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Biomedical subjects

F P Stuart

Publications and source records attributed to F P Stuart.

At least 91 records · Page 5Linked to original sources
PubMed1977

Progress in legal definition of brain death and consent to remove cadaver organs.

The availability of cadaver kidneys for transplantation falls far short of the needs of a rapidly expanding population of patients on chronic hemodialysis. Kidneys with the least ischemic injury come from donors with fatal head injury or stroke; such kidneys can be removed from a "beating-heart" cadaver after declaring death on the basis of brain death. To clarify the legal status of brain death and to encourage salvage of transplantable kidneys with minimal ischemic injury, 12 states already have codified the concept of brain death. Although the first few laws were lengthy and included medical terms, six of the last seven laws have used one or two models proposed by the American Bar Association (ABA) and the Institute of Society, Ethics and Life Sciences, Hastings-on-Hudson, N. Y. The ABA proposal is the simpler of the two models and should provide the basis for future state laws. In addition, the National Conference of Commissioners on Uniform State Laws plans to present a model law to define death and the liabilities of a physician who declares death on the basis of brain death by mid 1977. While state legislatures have written laws that establish the legality of the concept of brain death, medical groups have sought to define the medical criteria for its determination. The most recent list of criteria comes from a National Institutes of Health-supported Collaborative Study on Cerebral Survival, as follows: (1) unresponsivity, (2) apnea, (3) dilated pupils and absent cephalic reflexes, (4) electrocerebral silence, (5) a confirmatory test of absent cerebral blood flow (angiography, isotope bolus curve, retinoscopy, or echoencephalography).

Brain Death↗
PubMed1977

Conversion of a Scribner shunt to an arteriovenous fistula for chronic dialysis.

Since July, 1972, we have converted 14 Scribner shunts, which we had used for the initiation of hemodialysis in 14 patients with end-stage renal disease, to arteriovenous fistulas in the same peripheral artery and vein of the shunts for maintenance chronic dialysis. The shunts were converted to fistulaes electively in three patients and because of malfunction in 11. We did not convert infected shunts. Dialysis was resumed within 24 to 72 hours of conversion to a fistula in all 14 patients. Thirteen patients were followed from 14 to 1,505 days with pump speeds of about 300 cc/minute. The fistulas continued to function without complication. One patient developed a small pseudoaneurysm, which required excision. The overall patency rate was 93%. The autogenous peripheral vessels of a patient on chronic hemodialysis are a limited resource. This conversion or recycling technique will give the patient a preferred vascular access for dialysis for prolonged periods.

Adolescent↗
PubMed1976

Prediction of azathioprine intolerance in transplant patients.

One cause of transplant rejection is curtailment of immunosuppressive therapy due to leucopenia. To determine those patients most apt to develop leucopenia due to azathiprine the granulocyte response to intravenous injections (i.v.) of hydrocortisone was evaluated in 10 patients who had rejected their grafts at least six month previously. 5 patients who had rejected their grafts with concomitant severe leucopenia had an inadequate response to hydrocortisone, while in the other 5, who had tolerated the drug, the response was similar to that of normal controls. Based on these observations, all the transplant candidates underwent the hydrocortisone stimulation test the results of which were correlated with their subsequent clinical course. All medical decisions were based on events other than the steroid test. 8 leucopenic patients underwent splenectomy. 6 improved their granulocyte response to hydrocortisone and tolerated azathioprine after transplantation. 2 patients who underwent splenectomy and an unoperated leucopenic man were unresponsive to the hydrocortisone test, did not tolerate azatioprine after transplantation and rejected their grafts. 4 candidates with normal responses to i.v. hydrocortisone received transplants uneventfully. In all 13 patients transplanted since the beginning of this study, the hydrocortisone test correctly predicted their tolerance to azathioprine.

Azathioprine↗
PubMed1976

Cellular and humoral immunity after allogeneic renal transplantation in the rat. V. Appearance of anti-idiotypic antibody and its relationship to cellular immunity after treatment with donor spleen cells and alloantibody.

Enhancement of LBN F1 renal allograft survival in Lewis (L) rats is achieved by injecting the recipient i.v. with donor antigen (LBN F1 spleen cells) 1 day before transplantation and antidonor antibody (L anti-BN alloantiserum) at the time of transplantation. Treatment with this combination of antigen and antibody also induces the recipient to make L anti-(L anti-BN) anti-idiotypic antibody that reaches peak titers within 10 days. The degree of graft enhancement achieved was increased greatly by delaying transplantation until the peak of the anti-idiotypic antibody response 10 days after treatment with antigen and antibody. Two in vitro assays for cellular immunity (51Cr release and microcytotoxicity) failed to demonstrate antidonor activity in spleen cells from recipients for which transplantation had been delayed 10 days. The close correlation of enhancement, absence of cellular immunity in vitro, and the kinetics of the anti-idiotypic antibody response suggest that anti-idiotypic antibody may prevent either sensitization and generation of effector T lymphocytes or the destructive potential of sensitized cells.

Animals↗
PubMed1976

Immunological enhancement of renal allografts by antireceptor antibody.

Lewis (L) rats treated with donor antigen [Lewis Brown-Norway (LBN) spleen cells] and antidonor antibody (L anti-BN serum) produce L anti-(L anti-BN) antibody that reaches peak titers 10 days later. The antiantibody functions as an antibody against cell-surface receptor molecules on Lewis recognition lymphocytes for BN antigen. LBN kidneys grafted at the time of peak antireceptor titer are not rejected and function indefinitely. Homeostasis of enhanced kidneys in long-term graft recipients was evaluted by four sets of experiments with the following results: (1) adoptive transfer of spleen cells from long-term recipients causes fatal graft-vs.-host disease in LBN and LDA hosts; (2) adoptive transfer of spleen cells from long-term recipients to new, otherwise untreated Lewis recipients of LBN kidneys delays rejection and prolongs recipient survival; (3) adoptive transfer of sensitized spleen cells to long-term recipients causes no apparent injury to enhanced LBN kidneys; (4) splenectomy in long-term recipients did not lead to deterioration of enhanced kidneys. It appears that long-term recipients maintain a delicate balance of effector and suppressor cells with respect to donor antigens.

Animals↗
PubMed1976

New approaches to immunosuppression in renal transplantation.

Although the incidence of 1 year kidney graft survival has been on a plateau for the past 7 or 8 years, the likelihood of recipient survival has increased. These observations reflect the limits of our current nonspecific immunosuppressive techniques and the acquisition of knowledge about when to discontinue their use and allow rejection of the kidney rather than death from sepsis. Yet, there are many leads from the laboratory which, when applied clinically in the next few years, should allow safe kidney transplantation to become a routine clinical event. Among these are safer, more effective antilymphocyte preparations; precise indications for splenectomy; accurate identification of presensitized states in potential recipients; methods of reducing the immunogenicity of grafts by removing donor passenger leukocytes or flushing the kidney with substances that alter surface antigens; and possibly new classes of chemical immunosuppressive drugs. In addition, it is likely that techniques will evolve for selective suppression of the immune response to donor antigens. This will be achieved by using cytotoxic agents coupled to donor antigen to destroy specific antigen recognition lymphocytes. Other forms of noncytotoxic donor antigen and antibody with or without ALS will be used to manipulate the recipient's immune response prior to and after transplantation. These manipulations will leave intact most of the potential for immune response to antigens other than those introduced with the graft. Together, these manipulations and their effect in experimental animals have been called immunologic enhancement. Intentional enhancement in man by means of antigen treatment or passive immunization has just barely begun. Clinical trials will be difficult and, initially at least, they will be confined to only a few transplantation centers. Yet, the "antigen pretreatment" of natural pregnancy, blood transfusion, prior unsuccessful organ transplantation, and bacterial infection have at times inadvertently conditioned a potential host so as to allow enhancement of a subsequent graft. It is likely that much can be done with current clinical assays of cellular and humoral immunity to detect those patients who are already conditioned to enhance a subsequent graft.

Animals↗
PubMed1973

Specific suppression of immune responses.

The models we have discussed in detail demonstrate specific suppression of immune reactivity produced in normal adult animals by antibody and antigen. The mechanism of homeostasis of suppression in these models depends on continued exposure to antigen and on an active response by the host. The active response may include production of antibody directed against specific receptors as well as antibody directed against antigen. Thus, specific regulation of both antibody and cell mediated immunity to an antigen might be achieved by the use of only the biological agents of the response: antigen, antibody, and possibly antibody to receptors. The general implication is that these same biological agents are responsible for autoregulation of immune reactions occurring in nature. Presumably, these agents may be used to suppress or reverse immune responses for appropriate clinical objectives.

Animals↗