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1.
Comput Biol Med ; 81: 24-31, 2017 02 01.
Artigo em Inglês | MEDLINE | ID: mdl-28011418

RESUMO

This paper describes a novel temporal logic-based framework for reasoning with continuous data collected from wearable sensors. The work is motivated by the Metabolic Syndrome, a cluster of conditions which are linked to obesity and unhealthy lifestyle. We assume that, by interpreting the physiological parameters of continuous monitoring, we can identify which patients have a higher risk of Metabolic Syndrome. We define temporal patterns for reasoning with continuous data and specify the coordination mechanisms for combining different sets of clinical guidelines that relate to this condition. The proposed solution is tested with data provided by twenty subjects, which used sensors for four days of continuous monitoring. The results are compared to the gold standard. The novelty of the framework stands in extending a temporal logic formalism, namely the Event Calculus, with temporal patterns. These patterns are helpful to specify the rules for reasoning with continuous data and in combining new knowledge into one consistent outcome that is tailored to the patient's profile. The overall approach opens new possibilities for delivering patient-tailored interventions and educational material before the patients present the symptoms of the disease.


Assuntos
Diagnóstico por Computador/métodos , Diagnóstico por Computador/normas , Aprendizado de Máquina , Síndrome Metabólica/diagnóstico , Monitorização Ambulatorial/métodos , Monitorização Ambulatorial/normas , Reconhecimento Automatizado de Padrão/métodos , Algoritmos , Diagnóstico por Computador/instrumentação , Europa (Continente) , Humanos , Monitorização Ambulatorial/instrumentação , Reconhecimento Automatizado de Padrão/normas , Guias de Prática Clínica como Assunto , Reprodutibilidade dos Testes , Sensibilidade e Especificidade
2.
Arch Gerontol Geriatr ; 43(3): 301-12, 2006.
Artigo em Inglês | MEDLINE | ID: mdl-16448711

RESUMO

It is known that the circulating levels of leptin, the adipocyte hormone implicated in the control of energy balance, are correlated with fat body mass (FBM), although the influences of other physiological conditions are not fully understood. We investigated the relationships of serum leptin concentration with age, gender, and 36 hormone-metabolic parameters in a sample of a well defined healthy population (n=246; age range 20-93 years), and in subgroups of lean individuals according to their body mass index (BMI), within similar age range and gender distribution. Only insulin secretion (positively) and testosteronemia (negatively, in males) show direct correlations. The other relationships are not significant but throughout collaborating variables, such as serum lipids, especially through FBM, lean body mass (LBM) through insulin secretion, and gender through FBM. In males, LBM correlates with insulin secretions, s-IGF-1 and with s-testosterone. The relationship between insulin secretion and LBM persists up to advanced age. From the present study it may be concluded that the positive relationship of leptin with insulin secretion and the negative one with testosterone, indicate direct implications of leptin in insulin signaling, as well as in male sexual development. Finally, the fact that the amount of secreted insulin depends on LBM and the latter on testosterone and IGF-1, indicates the importance of muscle mass in the control of insulin secretion.


Assuntos
Envelhecimento/sangue , Leptina/sangue , Obesidade/sangue , Tecido Adiposo/metabolismo , Adolescente , Adulto , Fatores Etários , Idoso , Idoso de 80 Anos ou mais , Biomarcadores/sangue , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Prognóstico , Radioimunoensaio , Valores de Referência , Fatores de Risco , Fatores Sexuais
3.
Adv Gerontol ; 16: 14-20, 2005.
Artigo em Inglês | MEDLINE | ID: mdl-16075672

RESUMO

BACKGROUND: This is a theoretical approach on the question on how much maximally may extend the life of human individual. The starting point of this work was the biological consideration of two changes in human characteristics which took place during the last century up to now, namely human beings lived remarkably longer and are becoming taller. METHODS: Demography data and Gompertz deduced mathematics, either related to growth or survival, were the two columns on which the basis of this study has been supported. Respective equations were adapted to the purpose searched applying parameters of. normal body growth and cell growth in vitro. Having individual age on the abscisse, that of its crossing point with ordinate value indicates the age in which no more cell activity should exist, either of proliferation or migration. RESULTS: Despite rising life expectancy, whose extrapolation leads to remarkable enhance for future values, life span calculations with the help of our mathematic models do not indicate an extent beyond the limit of 120 years. Nevertheless hypothetically there is the exception of prolonging life out of the mentioned limit when growth and ageing would be proportional interrelated. Furthermore, when proliferation results of in vitro smooth muscle cell cultures were related to age of donor, its linear regression crosses the x-axis at an age of 110.16 years (mean value of different procedures of measurement) . This limit is not far from that using other cell activity parameters as migration (117.7 years when cessation) or such state of senescent (98 years when all cells involved). Nevertheless with the help of Gompertz equation putting growth in the ordinate (proliferation activity) instead mortality and donor age in the x-axis, the follow up of the curve is similar to that known of survival up to the age of 80. But this procedure does not seem adequate to obtain information on the limit of life potential because of later this curve becomes very flat reaching the end at age around 180; this seems not to be real but due to an artefact. Finally IGF-1 prolongs the cessation ( x-axis crossing point) of cell growing activity up to donor age of around 126.4 years. CONCLUSIONS: Human life span seems to be limited up to around 120 years, but growth process modulating factors could theoretically enhance it.


Assuntos
Estatura , Expectativa de Vida , Longevidade/fisiologia , Modelos Teóricos , Biomarcadores , Movimento Celular/fisiologia , Proliferação de Células , Células Cultivadas , Humanos , Células Musculares/fisiologia , Espanha
4.
Rev. esp. geriatr. gerontol. (Ed. impr.) ; 40(3): 178-183, mayo-jun. 2005. tab, graf
Artigo em Espanhol | IBECS | ID: ibc-037350

RESUMO

Objetivos: la obesidad reduce el potencial de vida y acelera la tasa de envejecimiento biológico. Los factores esencialmente implicados son la resistencia a la insulina, que condiciona la aterosclerosis, y la resistencia a la leptina, que conduce a la pérdida de la homeostasis ponderal. La finalidad de este estudio es valorar la relación entre leptinemia y secreción de insulina, por un lado, y también la relación de ambos parámetros hormonales con la ingesta y la masa corporal, por el otro. Pacientes y método: en 38 personas con índice de masa corporal (IMC) de 35-86, de ambos sexos y con una edad de 19-63 años, se determinaron la leptinemia, la secreción de insulina mediante el péptido-C urinario y la glucemia basal, tras una ingesta ad libitum. A continuación se realizó un seguimiento durante un máximo de 3,4 años y se repitieron las citadas determinaciones y del IMC con el ritmo aproximado de cada 6 meses, siempre bajo una ingesta moderadamente hipocalórica. Resultados: la leptinemia se relaciona significativamente con el IMC sólo en las mujeres. Por el contrario, en ambos sexos hay correlación significativa entre leptinemia y secreción insulínica, aun cuando la respuesta de la leptina al contenido calórico de la dieta parece más inmediata, tanto en su descenso como, al revés, cuando ha habido transgresión dietética. Efectivamente, el descenso de la leptinemia como respuesta a la reducción calórica es independiente del comportamiento ponderal, y esta disminución se puede producir sin ningún cambio objetivable del peso corporal. Al comparar los valores iniciales con los obtenidos al final del seguimiento de todos los obesos estudiados, se observa una tendencia hacia la normalización en los parámetros señalados, pero sólo es manifiesta y, por tanto, estadísticamente significativa en el caso de la leptinemia. Conclusiones: la reducción calórica interviene de forma directa y decisiva en el proceso de normalización de la hiperleptinemia. Se postula aquí un mecanismo reparador de la resistencia hipotalámica al efecto de la leptina, del que indirectamente dependería el restablecimiento de la sensibilidad insulínica con la normalización ponderal y glucémica


Objectives: obesity reduces life potential through increasing aging rates. Leptin and insulin resistance are here especially involved. The former produces impairment of body weight homeostasis, whereas the latter a propensity to develop atherosclerosis. We studied, on the one hand, the relationship of leptinemia with insulin secretion, on the other hand, that of both hormone parameters with food intake and body weight. Patients and method: in 38 individuals of both genders with body mass index (BMI) of 35-86, serum leptin, daily insulin secretion through urinary C-peptide, and basal glycaemia under ad libitum diet were determined in basal conditions. Then, under mild hypocaloric diet, a follow up was begun with repetition of the mentioned determinations including BMI, approximately every 6 months during a maximum time of 3.4 years. Results: leptinemia is statistically significantly related to BMI, but only in females. Nevertheless, there is a significant correlation between serum leptin and insulin secretion in both gender, but the response of leptinemia to caloric content of diet seems to appear more rapidly than in the case of insulin secretion. The decline in leptinemia following caloric restriction is independent of body weight behaviour, so that this decrease can be observed without any major change in body weight. Comparing the initial values with those at the end of the follow up period under slight caloric restriction, all parameters tend to normalization, but only serum leptin shows a statistically significant clear decrease. Conclusions: caloric restriction appears to act directly on the normalization process of hyperleptinemia. Finally, it is postulated that this phenomenon would be part of a sort of repair mechanism to the hypothalamic leptin resistance of obesity, on which indirectly depends, or follows, the recovery of insulin sensitivity linked to weight and glycaemic normalization


Assuntos
Masculino , Feminino , Adulto , Pessoa de Meia-Idade , Humanos , Leptina/sangue , Insulina/sangue , Obesidade/fisiopatologia , Envelhecimento/fisiologia , Resistência à Insulina/fisiologia , Estudos de Casos e Controles , Índice de Massa Corporal
7.
Int J Clin Pharmacol Ther ; 41(9): 386-91, 2003 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-14518598

RESUMO

During the atheroma plaque formation, smooth muscle cells (SMC) have to change their differentiated phenotype in order to proliferate, migrate and synthesize collagen. These phenotypic changes are stimulated by insulin and IGF-1, and we have studied the effect of L-type calcium channel blockade produced by diltiazem on such changes. Mitotic activity was measured using bromodeoxyuridine DNA incorporation, the migration capability as chemotaxis index in a Boyden chamber, and cytoskeleton changes related to SMC movement in immunofluorescence studies. Diltiazem (10(-7)-10(-6) M) reduced insulin-induced mitotic activity in cultured human vascular SMC more effectively than in IGF-1-induced mitotic activity, but at 10(-5) M, the inhibitory effects were similar. Diltiazem also showed a clear inhibition of migration ability, both under basal conditions (p < 0.05) and after addition of insulin (p = 0.0001) and IGF-1 (p < 0.0001). Finally, diltiazem inhibited membrane ruffling induced both by insulin and IGF-1 in a similar manner, and similar results were obtained with SMC from rat aorta. We conclude that substances blocking the L-type calcium channels such as diltiazem, could inhibit those processes which in vivo lead SMC to form the atheroma plaque.


Assuntos
Actinas/metabolismo , Bloqueadores dos Canais de Cálcio/farmacologia , Diltiazem/farmacologia , Fator de Crescimento Insulin-Like I/farmacologia , Insulina/farmacologia , Miócitos de Músculo Liso/efeitos dos fármacos , Animais , Divisão Celular/efeitos dos fármacos , Divisão Celular/fisiologia , Membrana Celular/efeitos dos fármacos , Membrana Celular/metabolismo , Células Cultivadas , Quimiotaxia/efeitos dos fármacos , Quimiotaxia/fisiologia , Citoesqueleto/efeitos dos fármacos , Imunofluorescência , Humanos , Insulina/fisiologia , Fator de Crescimento Insulin-Like I/fisiologia , Miócitos de Músculo Liso/fisiologia , Miócitos de Músculo Liso/ultraestrutura , Ratos
8.
Rev. esp. geriatr. gerontol. (Ed. impr.) ; 38(1): 25-29, ene. 2003. graf
Artigo em Espanhol | IBECS | ID: ibc-21816

RESUMO

Los resultados de tratamientos hormonales en la osteopororis son contradictorios, en especial si la manifestación ósea está relacionada con el envejecimiento. Además, los estudios en humanos sólo permiten objetivar el comportamiento de indicadores humorales o urinarios, pero no la medición directa en el hueso del recambio metabólico. Por ello, es preciso tratar de dilucidar aspectos sobre la efectividad y el posible mecanismo, especialmente con la ayuda de modelos de experimentación animal. En este trabajo se estudia el efecto desarrollado en la osteoporosis experimental de la rata por los dos tipos de hormonas anabolizantes: hormona de crecimiento (GH) y el andrógeno metilandrostenolona. El efecto registrado será comparado con el del glucocorticoide prednisolona, como representante de las sustancias estimulantes del catabolismo. Mientras que la GH induce la deposición de colágeno en el hueso sin lugar a dudas, el efecto de la metilandrostenolona es menos seguro, dependiendo de las condiciones que afectan al hueso. Sorprende observar que esta sustancia estimula el catabolismo óseo, siendo sus consencuencias distintas en función del estado inicial del hueso. En el hueso sano, y eventualmente en el osteoporótico en vía de recuperación, metilandrostenolona estimula el recambio, favoreciendo la colagenización. En el osteoporótico bajo los efectos de la noxa patogénica, puede conducir a la pérdida de la sustancia fundamental. La prednisolona no da lugar a resultados catabólicos propiamente dichos, sino que se limita a inhibir la mineralización. No obstante, el resultado es distinto cuando el hueso se encuentra sometido a los efectos de la noxa osteoporótica, es decir, protege contra sus consecuencias. Por consiguiente, en referencia al hueso, posiblemente sólo haya un anabólico, que es la GH (o IGF-1 como efector específico). En cambio, el andrógeno no produce una clara respuesta anabólica, ni el glucocorticoide una respuesta catabólica (AU)


Assuntos
Animais , Ratos , Envelhecimento/fisiologia , Osteoporose/tratamento farmacológico , Anabolizantes/farmacologia , Colágeno , Prednisolona/farmacologia , Androstenóis/farmacologia
9.
Rev. esp. geriatr. gerontol. (Ed. impr.) ; 37(6): 311-315, nov. 2002. graf, ilus
Artigo em Espanhol | IBECS | ID: ibc-19186

RESUMO

La deformidad articular, sin la inflamación como causa primaria, es un proceso regresivo que suele acompañarse de disminución de la resistencia del hueso, producida, por ejemplo, por la osteoporosis. Debido a que el envejecimiento se acompaña de una gran susceptibilidad para esta afección, se comprende que también lo haga para la deformidad articular, cuyas características anatomopatológicas son compatibles con la artrosis. Es también lógico que la carga y la intensidad del trabajo articular sea, a largo plazo, un importante factor coadyuvante. No obstante, la resistencia ósea perdida aumenta proporcionalmente el papel agravante de los factores señalados. Por otro lado, es también conocido que la actividad muscular protege el hueso frente a la desmineralización. En este trabajo se estudia, con la ayuda del modelo de la osteoporosis experimental de la rata, el efecto de la tensión muscular sobre el recambio de colágeno óseo, así como su papel en la aparición de la deformidad articular. La sección del musculo gastrocnemio protege contra la afección articular en la zona rotuliana, pero aumenta la tasa de desintegración colágena de la tibia y el peroné. Es decir, como la tasa de sintesis colágena es menor que la del catabolismo, se comprende que los huesos del lado del músculo seccionado sean más frágiles. Sin embargo, no se apreció deformidad articular. En el hueso sano se observa un comportamiento similar respecto al recambio de colágeno, pero la tasa de desintegración no sobrepasa la de síntesis, y las magnitudes metabólicas son claramente superiores a las de la osteoporosis. Se concluye que, aunque la ausencia de tensión muscular y de correspondiente actividad, protegen en la zona determinada contra la degeneración articular, en cambio, empeoran la situación metabólica del hueso en cuestión (AU)


Assuntos
Animais , Masculino , Ratos , Envelhecimento/fisiologia , Colágeno/metabolismo , Osteoporose/metabolismo , Contração Muscular/fisiologia , Osteoartrite/etiologia , Ratos Sprague-Dawley , Modelos Animais de Doenças , Osso e Ossos/química , Osteoartrite/metabolismo
10.
Rev. esp. geriatr. gerontol. (Ed. impr.) ; 36(supl.5): 13-19, dic. 2001. graf
Artigo em Espanhol | IBECS | ID: ibc-150967

RESUMO

En este trabajo se analizan datos y teorías del envejecimiento con la finalidad de explicar su etiología. Se concluye que ninguna de las teorías aclara la causa del envejecimiento; sí, en cambio, sus mecanismos de acorde con cada una de ellas. Es decir, todas son complementarias al respecto. Por el contrario, parece posible acercarse a la explicación etiológica del envejecimiento constatando el comienzo del mismo. Considerando que se trata de un proceso regresivo, tal regresión no aparece antes de finalizar el crecimiento y la diferenciación, sino después de alcanzar el organismo la optimización biológica. De aquí que el declive en la secreción de hormona de crecimiento no sólo marque tal comienzo, sino represente al primer eslabón en la cascada de sucesos que implica el envejecimiento. Aceptando que en la vida de un ser sólo el proceso de crecimiento y diferenciación obedece a un programa genéticamente determinado, se puede concluir que mediante el mismo se fija la duración de la vida adulta y así de la del envejecimiento. La tasa de envejecimiento dependería de la regulación, es decir, del efecto de los mecanismos adaptativos contra la agresión externa y de reparación del desgaste cuya mayor o menor eficacia habría sido también establecido previamente, en el primer período de vida (AU)


This paper analyzes the data and theories of aging in order to explain its etiology. It concludes that none of the theories clarify the cause cause of aging, but rather, on the other hand, its mechanisms. That is, all are complementary in this regards. On the contrary, it seems possible to approach the etiological explanation of aging by detecting its onset. Considering that it deals with a regressive process, such regression does not appear prior to the end of growth and differentiation, but after the body reaches biological optimization. Thus the decline in the growth hormone secretion not only marks this onset but also represents the first step in the cascade of events that imply aging. Accepting that only the process of growth and differentiation obeys a genetically determined program in the life of a human being, it can be concluded that the duration of the adult life and of aging is established by it. The aging rate would depend on the regulation, that is, on the effect of the adaptive mechanisms against external aggression and repair of wear, whose greater or lesser efficacy would have been previously established, in the first period of life (AU)


Assuntos
Humanos , Masculino , Feminino , Idoso , Idoso de 80 Anos ou mais , Envelhecimento/genética , Envelhecimento/patologia , Hormônios/deficiência , Morte , Células Epiteliais/citologia , Células Epiteliais/metabolismo , Articulações/citologia , Hormônios Esteroides Gonadais/genética , Sistemas Neurossecretores/citologia , Envelhecimento/metabolismo , Envelhecimento/psicologia , Hormônios/metabolismo , Células Epiteliais/classificação , Células Epiteliais/fisiologia , Articulações/crescimento & desenvolvimento , Hormônios Esteroides Gonadais/metabolismo , Sistemas Neurossecretores/metabolismo , Biografias como Assunto
11.
Mech Ageing Dev ; 110(1-2): 49-55, 1999 Oct 01.
Artigo em Inglês | MEDLINE | ID: mdl-10580691

RESUMO

This work studied the proliferation activity in cultures of vascular smooth muscle cells (SMC) from individuals of different ages. The cells derived from arteries of 12 donors of both sexes from 45 to 91 years of age. The main parameter considered was the 'proliferation rate' (cells grown per day in the different culture passages) taking into account the age of the donor. No significant relationship between age of the donor and the cell life in proliferation was found. On the contrary, the mean time of passage duration for reaching the maximum of proliferation as well as its 'efficiency' (maximum of proliferation rate registered/mean time of passage duration) show a statistically significant dependence on the age of the donor. Furthermore, the proliferation rate measured in each passage is statistically significant related to donor age. The regressions obtained show a similar negative slope (VC 4%). Considering the first five culture passages, the regression crosses the x-axis at the age of 105.6+/-11.7 years. This age in which no proliferative activity of human SMC would be expected lies near the limit of maximum life potential for human beings. Our results suggest that with advancing donor age there is an increasing number of senescent SMC either primarily transferred or appeared in the culture. Vascular SMC of individuals whose life is near the end would almost be all senescent and therefore show extremely low proliferation rates in the culture. If the proliferative activity of arterial SMC is a condition for atherogenesis, the proportion of senescent cells would be inversely related to the propensity of developing the atheroma because of the inability of these cells to divide.


Assuntos
Envelhecimento/fisiologia , Músculo Liso Vascular/fisiologia , Idoso , Idoso de 80 Anos ou mais , Divisão Celular/fisiologia , Células Cultivadas , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Músculo Liso Vascular/citologia
12.
Gerontology ; 44(3): 144-8, 1998.
Artigo em Inglês | MEDLINE | ID: mdl-9592685

RESUMO

The process of aging results in an increase in collagen in arterial walls, but the blood levels of insulin-like growth factor 1 (IGF-1) decrease remarkably as adults age. There is an almost simultaneous increase in insulin secretion, particularly in obese individuals. It is not known if, under these hormonal conditions, the enrichment of collagen in the arterial wall is due to insulin. We studied the effect of insulin on the production of collagen in vascular smooth muscle cells (VSMC) from elderly persons with high levels of insulin secretion after blocking the insulin receptors with a monoclonal antibody. Results were compared to those without insulin receptor blockage and to those with IGF-1. Despite the inhibition of 14C-glucose uptake, insulin clearly stimulated the release of procollagen III, and increased the collagen synthesis. The hydroxyproline labelling rate from 3H-proline increased to more than twice the control values. IGF-1 is a more potent effector than insulin, but the effect of insulin on the rate of collagen production became similar to IGF-1 when the specific receptors were blocked. The results indicate that under special conditions that occur with aging, insulin interacts with nonspecific receptors in VSMC, especially IGF-1, stimulating these cells to produce collagen.


Assuntos
Envelhecimento/fisiologia , Colágeno/biossíntese , Insulina/farmacologia , Músculo Liso Vascular/metabolismo , Idoso , Idoso de 80 Anos ou mais , Anticorpos Monoclonais/imunologia , Feminino , Artéria Femoral/citologia , Humanos , Hidroxiprolina/metabolismo , Fator de Crescimento Insulin-Like I/farmacologia , Masculino , Pessoa de Meia-Idade , Músculo Liso Vascular/citologia , Concentração Osmolar , Pró-Colágeno/biossíntese , Receptor de Insulina/imunologia
13.
Gerontology ; 44(3): 149-52, 1998.
Artigo em Inglês | MEDLINE | ID: mdl-9592686

RESUMO

We examined the mechanisms by which insulin may be atherogenic during aging. We postulated that an increase in insulin secretion during aging produces growth factor effects on vascular smooth muscle cells (VSMCs), promoting these cells to synthesize collagen and to migrate. We have previously demonstrated that insulin stimulates collagen synthesis and release in senescent VSMCs that were obtained from a human organism with high levels of insulin secretion. Using the same experimental model, we now study the effects of insulin on VSMC migration. We demonstrate that insulin has a chemoattractant effect on VSMCs which occurs through insulin binding to its own specific receptors as opposed to its effect on collagen production. Blocking the insulin receptor significantly eliminates the insulin effect on cell migration. At the same molarity, the chemotactic effect of insulin is less pronounced than that of insulin-like growth factor-1. In spite of different mechanisms, there is a remarkable correlation between the insulin effects on collagen secretion and cell migration (r2 = 97%, p < 0.0005). Our results indicate that distinct but closely related mechanisms may exist by which insulin becomes atherogenic. Our results also suggest the importance of normal aging processes in the development of atherosclerosis.


Assuntos
Envelhecimento/fisiologia , Insulina/farmacologia , Músculo Liso Vascular/fisiologia , Idoso , Movimento Celular/efeitos dos fármacos , Fatores Quimiotáticos/farmacologia , Colágeno/metabolismo , Humanos , Músculo Liso Vascular/citologia , Músculo Liso Vascular/efeitos dos fármacos , Fenótipo
14.
Arch Gerontol Geriatr ; 22(1): 39-47, 1996.
Artigo em Inglês | MEDLINE | ID: mdl-15374191

RESUMO

The urinary C-peptide excretion was measured in a healthy standardized population sample of 160 subjects from 20 to 90 years of age, homogeneously distributed by age and sex. Urinary C-peptide excretion corresponded to 7% of the total amount released. The daily C-peptide excretion was 61.23 +/- 2.2 (S.E.) microg in the whole sample which corresponds to 41.9 +/- 1.5 IU of insulin secreted/day (I(CP)d), without sex differences. There is an increase of the I(CP)d value from the young to the healthy middle-aged person, but when the results were corrected for standard amounts of excreted creatinine (1 g) and urea (22 g) the age-dependent increase is to be observed during the whole adult life span. Assuming that cross-sectionally observed data are representative of the individual changes, it is concluded that age alone increases insulin secretion. The results which may be useful as reference values for clinical application were as follows: (A) in 5 diabetes type II patients in which the I(CP)d value was measured several times a week, the intraindividual variation coefficient was 10.9 +/- 7.2%;(B) in a sample of 47 type II diabetic patients of both sexes, between 51 and 70 years of age, a clear correlation was found between I(CP)d and the results of the glucagon stimulation test, mainly regarding the relationship between I(CP)d and the planimetrically measured area under the curve (r = 0.7, P < 0.0001); (C) in 7 obese non-diabetic individuals of similar ages the influence of the hypocaloric diet on the I(CP)d value was more evident than the use of C-peptide blood determinations before or after glucagon. Finally, the I(CP)d values of type II diabetes patients with insulin requirement (n = 27) were significantly lower than in the healthy control group (31.1 +/- 24.0 vs. 45.0 +/- 20.4), while diabetic patients without insulin requirement showed significantly higher values (73.0 +/- 33.0) (n = 27). These clinical studies primarily focused on the physiology of human ageing justify the measurement of C-peptide urinary excretion for evaluating daily insulin secretion in patients with type II diabetes.

15.
Rev Med Chil ; 124(1): 124-6, 1996 Jan.
Artigo em Espanhol | MEDLINE | ID: mdl-8762630

RESUMO

Augusto Orrego Luco born in 1848 and dead in 1933 in Valparaiso, was one of the greatest clinicians and researchers of chilean medicine during the late nineteenth and early twentieth century. Besides being a psychiatrist he contributed to literature, history, politics and medicine. He received his medical degree in 1874 and, apart from being an anatomist, soon became interested in mental illnesses. The title of his thesis was "Mental Hallucinations". He worked in the insane asylum after José Ramón Elguero. Later, in 1891, he was the successor of professor Carlos Sazie at the Hospital for Nervous and Mental Illnesses. Orrego Luco was influenced by french neurology of Jean Martin Charcot and taught a preferentially neurological psychiatry, based on the anatomo-clinical method. His original works were on traumatic hysteria, the mechanism of hypnosis, hysterical hemiplegia, causes of mental hallucinations, syphilitic etiology of Tabes and anatomy of cerebral sulci. In his work about mimical neuroses, he considered and obligation not to discriminate between organic and non-organic patients, because both suffer, he claimed. Presently, Orrego Luco is considered the creator and instigator of the Psychiatry chair, turning it into one of the main medical specialties in Chile.


Assuntos
Psiquiatria/história , Chile , História do Século XIX , História do Século XX , Humanos
16.
Mech Ageing Dev ; 82(1): 19-29, 1995 Jul 28.
Artigo em Inglês | MEDLINE | ID: mdl-7475354

RESUMO

Total and nuclear androgen receptors (AR) were studied from epithelial cells in internal and external prostatic zones in 51- to 86-year-old individuals with benign prostatic hyperplasia (BPH) (n = 68) and prostatic cancer (n = 9). We focussed on the role played by androgens on those processes, despite the fact that at these ages, its secretion has normally decreased. In BPH, the nuclear AR do not change, but total measured androgen receptors rise with age (r = 0.5, P < 0.01). Total or nuclear AR do not correlate with gland volume, despite its increase with age (r = 0.8, P < 0.05). In prostates less than 180 cc in volume, there is a significant correlation between size, serum total testosterone level (r = 0.53, P < 0.05) and prostatic specific antigen (PSA) (r = 0.63, P < 0.05). The amount of nuclear AR in cells from the external zone (infiltrated by cancer or healthy) is two times greater than in those from the internal region. Total receptor content of the external zone cells is also high, but the sample is too small to demonstrate an age dependence. The results suggest that ageing is accompanied by an accumulation of non-nuclear AR in the cytosol, that does not play a role in the development of BPH because the amount of nuclear receptors remains unaltered. The enrichment in nuclear receptors of the external zone cells, independently of the presence of cancer, points to a greater androgen dependence in these cells than in cells of the internal region.


Assuntos
Envelhecimento/fisiologia , Próstata/metabolismo , Hiperplasia Prostática/metabolismo , Neoplasias da Próstata/metabolismo , Receptores Androgênicos/metabolismo , Idoso , Idoso de 80 Anos ou mais , Epitélio/metabolismo , Epitélio/patologia , Humanos , Masculino , Pessoa de Meia-Idade , Próstata/patologia , Hiperplasia Prostática/patologia , Neoplasias da Próstata/patologia
17.
Gerontology ; 41(5): 243-51, 1995.
Artigo em Inglês | MEDLINE | ID: mdl-8537007

RESUMO

The aim of this work was to investigate to what extent age-dependent anthropometric changes are causally related to changes in dietary habits. In a randomly obtained sample of 246 healthy adults in the age range of 20-90 years from a well-defined agrarian population, the intake of proteins, fat and carbohydrates in males decreases with age (r = -0.65, p < 0.001; r = -0.65, p < 0.001; r = -0.5, p < 0.01, respectively), but in females it remains unaltered (e.g. the mean +/- SD daily protein intake in young adult females is 74 +/- 31 vs. 71 +/- 11 g in individuals over 80); in males it decreases from 140 +/- 34 to 71 +/- 13 g. On the contrary, in both sexes the muscle-mass-related measurements decrease (r = -0.45, p < 0.001; vs. r = -0.41, p < 0.001; mean values of the quotient lean body mass with body length in young adult females and males were 41.9 +/- 4.4 and 52.7 +/- 5.9 vs. 35.0 +/- 3.1 and 43.2 +/- 5.0, respectively, in individuals over 80, p < 0.001 in both sexes). From 35 onwards, the daily urea excretion-as a marker of the protein degradation rate-declines significantly with age, but without a clear correlation to the protein intake (r = 0.38), as occurs during young adulthood (r = 0.63). Furthermore, body fat content tends to increase with age, but the differences are statistically significant only in males of very advanced age (p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)


Assuntos
Envelhecimento/fisiologia , Antropometria , Dieta , Adulto , Distribuição por Idade , Idoso , Idoso de 80 Anos ou mais , Índice de Massa Corporal , Dieta/tendências , Feminino , Humanos , Modelos Lineares , Masculino , Pessoa de Meia-Idade , Amostragem , Distribuição por Sexo
18.
Arch Gerontol Geriatr ; 19(3): 235-42, 1994.
Artigo em Inglês | MEDLINE | ID: mdl-15374269

RESUMO

Ten prevalences of disease or functional affections due to degenerative processes that statistically show a significant age-dependent behaviour were taken as variables for a biological aging study of a population living in a district of Madrid. The cross-sectional procedure consisted in grouping the disease prevalences by age decades and calculating aging by the vector-analytical mathematical method in which the age-dependent prevalence was the result of one of the total of 10 vector components. The progressive accumulative increase of the vector distances from the origin as well as the distances among the vectors in relation to the population age was considered as biological aging. On the basis of similar mathematical models the results were compared with those obtained from other populations in which different indicators were used; the results are concurrent, but show here a greater aging acceleration than when the population was composed solely of healthy individuals. This is considered a logical consequence due to the sample composition. The presented procedure, focussed epidemiologically, can be useful in comparing aging of populations.

19.
Z Gerontol ; 27(3): 172-6, 1994.
Artigo em Alemão | MEDLINE | ID: mdl-8091834

RESUMO

This work studies the follow-up of vitality using parameters related to the arterial wall. This study is based on the application of several mathematical models and different calculation procedures. Humoral parameters together with measurements of the daily insulin secretion (own methodology based on the C-peptide elimination) were applied for the calculations using the exclusively healthy population. In the case of the non-selected population the percentage of disease prevalences due to vascular affections were applied for calculations.


Assuntos
Arteriosclerose/fisiopatologia , Longevidade/fisiologia , Adulto , Idoso , Idoso de 80 Anos ou mais , Peptídeo C/sangue , Metabolismo Energético/fisiologia , Feminino , Humanos , Insulina/sangue , Masculino , Pessoa de Meia-Idade , Modelos Teóricos , Músculo Liso Vascular/fisiopatologia
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