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Biomedical subjects

H Kashiwa

Publications and source records attributed to H Kashiwa.

18 recordsLinked to original sources

Improved shoulder contour following forequarter amputation with an osteomyocutaneous free flap from the amputated extremity: two cases.

To cover a large soft-tissue defect and to reconstruct the shoulder contour after forequarter amputation, we used an osteomyocutaneous free flap incorporating an elbow joint from the amputated extremity in two patients. These flaps were well vascularised and reliable. They provided excellent coverage of large soft-tissue defects and they maintained shoulder contours. This procedure is useful for reconstruction after extended forequarter amputation and chest wall resection.

Adolescent↗

Morphometrical study of the arterial perforators of the deep inferior epigastric perforator flap.

Although abdominal perforator flaps based on a cutaneous branch of the deep inferior epigastric artery (DIEP flaps) have many advantages, preparing these flaps is technically difficult and requires great skill, especially as the portion of the artery running under the anterior rectus abdominis sheath must be operated upon "blind". To allow easier preparation and elevation of a DIEP flap pedicle, we propose that the arterial perforator should: 1) be more than 1.0 mm large; 2) run a straight intramuscular course, parallel to the rectus abdominis m. fibers, with no large muscular branches; and 3) have only a short portion running immediately under the anterior rectus abdominis sheath. We examined 329 perforators (more than 0.5 mm in diameter at the anterior sheath) in 66 rectus abdominis mm. from 33 cadavers among them: 1) 52 "large" perforators were over 1.0 mm in diameter; 2) 107 "suitable" perforators ran parallel to the muscle fibers without giving off large muscular branches; and 3) 35 "ideal" perforators combined these characteristics. The ideal perforators were usually located in the mid-abdominal region, 10-30 mm lateral to the umbilicus. The suitable perforators were usually present, often in combination with the ideal perforator(s), in a restricted area 20 mm cranial and 40-50 mm lateral to the umbilicus. We classified the course and ramification pattern of the deep inferior epigastric a. into six patterns, depending on whether the anastomosis was sited in the medial or lateral branch and the level at which the branches originated.

Aged↗

Sonographic assessment of osteochondritis dissecans of the humeral capitellum.

OBJECTIVE: The purpose of this study was to determine the efficacy of sonography for revealing osteochondritis dissecans of the humeral capitellum. SUBJECTS AND METHODS: Twenty-seven patients with capitellar osteochondritis dissecans (27 males; range, 11-20 years; mean age, 14 years) underwent radiography and sonography performed with a 7.5-MHz mechanical sector probe. Lesions were assessed as stable or unstable. The sonographic assessment was compared with radiographic assessment in 27 patients, MR assessment obtained in 10, and surgical findings in 15. RESULTS: Sonographic assessment agreed with radiographic assessment in 23 of the 27 patients, MR assessment in nine of the 10, and surgical findings in 14 of the 15. Sonography revealed that two lesions, which had been underestimated on radiography, were unstable. CONCLUSION: Sonography facilitates the assessment of capitellar lesions so that treatment can be optimized.

Adolescent↗

Thumb polydactyly.

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Journal Article↗

Familial congenital diaphragmatic hernia in the pig--studies on pathology and heredity.

Thirteen cases of congenital diaphragmatic hernia were encountered in one of the three pig families, established by us as a disease model of ano-rectal malformations. Five were males and 8 were females. The age at the onset of symptoms ranged between one and 4 months after birth. On the laterality, 7 had right side, 5 had left side and one had bilateral hernias. No hernial sac was observed. Herniated organs were intestine in the right and stomach in the left side. Thus congenital origin with late onset was suggested as a cause of the disease. In the studies of the heredity, there was no linkage between ano-rectal malformations and diaphragmatic hernia. Double recessive genes were supposed as a mode of inheritance, according to the statistical calculation. An effort is being made to produce a model of congenital diaphragmatic hernia from the pig family.

Animals↗

Dermal penetration enhancement by crude drugs: in vitro skin permeation of prednisolone enhanced by active constituents in cardamon seed.

Several extracts of crude drugs were prepared and tested as penetration enhancers for the diffusion of prednisolone through mouse skin in vitro. The acetone extract of cardamon seed (Eelettaria cardamomum) was selected for further study to identify the active principles. The result showed that terpineol and acetyl terpineol are the active components in cardamon seed.

Animals↗

Effect of protein kinase C inhibitor (H-7) and calmodulin antagonist (W-7) on pertussis toxin-induced IL-1 production by human adherent monocytes. Comparison with lipopolysaccharide as a stimulator of IL-1 production.

Human adherent monocytes stimulated with 1 microgram/ml pertussis toxin (PT) produced interleukin-1 (IL-1), as measured by thymocyte co-stimulation assay and enzyme-linked immunosorbent assay (ELISA), specific for IL-1 alpha and IL-1 beta. To clarify the role of protein kinase C (PKC) and calmodulin in IL-1 production, we investigated the effects of a PKC inhibitor, H-7, and a calmodulin antagonist, W-7 on PT- and lipopolysaccharide (LPS)-induced IL-1 production by monocytes. Addition of 10 microM and 20 microM H-7 to the culture medium markedly suppressed both PT- and LPS-induced IL-1 production. PT-induced IL-1 production was significantly suppressed by 5 microM and 10 microM W-7. However, LPS-induced IL-1 production was not suppressed by W-7 at the concentrations tested. When monocytes were labelled with Quin 2/AM, IL-1 production by monocytes stimulated with PT and LPS was markedly suppressed. These results indicate that different pathways are involved in the IL-1 production by PT and LPS; both calmodulin- and PKC-dependent processes are necessary for the IL-1 production induced by PT, whereas LPS-induced IL-1 production is dependent on the PKC. Inhibition of IL-1 production by interfering with intracellular Ca2+ trafficking in Quin 2/AM-loaded monocytes may be associated with the inhibition of PKC and calmodulin activity.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

Regulation of B cell maturation and differentiation. I. Suppression of pokeweed mitogen-induced B cell differentiation by tumor necrosis factor (TNF).

Growth and differentiation of B cells into Ig-secreting plasma cells is regulated by both T cells and macrophages and/or their secreted factors. Although the regulatory role of various cell-derived factors has been examined, the involvement of the macrophage-derived factor, TNF, in human B cell growth and differentiation has not yet been investigated. In the present study we examine the role of rTNF in polyclonal B cell response of human PBL induced by PWM. The addition of rTNF at the initiation of the culture resulted in the dose-dependent inhibition of the generation of both IgG and IgM PFC. Inhibition of PFC development followed the same dose response as rTNF-mediated cytotoxicity against a TNF-sensitive tumor target. The mechanism of rTNF-mediated suppression was examined in different experimental systems. Recombinant TNF did not affect the viability or proliferation of either the T cell or B cell subpopulations, suggesting that TNF does not mediate its suppressive effect by cytotoxic mechanisms. Kinetic studies in which rTNF was added at different times after initiation of culture indicated that inhibition can be observed as late as 4 days of culture and suggested that TNF acts at a late phase of the growth and differentiation pathway of B cells. In further studies we examined the cellular level of TNF-mediated suppression. The addition of rTNF to supernatants containing helper factors and enriched B cells resulted in no inhibition, suggesting that TNF does not act at the B cell level. This was confirmed by demonstrating that rTNF does not inhibit spontaneous PFC development by the CESS B cell line. The effect of TNF on T cell subpopulations was examined by using normal or irradiated T cells, which inactivate suppressor cells. Addition of rTNF to B cells combined with either T cell population suppressed both IgG and IgM PFC development, indicating that the target cell for suppression is the T helper cell but not ruling out an effect on macrophages or the T suppressor cells. Combined, the observed results demonstrate that rTNF suppresses PWM-induced B cell differentiation without affecting B cell proliferation. TNF appears to mediate the suppression by acting directly on T helper cells or else by regulating the production of factors controlling T cell activation and lymphokine secretion.

Antibody Formation↗

Inhibition by adenine of in vitro immunological functions of normal and adenine phosphoribosyltransferase-deficient human lymphocytes.

Exogenous adenine strongly inhibited mitogen-stimulated transformation, cytoplasmic immunoglobulin production, and natural killer activity of human mononuclear leukocytes at the high concentration of 1.0 mM. These inhibitions by adenine were not due to cytotoxicity, because the viability of cultured cells was not affected by adenine up to 1.0 mM. As the magnitude of inhibition by adenine of these in vitro immunological functions was similar in normal and adenine phosphoribosyltransferase-deficient cells, its inhibition was not mediated by corresponding nucleotides. Adenine at the concentration of 0.1 mM caused 50% inhibition of cytoplasmic immunoglobulin production without alternating cell proliferation or viability. This suggests that an appropriate concentration of adenine may inhibit the differentiation of B cells to plasma cells rather than affecting cell proliferation. Understanding the mechanisms of adenine inhibition may lead to new approaches for the regulation of immune responses.

Adenine↗

Natural killer activity in two cases of ataxia telangiectasia.

We report two cases of ataxia telangiectasia in which a small number of T cells and a slightly diminished response to phytohaemagglutinin or concanavalin A were observed. In one case, serum IgA was undetectable. In spite of T and/or B cell involvement, natural killer activity and the percentage of natural killer cells determined by monoclonal antibodies Leu 7 were normal in both cases.

Adolescent↗

LPF-induced T cell colony formation: effect of PMA and interleukin-2, and surface marker analysis.

We demonstrated that a primary exposure to the lymphocytosis promoting factor (LPF) of Bordetella pertussis-induced T cell colony formation. Colony formation was observed when mononuclear cells (MNC) were cultured at concentrations of more than 1 X 10(6)/ml, and reached a peak on day 8. However, the number of colonies generated with LPF was about one-third induced with phytohaemagglutinin (PHA). Removal of monocytes from MNC or T cells resulted in the failure of colony formation, but colony growth could be restored by the addition of monocytes or B enriched cells, indicating that they were required for the optimal colony growth induced by LPF. In the absence of accessory cells, optimal colony growth from monocyte depleted T cells could be obtained when an appropriate concentration of phorbol myristate acetate (PMA) or interleukin-2 (IL-2) was added in the cultures with LPF. PMA did not enhance LPF-induced colony formation in the cultures containing a sufficient amount of exogeneous IL-2. These findings suggest that IL-2 is essential to LPF-induced colony formation. Surface marker analysis showed that most of LPF-induced colony cells were T cells. The percentages of T4+ and T gamma cells of LPF-induced colony cells were more, and T8+ cells less, than those of PHA-induced colony cells. Ia1, T9 and Tac antigens were detected on many colony cells induced by LPF or PHA. These results indicate that the phenotype of LPF-induced colony cells differs from those of PHA, but the sequential antigen expression on lymphocytes triggered by IL-2 might be similar in both LPF- and PHA-induced colony formation.

Antigens, Surface↗

Insulin resistance in an infant with leprechaunism.

A Japanese female infant with typical features of leprechaunism exhibited glucose intolerance despite marked hyperinsulinemia, indicating insulin resistance. Circulating insulin appeared to be chemically and biologically normal. There was no evidence of antagonism of insulin action or circulating antibodies to insulin or insulin receptors. Insulin receptor assay of her erythrocytes showed very low affinity despite a six-fold increase in the number of receptors as compared with those of normal adult controls. Our studies indicate that insulin resistance in this patient appears to be due to a qualitative abnormality of insulin receptors or to a postreceptor defect.

Abnormalities, Multiple↗

The mitogenic effect of the lymphocytosis promoting factor from Bordetella pertussis on human T gamma and non-T gamma cells.

We studied the effect of lymphocytosis promoting factor (LPF), derived from the supernatant fluid of a culture of phase I Bordetella pertussis strain Tohama, on human lymphocyte proliferation. LPF was a potent mitogen for human mononuclear cells, specifically T cells. LPF failed to induce cytoplasmic immunoglobulin production by B cells. Removal of the monocytes from the T cell fraction diminished responses to LPF, but the response could be restored completely by the addition of 5.0% monocytes. These results suggest that LPF-induced cell proliferation is at least partially dependent on monocytes. In contrast to PHA, LPF stimulated T gamma cells to a greater extent than non-T gamma cells, but the magnitude of the T gamma or non-T gamma cell response was less than that of T cells, indicating that synergistic interactions between T gamma and non-T gamma cells are required for maximal response.

Bacterial Toxins↗

Comparison of phorbol myristate acetate and phytohaemagglutinin as stimulators of in vitro T lymphocyte colony formation of human peripheral blood lymphocytes. I. Surface markers of colony cells.

Human T lymphocyte colonies were grown in methylcellulose semi-solid cultures in the presence of phytohaemagglutinin (PHA) and/or phorbol myristate acetate (PMA). Surface marker analysis showed lower percentages of OKT3- and OKT4-positive cells in PMA-induced colonies than those in PHA-induced colonies. The percentage of OKIa1-positive cells in PMA-induced colonies was approximately twice that in PHA-induced colonies. The percentage of OKT9-positive cells in PMA-induced colonies was significantly lower than that in PHA-induced colonies. These data suggest that the subsets of PMA-induced colony cells express a more immature phenotype than that of PHA-induced colony cells and that, among PMA-induced colony cells, there are fewer T cells in the proliferative status at the time tested. When 3 X 10(5)/ml monocyte-depleted T cells, at which concentration of seeded cells neither PHA nor PMA could induce colony growth, were cultured in the presence of both PHA and PMA, T cell colony growth was observed. In T cell colonies induced by a combination of PHA and PMA, the percentages of OKT3-, OKT4- and OKT8-positive cells were different from those in colonies induced by either PHA or PMA alone. These results suggest that PMA acts not only as a substitute for monocytes and/or interleukin-1, but may directly affect lymphocyte proliferation induced by a combination of PHA and PMA.

Antibodies, Monoclonal↗

Effects of tunicamycin and various monosaccharides on phytohaemagglutinin-induced autorosette formation.

The structural characteristics of autologous red blood cell (ARBC) receptors on human peripheral blood lymphocytes (PBL) induced by phytohaemagglutinin (PHA) were examined. Tunicamycin, which is known to be a blocker of the protein glycosylation of N-glycosidic type glycoprotein, significantly inhibited the production of ARBC receptors. When trypsinized PBL were cultured in the presence of tunicamycin, the inhibitory effect was enhanced. When several monosaccharides were added to the mixture of ARBC and PBL pre-treated with PHA for 24 h, D-mannose caused the most inhibition, and galactose and D-fucose also caused significant inhibition. These data suggest that N-glycosidic type glycoproteins play an important role in binding sites to ARBC on PBL surface membranes and that more than one type of glycose may be involved.

Adult↗

Induction of human T-lymphocyte colonies by phorbol myristate acetate.

Colony growth of human lymphocytes by phorbol myristate acetate (PMA) was studied. PMA was able to induce lymphocyte colony growth in methylcellulose semi-solid cultures in the absence of lectin mitogens, phytohaemagglutinin or concanavalin A. PMA-induced colonies were found in cultures of mononuclear cells, monocyte-depleted mononuclear cells and the T-enriched cell fraction, whereas no colonies were obtained from the non-T cell fraction. At least one million mononuclear cells were required to form colonies by PMA. The colony cells were mainly T cells as judged from sheep red blood cell rosette formation. Surface immunoglobulin positive cells and peroxidase positive cells were not detected in colony cells. Non-specific esterase positive cells were only found to be less than 1% of colony cells. T cells formed more colonies than did mononuclear cells, presumably because of a concentration of colony forming cells and/or co-operating cells. Colony formation by PMA was induced from monocyte-depleted mononuclear cells and monocyte-depleted T cells, suggesting independence of monocytes. When mononuclear cells were precultured at 37 degrees for 5 min or 30 min with PMA and then cultured in the semi-solid medium without PMA, only a small number of colonies grew. Further studies of PMA-induced T-cell colonies will provide information the identification and characterization of immunological states in various immunological diseases.

Cells, Cultured↗