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Biomedical subjects

J R Ward

Publications and source records attributed to J R Ward.

At least 127 records · Page 7Linked to original sources
PubMed1977

Mycoplasma-dependent activation of normal lymphocytes: mitogenic potential of mycoplasmas for mouse lymphocytes.

Nonviable preparations of a wide variety of glucose-utilizing mycoplasma species, including Acholeplasma laidlawii and Spiroplasma citri, were found to be mitogenic for mouse lymphocytes. Particularly strong reactions were obtained with Mycoplasma synoviae, M. gallisepticum, M. pneumoniae, S. citri, and a strain of M. fermentans that was previously isolated from a leukemic patient. Nonviable preparations of arginine-utilizing mycoplasmas inhibited the uptake of [3H]thymidine by lymphocytes, but this effect could be reversed by heat treatment or arginine supplementation, and a stimulatory effect was then observed. Viable M. arthritidis was also found to have a mitogenic effect, as detected by an increased uptake of [3H]thymidine by normal lymphocytes and by autoradiographic techniques in which an increase in the numbers of transformed cells was seen. These observations provide the potential for enhanced immunological responsiveness or lymphokine-mediated inflammation in mycoplasma-infected hosts.

Acholeplasma laidlawii↗
PubMed1977

Septic arthritis: a complication of rheumatoid arthritis.

Eighteen cases of long-standing rheumatoid arthritis and superimposed pyarthrosis were reviewed to determine the most distinguishing radiographic features. Soft-tissue changes allowed earlier diagnosis in the knee and ankle joints and consisted of large asymmetrical joint effusion and fat-pad edema. Bony articular changes were more helpful than soft-tissue changes in the wrist and hip because of the paucity of adjacent extracapsular fat and were associated with delayed radiographic recognition of superimposed pyarthrosis. These changes are presumptive evidence of complicating septic arthritis and their presence necessitates needle aspiration and culture of the joint for proper definitive treatment.

Adult↗
PubMed1977

Isolated subcutaneous nodules (pseudorheumatoid).

Ten patients with isolated subcutaneous nodules histologically similar to rheumatoid nodules were studied. Because of the intense fibroblastic reaction in one such nodule, it was initially mistaken for a fibrosarcoma. The nodules tended to be multiple and recurrent, with eventual spontaneous regression, and they were not associated with any systemic illness. The etiology of these lesions is unclear but the possibility of subsequent development of systemic rheumatoid disease is remote.

Adolescent↗
PubMed1977

Joint pain of recent onset.

A joint pain of recent onset is a common and often challenging problem to the family physician. The many etiologies of acute arthritis require a systematic approach to a careful definition of the problem which is essential to safe and effective therapy. The proper evaluation of joint pain of recent onset requires a detailed history and physical examination as well as a rationally selected battery of laboratory studies. This paper provides the busy physician with a specific approach to the diagnosis of acute joint pain as the basis for precise management.

Arthritis, Infectious↗
PubMed1976

Arthritis of mice induced by Mycoplasma arthritidis. Humoral antibody and lymphocyte responses of CBA mice.

Peak arthritis occurred 7 days after intravenous injection of CBA mice with Mycoplasma arthritidis and persisted in some animals for 84 days. A marked leucocytosis was apparent for the first 21 days. Complement-fixing antibodies reached a peak 14 days after injection of the organisms and persisted at high levels for 84 days. Metabolic-inhibiting and mycoplasmacidal antibodies were present but at much lower titres.

Animals↗
PubMed1976

Cytotoxic activity of rheumatoid and normal lymphocytes against allogeneic and autologous synovial cells in vitro.

The possibility that lymphocytes from patients with rheumatoid arthritis (RA) might be sensitized to RA synovial cell antigens was investigated with a 51Cr release cytotoxicity assay. Peripheral blood lymphocytes from rheumatoid and normal donors were tested for cytotoxic activity against their own synovial cells and against allogeneic rheumatoid and nonrhemuatoid synovial cells. In the allogeneic studies, the degree of cytotoxicity was significantly influenced by the age in culture (passage number) of the synovial target cells (P less than 0.001). When the passage number of the target cells was considered in the analysis, rheumatoid lymphocytes were found to have greater cytotoxic activity than normal lymphocytes against young cultures (low passage number) of both RA and non-RA synovial cells (P = 0.0042). Differences in susceptibility to lysis between RA and non-RA synovial cells were more susceptible to both RA and normal lymphocyte-induced lysis than were non-RA synovial cells (P = 0.0048). No evidence of cytotoxicity was detected when lymphocytes from nine RA patients and two osteoarthritis patients were reacted against their own synovial cells. Although the data demonstrated an increased cytotoxic activity of peripheral blood lymphocytes from some RA patients against allogeneic synovial cells, the fact that this reactivity was seen against both non-RA and RA synovial cells and was not demonstrated against autologous synovial cells argues against the presence of an immunospecific response of RA lymphocytes to RA synovial cell antigens.

Adult↗
PubMed1976

Infection in rheumatoid arthritis.

Sepsis is an unusually common cause of illness and death in RA. All sorts of infections occur, but pyarthrosis produces exceptional problems. Clinically, pyarthrosis, empyema, and purulent pericarditis mimic bland rheumatoid effusions. Aspiration of the attendant effusions is the only reliable diagnostic procedure. Subcutaneous nodules on the sacrum and back are easily overlooked. Necrosis and ulceration of these nodules may provoke septicemia. Those with Felty's syndrome do not uniformly have problems with recurrent infection. Splenectomy may not benefit such patients. The belief that corticosteroids cause increased infections in rheumatoid patients is not totally justifiable at present. Steroids can, however, disguise underlying sepsis and hamper proper diagnosis.

Adrenal Cortex Hormones↗
PubMed1975

New approaches to trials of antirheumatic drugs in rheumatoid arthritis.

While drug trials can be performed in different designs and sequences, the paramount consideration is careful definition of limited trial objectives such as efficacy, tolerance, and safety. Efficacy variables might include tests for analgesic effect, antiinflammatory activity, or specific antirheumatic action. Unless a drug has remarkable therapeutic effect, double-blind comparison with placebo or a standard reference drug such as aspirin is mandatory. Random assignment of patients to treatment groups must be assured and patients should not receive other antirheumatic drugs unless the trial is specifically designed to study drug interactions. Drug dosage poses a problem because average doses are usually employed. Compliance is monitored by several techniques including measurement of blood levels of test drugs in all study patients. Multicenter trials have several advantages: (1) averaging patient selection, (2) minimizing observer bias, (3) shortening time of trial by rapid entry of patients, (4) entering large number of patients, which can permit examination of "responders" versus "non-responders." Data analysis should employ proper statistical evaluations (nonparametric tests for nonnormally distributed variables). Duration of study period, trials to evaluate drug interactions, and variables used to measure drug effects will be discussed.

Anti-Inflammatory Agents↗
PubMed1975

Chronic proliferative arthritis of mice induced by Mycoplasma arthritidis: demonstration of a cell-mediated immune response to mycoplasma antigens in vitro.

Lymphocytes taken from mice chronically infected with Mycoplasma arthritidis exhibited a significant blastogenic response as measured by (3H)thymidine uptake when exposed in vitro to M. arthritidis antigens. The lymphocytes taken from 9 of 12 control mice of similar age exhibited an inhibition of (3H)thymidine uptake when exposed to M. arthritidis antigens.

Animals↗
PubMed1975

Arthritis of mice induced by Mycoplasma pulmonis: humoral antibody and lymphocyte responses of CBA mice.

Peak arthritis occurred 14 days after intravenous injection of Mycoplasma pulmonis and persisted in some mice at low levels for 84 days. A marked lymphocytosis occurred during the first week of infection with only a slight increase in polymorphonuclear leukocytes. Complement-fixing antibodies appeared in low titer 3 days after infection and moderate levels persisted for 84 days. The metabolic-inhibiting and mycoplasmacidal antibody responses were absent or minimal. M. pulmonis appeared to be mitogenic for mouse lymphocytes as evidenced by (i) increased uptake of [3H]thymidine for normal lymphocytes exposed to various concentrations of nonviable M. pulmonis antigen, and (ii) a 13-fold increase in [3H]thymidine uptake in lymphocytes taken from mice 3 days after infection with M. pulmonis in the absence of added antigen. Lymphocytes taken from infected mice transformed significantly more at all time periods than control lymphocytes when exposed to M. pulmonis antigen. This response was maximal at 3 days and minimal at 21 to 35 days after infection. Lymphocytes sensitized to M. pulmonis did not transform when exposed to M. arthritidis antigen or vice versa. M. pulmonis infection had no effect upon the mitogenic responses of lymphocytes to phytohemagglutinin or lipopolysaccharide. There was no statistically significant correlation between persistence of arthritis and degree of humor antibody or lymphocyte responses. However, persisting arthritis was associated with a higher incidence of mycoplasma isolations.

Animals↗
PubMed1975

Hematologic changes in chronic arthritis of mice induced by Mycoplasma arthritidis.

The arthritis caused by iv injection of M. arthritidis in mice was found to be associated with neutrophilia and lymphopenia without a change in the total WBC concentration. A mild anemia developed which was characterized by hypoferremia and plentiful RE iron but with an increased plasma total iron-binding capacity. This anemia therefore differs from the anemia of chronic disorders and indeed from any anemia which occurs in man.

Anemia↗
PubMed1973

[Factors influencing the susceptibility of mice to Mycoplasma arthritidis].

Concentrated broth constituents markedly enhanced the development of abscesses after subcutaneous injection of Mycoplasma arthritidis. Under appropriate conditions, both virulent and avirulent strains of M. arthritidis produced toxic effects in mice, as detected by the development of necrotic abscesses and death of the animals. The treatment of mice at birth with M. arthritidis antigens rendered the animals more susceptible to infection with M. arthritidis later in life, as evidenced by increased arthritis after intravenous injection. The injection of M. arthritidis into pregnant mice resulted in a high incidence of abortions. Comparative studies using different mouse strains showed that DBA mice were the most susceptible and BALB/c and C57BL mice were the most resistant to infection by M. arthritidis.

Abscess↗
PubMed1973

Fate of intravenously injected Mycoplasma arthritidis in rodents and effect of vaccines.

Virulent Mycoplasma arthritidis strain 158 P10 was rapidly eliminated from the peripheral circulation of rats and mice during the first 2 h after intravenous injection of the organisms. Characteristically after this time, the numbers of viable organisms remained remarkably constant through 48 to 72 h. The inability to clear the remaining mycoplasmas was not due to reticuloendothelial blockade but appeared to indicate the presence of a certain number of cells which were resistant to the clearance mechanism. Rat blood was usually devoid of mycoplasmas at 6 days and mouse blood was sterile by 14 days. An occasional transient mycoplasmemia occurred after these times. Avirulent M. arthritidis strain H606 was cleared more rapidly from rats in which it is non-arthritogenic. Different, but characteristic, clearance curves were obtained in mice using M. hominis, M. bovirhinis, and M. pulmonis. Active immunization procedures resulted in enhanced clearance of virulent M. arthritidis from rats. These procedures were less successful in mice. The results of passive immunization of normal rats and mice using convalescent serum indicated the presence of a serum factor which greatly enhanced clearance from rats but had only minimal effects in mice. This serum factor could not be correlated with metabolic-inhibiting antibody. Lymphocytes taken from convalescent rats enhanced the clearance rates of recipient rats. Mouse convalescent lymphocytes were without effect. The results indicated that mice are less able to control long-term infection by M. arthritidis than are rats.

Animals↗
PubMed1973

Interaction of Mycoplasma arthritidis and other mycoplasmas with murine peritoneal macrophages.

Neither mouse nor rat peritoneal macrophages were able to kill Mycoplasma arthritidis to any observable degree in the absence of specific hyperimmune rabbit antiserum. Although convalescent mouse and rat serum were somewhat inhibitory to M. arthritidis in the absence of macrophages, these sera did not promote active phagocytosis by peritoneal macrophages. In fact, the macrophages appeared to protect the mycoplasmas against the inhibitory effects of the antisera by stimulating their growth. Hyperimmune rabbit antiserum against M. arthritidis initiated phagocytic action and resulted in a 50-fold decrease in numbers of viable mycoplasmas by 6 h. In contrast with M. arthritidis, M. pulmonis rapidly adsorbed to the surface of peritoneal macrophages. Upon addition of specific rabbit antiserum, a rapid decrease in viable organisms occurred, and a more complete destruction of organisms ensued in comparison with M. arthritidis. M. gallinarum, as with M. arthritidis, did not adsorb to the macrophages to any great extent. Phagocytic action was observed only in the presence of homologous rabbit antiserum and was not marked until after 6 h of incubation.

Adsorption↗