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Biomedical subjects

M Nakai

Publications and source records attributed to M Nakai.

At least 109 records · Page 6Linked to original sources
PubMed1998

Carbendazim-induced abnormal development of the acrosome during early phases of spermiogenesis in the rat testis.

Effects of a single, high dose of orally administered carbendazim (100 mg/kg) on acrosome formation in the early phases of spermiogenesis were examined by electron microscopy and immunocytochemistry up to day 7.5 post-treatment. No obvious abnormality of acrosome development was noted in the Golgi phase spermatids on day 1.5 post-treatment. On day 3, step 1 spermatids were seen in stage III seminiferous tubules. In stage V tubules at this post-treatment interval, direct connections between the trans-side saccules of the Golgi stacks and the outer acrosomic membranes were observed in step 5 spermatids. Similar direct connections between these two organelles were also observed in the advanced round spermatids in later stages at days 4.5 and 7.5. On day 4.5, step 1 and 3 spermatids were seen in stage V tubules. On day 7.5, round spermatids with various abnormalities of acrosome development were observed in stage VII tubules, in addition to the discontinuous and granular acrosomes reported previously. These features were not observed in testes of control animals. In the immunocytochemical analysis using an antibody mMN7 that recognizes a protein delivered from the Golgi apparatus to the acrosome, spermatids exposed to carbendazim showed various abnormal immunostaining patterns in the acrosomes. On the other hand, strong immunoreactivity was observed in the Golgi saccules connecting to the acrosomes. These results suggest that in testis treated with carbendazim acrosome development is impaired during the early phases of spermiogenesis, and material supply from the Golgi apparatus to the acrosome is perturbed, which is a possible cause of the abnormal development.

Acrosome↗
PubMed1998

Beneficial effects of prostaglandin E1 on ischemic colitis following surgery on the abdominal aorta.

To determine the effects of prostaglandin E1 (PGE1) on the intestinal circulation, an experimental dog model of ischemic colitis following abdominal aortic reconstruction was made by ligating the inferior mesenteric artery (IMA) and the internal iliac artery, with the creation of a 50% stenosis in the superior mesenteric artery (SMA). The parameters of enteric ischemia included the blood flow of the SMA, the tissue blood flow in the small intestine and left colon, the mean stump pressure of the IMA (IMAP), and the IMAP/mean systemic blood pressure ratio. With the continuous infusion of 10 ng/kg per minute of PGE1 into the descending thoracic aorta, these values increased significantly on the seventh postoperative day compared with those on the day of operation. These results thus suggest that the continuous intraarterial infusion of PGE1 may reduce ischemic changes in the colon following abdominal aortic reconstruction.

Alprostadil↗
PubMed1998

Isoform-specific redistribution of calcineurin A alpha and A beta in the hippocampal CA1 region of gerbils after transient ischemia.

To investigate isoform-specific roles of Ca2+/calmodulin-dependent phosphatase [calcineurin (CaN)] in ischemia-induced cell death, we raised antibodies specific to CaN A alpha and CaN A beta and localized the CaN isoforms in the hippocampal CA1 region of Mongolian gerbils subjected to a 5-min occlusion of carotid arteries. In the nonischemic gerbil, immunoreactions of both isoforms were highly enriched in CA1 regions, especially in the cytoplasm and apical dendrites of CA1 pyramidal neurons. At 4-7 days after the induced ischemia, immunoreactivities of the CaN A alpha isoform in CA1 pyramidal cells were markedly reduced, whereas they were enhanced in the CA1 radiatum and oriens layers. In contrast, CaN A beta immunoreactivities were reduced in all layers of the ischemic CA1 region, whereas they were enhanced in activated astrocytes, colocalizing with glial fibrillary acidic protein. These findings suggest that up-regulation of CaN A alpha in afferent fibers in CA1 and up-regulation of CaN A beta in reactive astrocytes may be involved in neuronal reorganization after ischemic injury.

Animals↗
PubMed1998

[Studies for dynamics of reverse transcriptase inhibiting antibody in sera from HIV-1 infected individuals].

Antibodies inhibiting human immunodeficiency virus type 1 (HIV-1) reverse transcriptase activity (RTI-antibody), Binding inhibition antibody (BI-antibody) and polymerization inhibition antibody (PI-antibody) were investigated for their ability to inhibiting RT activity in 248 HIV-1 infected individuals and 99 healthy individuals. In BI-antibody, high titer samples were determined more in than in RTI- and PI-antibodies. No significance was indicated between AC, ARC and AIDS is any antibody, however, progression from AC to AIDS was poled to high titer and low titer in RTI- and BI-antibodies. Moreover, time course of each antibody levels in the same infected individuals were resulted in no change, going up or down through all the experimental term, though all samples were collected in AC. These results were suggested that the determination factor of each stage in HIV progression would be multiple, and that the various dynamics of RTI-, BI- and PI-antibodies in the same infected individuals might be caused in the term from HIV infection to AIDS progression, prognosis or appearing of the drug resistant strain but stages of the disease.

Acquired Immunodeficiency Syndrome↗
PubMed1998

Nuclear factor-kappa B contributes to excitotoxin-induced apoptosis in rat striatum.

Excitotoxin-induced destruction of striatal neurons, proposed as a model of Huntington's disease, involves a process having the biochemical stigmata of apoptosis. Recent studies suggested that transcription factor nuclear factor (NF)-kappa B may be involved in excitotoxicity. To further analyze the contribution of NF kappa B to excitotoxic neuronal death in vivo, changes in binding activities of NF kappa B and other transcription factors as well as the consequences of inhibiting NF kappa B nuclear translocation were measured after the infusion of quinolinic acid (120 nmol) into rat striatum. Internucleosomal DNA fragmentation and terminal transferase-mediated dUTP digoxigenin nick end labeling-positive nuclei appeared 12 hr later and intensified over the next 12 hr. NF kappa B binding activity increased several-fold from 2 to 12 hr, then gradually declined during the next 12 hr. Other transcription factor changes included AP-1, whose binding peaked about 6 hr after quinolinic acid administration, and E2F-1, which was only modestly and transiently elevated. In contrast, quinolinic acid lead to a reduction in OCT-1, beginning after 12 hr, and briefly in SP-1 binding. The NF kappa B, AP-1, and OCT-1 changes were attenuated both by the N-methyl-D-aspartate receptor antagonist MK-801 and the protein synthesis inhibitor cycloheximide. Moreover, quinolinic acid-induced internucleosomal DNA fragmentation and striatal cell death were significantly reduced by the intrastriatal administration of NF kappa B SN50, a cell-permeable recombinant peptide that blocks NF kappa B nuclear translocation. These results illustrate the complex temporal pattern of transcription factor change attending the apoptotic destruction produced in rat striatum by quinolinic acid. They further suggest that NF kappa B activation contributes to the excitotoxin-induced death of striatal neurons.

Animals↗
PubMed1998

Scanning electron microscopic study of the vascular supply of the equine hoof.

The blood supply in the equine hoof was studied by a microvascular casting corrosion technique and scanning electron microscopy in combination with observations of sections of the decalcificated digit. The dermal lamella was observed at the hoof wall and the dermal papilla at the other parts of the hoof. The microvascular architecture of the dermal lamella differed from that of dermal papilla. The vascular cast in the dermal papillar regions indicated that each papilla contained two central vessels (artery and vein), which ran parallel to each other, and the capillary plexus surrounding these vessels. In the dermal lamella region, the vessels consisted of thin parallel sheets arranged in vertical rows. Each sheet was made of branched arteries and veins, both of which were sandwiched between capillary plexus. At the distal and proximal parts of the wall, the vascular casts of the papillae merged to form the vascular sheets of the dermal lamella.

Animals↗
PubMed1998

Spermatids of prepubertal male rats are susceptible to carbendazim during early spermiogenesis.

The fungicide carbendazim, a male reproductive system toxicant, affects the adult testis, while prepubertal animals are assumed to be unsusceptible to the chemical. The present study was conducted to re-evaluate the susceptibility of rat prepubertal testis (25-30 days old) to carbendazim based on the incidence of spermatid abnormalities, including nuclear enlargement (megaspermatids) and binucleate round spermatids. In control prepubertal rats treated orally with corn oil vehicle alone, seminiferous tubules containing magno- and/or binucleate round spermatids were often observed in the groups at stages II-III, IV-V and VI-VII. At 3.0 days after treatment with carbendazim (100 mg/kg), seminiferous tubules containing spermatids with identical abnormalities were significantly increased, including groups at all stages. Significant increases were also observed at stages IV-V and VI-VII at day 4.5, and VI-VII at day 7.5. In contrast, the frequency of spermatids with these abnormalities was reduced in the groups at stages II-III and IV-V at day 7.5. These findings confirm that the prepubertal rat testis is susceptible to carbendazim during early spermiogenesis.

Animals↗
PubMed1998

Cellular characterization of the 91kDa-ectopic ascitic antigen sharing antigenicity with MRP8 in the human placenta as revealed by immunoelectron microscopical colloidal-gold techniques.

Cellular characterization of the 91kDa-ectopic ascitic protein that exhibits pregnancy-associated and tumour-related dynamics has been examined in the human placenta using an electron microscopic immunocolloidal-gold technique. This protein was initially isolated from the ascitic fluids of a patient suffered from ovarian and uterine cancers with mixed mesodermal tumours, and determined to be sharing antigenicity with the 28kDa-oncodevelopmental protein and a calcium-binding protein; MRP8/CFA, respectively. Placentas obtained were divided into three groups by their gestational periods. Small chorionic villous tissues were embedded in Lowicryl K4M resin or Epon 812 resin. Specific and higher labelings by gold-particles were obtained in sections of Lowicryl resin and, then, recognized in mesenchyme-derived cells and/or myeloid lineages; such as placental tissue macrophages (Hofbauer cells), fibroblasts, foetal myelomonocytic cells including endothelial cells, etc., in the first and second trimesters. So far, the pattern of antigenic appearances changed depending on the stage of gestation. On the other hand, 91kDa-protein was also determined in the syncytiotrophoblast, but not in cytotrophoblasts at whenever been examined. It is assumed that the antigenic expression in syncytiotrophoblasts might be reflected to be absorbed or incorporated from those of foetal or maternal origins, and the antibody used in this study should be sensitive to the antigenic epitope derived from those of myeloid lineages. In the light of these results, hypotheses concerning mechanisms of both transplacental permeability of substances by the placental barrier and cell/tissue differentiation by calcium-binding (and/or -depending) proteins such as 91kDa-protein, MRP8, etc.; presumable the S-100 protein family, are discussed further.

Antibody Specificity↗
PubMed1998

[Late results of acute aortic dissection: analysis of the patients longer than five years after the operation].

Between 1985 and 1992, 28 patients of acute type A aortic dissection were operated on at our department. Our surgical strategy for this disease is "limited aortic resection", that is to avoid replacement of the entire arch except for the patients with arch tear that cannot be resected without total arch replacement. There were one operative mortality due to post transfusion GVHD, and ten late mortality (rupture of the residual dissecting aneurysm 3; complication of the late reoperation 3; cerebrovascular disease 2; pulmonary infection 2). Actuarial survival rate of all cases is 92.9%, 62.9%, and 58.4% at 1, 5, and 10 years, respectively. Comparing the patients whose primary tear was resected or not resected, there was no difference in the rate of residual dissection (12/16, 75% vs 5/6, 83.3%; primary tear resected vs not resected), the rate of late reoperation (3/16, 18.8% vs 1/6, 16.7%), nor actuarial survival rate (90.5% vs 100%, 66.7% vs %, 53.6% vs 71.4%, at 1, 5, 10 years, respectively). There were three cases with Marfan's syndrome, and all three cases died of the rupture of the residual dissection. We will follow the policy of the "limited aortic resection" unless the operative mortality of the entire arch replacement is proved as good as that of the ascending or hemiarch replacement. Because of the poor late results of the patients with Marfan's syndrome, entire arch replacement at the initial surgery and aggressive reoperation for the residual dissection is necessary.

Acute Disease↗
PubMed1997

Characterization and evolution of a gene encoding a Trimeresurus flavoviridis serum protein that inhibits basic phospholipase A2 isozymes in the snake's venom.

The proteins that bind phospholipase A2 (PLA2) isozymes of Trimeresurus flavoviridis (habu snake, crotalinae) venom were fractionated from sera on four columns, each conjugated with one of four PLA2 isozymes. Five proteins, termed PLA2 inhibitors (PLI) I-V, were obtained as the binding components. The combinations of the binding components differed depending on the PLA2 isozymes. PLI-IV and PLI-V correspond to PLI-A and PLI-B, respectively, which were known to bind to a major [Asp49]PLA2, PLA2, and contained a segment similar to the carbohydrate-recognition domain of C-type lectins. PLI-I, which is a major component of inhibitory proteins against three basic PLA2 isozymes, PLA-B (a basic [Asp49]PLA2) and basic proteins I and II (both [Lys49]PLA2s), has been isolated, and its partial amino acid sequence has been determined. A cDNA encoding PLI-I was isolated from a T. flavoviridis liver cDNA library and sequenced. PLI-I cDNA encoded 200 amino acid residues, including a signal peptide of 19 amino acid residues. One sugar chain was predicted to occur at position 157. A gene coding for PLI-I was isolated. It is 9.6-kb long and consists of five exons and four introns. Comparison of the exon-intron structure of the PLI-I gene with those of genes encoding urokinase-type-plasminogen-activator receptor (uPAR), Ly-6, CD59 and neurotoxins showed that they have characteristic unit encoding approximately 90 amino acid residues, which is divided over two exons. This strongly suggests that the PLI-I gene belongs to the uPAR, Ly-6, CD59 and neurotoxin gene family. There are two types of structurally different inhibitors against PLA2 isozymes in T. flavoviridis serum with different evolutionary origins.

Amino Acid Sequence↗
PubMed1997

Lack of infectivity of HIV-1 integrase zinc finger-like domain mutant with morphologically normal maturation.

The integrase (IN) encoded by human immunodeficiency virus type-1 (HIV-1) is required for integration of the viral DNA into a host cell chromosome. The function of the highly conserved HHCC motif in the HIV-1 IN amino-terminal zinc finger-like domain is still unknown. In this study, we examined the effect of mutations in the HHCC motif on viral infectivity, adsorption to and entry into target cells, and morphology in the context of a full-length form of an HIV-1 molecular clone. A complete lack of infectivity and de novo synthesized viral DNA of the HHCC mutants were demonstrated in both cell-free and co-culture infection systems using MT-2 or HeLa-CD4-LTR-beta-gal as target cells. The levels of viral adsorption to and entry into the target cells were determined by measuring the cell-associated p24 level in target MT-2 cells shortly after infection. We detected comparable cell-associated p24 levels of MT-2 cells after infection with wild-type and the mutant viruses. Taken together, these results suggest that the replication of HIV-1 carrying point mutations in the HHCC motif was blocked at the step after adsorption/ entry and prior to the initiation of reverse transcription, presumably at the uncoating step. Furthermore, electron microscopy revealed that the observed complete lack of viral infectivity caused by introducing an amino acid substitution into the HHCC motif is not always accompanied by apparent abnormal morphology or maturation of virus particles.

Adsorption↗
PubMed1997

Glutamate metabotropic receptor agonist 1S,3R-ACPD induces internucleosomal DNA fragmentation and cell death in rat striatum.

Glutamate metabotropic receptor mediated mechanisms have been implicated in both neuroprotection and neurotoxicity. To characterize these mechanisms further in vivo, the effects of an intrastriatally injected metabotropic receptor agonist, trans-(1S,3R)-1-amino-1,3-cyclopentanedicarboxylic acid (1S,3R-ACPD), were studied alone and together with N-methyl-D-aspartate (NMDA) or kainic acid (KA) receptor agonists on DNA fragmentation and nerve cell death. 1S,3R-ACPD induced internucleosomal DNA fragmentation of striatal cells in a dose-dependent manner. TUNEL and propidium iodide staining showed DNA fragmentation and profound nuclear condensation around the injection site. Fragmented nuclei were occasionally seen under light microscopy. Internucleosomal DNA fragmentation induced by 1S,3R-ACPD was attenuated by the protein synthesis inhibitor cycloheximide as well as by the non-selective and selective metabotropic receptor antagonists L-(+)-2-amino-3-phosphonopionic acid (L-AP3), (RS)-aminoindan-1,5-dicarboxylic acid and (RS)-alpha-methylserine-o-phosphate monophenyl ester, respectively. The 1S,3R-ACPD (100-900 nmol) induced death of striatal neurons was suggested by the reduction in NMDA and D1 dopamine receptors by up to 13% (P < 0.05) and 20% (P < 0.05) as well as by the decline in GAD67 mRNA (25%, P < 0.01) and proenkephalin mRNA levels (35%, P < 0.01). Interestingly, 1S,3R-ACPD attenuated internucleosomal DNA fragmentation induced by NMDA, but potentiated that induced by KA. These results suggest that metabotropic receptor stimulation leads to the death of striatal neurons by a mechanism having the biochemical stigmata of apoptosis. Moreover, metabotropic receptor stimulation evidently exerts opposite effects on pre- or postsynaptic mechanisms contributing to the NMDA and KA-induced apoptotic-like death of these neurons.

Alanine↗
PubMed1997

Cloning of the cDNA encoding rat Presenilin-1.

We isolated rat presenilin-1 (PS-1; also called S182 previously) cDNA from total brain RNA by using a reverse transcription-polymerase chain reaction (RT-PCR) technique with primers homologous to the conserved sequences of human and mouse PS-1. Rat PS-1 cDNA encoded 468 amino acids (aa) and the deduced aa sequence was highly homologous to those of the human (88.4%) and mouse (92.7%). Northern blot analysis of the rat PS-1 cDNA revealed two mRNA species in rat neurotypic pheochromocytoma and glioma cell lines (PC-12 and C6, respectively) that migrated at rates corresponding to approximately 3.0 and 7.5 kb.

Alzheimer Disease↗
PubMed1997

Effects of carbendazim (methyl 2-benzimidazole carbamate; MBC) on meiotic spermatocytes and subsequent spermiogenesis in the rat testis.

BACKGROUND: Benzimidazole fungicide, carbendazim, is known to adversely affect Sertoli cells by disrupting microtubules, which induces sloughing of elongate spermatids in a stage-specific manner. This study determines the direct effects on dividing germ cells and the subsequent effects on spermiogenesis. METHODS: Carbendazim was administered orally to male rats (100 mg/kg), and their testes were processed for histological evaluation at various post-treatment intervals up to day 20.0. RESULTS: The sloughing of elongate spermatids was observed as reported previously. In addition to this Sertoli cell lesion, necrosis of dividing spermatocytes in stage XIV was observed at 8 hours post-treatment. At day 1.5, empty spaces of missing step 1 spermatids were seen in stage I. At days 4.5 and 7.5, normal round spermatids were missing, but large round spermatids (megaspermatids) and binucleate spermatids were common. The megaspermatid nucleus was approximately 33% larger in diameter than normal round spermatids. At day 10.5, megasteps 10-12 spermatids, binucleate spermatids, and three to four different steps of spermatids coexisting in the same tubule section were present in stages X-XII. In addition, abnormally shaped elongating spermatids were observed having distorted heads and nuclear invagination containing microtubules. At day 20.0, empty spaces of missing diplotene spermatocytes were seen in stage XIII. CONCLUSIONS: The present observations show that carbendazim has rapid direct effects on meiotic spermatocytes and latent effects on spermatids, leading to morphological abnormalities and failure of spermiogenesis. These effects are found independent of occlusions in the efferent ductules.

Animals↗
PubMed1997

The attenuating effect of carteolol hydrochloride, a beta-adrenoceptor antagonist, on neuroleptic-induced catalepsy in rats.

It is known that beta-adrenoceptor antagonists are effective in the treatment of akathisia, one of the extrapyramidal side effects that occur during neuroleptic treatment. Neuroleptic-induced catalepsy, a model of neuroleptic-induced extrapyramidal side effects, was considered suitable as a model for predicting neuroleptic-induced akathisia in humans, although neuroleptic-induced catalepsy was not considered a specific test for neuroleptic-induced akathisia. Therefore, the effects of carteolol, a beta-adrenoceptor antagonist, on haloperidol-induced catalepsy in rats were behaviorally studied and compared with those of propranolol and biperiden, a muscarinic receptor antagonist. Carteolol, as well as propranolol and biperiden, inhibited the haloperidol-induced catalepsy. The inhibitory effect of carteolol was almost comparable to that of propranolol, but was weaker than that of biperiden. Carteolol did not evoke postsynaptic dopamine receptor-stimulating behavioral signs such as stereotypy and hyperlocomotion in rats. Carteolol did not antagonize the inhibitory effects of haloperidol on apomorphine-induced stereotypy and locomotor activity in rats. In addition, carteolol did not evoke 5-HT1A receptor-stimulating behavioral signs such as flat body posture and forepaw treading and did not inhibit 5-hydroxytryptophan-induced head twitch in rats. Finally, carteolol did not inhibit physostigmine-induced lethality in rats. These results strongly suggest that carteolol improves haloperidol-induced catalepsy via its beta-adrenoceptor antagonistic activity and is expected to be effective in the treatment of akathisia without attenuating neuroleptic-induced antipsychotic effects due to its postsynaptic dopamine receptor antagonistic activity.

Adrenergic beta-Antagonists↗
PubMed1997

Daily wheel running activity modifies the period of free-running rhythm in rats via intergeniculate leaflet.

The period of free-running rhythms (tau) in rats, as measured using a running wheel, is different from that measured using an Automex. The aim of this work was to examine the effects of lesions of the intergeniculate leaflet (IGL) on the tau of these two activity rhythms. When blind rats were transferred from a cage with a running wheel to a cage without a running wheel, the tau lengthened. The tau of the wheel-running activity was associated with the number of wheel revolutions per day. A complete lesion of the IGL lengthened the tau of the wheel-running activity, and caused a reduction in the number of wheel revolutions per day in all rats. In rats housed in cages without a running wheel, locomotor activity was reduced by IGL lesions, although the tau was unaffected. When IGL-lesioned rats were transferred from a cage with a running wheel to a cage without a running wheel, no further change was observed. These results indicate that the tau is modified by the daily activity of wheel-running, but not by general locomotor activity, and that the IGL may be involved in this modification.

Animals↗
PubMed1997

Further observations on carbendazim-induced abnormalities of spermatid morphology in rats.

The effects of a microtubule poison, carbendazim, on rat spermiogenesis were examined for abnormalities of nuclei, acrosome and manchette in round and elongating spermatids in Stages VII-XII on days 7.5, 9.5, 10.0 and 10.5 post-treatment using routine electron microscopy. Spermatid nuclear abnormalities were observed in Stages IX-XI on day 9.5 and at greater post-treatment intervals. Nuclear abnormalities included nuclear distortions, various types of nuclear invaginations and abnormal positioning of the modified nuclear envelope. Acrosomal abnormalities were noted on day 7.5 and at greater intervals. Discontinuous, multiple granular and fragmentary acrosomes were observed in Stages VII-XI. In addition, spermatids with complete absence of acrosome (acrosome-deficient spermatids) were observed in Stages VII-X. Poorly-formed and absent ectoplasmic specializations were seen in the cytoplasm of Sertoli cells next to the acrosome-deficient spermatids. A major abnormality of the manchette was irregular positioning of the manchette microtubules in steps 9-11 spermatids on day 9.5 and at greater intervals, which resulted in nuclear invagination. The results indicate that carbendazim induces abnormalities in spermatid morphology that are common to those reported in testes treated with several chemical compounds and in testes of mutant animals.

Acrosome↗