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Biomedical subjects

K Sayama

Publications and source records attributed to K Sayama.

At least 73 records · Page 4Linked to original sources
PubMed1993

[Measurement of myeloperoxidase and thiobarbituric acid-reactive material in plasma and bronchoalveolar lavage in E. coli-induced acute lung injury].

Myeloperoxidase (MPO), which is exclusively contained in neutrophils, is released on their activation. Therefore, MPO may possibly be used as a parameter of neutrophil activation. Thiobarbituric acid-reactive material (TBARM) reflects lipid peroxidation and is a parameter of oxygen radical-mediated cell membrane damage. Using our guinea pig model of septic lung injury we measured MPO and TBARM in the setting of acute lung injury. The two experimental groups were saline controls (n = 8) and an E. coli septic group to which 2 x 10(9) live E. coli were administered intravenously (n = 8). Lung damage was assessed by measuring wet to dry lung weight ratio (W/D) and lung tissue to plasma accumulation of 125I-albumin (AL: albumin leakage). We measured MPO and TBARM in plasma and BAL fluid. Increased W/D and AL were observed in the E. coli group suggesting the development of acute lung injury. In the E. coli group, plasma MPO increased and MPO in BAL fluid was significantly increased as compared with the saline control group. There was no difference in plasma TBARM between the two groups, while TBARM in BAL fluid of the E. coli group was greater than in that of controls. Although BAL fluid TBARM correlated with both W/D and AL, there was no relation between BAL fluid MPO and either of these parameters. We conclude that TBARM in BAL fluid may be useful for assessing E. coli-induced acute lung injury in guinea pigs.

Animals↗
PubMed1992

Distribution of complement regulators (CD46, CD55 and CD59) in skin appendages, and in benign and malignant skin neoplasms.

Immunohistochemical studies were performed to establish the distribution of membrane cofactor protein (MCP; CD46), decay-accelerating (DAF; CD55) and homologous restriction factor (HRF20; CD59), in normal skin appendages, and in benign and malignant skin neoplasms. At least two of these regulators were detected on normal eccrine glands, apocrine glands and sebaceous glands. They were also found in cellular naevi (CN), seborrhoeic keratoses (SK), basal cell carcinoma (BCC), Bowen's disease (BD), squamous cell carcinoma (SCC) and Paget's disease (PD). Although there were slight differences in their distribution, these regulators were found in all the cells examined, indicating that they are essential factors in human skin as well as other organs, and in neoplasms, in preventing autologous complement attack.

Antigens, CD↗
PubMed1992

[Measurements of plasmin-alpha 2 plasmin inhibitor complex and FDP.D dimer levels in the fibrinolytic therapy of acute pulmonary thromboembolism].

The key enzyme for fibrinolysis is plasmin, which is converted from plasminogen by plasminogen activator. Activated plasmin lyses fibrinogen and fibrin to make fibrin degradation products(FDPs) and plasmin is inactivated immediately by alpha 2 plasmin inhibitor. As FDP.D dimer is derived solely from insoluble fibrin, FDP.D dimer is thought of as an index for clot lysis. We measured plasmin-alpha 2 plasmin inhibitor complex(PIC) and FDP.D dimer plasma levels in 3 patients with acute pulmonary thromboembolism treated with recombinant tissue plasminogen activator(tPA). Fifteen million units of tPA(TD-2061) were infused in one hour on the first, second and third hospital days. PIC and FDP.D dimer before tPA infusion showed slightly elevated values as compared to normal ranges. They increased markedly after tPA infusion. These findings suggest that the fibrinolytic system is slightly activated in the acute phase of pulmonary thromboembolism and also strongly activated by tPA infusion. Increased FDP D dimer suggests that fibrin clots are dissolved by activated plasmin. Improvement of arterial oxygen tension was observed after tPA infusion. As sustained higher FDP.D dimer means the existence of fibrin clots, heparin treatment should be continued for prevention of clot formation as long as FDP.D dimer shows higher value. In conclusion, PIC and FDP.D dimer are useful indices not only to detect the activated state of the fibrinolytic system but also to know clot lysis in tPA treatment.

Acute Disease↗
PubMed1991

Expression and characterization of membrane co-factor protein (MCP) in human skin.

Membrane co-factor protein (MCP; CD46) is an integral membrane protein with molecular weight (MW) of the two species of 63 kD and 55 kD, and regulates autologous complement activation, with the activity of factor I cofactor. The quantity of each species is genetically regulated, and two codominantly inherited allelic variants account for the three phenotypic patterns. By immunohistochemical study, MCP was found both in the intercellular spaces of the epidermis and on the endothelial cells in the dermis of normal human skin in vivo. The intensity of the staining pattern was higher in the basal layer than in the granular layer. By Western blot analysis with use of a monoclonal antibody, MCP in the epidermis appeared as several bands ranged from 60-50 kD, with a major band of 56 kD, which was different from those in either polymorphonuclear cells, platelets, and cultured keratinocytes. No other variants were found in the epidermis obtained from skin of 20 normal humans. Complement activation in human skin may be regulated at several steps, including DAF and HRF20, thereby protecting cells from autologous complement attack.

Antigens, CD↗
PubMed1991

Characterization of decay-accelerating factor (DAF) in human skin.

Decay-accelerating factor (DAF) is a 70-kD membrane glycoprotein that regulates autologous complement activation, by preventing assembly of alternative or classical C3/C5 convertases, and has been shown to have a wide tissue distribution. In this study, DAF antigen has been demonstrated at the intercellular spaces of normal human epidermis with monoclonal antibody against DAF using the peroxidase-anti-peroxidase method. The amount of DAF was greater at the granular layer than the basal cell layer as judged by intensity of the staining. Western blot analysis of DAF in the epidermis showed a 55-kD band, whereas that of buffy coat cells was approximately 67 kD. When DAF of the epidermis was treated with neuraminidase, the molecular weight was reduced to 53 kD, whereas that of buffy coat cells was 56 kD. These results indicated that the content of sialic acid of DAF in the epidermis was different from that of buffy coat cells. In phosphatidylinositol-specific phospholipase C (PIPLC)-treated normal human skin, DAF was not demonstrated in the epidermis, whereas DAF remained unchanged on the elastic fibers. After the treatment of the epidermis by PIPLC, DAF was released into the buffer shown by Western blot analysis. These results suggested that DAF on the epidermis was anchored to keratinocyte via phosphatidylinositol (PI), whereas the anchoring mechanism of DAF on the elastic fibers was not through PI.

Blotting, Western↗
PubMed1991

Mal de Meleda-like palmoplantar keratoderma.

A 38-year-old Japanese man was seen for severe palmoplantar keratoderma, extending to the dorsal aspects with red rims. He had had spontaneous amputations of the toes and surgical amputation of the right lower leg because of squamous cell carcinoma of the right sole. The clinical symptoms suggested those of mal de Meleda, except for the absence of consanguinity and of granular layers in the epidermis. The keratoderma improved with oral etretinate treatment.

Adult↗
PubMed1991

Diffuse neonatal hemangiomatosis with a giant cutaneous hemangioma on the axilla.

A case of diffuse neonatal hemangiomatosis is described. At birth, a giant tumor, 10 cm in diameter and 6 cm in height, was present on the left axilla and associated with thrombocytopenia. Numerous cherry-red papules were present on the skin and buccal mucosa. On the second day of life, the giant tumor was excised. Histological examination of the tissue revealed masses of endothelial cells embedded in fibrous tissues. Plain and enhanced computed tomography of the brain revealed a hemorrhage and two hemangiomas. The associations of intravascular papillary endothelial hyperplasia were discussed.

Axilla↗
PubMed1991

Morphea profunda.

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Adolescent↗
PubMed1991

Complement allotypes in Japanese patients with pemphigus and bullous pemphigoid.

The allotypes of C6, C7, factor B (BF) and factor I (IF) of the human complement system were studied in 11 Japanese patients with pemphigus (5 with pemphigus vulgaris and 6 with pemphigus foliaceus) and 17 with bullous pemphigoid (BP) to investigate the genetic background of these diseases. The allotypes were detected by using isoelectric focusing and immunoblotting. The frequency for IF*A allele in the pemphigus patients was significantly higher (p = 0.009) than that in healthy controls (n = 60). A significant association of IF A allotype with pemphigus was also observed (p = 0.027), with a relative risk of 6.3. There was no association between the C6, C7, BF or IF allotypes and BP. These data suggest that IF A allotype may be an etiological genetic factor in the development of pemphigus.

Alleles↗
PubMed1991

[Characterization of dominant hereditary cataract in DDD/1 mice].

We found a female cataractous DDD/1-nu/+ mouse and established a hairy mutant strain (DDD/1-Cti/Cti) with 100% incidence of cataract from it by repeating sibmating. Genetic studies demonstrated that a single autosomal semidominant gene controls cataractogenesis. This gene was named Cti. In homozygotes, DDD/1-Cti/Cti, the lenses began to opacify at 14 days of fetal life and were recognized clinically as cataract at 13-14 days of age when the eyes first open. The opacification became more and more intense with age and looked like mature cataract at 28-42 days of age. However, clarification of the opacified lenses commenced at the periphery after 56 days of age and expanded to the inside with time, and only an opaque spot was left at the center at 140 days of age. In heterozygotes, DDD/1-Cti/+, the lenses were recognizable as cataract after 28 days and became like mature cataract around 35 days of age. The opacity began to be lightened at 42 days and the lenses appeared normal at 56 days of age. Both lenses and eyeballs developed in similar courses in DDD/1(-)+/+, -Cti/+ and -Cti/Cti, although slightly retarded in the last. Microphthalmia was not accompanied even in DDD/1-Cti/Cti. The lens water content remained higher during the time when intense lens opacity continued in DDD/1-Cti/Cti and -Cti/+. Background genes appeared to affect the expression of Cti. DDD/1-Cti(-)+ mice may provide a model for researches into clarification of opaque lenses. A discussion concerning the possible allelism of Cti and Cts with Lop was made based on their phenotypic characteristics.

Animals↗
PubMed1991

[Marked difference in sensitivity to gamma-ray-induced cataract between BALB/c and CBA-C3H strain mice].

Nineteen BALB/c, 14CBA/KI, 12C3H/HeJ and 15 (CBA/Kl x C3H/HeJ) F1 female mice were irradiated with 850 rad gamma-rays and transferred with 10(7) syngeneic bone marrow cells 24 hrs later. The occurrence of cataract was examined in these animals. All the BALB/c mice showed visible lens opacification in both eyes between 113 and 149 days after irradiation. All the animals were autopsied 6 months after irradiation and examined for opacification of their lenses. The proportion of opaque lenses was 100, 7.1, 16.7 and 0% in BALB/c, CBA/Kl, C3H/HeJ and (CBA/Kl x C3H/HeJ) F1 mice, respectively. The results indicate that BALB/c mice are much more sensitive to radiation-induced cataractogenesis than CBA and C3H mice.

Animals↗
PubMed1990

Subclass characteristics of IgG autoantibodies in bullous pemphigoid and pemphigus.

Immunoglobulin (Ig) G subclasses in anti-basement membrane zone (BMZ) autoantibodies found in the sera of bullous pemphigoid (BP) and in anti-intercellular substance (ICS) autoantibodies of pemphigus were investigated using immunofluorescent (IF) staining. In BP, IgG4, IgG1, and IgG2 were detected in 13, 5 and 6 of 15 patients, respectively; IgG3 was not detected. In pemphigus, IgG4 was detected in all of 10 patients, IgG1 in 7, IgG2 in one, and IgG3 in one patient, respectively. In both BP and pemphigus, the most prominent subclass in intensity of IF staining was IgG4. Although one BP and one PV patient had only IgG4 autoantibodies, C3 deposition was detected. The quantification of IgG subclasses in the sera of the patients was performed by enzyme-linked immunosorbent assays (ELISA). Serum levels of IgG4 in both BP and pemphigus were elevated approximately 3-fold over those in normal controls; those of whole IgG and IgG1-3 were not significantly elevated. Using direct IF staining, the deposition of C3 at the BMZ and at the ICS was demonstrated in 9 of 10 BP and in 3 of 8 pemphigus patients, respectively. The prominent IgG subclasses of anti-BMZ and anti-ICS antibody were IgG4, a noncomplement-fixing antibody, suggesting that the deposition of C3 in the lesional skin occurred via the alternative pathway, or that small amounts of IgG1-3 subclass autoantibodies activated the classical pathway.

Autoantibodies↗
PubMed1990

Characterization of homologous restriction factor (HRF20) in human skin and leucocytes.

Homologous restriction factor with a molecular weight of 20 kD (HRF20) is a membrane protein that inhibits assembly of the membrane attack complex of homologous complement. Distribution of HRF20 in normal human skin was studied. The plasma membrane of keratinocytes was stained, and the intensity of the staining pattern was higher in the basal cell layer than in the granular layer. Endothelial cells of blood vessels in the dermis were also stained. The molecular weight of HRF20 on erythrocytes and epidermis is 16 kD, determined by Western blot analysis. Those of polymorphonuclear cells and lymphocytes appeared as two bands, a major band of 20 kD and a minor band of 16 kD. Susceptibility of HRF20 to phosphatidylinositol-specific phospholipase C (PIPLC) was examined. After PIPLC treatment of the sections, HRF20 was not detected on the epidermis and was very slightly expressed on the blood vessels. These results indicate that HRF20 attaches to keratinocytes and blood vessels via phosphatidylinositol, regulating the formation of membrane attack complexes of homologous complement on the cell membrane.

Blood Proteins↗
PubMed1990

Immunological properties of type IV collagen from mouse kidney.

Some immunological properties of mouse kidney type IV collagen (MKIVC) were investigated. In enzyme-linked immunosorbent assay (ELISA), rabbit anti-MKIVC antiserum reacted strongly with MKIVC but not at all with type I collagen or laminin of mouse origin. Thus, the purified MKIVC preparation was not contaminated with detectable amounts of other constituents of the extracellular matrix and the basement membrane including interstitial collagens, as suggested previously (T. Oikawa et al., Chem. Pharm. Bull., 34, 789 (1986)). In ELISA inhibition assay, human kidney type IV collagen (HKIVC) only partially inhibited the binding of MKIVC to anti-MKIVC antiserum. Similarly, HKIVC showed a far weaker binding capacity to the antiserum compared to MKIVC in ELISA direct binding assay. After the anti-MKIVC antiserum was absorbed with acetone powder of human kidney, the resulting antiserum still possessed a considerable binding activity to MKIVC but did not react with HKIVC. In accord with these findings, anti-MKIVC antiserum immunostained both mouse and human renal basement membranes, while it stained the former but not the latter after being absorbed with human kidney. Taken together, these results suggest that MKIVC possesses at least two antigenic determinants; one but not the other cross-reacts with human kidney basement membrane collagen.

Animals↗
PubMed1990

[Comparison of background factors relevant to mammary tumorigenesis between DDD/1-Mtv-2/Mtv-2 congenic and DDD/1 mice].

To elucidate the possible participation of the Mtv-2 gene in the background factors relevant to mammary tumorigenesis, DDD/1-Miv-2/Mtv-2 (DDD-Mtv-2) congenic and DDD/1 background mice were compared for endocrine and immune organs, mammary gland development, expression of mouse mammary tumor virus (MMTV)-gp 52 antigen, hyperplastic alveolar nodules (HAN) and mammary tumor incidence. The congenic strain had been established by introducing Mtv-2 from GRS/AJms (GR) into DDD/1 mice by repeated 12 backcrosses. Body, thymus, spleen, uterus, ovary, adrenal and pituitary weights, histology of the ovary and mammary gland development showed no differences ascribable to Mtv-2 between both strains of mice at 4,6 and 12 months of age. In contrast, MMTV-gp 52 antigen expression, HAN and mammary tumor occurred in DDD-Mtv-2 but not in DDD/1 mice. These results showed that the Mtv-2 gene stimulates mammary tumorigenesis by constitutional production of endogenous MMTV which transforms mammary epithelial cells but not by influencing the background factors relevant to mammary tumorigenesis. Furthermore, the expression of Mtv-2 appeared to be lower on the DDD/1 than on the GR background.

Animals↗