DOPA-related release of iron from ferritin, and lipid peroxidation of liposomes induced by the released iron. Iron release increased with increasing DA or DOPA concentrations. Effects of SOD and an oxygen-reduced environment indicated that superoxide was partly responsible for iron release. The released iron induced lipid peroxidation at relatively low concentrations of DA or DOPA, while at high concentrations, peroxidation was inhibited. These findings indicate that the risk of lipid peroxidation depends on the DA/iron or DOPA/iron ratio even if the iron concentration is low. Our findings suggest that DA-containing neurons are always at risk of oxidative damage. Furthermore, DOPA therapy may modify the nigral degeneration by reducing or accelerating ferritin iron-dependent lipid peroxidation.

Animals↗
PubMed1999

Carboxyl-terminal fragments of presenilin-1 are closely related to cytoskeletal abnormalities in Alzheimer's brains.

To clarify the role of presenilin-1 (PS-1) in the pathology of Alzheimer's disease (AD), we tested four antisera to PS-1. The specific antisera to the N-terminus (HSN-2) and C-terminus (HS-C) of PS-1 detected a 44/40kD holoprotein, a 25kD N-terminal fragment (NTF) and a 16kD C-terminal fragment (CTF) of PS-1 in COS-7 cells. The 25kD NTF and 16kD CTF were observed in human brains, and their amounts were not significantly different between the control and AD brains. The antibody HS-C labeled extensive neurofibrillary tangles, dystrophic neurites and curly fibers in the AD brains. In the paired helical filament (PHF) fraction containing A68 protein from AD brains, a smear pattern of CTFs was revealed. Antisera (HS-L292 and HS-L300) to cleavage sites of PS-1 also revealed immunoreactive neurofibrillary tangles in the AD brain sections and the smear pattern of CTFs of A68 protein fraction. The CTFs of PS-1 accumulate with PHF tau, suggesting a close relationship between PS-1 and cytoskeletal abnormalities in AD brains.

Aged↗
PubMed1999

Changes in the cytoskeletal proteins, sarcoplasmic reticulum, and capillaries in acute relaxant-steroid myopathy (ARSM) in contrast to the corticosteroid myopathy.

Since we reported a case of acute relaxant-steroid myopathy (ARSM) in 1994, we continued histological studies and compared the findings with those in a case of corticosteroid myopathy (CM). It was revealed that (1) dystrophin, spectrin, beta dystroglycan, and sarcoglycans on the cell surface were decreased, (2) regular arrangement of the sarcoplasmic reticulum was lost, and (3) some capillaries were degenerated. Since none of these changes were seen in CM, it became clear that ARSM is different from CM. It was estimated that continuous administration of non-depolarizing muscle relaxant produces a state akin to denervation. Combination of denervation, immobilization and circulatory disturbance in ARSM not only augments the effects of corticosteroids, but they produce changes different from CM, namely impairment of the cell membrane system (both internal and external) and capillary degeneration.

Capillaries↗
PubMed1999

Immunohistochemical and ultrastructural characterization of neuritic clusters around ghost tangles in the hippocampal formation in progressive supranuclear palsy brains.

We performed a detailed study of swollen neurite aggregation surrounding extracellular neurofibrillary tangles (ghost tangles, GTs) in brains of patients with progressive supranuclear palsy (PSP) by immunohistochemistry and electron microscopy (EM). The complex structures, designated as tangle-associated neuritic clusters (TANCs), were found in the hippocampus and parahippocampal cortex in all five PSP brains examined. TANCs measured from 20 to 40 microm across; twice as large as nearby neurons. Each neurite was globular or fusiform in shape, measured up to 10 microm in diameter, and was found between loosened fascicles of GTs or along their outer rims. There were several subsets of neurites that were argyrophilic or immunoreactive against antibodies to either phosphorylated tau protein, phosphorylated neurofilaments, ubiquitin, or synaptophysin. On EM, TANCs consisted of numerous axon terminals of varying size, which were filled with flocculate dense bodies, vesicular profiles, and synaptic vesicles, as well as normal-looking and degenerating cell organelles. Some axons had 13- to 15-nm-thick straight tubules that showed tau immunoreactivity; however, there was little neurofilament accumulation. Most of the swollen axon terminals conformed to the ultrastructural features of either reactive or degenerating terminals. The neurites identified by immunohistochemistry only represented a minority of the swollen axons visualized by EM. Tubules of GTs were dispersed in the extracellular space, but no amyloid fibrils were found. TANCs may constitute a distinctive form of neuronal degeneration in PSP cortices. We hypothesize that axon terminal accumulation may occur in response to GT-formation.

Aged↗