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Biomedical subjects

Y Sakagami

Publications and source records attributed to Y Sakagami.

At least 73 records · Page 4Linked to original sources

Cytokine production and surface antigen expression by peripheral blood mononuclear cells in postmenopausal osteoporosis.

It was reported earlier that IL-1 production by cultured monocytes and the ratio of helper (CD4) to suppressor (CD8) lymphocytes in peripheral blood are different in osteoporotic compared to nonosteoporotic subjects. We examined these and several other parameters related to the biosynthetic activity and differentiation status of peripheral blood mononuclear cells (PBMC) in untreated osteoporotic postmenopausal women (age 65 +/- 7, n = 46), nonosteoporotic postmenopausal women (age 55 +/- 3, n = 20), and nonosteoporotic premenopausal women (age 37 +/- 7, n = 8), as defined by spine density. We found that unstimulated monocytes from osteoporotics did not produce detectable IL-1 beta as determined by ELISA. In addition, there were no significant differences between osteoporotics and nonosteoporotics in IL-1 beta or IFN-gamma production by PBMC stimulated with OKT3, a monoclonal antibody to the T cell-receptor complex. The proliferative response of lymphocytes to OKT3 was significantly less (p < 0.02) in osteoporotics compared to nonosteoporotic post- and premenopausal women; multiple-regression analysis, however, indicated that this difference was not due to bone density but to age. Flow cytometric analysis of PBMC revealed no difference between osteoporotics and nonosteoporotics in the distribution of 18 phenotypic subsets determined, including CD4- or CD8-positive lymphocytes or the ratio of CD4 to CD8 cells. Further, there was no correlation of the surface markers with bone density, the exceptions being the subsets expressing the CD3/CD56 and CD8/CD56 markers, which were inversely related to spine density in the osteoporotic women.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

Stimulation of interleukin-6 production by either calcitonin gene-related peptide or parathyroid hormone in two phenotypically distinct bone marrow-derived murine stromal cell lines.

It was recently shown that interleukin-6 (IL-6) is produced by bone and bone marrow-derived stromal cells and that it plays an important role in osteoclast development. Here we examined whether parathyroid hormone (PTH), calcitonin (CT), or the calcitonin gene-related peptide (CGRP) influence IL-6 production by two murine bone marrow-derived stromal cell lines: the preadipocyte-like stromal cell line +/+ LDA11 and the fibroendothelial stromal cell line MBA 13.2. We found that CGRP (but not PTH or CT) exerted a dose-dependent increase in cAMP and IL-6 production in the +/+ LDA11 cells. In addition, CGRP had an inhibiting effect on the proliferation of this stromal cell line. CGRP, however, did not affect cAMP or IL-6 in the rat osteogenic sarcoma cell line UMR-106-06, which exhibits CT receptors, whereas CT stimulated both cAMP and IL-6 by the UMR-106-01 cells. In contrast to the specificity of the IL-6 response of the +/+ LDA11 cells to CGRP, IL-6 production by the MBA 13.2 stromal cells was stimulated by PTH whereas CGRP or CT had no effect. These data suggest that bone marrow-derived stromal cells express receptors for either CGRP or PTH in a phenotype-specific manner and that, acting via these receptors, CGRP and PTH stimulate IL-6 production by stromal cells. In addition, the evidence for specific receptors for the neuropeptide CGRP in bone marrow stromal cells and an effect of CGRP on IL-6 raises the possibility for a role of cytokines in a putative interplay between neuronal stimuli and bone.

Animals↗

[Cytologic atypical grade of exfoliative cytology versus histologic differentiation degree in prostatic carcinoma].

Our method of exfoliative cytology using a prostatic fluid collecting catheter is effective in detecting prostatic carcinoma. To presume histological diagnosis by means of the cytology we analyzed cytological findings of 62 cases of prostatic carcinoma in relation with their biopsy findings, clinical stages and clinical courses. In cases in which cellular atypism was low in the cytology the carcinoma was mostly well or moderately differentiated. Conversely, in cases in which the carcinoma was well differentiated atypism was mostly low in the cytology. In cases in which the cellular atypism was high the carcinoma was poorly differentiated, and vice versa. The poorer histological differentiation and the higher cytological atypism, the more advanced carcinoma and the higher death rate from the carcinoma. The tendency seemed to be more related with the cellular atypism than with the histological differentiation. Thus the cytological findings reflect the histology well and the degree of the histological differentiation can be presumed by the cytological atypism. The cellular atypism is not a less important factor than the histologic differentiation degree for determining the clinical stage and the prognosis.

Adenocarcinoma↗

Changes in leukotrienes and prostaglandins in the liver tissue of rats in the experimental massive hepatic cell necrosis model.

When heat-killed Propionibacterium acnes is intravenously injected into rats followed by an intravenous injection of a small amount of Gram-negative lipopolysaccharide (LPS) 7 days later, massive hepatic cell necrosis is induced and most of the rats die within 24 hours of LPS injection. Using this experimental model, we studied the changes in the levels of leukotrienes (LTs) and prostaglandins (PGs) in the liver tissue and bile of rats with experimentally-induced massive hepatic cell necrosis. Both the levels of LTs and PGs in the liver tissue and LTs in the bile increased before the microscopic appearance of hepatic cell necrosis. These results suggest that arachidonic acid metabolites may play an important role in the induction of liver cell injury.

6-Ketoprostaglandin F1 alpha↗

Control of expression of Agrobacterium vir genes by synergistic actions of phenolic signal molecules and monosaccharides.

Most virulence (vir) genes of Agrobacterium tumefaciens that are required for the formation of crown gall tumors are expressed in response to such plant signal molecules as acetosyringone and lignin precursors. The phenolic signals are transduced through a receptor VirA protein in the inner membrane of the bacterial cell. The expression of these genes triggers the transfer of a specific DNA segment, called transferred DNA (T-DNA), from the Ti plasmid to plant cells, and its integration into their nuclear DNA. We show here that a group of aldoses (L-arabinose, D-xylose, D-lyxose, D-glucose, D-mannose, D-idose, D-galactose, and D-talose) can markedly enhance acetosyringone-dependent expression of vir genes when the concentration of acetosyringone is limited (10 microM) but does not enhance the expression of noninducible genes. Likewise, a 2-deoxy-D-glucose, a nonmetabolized sugar, is also effective. When a deletion was introduced into the virA gene in the region encoding the periplasmic portion of the VirA protein, enhancement by glucose disappeared, but vir expression was induced by acetosyringone in this mutant. These results suggest that these sugars directly enhance a signaling process initiated by phenolic inducers that results in an increase in expression of the vir genes.

Journal Article↗

[Cytological changes in endocrine therapies of prostatic carcinoma].

We studied cytological changes by endocrine therapies of prostatic carcinoma in 31 cases. We originated a method of cytology, in which a prostatic fluid collecting catheter was used. This has been already reported in previous papers. By the therapies, carcinoma cells usually became edematous, swollen, squamous and finally keratinized and in the cytoplasm hematoxylin-stained granules often appeared. These findings were usually seen in two weeks after the onset of the endocrine therapy. But the degree of the changes differed among the cases and among the therapies. In some there was no response or only squamous metaplasia was found. Most of the carcinoma cells were viable. In these cases the therapies were thought to be ineffective and their mortality was high. On the contrary, in those with only keratinized cells, the therapies were thought to be effective and the mortality was low. We conclude that the cytological methods were useful for evaluating the therapies.

Aged↗

[A case of urachal abscess].

A 26-year-old male with urachal abscess was demonstrated. Ultrasonography, CT and MRI revealed that there was a mass at the supravesical region, which was connected to the umbilicus. However, a differential diagnosis as to whether the mass was a tumor or an abscess was difficult from these examinations. Thus we performed an open biopsy. A pathological examination revealed no malignant change in the biopsy specimen. On the other hand, the pathological diagnosis of a follicular tumor located at the roof of the urinary bladder was TCC G2, but we considered that, this change was a reactive hyperplasia with dysplasia resulting from chronic inflammation of urachal abscess. Thus, the complete excision of urachal abscess and partial cystectomy were performed. The serial sections of the bladder wall revealed no malignant changes. We reviewed similar cases reported in our country and discussed various factors causing urachal abscess, especially related to the infectious root.

Abscess↗

Estradiol receptors in the cytosol of peripheral blood mononuclear cells in hepatitis B virus carriers treated with interferon-alpha.

Estradiol receptors in the cytosol of peripheral blood mononuclear cells and the effects of interferon-alpha (IFN-alpha) on estradiol receptors were studied in asymptomatic hepatitis B virus (HBV) carriers, patients with chronic hepatitis B and normal controls. The level of estradiol receptors in the cytosol of mononuclear cells was significantly lower in asymptomatic HBV carriers and patients with chronic hepatitis B, compared to normal controls. This low level of cytosol estradiol receptors in patients with chronic hepatitis B was increased by the administration of IFN-alpha. In addition, when peripheral blood mononuclear cells from patients with chronic hepatitis B were incubated with IFN-alpha in vitro, the level of cytosol estradiol receptors also increased by increasing the concentration of IFN-alpha. We previously reported that the response of mononuclear cells to estrogen is impaired in HBV carriers, and our present results suggested that this may be due to the low level of estradiol receptors in the cytosol of mononuclear cells.

Carrier State↗

Effects of bile acids on liver cell injury by cultured supernatant of activated liver adherents cells.

When heat-killed Propionibacterium acnes (P. acnes) is intravenously injected into mice followed by an intravenous injection of a small amount of lipopolysaccharide (LPS) 7 days later, most of the mice die of massive hepatic cell necrosis within 24 hours of LPS injection. In addition, when the liver adherent cells including Kupffer cells are separated from the mice 7 days after P. acnes injection and incubated in vitro with LPS, remarkable activity of the cytotoxic factor is found in the culture supernatant. This cytotoxic factor is thought to cause liver injury. Using this experimental model, the effects of various bile acids on liver cell injury were studied. As a result, ursodeoxycholic acid and dehydrocholic acid suppressed liver cell injury induced by the cytotoxic factor. However, cholic acid, deoxycholic acid and chenodeoxycholic acid did not have any hepatocytoprotective effects.

Animals↗

The mutagenicity of refuse leachate from a municipal incinerator.

The mutagenicity of refuse leachate from a municipal incinerator was studied by liquid rec-assay and Ames assay. Volatile components were found to be negative, and nonvolatile components positive, in the Ames assay and the leachate was found to have DNA-damaging capacity in the liquid rec-assay with S-9 mix. PAHs derived from tobacco ash and carbonyl compounds generated by the putrefaction of foods were confirmed to be main contributors to DNA-damaging capacity and mutagenicity in refuse leachate.

Animals↗

Release of leukotriene B4 from rat Kupffer cells.

In order to examine the production of leukotriene B4 (LTB4) from Kupffer cells, Kupffer cells isolated from the normal rat liver were incubated with calcium ionophore A23187, opsonized zymosan, or platelet activating factor (PAF), and the amount of LTB4 in the culture supernatant was determined by the combined technique of reverse-phase high-performance liquid chromatography and radioimmunoassay. As a result, when activated in vitro with calcium ionophore A23187, Kupffer cells generated LTB4. When Kupffer cells were stimulated with calcium ionophore after 10-min preincubation with AA861, a selective 5-lipoxygenase inhibitor, the release of LTB4 from Kupffer cells was markedly suppressed. PAF, which is a phospholipid mediator having a wide spectrum of biological activities, significantly enhanced the release of LTB4 from Kupffer cells stimulated with calcium ionophore or opsonized zymosan. Even when the Kupffer cell were not stimulated with calcium ionophore or opsonized zymosan, LTB4 production was significantly increased by PAF. Thus, our studies indicate that Kupffer cells could generate LTB4 as well as polymorphonuclear leukocytes and macrophages. In addition, it is suggested that Kupffer cells may be able to modify inflammatory and immunological events in the liver tissue by the release of LTB4.

Animals↗

Mechanism of resistance to benzalkonium chloride by Pseudomonas aeruginosa.

The mechanisms of resistance of Pseudomonas aeruginosa to benzalkonium chloride (BC) were studied. The effluence of cell components was observed in susceptible P. aeruginosa by electron microscopy, but resistant P. aeruginosa seemed to be undamaged. No marked changes in cell surface potential between Escherichia coli NIHJC-2 and a spheroplast strain were found. The contents of phospholipids (PL) and fatty and neutral lipids (FNL) in the cell walls of resistant P. aeruginosa were higher than those in the cell walls of susceptible P. aeruginosa. The amounts of BC adsorbed to PL and FNL of cell walls of BC-resistant P. aeruginosa were lower than those for BC-susceptible P. aeruginosa. Fifteen species of cellular fatty acids were identified by capillary gas chromatography and gas chromatography-mass spectrometry. The ability of BC to permeate the cell wall was reduced because of the increase in cellular fatty acids. These results suggested that the resistance of P. aeruginosa to BC is mainly a result of increased in the contents of PL and FNL. In resistant P. aeruginosa, the decrease in the amount of BC adsorbed is likely to be the result of increases in the contents of PL and FNL.

Benzalkonium Compounds↗

Determination of the cleavage site involved in C-terminal processing of penicillin-binding protein 3 of Escherichia coli.

Chromatographic peptide mapping of lysyl endopeptidase digests of penicillin-binding protein 3 (PBP 3) of Escherichia coli revealed peptides that differed in retention time between the precursor and mature forms. The peptides were purified from a processing-defective (prc) mutant and a wild-type (prc+) strain. These peptides were identified as the C-terminal region of the precursor form and mature PBP 3 by amino acid sequencing. Each of the C-terminal peptides was cleaved into two fragments by trypsin digestion. By sequencing the resultant carboxyl-side fragment derived from the mature form, it was concluded that the C-terminal residue of mature PBP 3 was Val-577, and thus the Val-577-Ile-578 bond is the cleavage site for processing. This conclusion was consistent with the amino acid compositions of the relevant peptides, which suggested that the peptide from the cleavage site to the end of the deduced sequence (Ile-578-Ser-588) was present in the precursor but absent in the mature form. One lysyl peptide bond resisted both lysyl endopeptidase and trypsin and remained uncleaved in the peptide analyzed above.

Acyltransferases↗

Distinct target cells and effects of 1 alpha,25-dihydroxyvitamin D3 and glucocorticoids in the rat thymus gland.

Thymocytes are known to possess receptors for glucocorticoids (GC) as well as for alpha, 25-dihydroxyvitamin D3 [1,25-(OH)2D3]. We have now investigated the distribution of the receptors for GC and 1,25-(OH)2D3 in rat thymocytes and compared the effects of the two steroid hormones on short term primary cultures of these cells. We report that in thymic cells, as in other tissues, 1,25-(OH)2D3 and GC bind specifically to distinct receptor molecules which exhibit sedimentation coefficients of 3.3S and 3.7S, respectively. Furthermore, the thymocytes that express the 1,25-(OH)2D3 receptor belong to a different and distinct subpopulation than the cells that express the glucocorticoid receptor. Specifically, by separating the thymocytes into two subsets by means of agglutination with the lectin peanut agglutinin (PNA), we have determined that the 1,25-(OH)2D3 receptor-positive cells belong to the PNA-negative medullary mature subset, whereas the GC receptor-positive cells belong to the PNA-positive cortical immature subset of thymocytes. Finally, we have compared the effects of the two steroid hormones on primary cultures of each of the two subsets as well as on unseparated thymocytes and found that GC act on PNA-positive cells to induce cell lysis; this leads to an enrichment in 1,25-(OH)2D3 receptor-positive thymocytes, as indicated by an apparent increase (6-fold) in the 1,25-(OH)2D3 binding in the cells surviving at the end of the culture. In contrast, we found that 1,25-(OH)2D3 acts on the PNA-negative cells to decrease the rate of cell lysis. These data indicates that the target cells for GC and 1,25-(OH)2D3 in the thymus are distinct and that these two hormones exert a different regulatory influence on the gland.

Animals↗

[Effects of the cholestatic factor and the prostaglandin E1 derivative on the level of cAMP in isolated hepatocytes of rats].

It has been reported that cAMP in hepatocytes plays an important role in bile discharge. Therefore, in order to examine the action mechanism of the cholestatic factor, we studied the effect of the cholestatic factor and prostaglandin E1 derivative which inhibits the activity of the cholestatic factor on the cAMP level in hepatocytes. As a result, the cAMP level in hepatocytes was decreased by treatment with the cholestatic factor, but was increased by the prostaglandin E1 derivative. Furthermore, the cAMP level which was decreased by the cholestatic factor returned to the original level by treatment with the prostaglandin E1 derivative. Because the increase in the cAMP level in hepatocytes promotes the bile acid independent bile discharge, it is suggested that the cholestatic factor reduces the bile flow by the decrease in the cAMP level in hepatocytes, and that the prostaglandin E1 derivative competes with the action of the cholestatic factor through the increase in the cAMP level in hepatocytes.

Alprostadil↗

Serotonin and tryptamine metabolism in the acute hepatic failure model: changes in tryptophan and its metabolites in the liver, brain and kidney.

When heat-killed Propionibacterium acnes, a gram-positive anaerobe, is intravenously injected into mice followed by an intravenous injection of gram-negative lipopolysaccharide (LPS) 7 days later, most of the mice die of massive hepatic cell necrosis within 24 hours of LPS injection. Using this experimental model, acute hepatic failure was induced in mice, and the tryptophan metabolism in the liver, brain and kidney was studied. As a result, the tryptophan level was remarkably high in all three organs, and the metabolism of both the tryptamine pathway and serotonin pathway was induced. However, in the brain, the tryptamine metabolism was more induced compared to the serotonin, suggesting that the metabolites of tryptamine, may be involved in hepatic encephalopathy.

Acute Disease↗

[Changes in production of platelet activating factor by adherent hepatocytes of mice with experimental liver failure].

It is thought that the platelet activating factor (PAF) enhances the immune response and inflammatory reaction. We studied the production of PAF from liver adherent cells. As a result, liver adherent cells produced PAF, when they were stimulated with calcium ionophore. In addition, when mice were treated with heat-killed Propionibacterium acnes and the mononuclear cells were infiltrated into the liver, a significantly larger amount of PAF was produced compared to normal mice.

Acute Disease↗