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S H Yoshida

Publications and source records attributed to S H Yoshida.

At least 19 recordsLinked to original sources
PubMed2001

Sonographic determination of fetal size from 20 weeks of gestation onward correlates with birth weight.

OBJECTIVE: To evaluate the clinical efficacy of ultrasonographic measurement of fetal weight, estimated fetal weight (EFW) was analyzed in relation to birth weight. METHOD: Data were collected retrospectively from the medical records of 548 term pregnancies unassociated with fetal malformations. The subjects underwent sonographic examinations from 20-23 weeks onward at 4 weeks intervals for the estimation of EFW. Subjects were divided into 6 subgroups based on birth weight deviation (BWD) (A: - 3.0 < or = BWD < -2.0; B: -2.0 < or = BWD < -1.5; C: -1.5 < or = BWD < -1.0; D: - 1.0 < or = BWD < -0.5; E: -0.5 < or = BWD < + 0.5 and F: + 0.5 < or = BWD). Distribution and changes in EFW deviation (EFWD) with gestational age were analyzed related to BWD. RESULT: A difference in fetal growth based on EFWD was noted in small for gestational age (SGA) cases compared to non-SGA cases, and the difference was observed as early as 20-23 weeks. EFWD was significantly correlated with BWD from 20-23 weeks to term. CONCLUSION<==: Sonographic determination of fetal growth from 20 weeks of gestation onward correlated with birth weight deviation, and this emphasized the clinical value of evaluating fetal growth during the latter half of pregnancy.

Adult↗
PubMed1997

Cytotoxic activity generated from channel catfish peripheral blood leukocytes in mixed leukocyte cultures.

In previous work, lysis of allotargets was routinely observed with PBL from nonimmune channel catfish. In the work reported here, greatly increased (approximately 100-fold) cytotoxic responses were generated by stimulation of channel catfish PBL with irradiated cells of allogeneic cloned B cell lines in mixed leukocyte cultures (MLC). This increased cytotoxicity did not appear to be simply a consequence of cell proliferation since stimulation of catfish PBL proliferative responses with polyclonal mitogens did not result in increased lysis. Somewhat surprisingly, the MLC-generated cytotoxicity did not exhibit allospecificity; i.e., allogeneic targets from other fish were as susceptible to lysis as were the cells used as stimulators. This apparent lack of allospecificity in MLC-generated cytotoxicity was confirmed by "cold" target inhibition assays. However, autologous targets were not killed, clearly demonstrating that MLC-generated effectors could distinguish "self" from "nonself" at the level of lysis/recognition. Although their origin is unresolved, the MLC-generated effectors may be a source of highly enriched fish cytotoxic cells and thus facilitate directly addressing questions pertaining to the evolution of such cells.

Animals↗
PubMed1996

The influence of petrochemicals and stress on the immune system of seabirds.

There is increasing attention directed to the role of environmental pollutants in altering immune function. Only with the identification of the responsible environmental toxicants, and an understanding of their mechanisms of action, can we hope to treat immunotoxic injuries. This situation is exemplified by the exposure of wild birds to oil spills, the subsequent potential for direct toxicity from the oil, and the secondary toxicity of stress-induced immune modulation. Immunosuppressive mechanisms related to oil ingestion and handling stress are implicated in the morbidity and mortality of seabirds during care and following reentry into the wild. This does suggest that improvements in the treatment of these affected animals will enhance their survival and well-being. However, a survey of the literature shows that the implementation of better techniques are hampered by inadequate information on the immunological consequences of oil contact with seabirds. Marine oil pollution is a constant occurrence and will continue as long as oil and oil products are important commodities transported by sea routes. Among the numerous negative consequences of oil pollution are its effects on marine wildlife. There is much evidence that oil spills are responsible for massive seabird deaths. However, the constant, low level releases of petrochemicals probably contribute to the harmful effects of oil pollution on seabird populations. In an attempt to rectify the damage inflicted on seabirds by accidental oil discharge, rehabilitation centers are established for the cleaning and care of affected wildlife. Unfortunately, there is evidence that the ingestion of oil by preening and the handling stress undergone by birds in these centers lowers their ability to survive and reproduce following release to their native habitats. Although the reasons for this are unclear, there is the suggestion that both oil and handling will induce immunosuppressive mechanisms that ultimately predispose birds to infections and immune-mediated diseases, as well as reproductive, behavioral, and other problems. Thus, there are questions concerning the effectiveness of intervention measures currently being used in the rehabilitation of seabirds.

Animals↗
PubMed1996

Dietary Juniperis virginiensis seed oil decreased pentobarbital-associated mortalities among DBA/1 mice treated with collagen-adjuvant emulsions.

The propensity of the fatty acid 5,11,14-eicosatrienoic acid (5,11,14-ETA) to replace arachidonic acid in cell membranes, and its inability to be converted to bioactive eicosanoids, suggest that it may be useful in the treatment of autoimmune disorders. Previously, dietary application of oils extracted from 5,11,14-ETA-rich Platycladus orientalis delayed the onset of autoimmune disease in New Zealand Black mice. To gain more knowledge of the efficacy of this fatty acid toward alleviating immunological disorders, a similar oil was used to examine its effects on collagen-induced arthritis in DBA/1 mice, a model characterized by synovial proliferation and joint infiltration by inflammatory cells. Mice were fed AIN76A diet supplemented with 4% (w/w) of either an oil extracted from the seeds of Juniperis virginiensis (0.4% 5,11,14-ETA); a control oil consisting of equal parts olive, linseed and safflower oils; fish oil (90% fish oil and 10% safflower oil); or safflower oil. Mice were immunized with three injections of collagen-adjuvant emulsions, the first injection was intradermal, and the two subsequent injections were intraperitoneal. Mortalities were recorded following a secondary pentobarbital administration intraperitoneally. Mice from the J. virginiensis group had the lowest mortalities (25%) while safflower oil-fed mice had the highest (59%; p < 0.05). While the J. virginiensis group had the lowest mean CD4/CD8 T lymphocyte ratio, the fish oil group had the highest. These observations suggest that manipulation of eicosanoid production by different dietary lipids had different effects on immune responses, possibly through alterations in T lymphocyte subsets. Hypothetically, a downregulation of prostaglandin E2 release could increase the ratio of T helper 1 to T helper 2 lymphocytes and thereby modulate anaphylactic responses. Also, lowered pro-oxidant status may decrease CD4/CD8 T cell ratios and modify immune function.

Animals↗
PubMed1995

Silicone breast implants: immunotoxic and epidemiologic issues.

Silicone gel implants for breast augmentation and reconstruction have been in use since 1962. Significant local complications include capsular contracture, rupture, gel "bleed", and spread of the implant material to regional lymph nodes (1-7) as well as histologic findings of foreign body granulomas in the capsular tissue and in lymph nodes (7-9). Through magnetic resonance spectroscopy and atomic emission spectroscopy, silicon compounds were found in the blood of some women with silicone breast implants; silicone and silica have also been found in liver (10). Well-publicized case reports have raised significant concerns regarding an association between implants and systemic disease. However, despite the availability of silicone implants for over 30 years, controlled epidemiological studies were not carried out until 1992. Currently available epidemiologic data are extremely limited. In part, because the majority of implants were used after 1981, the incidence of long-term problems is not yet known. In 1992, due to the unavailability of studies demonstrating the safety of implants, the U.S. Food and Drug Administration advised that silicone breast implants should be used only in reconstructive surgery and as part of clinical trials (11). This decision spurred a wave of research on the bioreactivity of silicone and clinical observations of patients with implants. Herein, we review the adverse immune effects following contact with silicone as well as the epidemiologic data available.

Animals↗
PubMed1995

Thymic microenvironmental abnormalities in MRL/MP-lpr/lpr, BXSB/MpJ Yaa and C3H HeJ-gld/gld mice.

Efforts to define the stromal architecture of thymic tissues of normal mice have used a panel of monoclonal antibodies (MTS series) to examine the localization of cell subtypes, including reagents that define thymic epithelial and stromal elements. Recent work with these MTS mAbs disclosed significant abnormalities in the thymic cortex of New Zealand mice including the appearance of medullary type epithelial cells in the cortical areas and the presence of epithelial free spaces or 'cortical holes'. To determine whether such abnormalities are unique to NZB mice or are found in other models of murine lupus, we examined the thymi of MRL/MP-lpr/lpr BXSB/MpJ Yaa, C3H/HeJ-gld/gld and C57BL/6 control mice. Thymi from all models of murine lupus showed dramatic alterations in the thymic microarchitecture. For example, staining with MTS10, a mAb which is specific for subcapsular and medullary epithelia, was decreased in the subcapsular and medullary regions. Moreover, there was increased staining in the thymic cortex, suggesting an abnormality in the localization of MTS10-reactive cells. Moreover, all three murine lupus strains demonstrated 'cortical holes' or cortical epithelial cell-free regions. By using MTS33, MTS35 and flow cytometry, both C3H/gld and BXSB/Yaa, but not MRL/lpr mice, showed decreased cortical thymocyte frequencies. Possible defects in the maturation of double-positive thymocytes to single-positive status in C3H/gld mice is implied by abnormally high levels of double-positive cells and low levels of single-positive cells. Finally, MRL/lpr thymocytes had lowered frequencies of CD3-4+8+ and increased levels of TCR-alpha/beta high cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Decrease of 12-hydroxyeicosatetraenoic acid production in mouse lungs following dietary oleic anilide consumption: implications for the toxic oil syndrome.

A study was performed to examine the ability of dietary oleic anilide to alter 12-hydroxyeicosatetraenoic acid (12-HETE) production. The structure of oleic anilide, synthesized by reacting oleic acid with aniline, was confirmed by mass spectrometry. The purity of oleic anilide, 75%, was measured by gas chromatography. Oleic acid, which constituted the remaining 25%, is a major component of the rapeseed oil vehicle. Balb/c mice were fed oleic anilide as 0.75% of their diet by weight for three weeks. Their lungs were excised and examined for 12-HETE production in vitro. The 12-HETE levels were significantly (p < 0.01) lower in mice fed oleic anilide than in mice fed the oleic acid control diet. This result illustrates eicosanoid production as a target of fatty acid anilide toxicity. The fatty acid composition, including arachidonic acid, of mouse lungs from both dietary groups was not different. This confirms the availability of substrate for 12-lipoxygenase in both groups. Spleen weights were higher in mice fed oleic anilide than in control mice (p < 0.005). These observations are relevant to immunoregulation and the autoimmune syndromes noted in patients of the Toxic Oil Syndrome (TOS).

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1995

Immunopathologic effects of silicone breast implants.

Silicone-gel breast implants have been associated with a myriad of autoimmune and connective tissue disorders by anecdotal reports and small observational series. To date, no prospective epidemiologic studies have been done to substantiate these observations, but an increasing body of literature is being developed and older studies are being recognized that point to immunotoxic or inflammatory effects of these breast implant components. The development of disease due to implants would depend on the interaction of genetic host factors so that only a few patients would potentially be at risk. Based on the example of other chemically mediated disorders, such as scleroderma in association with silica exposure, latency periods of more than 30 years before disease develops may be possible. Herein we review studies on silicone and immunity.

Animals↗
PubMed1994

Dietary Platycladus orientalis seed oil suppresses anti-erythrocyte autoantibodies and prolongs survival of NZB mice.

Dietary fish oils rich in 20:5(5,8,11,14,17) and 22:6(4,7,10,13,16,19) are known to replace arachidonic acid [20:4(5,8,11,14)] and to improve the immunopathology of New Zealand mice. However, in humans, similar dietary strategies may be impractical because of the high levels of fish oils required. In contrast, we believe that beneficial effects in humans may be attainable using new exotic fatty acids. Toward this end, we have focused on 5,11,14-eicosatrienoic acid [5,11,14-ETA, 20:3(5,11,14)]. This fatty acid is structurally analogous to 20:4(5,8,11,14) but lacks the delta-8 double bond essential for conversion to eicosanoids. To examine our hypothesis, diets containing the oil of Platycladus orientalis containing 3% 5,11,14-ETA, a matched control oil, fish oil, or safflower oil were fed to NZB mice. There was a dramatic delay in both the onset and the titer of direct Coombs' tests in mice fed P. orientalis oil. These were directly reflected by the abundance of 5,11,14-ETA in serum lipids. Most striking was the accumulation of 5,11,14-ETA in serum and tissue phospholipids. Though constituting only 3% of dietary fatty acids, 5,11,14-ETA was the most abundant long chain polyunsaturated fatty acid in the serum phospholipids, suggesting that it very successfully competed with 20:4 as a constituent of membrane lipids. 5,11,14-ETA was incorporated into all tissue phospholipids examined except brain phosphatidyl inositol. Among tissues, liver showed the highest incorporation of 5,11,14-ETA into phosphatidylcholine (PC), phosphatidylserine (PS), and phosphatidylinositol (PI), yet spleen PE had a higher quantity of ETA than other tissues. Lesser arachidonate in spleen PS, heart PC, and heart PI showed the evidence of replacement by 5,11,14-ETA. The data presented illustrates how new nutrition can modify autoimmune responses and emphasizes the need for further studies based on new nutritional strategies.

Anemia, Hemolytic↗
PubMed1994

The contribution of H-2bm12 and non H-2 background genes on murine lupus in NZB.H-2bm12/b mice.

We have previously demonstrated the influence of the I-Abm12 gene mutation on the appearance of IgG anti-dsDNA antibodies when placed on an NZB genetic background. To further enhance our understanding of the interaction of the bm12 mutation on disease expression, lethally irradiated NZB.H-2bm12/b F1 mice were reconstituted with T-cell-depleted bone marrow cells from 3- to 6-week-old donors of four different congenic strains, NZB.H-2bm12, NZB.H-2b, B6.C-H-2bm12 and C57BL/6 (H-2b) mice. All animals when then serially followed for the appearance of IgM and IgG anti-ss and dsDNA antibodies. Significant alterations of T-cell subsets, high levels of IgG anti-dsDNA antibodies and proteinuria were found only in recipient NZB.H-2bm12/b F1 mice that were reconstituted with T-cell-depleted NZB.H-2bm12 bone marrow cells. Such activity was not found in F1 mice engrafted and fully reconstituted with NZB.H-2b, B6.C-H-2bm12 or C57BL/6 (H-2b) T-cell depleted bone marrow cells. Additionally, to evaluate the importance of the NZB background (non-H-2) genes, we transferred T-cell-depleted bone marrow cells from NZB.H-2bm12 mice into H-2 compatible B6.C-H-2bm12 mice and vice versa. Without NZB background genes, an increase in CD4- CD8- T cells, IgG anti-dsDNA, splenomegaly, and proteinuria were not observed. These data suggest that the H-2bm12 gene and the NZB background genes in bone marrow-derived cells are both necessary for the altered expression of T-cell subsets and anti-DNA production.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Activation of autoreactive T-cell clones from NZB.H-2bm12 mice.

We have previously established H-2bm12-restricted autoreactive T-cell clones from NZB.H-2bm12 mice which induce in-vitro production of IgG anti-dsDNA antibodies by syngeneic B cells. However, the mechanism underlying the activation of autoreactive T cells is not clear. We have taken advantage of the existence of L cells which were co-transfected with the A alpha b gene and independent A beta genes comprising all the permutations of amino acid residues distinguishing A beta b from A beta bm12. Using this panel of L cells expressing recombinant I-A molecules, 6/6 autoreactive T-cell lines responded significantly to the FT7.2 L cell transfectant expressing wild-type I-Abm12 as well as control APC from NZB.H-2bm12 or B6.C-H-2bm12 mice, but not to the other recombinant L-cell transfectants or to allogeneic APC. The fixation of APC with paraformaldehyde prior to co-culture led to dramatically diminished reactivity of all the autoreactive cloned T-cell lines tested. Interestingly, the inability of FT7.2 L cells to induce T-cell activation after paraformaldehyde fixation could be reconstituted by the addition of B/monocyte cells, but not T cells, from NZB.H-2bm12, NZB.H-2b or NZB(H-2d) mice and to a significantly lesser extent, from C57BL/6 (H-2b) and BALB/c (H-2d) mice. Conversely, when treated with either mitomycin C or cycloheximide, before incubation with autoreactive T cells and fixed FT7.2 cells, the ability of spleen cells from NZB.H-2b mice to reconstitute reactivity was reduced. Controls for these observations included KLH-specific T-cell clones from NZB.H-2bm12 mice, the T-cell hybridoma H66.3.6.54 specific for beef insulin and restricted to I-Ab, the IBM026 hybridoma specific for OVA and restricted to I-Abm12, and the TH2.2 hybridoma, and I-Ab antigen-presenting cell line.

Animals↗
PubMed1994

The toxic oil syndrome: a perspective on immunotoxicological mechanisms.

The etiologic agents responsible for the development of autoimmune diseases are generally unknown. Clearly, developing an understanding of causative agents will be essential for the development of strategies for therapy, if not prevention, of these health problems. The immune system is a target of many toxicants, including those obtained through diet. One important example of the immunologic effect of dietary toxins is provided by the toxic oil syndrome (TOS). The intentional denaturation of rapeseed oil with aniline resulted in the production of fatty acid anilides. The unintentional consumption of this adulterated oil in Spain caused a mass poisoning whose effects continue to the present. Among other clinical signs, a majority of TOS patients had characteristics of type 1 hypersensitivities. A smaller number of people developed symptoms of autoimmune diseases including scleroderma. These observations highlight the probability that environmental chemicals may be a major source of etiologic agents for autoimmune disease. In this review, the authors provide an overview of some of the more important features of TOS as they pertain to immunity. The authors also speculate on the immunopathologic mechanisms by which the TOS progressed, with emphasis on oxidative stress as a central byproduct of anilide-induced injury.

Aniline Compounds↗
PubMed1994

Immunotoxicity of silicone: implications of oxidant balance towards adjuvant activity.

A variety of mechanisms can be proposed to explain the potential effects of silicone and silicone by-products on the immune response. In this paper, we discuss information on the chemistry of silicon and silicone gels/elastomers, and the manufacture of silicone breast implants as they pertain to the bioreactivity of silicone. Moreover, with reference to silicone-mediated human adjuvant disease, an overview of experimental adjuvant-induced arthritis is presented; comparisons with graft-versus-host disease and chemically induced autoimmunity then follow. Particular attention is paid to similarities in the characteristics of silicone and classic lipid adjuvants. For example, macrophage activation is presumed to be a central event in silicone-induced autoimmunity. Since those genes uniquely expressed in macrophages activated by plastic adherence are similar to those induced by lipopolysaccharide, adherence to silicone rubber may initiate an inflammatory response by the same mechanism. Macrophage effects would also include the erosion of implants through the generation of oxidants and localized pH changes. The degradation products of silicone are also implicated in the adjuvant effects of silicone implants. There is evidence to suggest that oxidants produced by inflammatory cells preferentially inactivate CD8+ suppressor T cells. This could then lead to an inflammatory state, perhaps through oxidant-induced transcription factors such as NF-kB, resulting in a long-term pro-oxidant imbalance that manifests itself as a breakdown in immunological self-tolerance. The authors hypothesize that autoreactivity following oxidant stress evolved to enhance inflammatory repair mechanisms after tissue, cell or molecular damage by oxidants.

Animals↗
PubMed1994

Remission of sarcoidosis following removal of silicone gel breast implants.

We report herein a patient with debilitating multisystem sarcoidosis. Interestingly, dermal lesions and enlarged lymph nodes resolved and her clinical condition dramatically improved following removal of silicone gel breast implants. Of note, the capsular tissue surrounding the breast implant demonstrated a granulomatous foreign-body response. The potential harmful effects of silicone may include an acceleration of an already existing hypersensitivity response.

Adult↗
PubMed1993

The contribution of I-Abm12 to phenotypic and functional alterations among T-cell subsets in NZB mice.

To further understand the contribution of I-A to the development of disease in murine lupus, we compared the incidence and/or titers of natural thymocytotoxic autoantibodies (NTAs), autoantibodies to red blood cells, gp70 immune complexes (gp70), antibodies to Sm, and rheumatoid factor in NZB (H-2d), NZB.H-2b and NZB.H-2bm12 mice. There were striking and significant differences among the three NZB strains in several of these parameters. NZB (H-2d) and NZB.H-2bm12 mice had a 100% incidence of NTA. In contrast, NZB.H-2b mice were found to have NTA in only 36% of animals at 8-10 months of age. Furthermore, the NTA titers of NZB.H-2bm12 mice were relatively low. There were also distinct differences between these strains with respect to the presence of antibodies to anti-erythrocytes (positive Coombs' test). NZB (H-2d) and NZB.H-2bm12 both had high titers of anti-erythrocyte autoantibodies (AEAs), whereas there was a delayed onset and lower titers in NZB.H-2b mice. Additionally, there was a dramatic increase in gp70 IC levels in NZB.H-2bm12 mice. In previous studies, NZB.H-2bm12 as well as NZB.H-2bm12 x NZB.H-2b F1 mice were found to produce high autoantibody titers to single-stranded (ss) and double-stranded (ds) DNA. Using unfractionated or fractionated splenic T cells (CD4+ CD8-, CD4- CD8+, or CD4-CD8-) from NZB.H-2b or NZB.H-2bm12 mice, we compared their relative abilities to cooperate with T-depleted splenocytes from NZB.H-2bm12 x NZB.H-2b F1 mice to produce antibodies to ss- and ds-DNA. Only T cells, including both CD4+ CD8- and CD4- CD8- populations, from NZB.H-2bm12 mice, were able to induce such autoantibody production among F1 splenocytes. Finally, marked alterations in splenic T cell subsets were found in NZB.H-2bm12 mice compared to NZB.H-2b mice, and to a lesser extent, in B6.C-H-2bm12 mice compared to C57BL/6 (H-2b) mice. These data further highlight the influence of I-A on autoimmunity and in particular the influence of the bm12 mutation on altering the natural history of disease expression in NZB mice.

Animals↗
PubMed1993

Anti-collagen autoantibodies are found in women with silicone breast implants.

There have been several anecdotal reports that silicone breast implants are associated with an increased incidence of autoimmune disease. Based upon these data as well as the theoretical potential of silicon and silicone immune interactions, we hypothesized that an immune response to a silicone breast implant would include host reactivity against components of the microenvironment within the implant milieu. To test this hypothesis, we obtained detailed histories and performed examinations of 57 consecutive, self-referred patients concerned about their breast implants. Eleven of these women were excluded for various reasons including previous exposure to bovine collagen. The remaining 46 women, as well as 45 normal women of approximately the same age and living in the same geographic region, were tested using a sensitive ELISA for the presence of autoantibodies to human native type I collagen, denatured type I collagen, native type II collagen and denatured type II collagen. Known positive and negative sera were included in all assays and the ELISA was performed and interpreted blindly. Positive sera were defined as an ELISA value of three standard deviations above the mean of the normal controls. Using these stringent criteria, there was a statistically significant incidence of antibodies to collagen in women with silicone breast implants. In fact, 35% of women with silicone breast implants had such antibodies; this is higher than we have observed in any other autoimmune disease and is similar to that of chronic erosive rheumatoid arthritis. We believe that silicone breast implants, in genetically susceptible hosts, may pose a significant risk for immunopathology.

Adult↗