Reversible photocontrol of the coordination number of silicon in a tetrafluorosilicate bearing a 2-(phenylazo)phenyl group.
Explore the source record for details and available documents.
Journal Article↗
Biomedical subjects
F Komatsu
Publications and source records attributed to F Komatsu.
Multidrug resistance gene 1 expression in salivary gland adenocarcinomas and oral squamous-cell carcinomas.
In combined chemotherapy for head-and-neck cancer (HNC), salivary gland-cell adenocarcinoma (SGA) shows insufficient clinical outcome, and it has been suggested that the sensitivity and/or the mechanism of resistance to anti-cancer drugs are different between SGA and oral squamous-cell carcinoma (SCC). The aim of our study was to clarify whether P-glycoprotein (P-gp) expression is associated with multidrug resistance (MDR) in HNC and the difference in the process of its development between SGA and SCC. In immunohistochemical analysis, P-gp expression was found in the ductal cells of salivary glands but not in oral mucosal epithelium. In cancer tissues, a few SCC cells in 12 of 37 and most cells in all SGAs expressed P-gp. The intensive P-gp expression was significantly found in SGA compared with SCC. In an in vivo chemotherapeutic model using tumor-bearing nude mice, P-gp expression in counterparts was observed in only a few cells of the HSY line, while no P-gp expression was observed in Hepd cells. However, P-gp expression was developed in both HSY and Hepd cell lines after vincristine (VCR) treatment. RT-PCR showed that the mean ratios of mdr1 mRNA expression levels in HSY clones were 3.7-fold higher than those in Hepd clones after VCR treatment, while each cell line exhibited both induction and activated production of P-gp. These results suggest that P-gp-related MDR in SGA is an inherent phenotype caused by both high levels of P-gp induction and activated P-gp production during VCR treatment, while that in SCC is an acquired phenotype chiefly caused by induction of P-gp.
ATP Binding Cassette Transporter, Subfamily B, Mem↗
Large volume apheresis of autologous plasma and preparation of autologous fibrin glue from the plasma.
Autologous blood transfusion (ABT) is useful for prevention of undesirable effects of allogeneic blood transfusion. In our hospital, not only autologous whole blood but also autologous red blood cells, autologous fresh frozen plasma (Auto-FFP), and autologous fibrin glue (Auto-FG) are routinely produced for surgical patients. The Auto-FG is prepared from plasma which is separated from manually collected whole blood. However, when a large volume of Auto-FG is required, the plasma obtained by an apheresis method may be useful. Therefore, a pilot study was conducted to determine whether a collection of 2 U (160 ml) of red blood cells (RBCs) and 400 ml of plasma at 1 apheresis is acceptable. We first performed the apheresis on healthy donors, and then applied for autologous blood donation. The apheresis is safe. The collected plasma is used for the production of Auto-FFP and Auto-FG. The remaining RBCs also are used for ABT. The preparation of Auto-FG is simple, and it is effective for the reduction of allogeneic fibrin glue.
Adult↗
A case of aldosterone-producing adrenocortical adenoma associated with preclinical Cushing's syndrome and hypersecretion of parathyroid hormone.
A rare case of aldosterone-producing adrenocortical adenoma with preclinical Cushing's syndrome and hypersecretion of parathyroid hormone (PTH) is described. A 64-year-old male patient had a history of hypertension for two decades and hypokalemia for 4 years. He suffered from left hemiparesis and aphasia due to cerebral hemorrhage, but his appearance was not Cushingoid. His plasma renin activity was below the normal range, while plasma aldosterone concentration was high. They did not respond to furosemide-upright test. His plasma cortisol level in the morning was at the upper limit of the normal range, but it did not show a diurnal rhythm nor was it suppressed by 1 mg and 8 mg of dexamethasone. Computed tomography showed a low density tumor in the right adrenal gland. An adrenal scintigram under dexamethasone treatment revealed an uptake of the tracer on the right side, and plasma aldosterone and cortisol concentrations in the adrenal vein were higher on the right side than on the opposite. The diagnosis of right aldosterone-producing adrenal adenoma with an autonomous production of cortisol was confirmed by right adrenalectomy. Histological findings showed an adenoma consisting mostly of clear cells, but that the nests of compact cells were scattered. Analysis of an extract from the adenoma revealed that the adenoma contained an excess amount of aldosterone and that the cortisol/corticosterone ratio was higher than that of aldosterone-producing adenoma. Both serum calcium and PTH levels remained high one year after adrenalectomy. Ultrasonography revealed the swelling of a parathyroid gland on the left side, indicating the coexistence of an autonomous hyperparathyroidism.
Adenoma↗
[Enucleation of renal tumor using microwave tissue coagulator: a case report].
A 69-year-old man was referred to our department for a cystic tumor, 4.0 cm in diameter, in the lower portion of the right kidney, which was detected by computed tomography. The patient had been admitted to the department of surgery in our hospital for treatment of ileus caused by transverse colon cancer. With a diagnosis of cystic renal cell carcinoma. T2N0M0, in situ non-ischemic tumor enucleation was performed using a microwave tissue coagulator (Microtaze, Heiwa Electronics Industry Inc., Tokyo). The enucleation was accompanied by a defect of the renal pelvis, but it was easily repaired. The operation time was 120 minutes and blood loss was 110 cc. The histological diagnosis was renal cell carcinoma, pT2N0M0V1, expansive, alveolar type, clear cell subtype, G1 > G2. Diagnostic imaging done postoperatively showed no sign of damage to renal function. At the present time, the patient has been disease-free with interferon-alpha for 12 months and is being followed on an outpatient basis. In this report, the advantages of nephron-sparing surgery, especially in situ non-ischemic tumor enucleation using a microwave tissue coagulator for renal tumor are discussed. In particular, the technique of performing tumor enucleation with repair of the defect of renal pelvis used in this case may extend the indication of nephron-sparing surgery.
Aged↗
A pilot study of large volume apheresis of red blood cells and plasma during one donation by allogeneic blood donors.
UNLABELLED: As a pilot study, we assessed large volume apheresis of red blood cells (RBC) and plasma. The protocol was as follows: (a) 3-RBC group: 3 units (240 ml) of RBC were drawn, (b) RBC+P group: 2 units (160 ml) of RBC and 400 ml of plasma were drawn during one apheresis procedure, and (c) CONTROL GROUP: 400 ml of whole blood was drawn by a manual method. Each group contained 7 healthy male donors of body weight 54-65 kg. We were able to perform these apheresis procedures without serious complications. Recovery of RBC for the donors of the 3-RBC group was delayed, but the level returned to the pre-donation level within nine weeks. The decreased total protein and albumin in the RBC+P group recovered within one week. The apheresed RBCs demonstrated the same quality as the manually collected RBC. These findings suggest that this apheresis approach may be applicable for routine donation.
Adult↗
Adult-onset giant juxtaglomerular cell tumor of the kidney.
The juxtaglomerular cell tumor (JGCT) of the kidney is a rare neoplasm which commonly secretes renin. This tumor often occurs in teenagers. This paper documents the 14th adult-onset (over 30-years-old) case with a giant JGCT which measured 9.0 x 8.0 x 7.5 cm. Histologically, this tumor was composed of both vascular and tubular components. Immunohistochemically, the vascular component reacted with renin, cytokeratin 7, ulex europaeus agglutinin-1, vascular endothelial growth factor (VEGF) and Flk-1 (VEGF-R2), whereas the tubular component was positive for renin, epithelial membrane antigen (EMA), cytokeratin 7, alpha-1-antitrypsin, VEGF and Flk-1. This finding suggests that both vascular and tubular components of JGCT may promote neoplastic proliferation via an autocrine mechanism through the action of VEGF.
Female↗
CD18/CD54(+CD102), CD2/CD58 pathway-independent killing of lymphokine-activated killer (LAK) cells against glioblastoma cell lines T98G and U373MG.
For natural killer cell-mediated cytolysis (NK-lysis) and lymphokine-activated killer cell-mediated cytolysis (LAK-lysis), the co-stimulatory signals of CD18/CD54(+CD102) and CD2/CD58 pathways are essential. However, in this report, we describe a LAK-lysis that does not depend upon these two pathways. The killed cells were glioblastoma cell lines T98G and U373MG. The LAK cells were induced from peripheral blood lymphocytes in the presence of interleukin-2. 1) The T98G and U373MG did not express CD54 or CD102, but expressed CD58. 2) However, when they were pretreated with an anti-CD58 (TS2/9), the LAK-lysis was not blocked. 3) The LAK-lysis was markedly inhibited by pretreating with Concanamycin A and slightly inhibited by treating with antitumor necrosis factor-related apoptosis-inducing ligand (anti-TRAIL) antibody. 4) Nineteen percent of the LAK cells adhered to the T98G. The adhered LAK cells killed it. But nonadherent LAK cells could not kill the T98G or U373MG but killed lymphoblastoma cell lines Raji and NALM-6. These findings suggested that this type of the LAK-lysis might not depend upon the CD18/CD54(+CD102) pathway or CD2/CD58 pathway. The effector cells that killed the T98G and U373MG might not always be the same as the effector cells that killed the other cell lines. The LAK cells contain several subsets, and one of the subsets might kill these two target cell lines.
Antigens, CD↗
Cell-cell adhesion-independent killing due to lymphokine-activated killer cells against glioblastoma cell lines.
Lymphokine-activated killer (LAK) cells can kill several tumor cells. Their killing activity is generally due to cell-cell adhesion. Cell-cell adhesion of the LAK cells to the target cells is essential for LAK lysis. In this report, however, we describe that the LAK cells can also kill the target cells by cell-cell adhesion-independent killing. Killing occurred after the target cells were exposed to the LAK cells. When the LAK cells were added to glioblastoma cell lines T98G and U373MG (which proliferate by adhering to the bottom of a culture flask), the LAK cells killed them by cell-cell adhesion killing within 4 h (early killing). On the other hand, when small numbers of the LAK cells were added, some of the target cells escaped from the early killing. At 4 and 6 h after the adding the LAK cells, when the LAK cells were discarded from the flask by washing with PBS, the escaped cells still adhered and were alive. However, they ultimately died over the next 24-96 h (late killing). The late killing was the cell-cell adhesion-independent killing, because it occurred after the LAK cells were removed. In this killing, numerous granules and vacuoles appeared in the cytoplasm of the cells. The vacuoles enlarged and then the cells died. The cell death was different from apoptosis, because the nucleus was intact until the late stage and no DNA fragment laddering in the degenerated cells was recognized. The vacuoles were stained with acid phosphatase and the cell death was inhibited with 3-methyladenine (an inhibitor of lysosome), suggesting that the late killing may be autophagic cell death due to activated lysosome. Induction of late killing in tumor cells using the LAK cells may become one approach for cancer therapy.
Acid Phosphatase↗
Utility and quality of autologous fresh frozen plasma and autologous fibrin glue for surgical patients.
The quality of autologous fresh frozen plasma and autologous fibrin glue prepared in our hospital was evaluated. The Auto-FFP was separated from whole blood or collected using a cell separator and the Auto-FG was then prepared from the Auto-FFP. The Auto-FFP showed significantly higher levels of fibrinogen, Factor-V and Factor-VIII than commercially available FFP. The Auto-FG contained approximately 10 times the concentration of fibrinogen, Factor-VIII, Factor-XIII, von Willbrand factor and fibronectin and 1.5 times that of alpha 2-Plasminogen inhibitor compared to those of the Auto-FFP. When the Auto-FG was sprayed over diffusely bleeding sites from surgical wounds, hemostasis occurred within 5 s. These results suggest that Auto-FFP and Auto-FG may have sufficient utility and quality to reduce the use of allogeneic blood products.
Adult↗
Determination of serum hepatitis C virus (HCV) core protein using a novel approach for quantitative evaluation of HCV viraemia in anti-HCV-positive patients.
AIMS/BACKGROUND: Hepatitis C virus (HCV) infection is frequently diagnosed by detection of antibody to the HCV (anti-HCV). Recently, a method for detection of HCV core protein, "Imucheck F-HCV Ag Core Kokusai", has been developed. In this study, we evaluate the utility of this method. METHODS: HCV core protein levels in sera were determined using this following method; anti-HCV titres were measured by particle agglutination (PA) test and then quantitative HCV-RNA values were investigated using a competitive reverse transcription-polymerase chain reaction (RT-PCR) test. RESULTS: The HCV core protein was detected only in anti-HCV-positive sera. Of 490 anti-HCV-positive sera, 130 (26.5%) were positive by this method. Of 144 anti-HCV-positive/HCV-RNA-positive sera, 130 (90.3%) were positive by it. A significant correlation between the HCV core protein levels and quantitative HCV-RNA values was recognized (n= 110, r=0.86, p<0.01). A significant correlation between the HCV core protein levels and alanine aminotransferase titres was also observed (n=67, r=0.72, p<0.05). All 71 patients with chronic active hepatitis, cirrhosis and hepatocellular carcinoma were positive with this method, whereas 18 of 32 patients with chronic inactive hepatitis were positive. Twenty-three patients with chronic active hepatitis were treated with interferon-alpha. During therapy, some patients showed a negative conversion of HCV core protein. One (7.7%) of 13 patients with HCV genotype 1 and 5 (62.8%) of 8 patients with genotype 2 remained negative for 6 months after the therapy. CONCLUSION: This method may be useful for quantitative evaluation of HCV viraemia in anti-HCV-positive patients.
Adolescent↗
Characteristics of human T-lymphotropic virus type-1 (HTLV-1)-infected cell line MT-2, which is not killed by a natural killer cell line NK-92 but is killed by lymphokine-activated killer cells.
Natural killer (NK) cell-mediated cytolysis (NK-lysis) is triggered by costimulatory signals of adhesion molecules and is downregulated by negative signals of killer cell inhibitory receptors (KIRs). Recently, a NK cell line, NK-92, was established. This cell line can kill several tumor cells, which possess adhesion molecules CD54 and CD102. However, the NK-92 cannot kill a human T-lymphotropic virus type 1 (HTLV-1)-infected cell line, MT-2, although lymphokine-activated killer (LAK) cells can kill MT-2. In this report we investigated the reason for LAK sensitivity but NK-92 resistance of the MT-2. The MT-2 highly expressed CD54 and CD102, suggesting that the costimulatory signals may be intact. Then we tested the responsibility of the negative signals by determining HLA type of the MT-2 and KIRs of the effector cells. The MT-2 expressed HLA-A24, B40, B51, Cw3, and HLA-G. The NK-92 did not express KIR2DL1, KIR2DL2,3, nor KIR3DL1, but 24% of the cells weakly expressed CD94. The blocking tests against these HLA class I molecules and KIRs did not restore the NK-92 resistance, although blocking against HLA-G slightly increased its lysis. Finally, in order to eliminate the class I molecules from the cell surface, we treated the MT-2 using a buffered citric acid solution (pH 3.8). By using this treatment, the expression of class I molecules and HTLV-1 antigen decreased, and then the MT-2 was killed by the NK-92. These findings suggest that an aberrant class I molecule of the MT-2 transferred a negative signal to the NK-92 and induced the NK-92 resistance. It remains to be elucidated whether or not the HTLV-1 infection contributed to the alteration of the class I molecule.
Antigens, CD↗
[Direct and indirect anti-globulin test].
Explore the source record for details and available documents.
Coombs Test↗
[Anti-D human immunoglobulin test].
Explore the source record for details and available documents.
Humans↗
[Donath-Landsteiner test].
Explore the source record for details and available documents.
Autoantibodies↗
Enhancement of tumor cell lysis by natural killer cells after blocking of HLA-monomorphic determinant using F(ab')2 fragment of W6/32.
It has been known that negative signal of natural killer (NK) cells is triggered by HLA-polymorphic determinant (PMD) of target cells. However, it is not clear whether or not the negative signal is triggered by HLA-monomorphic determinant (MMD). In this study, we determined the interaction of NK receptor and MMD by mean of a blocking test. For the blocking, W6/32, which is an antibody to the MMD, was used. As target cells, we used a tumor cell line H42 and several cell lines. The H42 was established from a bladder cancer patient after radiation therapy. This cell line was demonstrated to be PMD negative but MMD positive and showed NK sensitivity. We had established one more cell line, H41, from the same patient before the radiation therapy. However, the H41 possessed both the PMD and MMD and exhibited NK resistance. Thus, the NK sensitivity of the H42 may be due to depression of the PMD. We performed a blocking test against the MMD of these cell lines. When the H42 was pretreated with F(ab')2 fragment of the W6/32, the killing by NK cells increased. Other cell lines, EB33, KMT-1, and HMy2-C1R, which possessed low levels of PMD, were killed moderately after the pretreatment, although the H41 and other cell lines (KO, MT-2, OKM-3T), which possessed high levels of PMD, were killed only slightly. These findings suggest that the negative signal may be triggered not only by the PMD but also by the MMD.
Adult↗
Timing of effective natural killer cell collection in cancer patients after high dose chemotherapy, compared to peripheral blood stem cell collection.
Natural killer (NK) and lymphokine-activated killer (LAK) activities in patients with seminoma were determined, and the timing of effective NK cell collection was evaluated, compared to autologous peripheral blood stem cell (PBSC) collection. After chemotherapy, patients were injected with granulocyte-colony stimulating factor (G-CSF). CD56 cells decreased in parallel with white blood cells and then were restored. After discontinuing the G-CSF, the CD56 cells increased and reached peak 3-5 days after PBSC collection. The peak showed higher levels than those at premedication. Recovery-peripheral blood lymphocytes (PBL) which were obtained 4 days after PBSC collection showed higher NK and LAK activities than the PBL obtained before chemotherapy (Before-PBL). They exhibited a high expression of CD2, CD18, CD29, and CD49d. Furthermore, the LAK cells generated from the Recovery-PBL could acquire 9.6 folds of killer unit compared with the Before-PBL-LAK. These results suggest that, in order to obtain large numbers of NK cells, Recovery-PBL collection may be more advantageous than PBL collection in no relation with the chemotherapy.
Antigens, CD↗
Relation of natural killer cell line NK-92-mediated cytolysis (NK-92-lysis) with the surface markers of major histocompatibility complex class I antigens, adhesion molecules, and Fas of target cells.
Natural killer (NK) cell line NK-92 has recently been established by Klingemann et al. In this study, we compared the NK-92-mediated cytolysis (NK-92-lysis) with the killing of healthy volunteers' NK cells and lymphokine-activated killer (LAK) cells. The NK-92-lysis was partially different from the NK- and LAK-lysis. 1) The NK-92 could kill most of major histocompatibility complex (MHC) class I antigen-positive tumor cells. 2) The NK cells killed a myeloid leukemia cell line K562, but the NK-92 showed low killer activity against it. 3) The LAK cells could not kill a CD58-deficient cell line OKM-2T, whereas the NK-92 could kill it sufficiently. 4) The NK-92 could not kill CD54-, CD102-deficient cell lines T98G and U373MG; however, the LAK cells could kill them. Blocking tests using specific antibodies revealed the reason for these differences. The K562 expressed relatively low levels of CD54 and CD102. When the K562 was pretreated with anti-CD54 and anti-CD102, the NK-92 could not kill it at all, whereas the NK cells could still kill it, although the killing level decreased. The NK-92 could not kill the anti-CD54- and anti-CD102-treated OKM-2T. The LAK cells could not kill anti-CD58-treated U373MG and T98G. These findings suggest that NK-92-lysis may require the CD54 and CD102 but that NK-lysis does not require them as much, whereas the LAK-lysis may be rather in relation with the CD58. The NK-92 has high killer activity, and may be applicable for clinical use. However, it should be considered that the NK-92 cannnot kill CD54-, CD102-deficient tumor cells.
Antigens, CD19↗