PubMed Health⌕ Search

Biomedical subjects

M E Cabrera

Publications and source records attributed to M E Cabrera.

41 records · Page 3Linked to original sources
PubMed1985

Cell markers and acute leukaemia subtypes in Chile.

A panel of monoclonal antibodies were used to define acute myeloblastic leukaemia (AML) and acute lymphoblastic leukaemia (ALL) with its different subgroups. Thirty-three patients were studied in a period of one year. ALL was diagnosed in 80% of the children and 20% of the adults. AML was present in 22% of the children and 78% of adults. In children, only one of seven was common ALL, three of seven were T-ALL and three of seven were B-ALL. Five of 12 were unclassifiable (U-ALL). In adults the 4 ALL were U-ALL.

Adolescent↗
PubMed1984

Treatment of severe or resistant corticosteroid-responsive dermatoses with Diprolene cream.

In an open study Diprolene Cream was administered to fifty patients with severe or resistant psoriasis, atopic dermatitis or other corticosteroid-responsive dermatoses. For a period of 14 days, patients applied 3.5 grams of medication twice daily. Efficacy was evaluated in forty-six patients, while tolerance and safety were evaluated in fifty patients. Therapeutic response in forty-one of forty-six patients was noted by treatment Day 3. By Day 14, mean total severity score of signs and symptoms in twenty-one patients with psoriasis was reduced by 88%. Similarly, in twenty-five patients with other severe or resistant corticosteroid-responsive dermatoses, a 99% decrease in the mean total severity score of signs and symptoms was evident. Of the patients evaluable for tolerance and safety, twenty-four of fifty reported transient, mild to moderate burning that occurred most often upon application of the study preparation. Therapy was not discontinued in any of these patients, and none required additional treatment for the local reaction. Morning plasma cortisol levels in monitored patients remained within normal limits throughout the study.

Adult↗
PubMedDate not supplied

Role of O2 in regulation of lactate dynamics during hypoxia: mathematical model and analysis.

The mechanistic basis of the relationship between O2 and lactate concentration in muscle is not fully understood. Although hypoxia can cause lactate (LA) accumulation, it is possible for LA accumulation to occur without hypoxia. Nevertheless, during conditions of low O2 availability, blood and tissue LA accumulation are used as indicators of hypoxia. To provide a framework for analyzing changes in energy metabolism and its regulation, we developed a mathematical model of human bioenergetics that links cellular metabolic processes to whole-body responses. Our model is based on dynamic mass balances and mechanistic kinetics in muscle, splanchnic and other body tissues for many substrates (glycogen, glucose, pyruvate, LA, O2, CO2, etc.) and control metabolites (e.g., ATP) through coupled reaction processes. Normal substrate concentrations in blood and tissues as well as model parameters are obtained directly or estimated indirectly from physiological observation in the literature. The model equations are solved numerically to simulate substrate concentration changes in tissues in response to disturbances. One key objective is to examine and quantify the mechanisms that control LA accumulation when O2 availability to the muscle is lowered. Another objective is to quantify the contribution of different tissues to an observed increase in blood lactate concentration. Simulations of system responses to respiratory hypoxia were examined and compared to physiological observations. Model simulations show patterns of change for substrates and control metabolites that behave similarly to those found experimentally. From the simulations, it is evident that a large decrease can occur in muscle O2 concentration, without affecting muscle respiration (Um,O2) significantly. However, a small decrease in Um,O2 (1%-2%) can result in a large increase in LA production (50%-100%). The cellular rate of oxygen consumption, Um,O2, which is coupled to ATP formation and NADH oxidation, can regulate other processes (e.g., glycolysis, pyruvate reduction) with high sensitivity through its effects on ADP/ATP and NADH/NAD. Thus, although LA metabolism does not depend directly on O2 concentration, it is indirectly affected by Um,O2, through changes in ADP/ATP, and NADH/NAD. Arterial LA concentration (Ca,LA) follows the pattern of change of muscle LA concentration (Cm,LA). Nevertheless, changes in Ca,LA, due to Cm,LA, are unlikely to be detected experimentally because changes in Cm,LA are small relative to the total LA concentrations in other tissues.

Adenosine Triphosphate↗