Nutrition in early life - "long term effects" - Keynote Address

Most estimates indicate that during the next 20 years most of the morbidity and mortality in the world will be related to chronic diseases, such as cardiovascular disease, diabetes mellitus, some cancers and mental health. The aetiology of each condition is complex and multifactorial, but recent evidence shows that nutritional exposure during early life might be critical in determining individual susceptibility to a range of other environmental factors in the generation of chronic disease in adulthood. It is proposed that the underlying susceptibility originates through "programming" during fetal and early infant life. Thus, in response to a limited availability of nutrients the fetus adapts and this adaption results in a permanent change in organ structure and metabolic function, giving rise to the hypothesis of "Fetal Origins of Adult Disease". Across Britain there is a two-fold variation in cardiovascular disease which cannot be adequately explained by variations in lifestyle. Early studies suggested they may be explained by differences in the physique and growth of young women, the growth of their babies in utero and during infancy, and the consequent lifelong differences in the physiology and metabolism of the offspring. Novel epidemiological studies by Barker and colleagues in Southampton allowed exploration of these ideas using detailed maternity and health visitors records which have been kept from the early years of this century. Babies born fifty years ago were traced and their size at birth and one year of age related to the occurrence of cardiovascular disease in later life. Amongst 10,000 men in Hertfordshire who had lower birthweight and remained lighter than average at one year of age the risk of death from heart disease was three times that of men at the upper end of normal. Small size at birth is also associated with high blood pressure and diabetes, high serum cholesterol and disordered blood coagulation. The lightest babies at birth were ten times more likely to develop the metabolic syndrome of hypertension, impaired glucose tolerance and raised blood lipid levels than those who were heaviest at birth. Stroke is also increased in those with a lower birth weight. These relationships are even more evident in babies in whom growth is disproportionate, thus thinner babies are more likely to develop non-insulin diabetes mellitus as adults.(Au) [truncated at 2500 characters]

Rabies without nwgri bodies: detection of rabies virus at autopsy by immunohistochemistry and in situ hybridization / Rabia sin cuerpos de Negri. Detección del virus rábico en autopsia por inmunohistoquímica y por hibridación in situ

El patólogo puede diagnosticar rabia en autopsia cuando reconoce cuerpos de Negri o si documenta la presencia de antígeno del virus por inmunofluorescencia en tejido fresco o congelado. Técnicas moleculares recientes permiten llegar al diagnóstico en ausencia de estos marcadores. Un muchacho de 13 años fue mordido por un perro rabioso y murió veinte días después a pesar de haber recibido un curso completo de vacuna antirrábica. En la autopsia se encontraron infiltrados inflamatorios en cerebro y médula espinal pero un extenso muestreo no reveló cuerpos de Negri. El cerebro y la médula habían sido fijados en formol y no había tejido fresco para inmunofluorescencia. Se identificó antígeno del virus de la rabia por tinciones con inmunoperoxidasa en cerebelo, hipocampo, bulbo y médula espinal. Se detectó asimismo la presencia de RNA genómico del virus y mRNA de la glicoproteína viral por hibridación in situ usando sonda tritiadas de RNA. En este caso se logró un diagnóstico específico de rabia mediante el uso de métodos de inmunohistoquímica y de hibridación in situ. Estas técnicas pueden ser de utilidad en estudios retrospectivos en material de archivo y particularmente cuando se carece de tejido fresco o congelado para inmunofluorescencia