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Query: UMLS:C0155339 (Brown)
 12,436 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect on the pulp of a high-copper amalgam was studied in buccal cavities in 16 pairs of human premolars, 32 teeth, restored with ANA 2000. To minimize the risk of bacterial contamination, the cavities were treated with a cleanser, Tubulicid, and the outer portion of the filling was replaced by zinc oxide-eugenol cement (ZOE), i.e. surface-sealing. In one cavity in each pair, the control, a thin lining was used. The teeth were extracted after 5-13 days, sectioned, stained with hematoxylin-eosin or Brown and Brenn and evaluated for the degree of pulpal inflammation and presence of bacteria. The results showed that regardless of whether lining was used or not, no inflammation or only a very few inflammatory cells were found in the 21 teeth in which the thickness of the remaining dentin varied from 0.15 mm to 0.5 mm, except for one pair showing slight to moderate inflammation. However, in this pair bacterial growth were found on the cavity walls. No other teeth showed bacterial growth. In the remaining eleven teeth the thickness of the remaining dentin was less than 0.08 mm, including five pulpal exposures. Slight to severe inflammation occurred in eight of these teeth. ANA 2000 per se did not seem to irritate the pulp except in very deep cavities or on direct exposures. The reason for this reaction is not known, but it might be attributable to the zinc content of the amalgam.
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PMID:Pulpal response to restoration of deep cavities with high-copper amalgam. 149 61

After 37 generations, the AA and ANA rat lines developed for high and low voluntary alcohol consumption, were revitalized by crossing with hybrid (Brown Norwegian X Lewis) rats. The line difference in alcohol consumption continued, although initially diminished, after revitalization. The greater acetaldehyde accumulation and longer loss of righting reflex after ethanol administration of the ANAs persisted after revitalization, but significant line differences in motor impairment were no longer found. The line characteristics for open-field test behavior were also different than before revitalization. Of the previously-observed line differences that have now been reexamined, the level of blood acetaldehyde during ethanol metabolism appears to be the most closely related to the genetically-determined factors influencing alcohol consumption.
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PMID:Revitalization of the AA and ANA rat lines: effects on some line characteristics. 654 12

Silicone, previously thought to be a biologically inert and harmless material, has now been reported to elicit antibody response and to be responsible for adjuvant disease in humans. The present study was designed to evaluate the immune function of forty individuals who had undergone silicone breast augmentation for a period of longer than ten years and who were compared with 40 sex and age-matched controls. The following immunological functions were studied: lymphocyte subset analysis, lymphocyte mitogenic response, NK cytotoxic activity and markers for autoimmunity such as ANA, rheumatoid factor immune complexes such as smooth muscle, myelin, and thyroid, and tissue antibodies. Results of lymphocyte subpopulation analysis showed significantly elevated T helper/suppressor ratio in 60% and significantly decreased T helper/suppressor ratio in 7.5% of the silicone implant group, while the control group showed increased helper/suppressor ratio only in 10% of tested individuals and no significant decrease in the T helper/suppressor ratio. There was 20% inhibition in T cell mitogenic responses in the silicone implant group, which is significant when compared to the controls. When NK cytotoxic activity was compared between the two groups, significant inhibition in the ability of lymphocytes to kill tumor target cells was observed in the silicone implant group. This inability of target cell lysis was attributed to the demonstrated lack of granularity of NK cells from the silicone implant group. There was significant increase in: immune complexes, anti-nuclear antibodies, anti-thyroid antibodies, anti-striated muscle cell antibody, and anti-myelin basic protein antibodies. These immunological abnormalities in individuals who underwent silicone breast augmentation indicate a mechanism of tissue injury to these patients, causing autoimmune diseases or syndromes. Since autoimmunity in some other conditions is associated with abnormalities in the HLA serotyping system, and since some collagen vascular diseases have been associated with a higher incidence of the HLA serotyping system, it is recommended that HLA studies be included in future investigations of immune-mediated abnormalities associated with silicone breast augmentation. Our findings here show definite abnormalities of the T helper/suppressor ratio, increased autoimmunity, as well as increased production of immune complexes. Silicone implants have been used in cosmetic and reconstructive surgery more than 30 years (Brown et al., 1960). The gel used in the implant is produced from silicone, which is then related with methyl chloride and polymerized to form stable polydimethylsiloxane (Brown, et al., 1960). There have been a number of reports describing the occurrence of connective tissue disease in patients after the implantation of silicone.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Immune functional impairment in patients with clinical abnormalities and silicone breast implants. 757 Jun 22

Silica and silicate may disturb immune function such as autoimmunity and tumour immunity. The main objective of this study was to examine the relation between sodium silicate and induction of autoimmunity in genetically susceptible rats. In this study, thirty Brown Norway rats were randomised into four treatment groups, the first and second group receiving 3 mg of sodium silicate (NaSiO(4)) (equivalent to 2 mg silica) in 0.2 mL of normal saline either per oral or subcutaneously, and the third and fourth group (control) receiving 0.2 mL of normal saline (0.9%) through the same corresponding route. A significant number of rats (80%) (P < 0.05) which received sodium silicate by the subcutaneous route showed a high level of serum ANA compared with controls. In the oral, sodium silicate group showed high serum ANA in an insignificant number of rats. Other autoantibodies in both groups (anti-dsDNA, anti-Smith, anti-SSA, anti-SSB) showed gradual increased post exposure, but the numbers of rats with positive titres post exposure was statistically not significant. Silica exposure in rats appears to induce the development of autoimmunity. A longer duration post exposure to silicate seems to be associated with greater risks.
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PMID:Induction of autoimmunity in Brown Norway rats by oral and parenteral administration of sodium silicate. 1931 93

Nickel sensitization is a growing problem and the most common cause of allergic contact dermatitis. The aim of this study was to investigate whether nickel chloride can induce autoimmunity and cutaneous sclerosis in immunosensitive rats. Nickel chloride, in a dose of 4.5 mg in 0.2 ml NS, was administered by the oral and subcutaneous routes to 20 Brown Norway rats. Autoantibodies (ANA, anti-RNP, anti-SCL70 and anti-centromere) were measured and compared in pre- and post-challenge serum samples. Histological studies were also performed in skin biopsies obtained from six positively responding rats and compared with an equal number of control rats at the 14th week post-challenge. Serum ANA was high in a significant number of rats in both the oral (P < 0.005) and subcutaneously nickel-treated groups (P = 0.02), while the anti-SCL70 was high in a significant number of rats in only the orally nickel-treated group (P = 0.04). Histologically, subcutaneous and oral nickel-treated groups showed sclerodermic features of the skin (P = 0.22, P = 0.5), respectively. It may be concluded that nickel chloride can induce scleroderma-related autoantibodies and cutaneous sclerosis. More prolonged duration of exposure is probably associated with greater risk. This is the first study showing the potential risk of nickel in triggering the development of cutaneous sclerosis in susceptible hosts.
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PMID:Nickel-induced allergy and contact dermatitis: does it induce autoimmunity and cutaneous sclerosis? An experimental study in Brown Norway rats. 1978 41