[Survey on mental health-related facilities in the secondary health service region].
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Community Mental Health Services↗
Biomedical subjects
K Asai
Publications and source records attributed to K Asai.
Tissue distribution of human gliostatin/platelet-derived endothelial cell growth factor (PD-ECGF) and its drug-induced expression.
Human tissue contents of gliostatin/platelet-derived endothelial cell growth factor (PD-ECGF) and its drug-induced expression in tumor cells were currently examined by a sandwich enzyme immunoassay (EIA) system and a reverse transcription-polymerase chain reaction (RT-PCR) method. Gliostatin/PD-ECGF was found to distribute in rather ubiquitous than specific human tissues and organs, with a relatively high levels in the tissues of digestive system (esophagus and rectum), brain, spleen, bladder and lung, but not in gall bladder, aorta, muscle, fat and kidney. Most of examined human tumor cell lines showed 4- or 5-fold higher contents (21.5 +/- 3.9 ng/mg protein) than normal tissue contents (4.4 +/- 1.1 ng/mg protein) on the average. While gliostatin/PD-ECGF is known to lack a signal sequence, some tumor cells (A431 and MKN74) appeared to release it into the conditioned medium. Expression of gliostatin/PD-ECGF in epidermoid carcinoma cell (A431) and stomach cancer cell (MKN45) was induced by dibutyryl cyclic AMP and phorbol ester, and uniquely in MKN45 by hydrocortisone. In particular, this hydrocortisone specifically caused an increase of the apparent secretion of MKN74 without its cytotoxic effects, suggesting a possible secretion of gliostatin/PD-ECGF in the restricted but not universal cell line. Biological significance on the chemical induction of gliostatin/PD-ECGF in tumor cells and on its extracellular secretion are discussed.
Cell Line↗
Heat shock-mediated cell cycle arrest is accompanied by induction of p21 CKI.
Heat shock induces several events in cells including a series of gene expressions and cell cycle arrest. Recently, several types of cell cycle arrest have been related to the function of cyclin-dependent kinase inhibitors (CKI). Here we show that heat shock treatment up-regulates p21 CKI mRNA and protein in A172 glioma cells and arrests the cell cycle at the G1 phase, p53-deficient cell lines, MDAH041 and T98G, also showed a significant increase in p21 CKI expression after heat stress, indicating that the induction involves a p53-independent pathway. The kinetics of this transient induction, which is not affected by cycloheximide, demonstrate that p21 CKI is an immediate-early response gene.
Cell Cycle↗
Morphological study of cytotoxicity produced by PSK-induced polymorphonuclear leukocytes (PMNs) and Nocardia rubra cell wall skeleton.
The morphologic changes in PMNs induced by an i.p. injection of PSK, a polysaccharide from the mycelia of Coriolus versicolor, and tumor cells undergoing cell death, were evaluated by immunohistochemical staining and electron microscopy. Male C3H/He mice, 8-10 -weeks old, received an i.p. injection of 125 mg/kg of PSK. Their PMNs were obtained 6 h after the PSK injection by peritoneal lavage. N-CWS (Nocardia rubra cell wall skeleton) was added at the start of the chromium release assay using the MM46 mammary carcinoma cell line, which is syngeneic to C3H/He mice, as target cells. During the cytotoxic assay, the cells were fixed at various time points. The MM46 cells expressed ICAM-1 while the PMNs expressed both ICAM-1 and LFA-1 as determined by immunohistochemical staining and immunoelectron microscopy using anti-ICAM-1 and anti-LFA-1 antibodies. PMNs with ruffle-like microvilli adhered to the MM46 tumor cells 30 min after the addition of N-CWS. Immunoelectron microscopic findings suggested that the adhesion molecules were LFA-1 on the PMNs and ICAM-1 on the MM46 tumor cells, but cell fusion between the PMNs and tumor cells was not observed. The MM46 tumor cells gradually lost their microvilli, which showed cell damage, and died 6-7 h after the addition of the N-CWS. This time course of tumor cell death is compatible with the results of the cytotoxic assay. Pretreatment of PMNs by anti-LFA-1 antibody suppressed 1% lysis of MM46 tumor cells from 90% to 10% (p < 0.01). These data suggest that adhesion molecule on the surface of PMNs such as LFA-1 might play an important role on signal transduction of these PMNs cytotoxic function in this experimental system.
Adjuvants, Immunologic↗
Induction of gene expression for nitric oxide synthase by immunomodulating drugs in the RAW264.7 murine macrophage cell line.
We have elucidated the direct effects of PSK (a protein-bound polysaccharide) and OK-432 (a streptococcal preparation), both immunomodulating drugs, on the gene expression for an inducible nitric oxide synthase and on the production of nitric oxide (NO) in the RAW264.7 murine macrophage cell line. As determined by northern blot analysis, both immunomodulating drugs were potent inducers of gene expression for inducible NO synthase when cells were costimulated with interferon-gamma (IFN gamma). Expression of mRNA for the enzyme occurred in a dose-dependent manner after 3 h, when 10-50 micrograms/ml PSK or 0.001-1 KE/ml OK-432 was used. Furthermore, NO was also produced in response to these drugs, as detected by the Griess reagent reaction. The enhancement of NO synthesis was thought to be mediated, in part, through tumor necrosis factor alpha (TNF alpha) induction by these agents, since a neutralizing antibody to TNF alpha significantly suppressed NO production in RAW264.7 cells stimulated with PSK or OK432 in combination with IFN gamma. We speculate that NO production may play a role in tumoricidal and microbicidal activities of PSK or OK-432 in vivo.
Adjuvants, Immunologic↗
Efficacy of in vitro sensitized cells generated by in vivo priming with OK-432 for adoptive immunotherapy of the poorly immunogenic B16-Bl6 melanoma.
We investigated the efficacy of the streptococcal preparation OK-432 as an adjuvant for in vivo priming in induction of sensitized cells for adoptive immunotherapy of the poorly immunogenic B16-BL6 (BL6) melanoma. C57BL/6 (B6) mice were immunized subcutaneously (s.c.) with 3 x 10(6) viable BL6 tumor cells admixed with various doses of OK-432 ranging from 1 to 100 micrograms in the foot-pad. Draining popliteal lymph nodes (LNs) were harvested 7 days after immunization and LN cells were further sensitized with irradiated tumor cells in the presence of 60-300 IU/ml of IL-2 for 11 days. These in vitro sensitized (IVS) cells (2 x 10(6)) were transferred intravenously (i.v.) to B6 mice bearing 4-day pulmonary metastases established by i.v. injection of 2-4 x 10(5) viable BL6 cells. The mice were also received intraperitoneally (i.p.) 4 x 10(4) IU/day of IL-2 for 4 days after adoptive transfer. Transfer of IVS cells from mice immunized by s.c. injection of tumor cells admixed with 10 micrograms of OK-432 significantly reduced the numbers of BL6 pulmonary metastases compared with that of control IVS' cells without the administration of OK-432 (P = 0.003). These effective IVS cells also significantly prolonged the survival of treated animals (P = 0.003). Functional IVS cells required in vitro stimulation with tumor cells. However, addition of OK-432 in the vaccine resulted in no enhancement of in vitro cytotoxicity and no characteristic change of phenotype of IVS cells. These results suggest that in vivo priming of OK-432 facilitates the sensitization of tumor-reactive T-cells. The procedure of in vivo priming with OK-432 may be beneficial in the adoptive immunotherapy of melanoma.
Animals↗
Does inhibition of coronary nitric oxide synthesis alter coronary vascular tone in normal dogs?
To examine whether endothelial nitric oxide formation contributes to the vascular tone of resistance coronary vessels in vivo, we administered NG-nitro-L-arginine methyl ester (L-NAME) (10 and 100 micrograms/kg/min), a nitric oxide synthase inhibitor, as well as D-enantiomer into the left circumflex artery in normal dogs. Intracoronary L-NAME, which was associated with dose-related reductions in acetylcholine-induced coronary vasodilation, significantly reduced the baseline left circumflex blood flow by 6% and increased coronary vascular resistance of the left circumflex artery by 6%. D-enantiomer was ineffective in altering baseline coronary blood flow and vascular resistance of the left circumflex artery. These results indicate that continuous nitric oxide formation in the vasculature is important in the regulation of the coronary vascular tone of resistance vessels in vivo, and serves to maintain the vessels in a dilated state.
Animals↗
[Patency of the ostium of the frontal sinus after endoscopic endonasal surgery for chronic sinusitis].
We examined the patency of the ostium of the frontal sinus after endoscopic endonasal surgery for chronic sinusitis. This study involved one hundred and seventy-two nasal sides of ninety cases who underwent surgery in this unit in the preceding three-year period by the designated three surgeons. All patients were followed up for more than one year after surgery. We obtained a high postoperative patent rate of 90.1%. However, communication between the frontal and ethmoidal sinus could not be confirmed in 9.9% of the cases due to the presence of polyp or adhesion in the middle meatus. Cases with preoperative severe lesion of the frontal sinus showed significantly lower rates of patent than cases with preoperative mild and/or no lesion. In cases where the opening of the ostium could not be sufficiently widened during surgery because the size around the ostium was already small, lower patent rates resulted. However, even in such cases, scraping or curetting of the surrounding bone should be avoided, because it may cause postoperative narrowing of the ostium due to new bone formation. Cases with unsatisfactory results caused by pathological changes in the middle meatus showed significantly lower patent rates than cases with satisfactory postoperative results. It is recommended that accurate cleaning of the ethmoid sinus and adequate postoperative treatment be considered important. Endoscopic endonasal opening of the ostium of the frontal sinus is shown to be a safe and reliable procedure, which can be performed with clear visualization.
Adolescent↗
Physiological concentration of 17 beta-estradiol inhibits chemotaxis of human monocytes in response to monocyte chemotactic protein 1.
While estrogen is known to retard the development of atherosclerosis, the exact mechanism is unknown. The migration of monocytes into the arterial intima is important in the pathogenesis of atherosclerosis. Monocyte chemotactic protein 1 (MCP-1) is suggested to be a real chemotactic factor that is released from monocytes, endothelial cells, and smooth muscle cells. We investigated the effect of 17 beta-estradiol on the migration of human monocytes in response to MCP-1, using a modified Boyden chamber. A physiological concentration of 17 beta-estradiol (10(12) - 10(4)M) inhibited the migration of monocytes exposed to MCP-1. Two estrogen receptor antagonists, tamoxifen and clomiphene, each restored monocyte chemotaxis to MCP-1 to control level, even in the presence of 17 beta-estradiol, suggesting that estrogen receptors are related to the effect of 17 beta-estradiol. Progesterone and testosterone had no measurable effect on monocyte migration. These findings suggest that inhibition of the chemotactic response of monocytes exposed to MCP-1 may be one mechanism for the anti-atherogenic effect of 17 beta-estradiol.
Arteriosclerosis↗
Extraction of hidden Markov model representations of signal patterns in DNA sequences.
We have developed a method to extract the signal patterns in DNA sequences. In this method, the Genetic Algorithm (GA) and Baum-Welch algorithm are used to obtain the best Hidden Markov Model (HMM) representations of the signal patterns in DNA sequences. The GA is used to search the best network shapes and the initial parameters of the HMMs. Baum-Welch algorithm is used to optimize the HMM parameters for the given network shapes. Akaike Information Criterion (AIC), which gives a criterion for the balance of adaptation and complexity of a model, is applied in the HMM evaluation. We have applied the method to the extraction of the signal patterns in human promoters and 5' ends of yeast introns. As a result, we obtained HMM representations of characteristic features in these sequences. To validate the efficiency of the method, we have performed promoter recognition using obtained HMMs. Two entries including nine promoters are selected from GenBank 76.0, and it is observed that the HMM can predicts eight promoters correctly. These results imply that the method is efficient to design preferable HMM networks, and provides reliable models for the recognition of the signal patterns.
Algorithms↗
Expression of cyclooxygenase-1 and -2 in human colorectal cancer.
Several studies indicate that nonsteroidal anti-inflammatory drugs including indomethacin, aspirin, sulindac, and piroxicam reduce the risk of colon cancer. Furthermore, nonsteroidal anti-inflammatory drugs that inhibit the cyclooxygenase (COX) enzyme were shown to inhibit the development of colon cancer in animal models of carcinogenesis. Non-steroidal anti-inflammatory drugs inhibit the enzymatic activity of both the constitutive (COX-1) and inducible (COX-2) isoforms of COX enzyme. We have investigated the expression of COX-1 and COX-2 polypeptides in human colon cancer tissues using immunohistochemistry. Enhanced COX-2 expression was observed in colon cancer tissues from 15 subjects with clinically diagnosed colorectal cancer. Marked COX-2 expression was observed in cancer cells, inflammatory cells, vascular endothelium, and fibroblasts of the lesional tissues compared with the nonlesional and normal colon tissues. The extent and intensity of the immunoreactive COX-2 in cancer cells was much greater than that of the other cell types. In contrast, the expression of COX-1 polypeptide was weak in both normal and cancerous specimens. These data suggest that the enhanced expression of the COX-2 gene in colon cancer tissues may contribute to the enhanced synthesis of prostaglandin E2 by the colon cancer tissues. Enhanced expression of COX-2 may play a role in the pathogenesis of colon cancer. Furthermore, selective inhibition of COX-2 may prove to be more efficacious in the retardation of colon cancer development.
Adenocarcinoma↗
Case 42-1994: Mycoplasma pneumonia and transverse myelitis.
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Adult↗
Induction of angiogenesis by smooth muscle cell-derived factor: possible role in neovascularization in atherosclerotic plaque.
The development of atherosclerotic plaque is associated with neovascularization in the thickened intima and media of vascular walls. Neovascularization may have a role in the progression of atherosclerotic plaque as well as in the development of intraplaque hemorrhage. However, the mechanism and stimulus for neovascularization in atherosclerotic plaque are unknown. We postulated that smooth muscle cells (SMCs), a major cellular component in the vascular wall, might contribute to the induction of neovascularization in atherosclerotic plaque through the secretion of an angiogenic factor. We observed that endothelial cells (ECs) cultured on collagen gel with SMC-conditioned medium became spindle shaped, invaded the underlying collagen gel, and organized a capillary-like branching cord structure in the collagen gel. The conditioned medium also stimulated EC proliferation and increased the EC-associated plasminogen activator activity. The angiogenic factor in SMC-conditioned medium was retained in a heparin-Sepharose column and eluted with 0.9 M NaCl. Neutralizing anti-vascular endothelial growth factor (VEGF) antibody attenuated the angiogenic activity in the conditioned medium, including the induction of morphologic changes in ECs, mitogenic activity, and increased plasminogen activator activity associated with ECs. Immunoblotting analysis confirmed the secretion of VEGF from SMCs. These observations indicate that SMC may be responsible for the neovascularization in atherosclerotic plaque through the secretion of VEGF.
Arteriosclerosis↗
Spontaneous resolution of symptoms in an infant with a congenital dural caroticocavernous fistula.
We report a 5-week-old boy with a congenital dural caroticocavernous fistula (CCF). He had gradually progressive proptosis, dilated conjunctival veins, chemosis, abducens nerve palsy and an objective bruit. Angiography of the right common carotid artery revealed fistulous communication in the cavernous sinus (CS) region. The CS was fed by the middle meningeal artery and drained through the superior ophthalmic vein and the superior petrosal vein. The child's symptoms and signs disappeared within a few weeks and did not recur over 11 months. At that time, however, angiography still showed a small communication between the right external carotid artery and the CS.
Arteriovenous Fistula↗
Adoptive immunotherapy of poorly immunogenic tumors with in vitro sensitized cells generated by intratumoral administration of biological response modifiers.
We investigated the efficacy of intratumoral administration of biological response modifiers (BRM) in induction of in vitro sensitized (IVS) cells for adoptive immunotherapy of the poorly immunogenic MCA 102 sarcoma and B16-BL6(BL6) melanoma. We used the bacterial immunoadjuvant Nocardia rubra cell wall skeleton (N-CWS), and a streptococcal preparation, OK-432, for MCA 102 and BL6, respectively. After C57BL/6(B6) mice were inoculated subcutaneously (s.c.) with viable MCA 102 or BL6 tumor cells in the foot-pad, mice were injected intratumorally (i.t.) with N-CWS ranging from 10 to 400 micrograms or OK-432 ranging from 1 to 100 micrograms. Draining popliteal lymph nodes (LN) were harvested 7 days after i.t. administration of BRM, and LN cells were cultured with irradiated tumor cells in the presence of IL-2 for 11 days. These IVS cells (7.5 x 10(6) or 2 x 10(6)) were transferred intravenously (i.v.) to B6 mice with 4 day pulmonary metastases established by i.v. injection of viable MCA 102 cells (1 x 10(6)) or viable BL6 cells (3 x 10(5)). The mice were also received intraperitoneally 4 x 10(4) IU/day of IL-2 for 4 days after adoptive transfer. The transfer of IVS cells from mice immunized by i.t. injection of 100 micrograms of N-CWS 1 week after inoculation of tumor cells significantly reduced MCA 102 pulmonary metastases, compared with control IVS cells without administration of N-CWS. Moreover, the transfer of IVS cells from mice immunized by i.t. injection of 10 micrograms of OK-432 3 days after inoculation of tumor cells significantly reduced BL6 pulmonary metastases compared with control IVS cells without administration of OK-432. The administration of N-CWS resulted in no enhancement of in vitro cytotoxicity. Although the administration of 10 micrograms of OK-432 augmented in vitro cytotoxicity of IVS cells against BL6, cytotoxic activity was lower than that of IVS cells immunized with N-CWS. The major phenotype was CD8+ cells in IVS cells immunized with N-CWS or OK-432. These results suggest that i.t. administration of N-CWS and OK-432 facilitates the production of sensitized T-cells, and this administration route of BRM may be useful in the adoptive immunotherapy of human cancer.
Adjuvants, Immunologic↗
Specific binding of a synthetic peptide derived from an antibody complementarity determining region to phosphatidylserine.
We have established a series of monoclonal antibodies that bind to phosphatidylserine (PS). One mAb, PS4A7, showed a strict specificity for PS and distinguished the stereospecific configuration of its serine moiety. We determined the amino acid sequences of the heavy and light chain variable regions of PS4A7, and examined the reactivity of the synthetic peptides corresponding to the complementarity determining region (CDR) of the mAb with phospholipids. We found that a 12-amino acid synthetic peptide corresponding to the third CDR of the heavy chain (amino acid residues 93-102, referred to as CDR3-H) bound specifically to PS. Although the affinity of the peptide to PS was markedly lower, the peptide was shown to bind to 1,2-diacyl-sn-glycero-3-phospho-L-serine (PS), but not to 1,2-diacyl-sn-glycero-3-phospho-D-serine, showing a similar specificity to that of PS4A7. The specific binding of the CDR3-H peptide to PS was confirmed by ELISA and TLC-immunostaining assay. The interaction between the CDR3-H peptide and water-soluble PS-derivatives was investigated by inhibition of the ELISA. PS effectively inhibited the binding and phosphoserine showed a weak but significant inhibition, but no appreciable inhibition was observed with serine. These observations suggest that the CDR3-H peptide plays a major role in the interaction of PS4A7 with the phosphoserine residue of the PS molecule.
Amino Acid Sequence↗
A case of distal 9q trisomy syndrome associated with an unusual inheritance of ABO blood type.
A male infant with distal 9q trisomy syndrome associated with an unusual inheritance of ABO blood type is reported. His clinical features were concordant with those of distal 9q trisomy syndrome. His karyotype was 46,XY, -10, +der (10) t(9;10) (q22.3;q24.3) confirmed by G-banding and high resolution methods. His father had the balanced translocation t(9;10) (q22.3;924.3). He had a blood type of AB, despite his father's blood type of AB and his mother's blood type of O. The gene of ABO blood type is located at 9q34.1-q34.2. Therefore, he would have received A and B type alleles from his father. 9q trisomy syndrome should be carefully investigated with ABO blood type.
ABO Blood-Group System↗
Effects of spo0 mutations on spo0A promoter switching at the initiation of sporulation in Bacillus subtilis.
Transcriptional analyses of the Bacillus subtilis sporulation initiator gene spo0A revealed that promoter switching from the vegetative (Pv) to the sporulation-specific (Ps) promoter did not occur in the spo0A, spo0B, spo0E, spo0F, and spo0H mutants. The sof-1 mutation in spo0A restored the promoter switching in the spo0F mutant. These results strongly suggest that Spo0A plays a central role in the regulation of its own promoter switching.
Bacillus subtilis↗