Numerical Simulation of a Physiological Mathematical Model of Energy Consumption in a Sarcomere / Simulación Numérica de un Modelo Matemático Fisiológico de Consumo de Energía en un Sarcómero

ABSTRACT The paradigm of biological systems provides a framework to quantify the behavior of biological processes. Mathematical modeling is one of the analytical tools of biological systems used to reproduce the variables of a system for prediction. This article presents the analysis of muscular contraction, the physiological process responsible of generating force in skeletal muscle, from the point of view of mathematical modeling. The aim is to provide numerical evidences about the force generated by the sarcomere, and the energy required to produce such a force. The proposed scheme includes a model to activate the contractile cycle, based on the action potential that reaches the neuromuscular junction, the calcium release into the sarcoplasm, the contraction response, and the quantification of the energy that the sarcomere requires to perform mechanical work. The results shows that the proposed scheme is acceptable because it reproduces experimental data of force, velocity, and energy reported in the literature. The results of the proposed scheme are encouraging to scale the model at the muscle or muscle group level, in such a way that the quantification of energy can be an alternative to the indirect estimation methods of energy consumption that currently exist.

Endometrial autoantigens eliciting immunoglobulin (Ig)G, IgA, and IgM responses in endometriosis.

Endometrial antigens from patients with endometriosis and fertile controls were tested against immunoglobulin (Ig)G, IgA, or IgM in endometrium, serum, and peritoneal fluid (PF) of the patients and controls by Western blot analysis. Endogenous IgG was detected in 78% of the endometria or endometriosis implants from the patients and 22% of the endometria from the controls. Endometrial IgA and IgM were detected in few controls and patients. Immunoglobulin G in the serum and/or PF of patients with endometriosis was specifically directed against antigens with molecular weights of 34, 42, 82, 94, 110, 120, and 140 kd found in the patients' endometrium or endometriosis implants. Immunoglobulin A and IgM in the serum or PF of the patients and controls were nonspecific in their reactivity. Endometrial antigens found in endometrium or implants of patients with endometriosis, and eliciting IgG responses, may be relevant to autoimmunity in endometriosis.

Clinical manifestations of hormonal changes in the menstrual cycle.

The human female reproductive cycle is the result of repeated interactions--giving positive and negative feedback--of pituitary gonadotropic hormones and ovarian sex steroid hormones. If any of the pituitary or ovarian hormones becomes tonically elevated or suppressed, ovulation will cease. The charge to the clinician in evaluating disorders of ovulation is to determine which hormone(s) is tonically elevated or suppressed. Sex steroid hormones exert effects on their target tissues that can be observed directly. These changes aid the clinician in evaluating disorders of ovulation and establishing which hormone(s) is tonically elevated or suppressed. Changes in thermoregulation can be detected by the basal body temperature record. Changes in the vagina can be detected by cytologic examination. Changes in the endometrium can be observed by obtaining a biopsy specimen for histologic examination. Premenstrual molimina suggest to the woman and her clinician that ovulation has occurred. Utilization of these changes in clinical practice aids the clinician in making a specific diagnosis of the cause of anovulation and in developing a treatment plan. Moreover, when the woman is aware of these clinical changes, it makes her a more involved participant in her health care.

Immunological aspects of surgically induced experimental endometriosis: variation in response to therapy.

Elevated endometrial antibody titers were detected in serum and peritoneal fluid of rabbits with experimentally induced endometriosis. Surgical extirpation of implants or suppression with gonadotropin-releasing hormone agonist resulted in decreased endometrial antibody titers, whereas the antibody titers in untreated rabbits with endometriosis increased significantly. Endometrial implants and normal endometrial tissue had similar proteins by polyacrylamide gel electrophoresis. However, the serum and peritoneal fluid from rabbits with experimentally induced endometriosis had gamma G immunoglobulin antibodies to an endometrial protein with molecular weight of approximately 40 kD. These antibodies were absent in rabbits without endometriosis. Isolation of endometrial antigens eliciting the humoral immune response in endometriosis may aid in the development of a specific antibody marker for endometriosis.

Endometrial antigens involved in the autoimmunity of endometriosis.

Serum and peritoneal fluid from five fertile women without endometriosis and serum (n = 23) and peritoneal fluid (n = 12) from infertile women with endometriosis were tested for the presence of antibodies against endometrial tissue antigens by a Western blot analysis. Antigens with molecular weights (MW) of 19, 31, 38, and 42 kd reacted with antibodies in the serum and peritoneal fluid from both fertile and infertile women. Antibodies in 20 of 23 (87%) sera and all 12 (100%) peritoneal fluid samples from endometriosis patients reacted against endometrial antigens with molecular weights (MW) of 26 kd and/or 34 kd. Serum from 10 patients (43%) and peritoneal fluid from 6 patients (50%) also had antibodies to an endometrial antigen with MW of 21.5 kd. Reactivity to other endometrial antigens with MW 16, 24, 48, and 75 kd was also noted in patients with endometriosis. Antibodies in the serum and peritoneal fluid from fertile women failed to react against these antigens. It is concluded that the humoral and local endometrial autoimmunity detected in patients with endometriosis is primarily directed against antigens with MW of 26 and 34 kd.