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Biomedical subjects

B J Steinberg

Publications and source records attributed to B J Steinberg.

12 recordsLinked to original sources
PubMed1989

Successful periodontal treatment for the elderly.

The demographic reality of a rapidly growing elderly population segment presents the practicing dentist with certain imperatives and challenges. Familiarity with the healthy aging process and common medical conditions of the aged is becoming increasingly essential. Customized treatment plans and modifications in techniques and home care aids require flexibility and creativity. In addition, it should not be overlooked that this demographic reality also presents the practicing dentist with new opportunities for practice-building as well as personal and professional satisfaction.

Aged↗
PubMed1987

Patient evaluation.

This article has focused on the various aspects of patient evaluation that is a vital component in the total care of the dental patient. It must be emphasized that dentists are ultimately responsible for the overall management of the patients that they are treating, and only by careful selection and treatment plan can the practitioner maximize the benefits while minimizing the dangers inherent in outpatient anesthesia.

Aged↗
PubMed1984

Physical evaluation.

Explore the source record for details and available documents.

Clinical Laboratory Techniques↗
PubMed1982

Ability of the xid gene to prevent autoimmunity in (NZB X NZW)F1 mice during the course of their natural history, after polyclonal stimulation, or following immunization with DNA.

F1 hybrid offspring of New Zealand Black mothers and New Zealand White fathers [(NZB X NZW)F1] female mice develop antibodies to single-stranded (ss) and native DNA, immune complex glomerulonephritis, massive proteinuria, and premature death with renal failure. By a series of matings, congenic (NZB X NZW)F1 . xid/xid mice were prepared. These mice were different from (NZB X NZW)F1 mice in having the X chromosome-linked immune deficiency gene, xid, in homozygous form. Such congenic (NZB X NZW)F1 . xid/xid females failed to develop antibodies to single-stranded or native DNA. They also failed to develop fatal renal disease as measured by proteinuria, glomerular histology, glomerular immunofluorescence, and survival. To control for unknown genetic factors, studies were performed with littermates that were derived by mating NZB . xid/+ females with NZW . xid/Y males such that the resulting offspring were either (NZB X NZW)F1 . xid/xid (and therefore "defective") or (NZB X NZW)F1 . xid/+ [phenotypically like (NZB X NZW)F1]. In these and in additional studies, mice were housed in the same cages and identified by ear tagging so as to avoid possible environmental variations from cage to cage. In these studies, xid/xid mice failed to develop the characteristic signs of autoimmunity, whereas the controls did. Similar results were also obtained with (NZW X NZB)F1 xid/xid mice compared with (NZW X NZB)F1 xid/+ mice. The effect of xid/xid upon (NZB X NZW)F1 mice was further investigated by assessing responses to immunization and polyclonal B cell activation in vivo. The xid/xid mice failed to produce anti-ssDNA following immunization with ssDNA complexed to a protein carrier in fluid form or even emulsified in adjuvant. Finally, the xid/xid mice failed to produce antiDNA in response to multiple injections of the polyclonal activator, bacterial lipopolysaccharide (LPS), or the polyclonal activator, polyribose inosinic acid . polyribose cytidylic acid. However, the xid/xid mice were neither generally hyporesponsive nor unable to recognize LPS because they made normal antibody responses following immunization with LPS to which multiple trinitrophenyl groups were chemically attached. We conclude from these studies that xid/xid, which is known to cause the deletion of a B cell subset, has a profound affect upon (NZB X NZW)F1 mice, rendering them insusceptible to the naturally occurring autoimmune disease characteristic of (NZB X NZW)F1 mice, and preventing them from producing antibodies to DNA despite purposeful immunization and polyclonal B cell activation. These results force a reevaluation of previous concepts regarding the mechanisms by which xid/xid might interfere with the development of autoimmunity, and a consideration of therapeutic implications.

Animals↗
PubMed1982

Studies of immune abnormalities in systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) in humans and in mice appears to be a syndrome with different cellular bases. In individuals, the illness is influenced by a variety of factors, including genetic, hormonal, immune, and environmental. In mice, SLE can be induced with polyclonal B-cell activators and thymectomy. Retardation of disease occurs with the gene xid on an NZB background. Tolerance studies indicate that tolerance depends upon a normal thymus. In addition, females can be nontolerant with a single immune defect, whereas males can become tolerant with only one defect; they become nontolerant with two immune defects. These studied may help to explain the prevalence of SLE in females and the protective effects of androgens. Human SLE is characterized by excessive B cell activity and impaired T cell activity, especially in active disease. A scheme by which the disease becomes activated is put forth. The details of cell-cell dialogue are becoming clearer with study of the autologous mixed lymphocyte reaction. T 4+ cells provide helper signals for T 8+ cells. Macrophages and T cells combine to regulate the AMLR. The AMLR itself gives rise to a variety of functional cells and serves as an amplification system. This system is defective in active SLE. Preliminary attempts have been made to separate human SLE into subgroups on the basis of the ratio of helper to suppressor cells (RT). A low RT is associated with renal disease, whereas a high RT characterizes patients with a multisystem illness with less important kidney involvement.

Androgens↗