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S Yamada

Publications and source records attributed to S Yamada.

At least 613 records · Page 34Linked to original sources

Subcellular localization of the major autolysin, ATL and its processed proteins in Staphylococcus aureus.

The Staphylococcus aureus autolysin gene, atl, encodes a unique 138-kDa protein (ATL) with amidase and glucosaminidase domains. ATL has been suggested to undergo proteolytic processing to generate two extracellular peptidoglycan hydrolases, 51-kDa endo-beta-N-acetylglucosaminidase (51-kDa GL) and 62-kDa N-acetylmuramyl-L-alanine amidase (62-kDa AM). To investigate cell-associated bacteriolytic enzymes for atl gene products, proteins were extracted from the cells as follows. The cells were exposed to 3 M LiCl followed by 4% SDS. Thereafter, the cells were disrupted and again extracted with 4% SDS. Whole SDS-stable cell-associated bacteriolytic proteins were extracted without disrupting the cells. Exposure to 3 M LiCl released major 138-, 115-, 85-, 62- and 51-kDa bacteriolytic proteins, and subsequent 4% SDS extraction released major 138- and 115-kDa bacteriolytic proteins. These bacteriolytic proteins were missing in extracts of atl mutant RUSAL2 (S. aureus RN450 atl::Tn551). Immunoblotting studies suggest that these are all atl gene products: the 138-kDa protein is an ATL with a cleaved signal sequence; the 115- and 85-kDa proteins are intermediates; and the 51- and 62-kDa proteins are cell-associated 51-kDa GL and 62-kDa AM, respectively. The trypsin susceptibility of these proteins suggests that they are located outside the cell membrane. Differences in extractability and immunoelectron microscopic studies suggest that atl gene products are associated with cells in two different ways, LiCl extractable and non extractable. We suggest that the 138-kDa ATL undergoes processing through intermediate proteins (115- and 85-kDa proteins) to mature as the active cell cluster-dispersing enzymes 51-kDa GL and 62-kDa AM on the cell surface.

Amino Acid Sequence↗

Effects of all-trans retinoic acid on choriocarcinoma cells in vitro.

OBJECTIVES: To determine the activities of all-trans retinoic acid (RA) on choriocarcinoma cells in vitro. METHODS: The antiproliferative effect of all-trans RA on 4 choriocarcinoma cell lines was measured by the MTT assay. The effect of all-trans RA combined with methotrexate or actinomycin-D was then examined. The effect of all-trans RA on hCG secretion was also studied. The gene expression of retinoic acid receptors (RARs) was examined by RT-PCR. RESULTS: All-trans RA inhibited cell proliferation dose- and time-dependently; a 6-day exposure to 1 microM all-trans RA suppressed the cell growth by 67.8%-82.0% compared to the controls. An enhanced effect was observed in the combined administration of all-trans RA and methotrexate or actinomycin-D. The secretion of hCG increased 4-fold to 9-fold by the addition of 1 microM all-trans RA. RARs genes were expressed in all cell lines. CONCLUSION: The anticancer activity presented here appears to warrant further evaluation of all-trans RA as adjuvant therapy for choriocarcinoma.

Antineoplastic Agents↗

A case of uterine choriocarcinoma with spontaneous rupture twenty-three years following the antecedent pregnancy.

A 53-year-old woman went into shock with a spontaneous uterine rupture due to choriocarcinoma that occurred 23 years after an elective abortion in the first trimester, and she underwent an emergency hysterectomy. After 4 courses of uneventful postoperative chemotherapy, she suffered from severe pneumonia. Fortunately, however, she recovered and has remained in complete remission at 2.5 years follow-up. This is a case of uterine choriocarcinoma with a spontaneous rupture after the longest latent period yet reported.

Abortion, Induced↗

Malignant melanoma of the uterine cervix: a case report.

We present case of a 57-year-old Japanese woman a 9 cm-size primary malignant melanoma of the uterine cervix. MRI demonstrated a low-signal T1-weighted spin echo image and hyperperfusion indicated by Gd-DTPA enhancement. The sequence analysis of the MTS1/CDK4I gene revealed no deletion or mutation. The results of cytological, pathological, and electron microscopy tests are also presented.

Antineoplastic Combined Chemotherapy Protocols↗

Pharmacological profile of TH-142177, a novel orally active AT1-receptor antagonist.

The pharmacological properties of TH-142177 (N-n-butyl-N-[2'-(1-H-tetrazole-5-yl) biphenyl-4-yl]-methyl-(N-carboxymethyl-benzylamino)-acetamide), a novel antagonist of the angiotensin II (AII) AT1 receptor, were studied in vitro and in vivo, and compared to those of losartan. In the rat isolated aorta, TH-142177 produced parallel shifts to the right of the concentration-response curves for AII-induced contractions without affecting the maximal response (pA2 = 9.07). The inhibitory potency of TH-142177 in the aorta was about three times greater than that of losartan. TH-142177 completely inhibited the specific binding of [125I]AII to AT1 receptor in rat aortic membranes (Ki = 1.6 x 10(-8) M), whereas specific [125I]AII binding to AT2 receptor in bovine cerebellum and human myocardium was not affected by concentrations of TH-142177 up to 10(-5) M. Losartan also inhibited the [125I]AII binding to rat aortic membranes (Ki = 2.2 x 10(-8) M). Following the intravenous administration to anesthetized normotensive rats, TH-142177 dose-dependently inhibited the increase in systolic blood pressure induced by an intravenous bolus injection of AII that was 1.5 times less potent than losartan. Furthermore, the oral administration of TH-142177 to conscious renal hypertensive rats exerted a dose-dependent reduction of systolic blood pressure without significantly effecting the heart rate. TH-142177 was at least three times more potent than losartan. These results demonstrate that TH-142177 is a potent and selective antagonist of AT1 receptors and by oral administration has a long-lasting antihypertensive activity.

Angiotensin II↗

Role for the S-layer of Campylobacter rectus ATCC33238 in complement mediated killing and phagocytic killing by leukocytes from guinea pig and human peripheral blood.

OBJECTIVE: The role of the S-layer of Campylobacter rectus ATCC 33238 in complement-mediated killing and interaction with leukocytes of the intraperitoneal cavity from guinea pigs and human peripheral blood was studied in vitro. MATERIALS AND METHODS: Rabbit polyclonal anti-serum to whole C. rectus cells, a monoclonal antibody which recognizes 150 KDa S-layer protein antigen and a monoclonal antibody against lipopolysaccharide (LPS) were prepared. Sensitivities of C. rectus cells against complement mediated killing and phagocytic killing by peritoneal leukocytes of guinea pig and human peripheral leukocytes were examined in the presence or absence of a specific antibody. RESULTS: C. rectus ATCC 33238 cells were moderately sensitive to complement mediated killing in the presence of rabbit polyclonal antibody against whole cells, and slightly sensitive in the presence of monoclonal antibody against S-layer. Ingestion and phagocytic killing of C. rectus cells by leukocytes were enhanced by the rabbit anti-serum and monoclonal antibody against S-layer, but not by the monoclonal antibody against LPS, pre-immune rabbit serum or control ascites. Viability of leukocytes was dependent on the number of ingested C. rectus cells. CONCLUSIONS: The present study demonstrates that S-layer possessing C. rectus cells are resistant to complement mediated killing and phagocytic killing by leukocytes in the absence of specific antibody.

Animals↗

Antagonistic effects of OPC-14597, a novel antipsychotic drug, on quinpirole- and (-)-sulpiride-induced changes in evoked dopamine release in rat striatal slices.

The effects of a newly synthesized quinolinone derivative, 7-[4-(4-(2,3-dichlorophenyl)-1-piperazinyl) butoxy)-3,4-dihydro-2-(1H)-quinolinone (OPC-14597), a novel antipsychotic drug, on electrically evoked dopamine release in rat striatal slices were investigated. OPC-14597 (0.1-10 microM) had no effect on the dopamine release evoked in the striatal slices. The decrease induced by quinpirole, a dopamine receptor agonist, in evoked dopamine release was attenuated by superfusion with OPC-14597 (1 and 10 microM) which by itself had no effect on evoked dopamine release. The increase induced by (-)-sulpiride, a dopamine receptor antagonist, in evoked dopamine release was, moreover, also attenuated by 1 and 10 microM OPC-14597. These findings indicate that OPC-14597 antagonizes both dopamine agonist- and antagonist-induced changes in evoked dopamine release in striatal slices in rats.

Animals↗

A novel member of the subtilisin-like protease family from Streptomyces albogriseolus.

We previously isolated three extracellular endogenous enzymes from a Streptomyces albogriseolus mutant strain which were targets of Streptomyces subtilisin inhibitor (SSI) (S. Taguchi, A. Odaka, Y. Watanabe, and H. Momose, Appl. Environ. Microbiol. 61:180-186, 1995). In the present study, of the three enzymes the largest one, with a molecular mass of 45 kDa (estimated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis), termed SAM-P45, has been characterized in detail. The entire gene encoding SAM-P45 was cloned as an approximately 10-kb fragment from S. albogriseolus S-3253 genomic DNA into an Escherichia coli host by using a shuttle plasmid vector. The amino acid sequence corresponding to the internal region of SAM-P45, deduced from the nucleotide sequence of the gene, revealed high homology, particularly in three regions around the active-site residues (Asp, His, and Ser), with the amino acid sequences of the mature domain of subtilisin-like serine proteases. In order to investigate the enzymatic properties of this protease, recombinant SAM-P45 was overproduced in Streptomyces coelicolor by using a strong SSI gene promoter. Sequence analysis of the SAM-P45 gene and peptide mapping of the purified SAM-P45 suggested that it is synthesized as a large precursor protein containing a large C-terminal prodomain (494 residues) in addition to an N-terminal preprodomain (23 and 172 residues). A high proportion of basic amino acids in the C-terminal prodomain was considered to serve an element interactive with the phospholipid bilayer existing in the C-terminal prodomain, as found in other membrane-anchoring proteases of gram-positive bacteria. It is noteworthy that SAM-P45 was found to prefer basic amino acids to aromatic or aliphatic amino acids in contrast to subtilisin BPN', which has a broad substrate specificity. The hydrolysis by SAM-P45 of the synthetic substrate (N-succinyl-L-Gly-L-Pro-L-Lys-p-nitroanilide) most preferred by this enzyme was inhibited by SSI, chymostatin, and EDTA. The proteolytic activity of SAM-P45 was stimulated by the divalent cations Ca2+ and Mg2+. From these findings, we conclude that SAM-P45 interacts with SSI and can be categorized as a novel member of the subtilisin-like serine protease family.

Amino Acid Sequence↗

Localized perforation of the cell wall by a major autolysin: atl gene products and the onset of penicillin-induced lysis of Staphylococcus aureus.

We investigated the cell surface localization of the atl gene products of Staphylococcus aureus exposed to a lytic concentration (4 MIC) of penicillin G (PCG) by means of immunoelectron microscopy using anti-62-kDa N-acetylmuramyl-L-alanine amidase or anti-51-kDa endo-beta-N-acetylglucosaminidase immunoglobulin G. Protein A-gold conjugates reacting with antigen-antibody complex localized at sites of defects of the cell wall at the nascent cross wall. Anti-62-kDa N-acetylmuramyl-L-alanine amidase or anti-51-kDa endo-beta-N-acetylglucosaminidase immunoglobulin G inhibited the decreased turbidity caused by PCG-induced lysis and the formation of defects in the wall. The autolysis-defective mutant, S. aureus RUSAL2 (atl::Tn551), exposed to 4 MIC of PCG resisted autolysis and formation of the wall defect. These results suggest that activation or deregulation of the atl gene products at localized sites where formation of new cross wall was disturbed by PCG causes small defects in the cell wall in situ, eventually leading to general autolysis.

Antibodies↗

Decreased beta-phenylethylamine in CSF in Parkinson's disease.

OBJECTIVE: To determine the concentrations of beta-phenylethylamine (PEA) in CSF in patients with Parkinson's disease, and to evaluate the relation between concentration of PEA in CSF and severity of Parkinson's disease. METHODS: Using gas chromatography-chemical ionisation mass spectrometry, CSF concentrations of PEA were measured in 23 patients with Parkinson's disease (mean age, 64.0 (SD 8.2) years), of whom three were at Hoehn and Yahr stage II, 11 were at stage III, and nine were at stage IV. Comparison was made with eight patients with neuropathy (mean age, 57.0 (SD 19.2) years) and 12 controls without neurological disease (mean age, 57.6 (SD 4.8) years). RESULTS: Concentrations of PEA in CSF in Parkinson's disease were significantly lower (mean 205 (SD 131) pg/ml) than in patients with peripheral neuropathy (433 (SD 254) pg/ml) and controls (387 (SD 194) pg/ml). The concentrations of PEA in CSF correlated negatively with Hoehn and Yahr stage (P<0.01). CONCLUSIONS: There are decreased CSF concentrations of PEA in patients with Parkinson's disease.

Aged↗

A case of scurvy rarely encountered in Japan.

We report a case of scurvy, which is rarely encountered in Japan. A 75-year-old male was hospitalized with diffuse subcutaneous hemorrhaging of both feet, pain on walking, and shortness of breath. A remarkably low serum level of vitamin C was confirmed. Administration of ascorbic acid dramatically improved his clinical symptoms. Improvement paralleled the increase of serum vitamin C level. This case underscores the important role of vitamin C on the integrity function of the vessel wall.

Aged↗

Inactivation of the tumor suppressor gene on 11q13 in brothers with familial acrogigantism without multiple endocrine neoplasia type 1.

Two of three brothers (the second and third brothers) and their uncle (their mother's brother) presented acrogigantism without multiple endocrine neoplasia type 1 (MEN 1). An invasive macroadenoma was found in the second brother, and it was histologically confirmed as a sparsely granulated GH cell adenoma. Two distinct microadenomas were found in the third brother, and these were histologically diagnosed as a mixed GH cell and PRL cell adenoma and a sparsely granulated GH cell adenoma, respectively. The loss of heterozygosity (LOH) was analyzed in two adenomas (GH cell adenoma from the second brother and a mixed GH cell and PRL cell adenoma from the third brother) by determining microsatellite polymorphisms of DNAs from tumors and patients' leukocytes. The LOH was found on the chromosome 11q13, whereas LOH was not detected on 1p31-36, 2p, 3p, 4, 5, 6p, 7, 8, 9p21-22, 12p, and 19q13 in both pituitary adenomas examined. The haplotype analysis showed that the same haplotype on 11q13 was found in their mother and the unaffected first brother as well as in the affected uncle and two brothers. The deleted alleles on chromosome 11q13 in the tumors of two affected brothers were, however, restricted to those transmitted from their unaffected father. These data suggest that inactivation of the MEN 1 gene or other tumor suppressor genes on chromosome 11q13 plays an important role for the development of our familial acrogigantism without MEN 1.

Adenoma↗

A novel transcript for the thyrotropin-releasing hormone receptor in human pituitary and pituitary tumors.

We measured the amounts of TRH receptor (TRHR) messenger ribonucleic acid (mRNA) in human normal pituitary and pituitary tumors and found a novel transcript of the TRHR gene. Competitive PCR revealed expression of the TRHR mRNA in all pituitary adenomas examined, and its level was variable and similar to that in the normal pituitary. When the C-terminal region was amplified by PCR, an additional short product was observed. Cloning and sequence analysis of this short fragment revealed that the deleted sequence corresponded exactly to the 5'-sequence of exon 3, indicating alternative splicing of the TRHR mRNA. This alternative splicing resulted in a frame shift, yielding a C-terminal truncated protein (HTRHR2) on translation. Expression analysis of HTRHR2 in Chinese hamster ovary cells showed no significant binding to [3HIMeTRH or response of intracellular calcium to TRH administration. However, the mRNA ratio of HTRHR2 vs. the wild type (HTRHR1) was significantly different among pituitary tumors. The highest ratio was observed in prolactinomas (30%), and almost no detectable expression was found in GH-producing tumors. These findings indicate that this novel transcript of the human TRH receptor gene is produced in a tumor-specific manner and may be a useful parameter for evaluation of individual pituitary tumors.

Adenoma↗

Laminin suppresses progesterone production by human luteinizing granulosa cells via interaction with integrin alpha 6 beta 1.

We previously raised a murine monoclonal antibody (mAb), OG-1, against human granulosa cells (GC) and reported that human GC express the OG-1 antigen with the highest immunoreactivity during the periovulatory phase. Later, we showed that the OG-1 antigen is identical to human integrin alpha 6, and that human GC express integrin alpha 6 beta 1, but not alpha 6 beta 4. In the present study, we examined the expression of laminin (LN), the ligand for integrin alpha 6 beta 1. Flow cytometry showed that LN was bound to the cell surface of some GC obtained from preovulatory follicles of patients undergoing in vitro fertilization. Immunohistochemistry showed that LN was detected between luteinizing GC in the early corpora lutea. To examine the effect of LN on steroidogenesis by human luteinizing GC, GC obtained from patients undergoing in vitro fertilization were cultured on mouse LN-coated or noncoated plastic dishes in medium containing 5% FCS for 24 h. In the absence or presence in hCG (1 IU/mL), GC cultured on LN-coated dishes produced 0.70- and 0.67-fold less progesterone than those on noncoated dishes, respectively (P < 0.05). We examined the effect of the interaction of integrin alpha 6 beta 1 and LN on steroidogenesis by human luteinizing GC. We cultured GC with 5 micrograms/mL of the anti-alpha 6 mAb GoH3, which inhibits the interaction between human integrin alpha 6 beta 1 and mouse LN, or with a control rat mAb (TER199) on mouse LN-coated dishes in serum-free medium for 24 h. In the absence or presence of hCG (1 IU/mL), GC cultured with GoH3 produced 1.97- and 1.94-fold more progesterone than the control cells (P < 0.01 and P < 0.05, respectively). In contrast, when GC were cultured on dishes coated with type IV collagen, progesterone production was not enhanced by GoH3. Furthermore, the anti-alpha 6 mAb OG-1, which does not inhibit the interaction between integrin alpha 6 beta 1 and LN, had no effect on the progesterone production by GC cultured on LN. These results indicate that LN suppresses the luteinization of human luteinizing GC via integrin alpha 6 beta 1 and that integrin alpha 6 beta 1 regulates the luteinization of human GC during the periovulatory phase.

Adult↗

Infrequent mutations of p27Kip1 gene and trisomy 12 in a subset of human pituitary adenomas.

To study the etiologic roles of genes on chromosome 12 for the pituitary tumorigenesis of adenomas, mutations of the p27Kip1 gene and allelic ratios of 18 microsatellite markers on the entire chromosome 12 were studied in 33 pituitary adenomas. The p27Kip1 gene on chromosome 12p12-p13 encoding an inhibitor of complexes between cyclins and cyclin-dependent kinases is supposed to function as the tumor suppressor gene. Among 31 sporadic and 2 familial pituitary adenomas, PCR-single strand conformation polymorphism analysis detected three polymorphic changes but no tumor-specific mutations of the p27Kip1 gene. Genotyping of 18 microsatellite markers on the entire chromosome 12 detected the uniformly decreased allelic ratios ranging from 54-66% in 8 of 33 pituitary adenomas (24%), although no loss of heterozygosity was detected. Fluorescence in situ hybridization confirmed trisomy 12 in all 5 available samples out of these 8 samples. Based on these, we conclude that not mutations of the p27Kip1 gene, but trisomy 12 may be etiologically important in a subgroup of pituitary adenomas.

Adenoma↗

3 beta,5 alpha-Dihydroxycholestan-6-one exists in human blood.

3 beta,5 alpha-Dihydroxycholestan-6-one was detected in fresh human plasma at the concentration of 14-44 ng/mL. The oxysterol binds specifically to phorbol ester specific binding protein in vitro, and may be an endogenous ligand of the protein.

Animals↗

Optical resolution of a 1,5-benzothiazepine derivative, a synthetic intermediate of diltiazem, by preferential crystallization and diastereomeric salt formation.

Practical preparation methods of an optically active intermediate of diltiazem, (+)-(2S,3S)-5-[2-(dimethylamino)ethyl]-2,3-dihydro-3-hydroxy- 2-(4-methoxyphenyl)-1,5-benzothiazepin-4(5H)-one [(+)-7], have been developed by the use of physicochemical and chemical resolutions. 1) The salt of (+/-)-7 with 3-amino-4-hydroxy-benzenesulfonic acid (AHS), was found to exist as a conglomerate and could be reproducibly resolved into (+)-7.AHS and (-)-7.AHS of 94-98% ee by a preferential crystallization procedure. 2) (+)-(1R)-3-Bromocamphor-9-sulfonic acid [(+)-BCS] was found to be an efficient resolving agent for (+/-)-7 and the diastereomeric resolution provided (+)-7.(+)-BCS.2H2O salt in > 43% yield and > 97% ee by fractional crystallization. It is presumed that the crystal water of (+)-7.(+)-BCS.2H2O plays an important role in the selective crystallization during this efficient resolution.

Crystallization↗