[Medical practice in the thought of Thomas Aquinas]. / L'arte del medico nel pensiero di Tommaso d'Aquino.

In the works of St. Thomas Aquinas there are many examples of medical practice, in the discussion of philosophical and theological questions. St. Thomas asserts that like the doctor causes the recovery of the patient, although it is the power of nature to perform, so does the teacher with his student; the teacher raises the knowledge in the student, even if it is the own reason to act. Like the patient can be recovered only by natural force or by this force with the help of the doctor, in the same way, knowledge can be achieved only through the natural reason of the student or with the help of the teacher. To define the relationship between the desired aim and the means to achieve it, St. Thomas suggests a fundamental principle of medical ethics. The doctor, which is minister of nature, if has no limit wishing the recovery of the patient, must have a measure in relation to the means used to obtain that goal. In fact, he must try to cure the patient in the best way he can, not using the "strongest" drug; in fact, the drug is not the aim but it is only one of the means to obtain health.

IL-10 and the cytokine network in the pathogenesis of human autoimmune hemolytic anemia.

In animal and human autoimmune hemolytic anemia (AIHA) immunologic tolerance loss against RBC self-antigens could be originated by several mechanisms: ignored self-antigens' epitopes, polyclonal lymphocyte activation, molecular mimicry between self- and foreign antigens, central or peripheral tolerance errors, or immunoregulatory disturbances including the alteration of a cytokine network. To identify the immunologic factors contributing to autoimmune onset and maintenance, several murine strains (such as NZB and NZB/NZW) that spontaneously develop a complex autoimmune syndrome, including AIHA, have been extensively studied. In human AIHA, the respective roles of IL-2, IL-4, IFN-gamma, IL-10, and IL-12 were investigated by examining the spontaneous and mitogen-induced (OKT3 or LPS) production of these cytokines. ELISA methods were used in PBMCs to evaluate whether the manipulation of IL-10/IL-12 balance can have an effect on the incidence of autoimmune diseases and whether this might be useful for the control of AIHA. Results affirmed that AIHA is a disease that exhibits an increased basal synthesis of IL-4 and decreased levels of IFN-gamma by AIHA PBMCs compared with controls and that there is a basal increase of Th2 cytokines. Th1-type cytokine decrease in the basal state occurred in parallel with an increase of constitutive IL-10 production and an IL-12 decrease. In conclusion, decreased production of Th1-type cytokines and the production of autoantibodies in AIHA may be secondary to the imbalance between IL-10 and IL-12, and the neutralization of IL-10 may be efficacious in diminishing the clinical pathology associated with Th2 subset prevalence. In the same way, the treatment with IL-12 could offer a second and independent level of blockade against the consequences of the overstimulation of B cells associated with AIHA.

Immunological tolerance loss vs. erythrocyte self antigens and cytokine network disregulation in autoimmune hemolytic anaemia.

Recent studies on animal and human autoimmune hemolytic anaemia (AIHA) suggest that the loss of immunological tolerance vs. erythrocyte (Er) self antigens (Ag) may be primed by different mechanisms: ignorance of Er self Ag, molecular mimicry between self and non-self Ag, polyclonal T and/or B cells activation, errors in central or peripheral tolerance, immunoregulatory disturbances including the alteration of cytokines network. In vitro stimulation by synthetic Rh peptides indicates that ignorant T and/or B cells from patients with AIHA may recognize criptic Er self Ag. The AIHA associated with bacterial or viral infections seems to be produced by polyclonal T and/or B cell activation against foreign Ag that mimics protein or carbohydrate epitopes on Er. Polyclonal activation of host B cell clones by donor T cells causes the AIHA in chronic graft-versus-host disease. Mouse lines expressing a transgene with autoantibody (autoAb) activity against murine Er have shown that non-deleted peripheral B cell clones may produce Er autoAb. In human a genetic defect of Fas/FasL autoreactive lymphocyte apoptosis may be associated with AIHA. Th1/Th2 cytokines or IL10/IL12 imbalance may induce AIHA: in NZB mice and in human AIHA there is an increased production of Th2 cytokines such as IL4 and IL10 but INF-gamma and IL12 reduced production. Particularly, IL10 seems to act as critical mediator for the Er autoAb production.

[Medical practice in Rome during the XVI century]. / La medicina a Roma nel secolo XVI. Malattie e medici di S. Filippo Neri.

S. Filippo Neri (1515-1595), founder of the Congregazione dell'Oratorio in Rome, was a longly debated clinic case for his various pathologies. Eminent scientists, like B. Eustachio and A. Cesalpino, treated him and drew up clinical reports, which were inserted in the Canonization Process and also published as scientific works, and which give useful informations about the history of medicine in the second half of the 16th century. Those reports relate, among others, about many diseases like frequent heart palpitation, shaking tremors heat flame and bronchitic fever episodes, that since hte age of thirty affected the saint. Autopsy revealed cardiac hypertrophia and pulmonary artery dilatation over twice the normal diameter. G. M. Lancisi was the first who formulated the hypothesis of an artery aneurysm, which, according to the present knowledge, can be produced by a post-stenotic dilatation of the pulmonary valve and/or pulmonary hypertension. Tremors and flames can be attributed to hyperthyroidism. Doctors who treated S. Filippo Neri and who shoved to be aware of his psychology, considered his pathology due to supernatural causes. Their conclusions can be understood basing on the medical way of thinking of that age, which was still linked to ancient medicine and limited by the biological and medical knowledge of the time.

IFN-gamma and TNF-alpha production in gamma-irradiated blood units by mononuclear cells and GVHD prevention.

Gamma-radiation of blood products is considered the mainstay of transfusion-associated graft-versus-host disease prevention. Previous studies have detected lymphocyte inhibition rate in blood components just one time after irradiation but there is evidence of cellular variability with production of cytokines at different storage time which could be related with irradiation activity and cellular damage repair. IFN-gamma, a Th1 cytokine, and TNF-alpha, a pro-inflammatory one, had a central role in the stimulation of cellular and inflammatory reactions. In this study whole blood was collected from five volunteer healthy donors and each donor bag was divided into two satellite bags: one of them was exposed to 137Cs-irradiation with a 2500 cGy dose. Samples for cytokine production, detected by ELISA methods, and proliferative response, evaluated by incorporation of H3 thymidine, were taken at the following storage time: 0, 24, 48, 72 and 96 h. The time-response curve of irradiated mononuclear cells from blood bags (BBMC) in mitogenic activation showed a time-related inhibition of cell proliferation with an enhanced response only after 24 h of storage and about 84% inhibition at 96 h. A similar pattern is follow by IFN-gamma production after OKT3 stimulation. TNF-alpha levels both in lipopolysaccharide stimulated or unstimulated cells were always high. This data suggest that BBMC cells maintain the ability to produce cytokines after gamma-radiation. On the ground of this study seems to be necessary to evaluate hypothetical risk associated with the administration of cytokine via irradiated blood components.