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Biomedical subjects

B Henderson

Publications and source records attributed to B Henderson.

At least 163 records · Page 9Linked to original sources
PubMed1988

Diet and high risk of stomach cancer in Shandong, China.

A case-control investigation involving interviews with 564 stomach cancer patients and 1131 population-based controls was conducted to evaluate reasons for the exceptionally high rates of stomach cancer in Linqu, a rural county in Shandong Province in northeast China. Daily consumption of sour pancakes, a fermented indigenous staple, was associated with a 30% increase in risk. Risks of stomach cancer were also increased by 2- to 3-fold among persons with prior chronic gastritis or gastric ulcer, by 80% among those with stomach cancer in a family member, by 50% among men who smoked one or more packs of cigarettes/day, by 40% among those who preferred salty foods, and by 50% among families with moldy grain supplies. In contrast, risks tended to decrease in proportion to increasing consumption of fresh vegetables and fruits. This protective effect was more pronounced for vegetables, with those in the highest quartile of intake at less than one-half the risk of those in the lowest. Stomach cancer risks also declined with increasing dietary intake of carotene, vitamin C, and calcium, but not retinol. These findings provide leads to dietary factors that contribute to the high rates in Linqu, where stomach cancer is the leading cause of cancer and has not yet begun to decline as in other parts of the world.

Adult↗
PubMed1988

Leucocyte infiltration and cartilage proteoglycan loss in immune arthritis in the rabbit.

1. The relationship between phagocytic leucocyte infiltration and cartilage degradation in immune arthritis has been investigated in groups of normal and neutropenic rabbits. 2. Injection of antigen into the knee joints of sensitized control animals induced joint swelling, prostaglandin E2 (PGE2) synthesis, leucocyte accumulation and proteoglycan loss from articular cartilage. 3. Intravenous injection of nitrogen mustard caused a selective depletion of circulating neutrophils and monocytes with little or no effect on platelets or lymphocytes. In neutropenic animals challenged with antigen, there was virtually no joint swelling, PGE2 synthesis or leucocyte infiltration but cartilage proteoglycan loss was unchanged after 1 day and increased by day 4 compared to control animals. 4. The numbers of circulating leucocytes returned to normal 3-4 days after nitrogen mustard treatment and leucocyte infiltration occurred in antigen-challenged joints but this was not accompanied by joint swelling. Subsequent intra-articular injection of PGE2 did, however, cause swelling. 5. Lysosomal enzyme levels in arthritic joint fluids were measured. The levels of beta-glucuronidase, which is released by activated phagocytes, were decreased in neutropenic animals but the levels of N-acetyl-beta-glucosaminidase, which is a marker of tissue damage, were not changed by neutrophil depletion. 6. Intra-articular injections of the cytokine interleukin-1 (IL-1) induced a pattern of leucocyte infiltration and cartilage proteoglycan loss similar to that seen in immune arthritis. In neutropenic animals, IL-1 did not cause significant accumulation of leucocytes in the joint but the loss of proteoglycan from cartilage was unimpaired. 7. These results indicate that both leucocyte infiltration and prostaglandin synthesis are required for joint swelling but that tissue degradation is mediated by resident cells. It is likely that release of IL-1 by synovial cells stimulates the synthesis and activation of metalloproteinases which initiate the process of tissue degradation.

Animals↗
PubMed1988

Quantitative histological analysis of antigen-induced arthritis in the rabbit.

Antigen-induced arthritis in the rabbit (AIAR) provides the closest experimental equivalent to human rheumatoid arthritis in terms of infiltration of synovial tissue by lymphoid cells. A method is described for quantitative histological analysis of AIAR. Measurements of total cell numbers, lymphocyte and polymorphonuclear leucocyte infiltration, and thickness of infiltrated synovium were obtained for ranges of antigen dosage and duration of arthritis. The method has been devised as part of a system for the analysis of joint swelling, synovial fluid biochemistry and cytology, cartilage proteoglycan chemistry and synovial histology on the same specimen.

Animals↗
PubMed1988

Studies on interleukin-1-induced arthritis.

IL-1 induces PMN and monocyte infiltration when injected into rabbit knee joints (1). This transient synovitis is associated with depletion of proteoglycan from the articular cartilage matrix. However, it is not clear whether the cartilage proteoglycan depletion is dependent on the infiltrating leucocytes. Consequently, we have investigated the effect of intra-articular injection of interleukin-1 in rabbits depleted of circulating PMN and monocytes with nitrogen mustard.

Animals↗
PubMed1988

Production of interleukin 1 in the joint during the development of antigen-induced arthritis in the rabbit.

Antigen-induced arthritis in the rabbit closely resembles rheumatoid arthritis. The levels of interleukin 1 (IL-1) in the synovial fluid and the synthesis of IL-1 by infiltrating cells in synovial fluid and by the synovial lining from control and inflamed joints has been assessed during the first month of this disease. A number of biological assays have been used to measure rabbit IL-1. Of these, only the assay using the murine thymoma cell line (EL-4 NOB-1) was able to detect IL-1 activity in the synovial fluid of arthritic joints, which was present only in the very early lesion. The leucocytes infiltrating the synovial cavity produced little IL-1 ex vivo in the acute lesion but released large amounts when arthritis was established. A similar finding was made with respect to the production of IL-1 by the synovial lining.

Animals↗
PubMed1988

The relationship between cell-mediated immunity and cartilage degradation in antigen-induced arthritis in the rabbit.

The relative contributions of cellular and humoral immunity to cartilage destruction in chronic arthritis has been investigated in a model of chronic synovitis in the rabbit. In this model, antigen-induced arthritis, immunization with ovalbumin in Freund's complete adjuvant (FCA) followed by intra-articular injection of this protein produces a chronic synovitis associated with loss of proteoglycan from articular cartilage. In addition, the synovial lining cell population is metabolically activated. Similar treatment of animals immunized with ovalbumin in Freund's incomplete adjuvant (FIA) produced a resolving arthritis which initially (over the first 7 days) appears to be identical to that in FCA-immunized animals, apart from the lack of activation of synovial lining cells. Following this initial synovitis the joints return to apparent normality apart from a persistent 'low grade' synovitis consisting mainly of a plasma cell infiltrate. The most striking finding in the FIA-immunized animals is the rapid loss (greater than 30% by day 7) and recovery of proteoglycan from the matrix of articular cartilage. These findings show that the perpetuation of chronic destructive synovitis in the rabbit requires the presence of active cellular immunity.

Acid Phosphatase↗
PubMed1988

Elevation of cathepsin L levels in the synovial lining of rabbits with antigen-induced arthritis.

The activity and distribution of the collagenolytic lysosomal enzyme, cathepsin L, has been assessed in the synovial lining of the rabbit during the initiation and development of chronic (antigen-induced) arthritis. Biochemical assay of homogenates of synovial lining revealed a marked increase in the activity of lysosomal enzymes, including cathepsin L, between 1 and 5 days following initiation of arthritis. Elevated levels of these enzymes were still present at 4 weeks duration of arthritis. Using a monospecific antibody to cathepsin L. enzyme was immunolocated only in synovial lining cells in normal joints. In arthritic joints the enzyme was found in synovial lining cells, synovial fibroblasts and in infiltrating macrophages. Measurement, by scanning and integrating microdensitometry, of the peroxidase-reaction product in synovial lining cells revealed an increased content of cathepsin L in these cells in the diseased tissues.

Acetylglucosaminidase↗
PubMed1988

Tolerogenic activity of polymerized type II collagen in preventing collagen-induced arthritis in rats.

Rats were exposed parenterally or pergastrically to polymerized type II collagen (POLCII) and became resistant to the subsequent induction of disease with arthritogenic type II collagen (CII) administered intradermally in Freund's incomplete adjuvant (FIA). POLCII was prepared by cross-linking native soluble arthritogenic CII, from bovine nasal septal cartilage, with glutaraldehyde. POLCII injected intradermally in FIA did not induce arthritis. Animals treated in this manner were resistant for a period of at least 100 days to induced disease. The change in the properties of the CII from an arthritogen to a tolerogen was related to the amount of glutaraldehyde (used to polymerize the CII) which was assumed to control the extent of cross-linking of the CII. Highly cross-linked POLCII administered pergastrically, like soluble CII, was not arthritogenic but was tolerogenic, inducing a state of unresponsiveness to a challenge with arthritogenic CII. In general serum anti-CII antibody levels were higher in arthritic than in tolerized non-arthritic rats. It is concluded that the breaking of self-tolerance to CII depends upon its physical state. When polymerized and insoluble, a form analogous to that in which it exists naturally, it is tolerogenic.

Animals↗
PubMed1987

Synthesis of arachidonate oxidation products by synovial joint tissues during the development of chronic erosive arthritis.

An animal model, antigen-induced arthritis in the rabbit, was used to investigate the synthesis of arachidonic acid oxidation products (eicosanoids) by tissues of the knee joints during the initiation and early phase of this developing chronic destructive lesion. High concentrations of immunoreactive prostaglandin E2 and immunoreactive leukotriene B4 were found to be present in the synovial fluid in the early lesion. These levels rapidly declined, as did the ability of the infiltrating cells of the arthritic joint fluids to synthesize leukotriene B4. Articular cartilage and synovial lining were maintained for 24 hours in nonproliferative organ culture, and the synthesis of eicosanoids was measured by assay of the culture fluids. The synovial lining was the major source of eicosanoids. Synthesis of prostaglandin E2, prostacyclin, thromboxane A2, and leukotriene B4 by the arthritic synovial lining was low during the first few days, but reached maximal values between day 5 and day 15 of disease duration. Maximal eicosanoid production occurred around the time that damage to articular cartilage and bone has been reported to occur, though it is not certain that these two events are linked. It was demonstrated that, in chronic lesions, the arthritic synovial lining was still producing elevated levels of eicosanoids compared with levels in the control tissue.

Animals↗
PubMed1987

PAF-acether in chronic arthritis.

Platelet activating factor (PAF-acether) is a potent pro-inflammatory mediator. The possible involvement of this molecule in the pathogenesis of chronic erosive arthritis has been investigated using an animal model, antigen-induced arthritis in the rabbit, which closely resembles rheumatoid arthritis. The arthritic joint fluids from rabbits with antigen-induced arthritis contained low levels of PAF-acether in the acute stages of the disease. However, PAF-acether was not detectable in the chronic stages of the lesion. The biologically inactive precursor/metabolite of PAF-acether, lyso-PAF-acether, was detectable in both control and arthritic joint washes. However, the levels of lyso-PAF-acether in the arthritic joint fluids were significantly elevated above those of control in the acute stages of the disease, but not in the chronic stages. Intra-articular injection of PAF-acether at doses up to 100 times the levels detected in the acute stages of this model did not induce joint swelling or leucocyte accumulation in normal rabbits. This study suggest that PAF-acether may contribute to the acute phase of antigen-induced arthritis but is less likely to be involved in the chronic processes.

Animals↗
PubMed1987

Pharmacokinetics of aspirin and salicylate in relation to inhibition of arachidonate cyclooxygenase and antiinflammatory activity.

Among the nonsteroid antiinflammatory drugs there is generally a close correlation between the potency of their inhibition of arachidonate cyclooxygenase, and thus prostaglandin production, and their antiinflammatory activity. One anomaly in this generalization is that whereas aspirin and salicylate are equipotent as antiinflammatory agents, salicylate is less active than aspirin in inhibiting prostaglandin production in vitro. Using rats, we have now measured the concentrations of aspirin and salicylate in plasma and in inflammatory exudates after their oral administration and determined their effects on thromboxane B2 production in clotting blood and prostaglandin (PG) E2 concentrations in the exudates. We have also investigated the effects of both drugs, at concentrations achieved in the exudates, on PGE2 production by nonproliferative explants of acutely inflamed tissues. Aspirin is rapidly metabolized, resulting in peak concentrations of salicylate in the plasma and exudate that exceeded peak concentrations of aspirin by 30- to 50-fold. Furthermore, concentrations of aspirin rapidly declined, whereas high concentrations of salicylate persisted in the plasma and in the exudate for up to 6 hr after a single administration of aspirin. Both drugs reduced PGE2 concentrations in inflammatory exudates by 50-70%, but aspirin was considerably more potent than salicylate in inhibiting thromboxane B2 production in clotting blood. The concentration of salicylate found in inflammatory exudates 6 hr after the administration of aspirin was sufficient to reduce PGE2 production in explants by more than 50%. We conclude that the antiinflammatory action of both drugs depends on the inhibition of PGE2 synthesis by salicylate.

Animals↗
PubMed1987

Inflammatory responses to intraocularly injected interleukin 1.

Intraocular injection of highly purified human interleukin 1 into the anterior chamber of the rabbit eye resulted in the accumulation of inflammatory cells. Peak cellular infiltration occurred at 4hr and cells were still present at 24h. Examination of ocular blood vessels in IL-1-injected eyes revealed no abnormalities. IL-1 had no effect on the protein content of the aqueous humour confirming that this monokine has no direct action on the blood-aqueous barrier. Comparison of the potency of IL-1 as a chemoattractant with the 5-lipoxygenase product, leukotriene B4 demonstrated that the former agent was more active by several orders of magnitude.

Animals↗
PubMed1986

Human interleukin 2. Quantitation by a sensitive radioimmunoassay.

Using polyclonal and monoclonal antibodies to human recombinant IL-2 (rIL-2), we developed a sensitive radioimmunoassay (RIA) for quantitation of human IL-2. In this assay, microtitration plates pre-coated with an anti-rIL-2 monoclonal antibody (35H10), recognizing residues 59-72 of human IL-2, are incubated with serial dilutions of test samples. Captured IL-2 is quantitated by adding an affinity-purified rabbit anti-rIL-2 antibody followed by an 125I-labeled goat anti-rabbit IgG. Antibodies to chemically synthesized IL-2 peptides could replace the polyspecific rabbit anti-rIL-2 antibody as the second specific reagent in the assay. This configuration was more sensitive than others tested, approaching the level of detection of the conventional IL-2 bioassay, thus allowing detection of as little as 100-200 pg IL-2. Serum or plasma fluids, however, inhibited the assay, reducing its sensitivity by approximately 5-fold. This RIA correlated well with the conventional bioassay in measuring IL-2 levels in sera from IL-2-treated patients. This, and similar, RIAs may serve as a useful adjunct or alternative to the conventional IL-2 bioassay in detecting and quantitating human IL-2 in culture supernatants and clinical samples.

Animals↗