Differential Stage-Specific Mortality as a Mechanism for Diversification.

AbstractIndividual variability in mortality is widespread in nature. The general rule is that larger organisms have a greater chance of survival than smaller conspecifics. There is growing evidence that differential mortality between developmental stages has important consequences for the ecology and evolution of populations and communities. However, we know little about how it can influence diversification. Using an eco-evolutionary model of diversification that considers individual variability in mortality, I show that commonly observed differences in mortality between juveniles and adults can facilitate adaptive diversification. In particular, diversification is expected to be less restricted when mortality is more biased toward juveniles. Additionally, I find stage-specific differences in metabolic cost and foraging capacity to further facilitate diversification when adults are slightly superior competitors, due to either a lower metabolic cost or a higher foraging capacity, than juveniles. This is because by altering the population composition, differential stage-specific mortality and competitive ability can modulate the strength of intraspecific competition, which in turn determines the outcome of diversification. These results demonstrate the strong influence that ecological differences between developmental stages have on diversification and highlight the need for integrating developmental processes into diversification theory.

Marine reserves promote cycles in fish populations on ecological and evolutionary time scales.

Marine reserves are considered essential for sustainable fisheries, although their effectiveness compared to traditional fisheries management is debated. The effect of marine reserves is mostly studied on short ecological time scales, whereas fisheries-induced evolution is a well-established consequence of harvesting. Using a size-structured population model for an exploited fish population of which individuals spend their early life stages in a nursery habitat, we show that marine reserves will shift the mode of population regulation from low size-selective survival late in life to low, early-life survival due to strong resource competition. This shift promotes the occurrence of rapid ecological cycles driven by density-dependent recruitment as well as much slower evolutionary cycles driven by selection for the optimal body to leave the nursery grounds, especially with larger marine reserves. The evolutionary changes increase harvesting yields in terms of total biomass but cause disproportionately large decreases in yields of larger, adult fish. Our findings highlight the importance of carefully considering the size of marine reserves and the individual life history of fish when managing eco-evolutionary marine systems to ensure both population persistence as well as stable fisheries yields.

The enrichment paradox in adaptive radiations: Emergence of predators hinders diversification in resource rich environments.

Adaptive radiations are known for rapid niche diversification in response to ecological opportunity. While most resources usually exist prior to adaptive radiation, novel niches associated with novel resources can be created as a clade diversifies. For example, in African lake cichlid radiations some species prey upon other species of the clade (intraclade consumers). Using a trait-based eco-evolutionary model, we investigate the evolution of intraclade consumers in adaptive radiations and the effect of this novel trophic interaction on the diversification process of the radiating clade. We find that the evolutionary emergence of intraclade consumers halts the diversification processes of other ecomorphs as a result of increased top-down control of density. Because high productivity enables earlier evolution of intraclade consumers, highly productive environments come to harbour less species-rich radiations than comparable radiations in less productive environments. Our results reveal how macroevolutionary and community patterns can emerge from ecological and microevolutionary processes.

Adaptive Evolution Can Both Prevent Ecosystem Collapse and Delay Ecosystem Recovery.

AbstractThere is growing concern about the dire socioecological consequences of abrupt transitions between alternative ecosystem states in response to environmental changes. At the same time, environmental change can trigger evolutionary responses that could stabilize or destabilize ecosystem dynamics. However, we know little about how coupled ecological and evolutionary processes affect the risk of transition between alternative ecosystem states. Using shallow lakes as a model ecosystem, we investigate how trait evolution of a key species affects ecosystem resilience under environmental stress. We find that adaptive evolution of macrophytes can increase ecosystem resilience by shifting the critical threshold, which marks the transition from a clear-water state to a turbid-water state to a higher level of environmental stress. However, following the transition, adaptation to the turbid-water state can delay the ecosystem recovery back to the clear-water state. This implies that restoration could be more effective when implemented early enough after a transition occurs and before organisms adapt to the alternative state. Our findings provide new insights into how to prevent and mitigate the occurrence of regime shifts in ecosystems and highlight the need to understand ecosystem responses to environmental change in the context of coupled ecological and evolutionary processes.

Fast environmental change and eco-evolutionary feedbacks can drive regime shifts in ecosystems before tipping points are crossed.

Anthropogenic environmental changes are altering ecological and evolutionary processes of ecosystems. The possibility that ecosystems can respond abruptly to gradual environmental change when critical thresholds are crossed (i.e. tipping points) and shift to an alternative stable state is a growing concern. Here I show that fast environmental change can trigger regime shifts before environmental stress exceeds a tipping point in evolving ecological systems. The difference in the time scales of coupled ecological and evolutionary processes makes ecosystems sensitive not only to the magnitude of environmental changes, but also to the rate at which changes are imposed. Fast evolutionary change mediated by high trait variation can reduce the sensitivity of ecosystems to the rate of environmental change and prevent the occurrence of rate-induced regime shifts. This suggests that management measures to prevent rate-induced regime shifts should focus on mitigating the effects of environmental change and protecting phenotypic diversity in ecosystems.

Interferon-alpha-2a as a salvage treatment for hemorrhagic enteritis associated with Epstein-Barr Virus reactivation: a case report.

Epstein-Barr virus [EBV] is a virus that infects almost all humans worldwide. After the acute phase of the infection, it stays in a latent form in B lymphocytes. EBV reactivation tends to occur in immunosuppressed patients. EBV reactivation may involve the gastrointestinal tract ; it has been associated mainly with colitis, but hemorrhagic enteritis has been poorly reported. Treatment usually includes antivirals. However, our patient did not respond to conventional treatment, so interferon alpha-2a was given as a salvage treatment. To our knowledge, this is the first reported case of hemorrhagic enteritis associated to EBV reactivation treated successfully with interferon alpha-2a.

Density-dependent effects of mortality on the optimal body size to shift habitat: Why smaller is better despite increased mortality risk.

Many animal species across different taxa change their habitat during their development. An ontogenetic habitat shift enables the development of early vulnerable-to-predation stages in a safe "nursery" habitat with reduced predation mortality, whereas less vulnerable stages can exploit a more risky, rich feeding habitat. Therefore, the timing of the habitat shift is crucial for individual fitness. We investigate the effect that size selectivity in mortality in the rich feeding habitat has on the optimal body size at which to shift between habitats using a population model that incorporates density dependence. We show that when mortality risk is more size dependent, it is optimal to switch to the risky habitat at a smaller rather than larger body size, despite that individuals can avoid mortality by staying longer in the nursery habitat and growing to safety in size. When size selectivity in mortality is high, large reproducing individuals are abundant and produce numerous offspring that strongly compete in the nursery habitat. A smaller body size at habitat shift is therefore favored because strong competition reduces growth potential. Our results reveal the interdependence among population structure, density dependence, and life history traits, and highlight the need for integrating ecological feedbacks in the study of life history evolution.

Ecological changes with minor effect initiate evolution to delayed regime shifts.

Regime shifts have been documented in a variety of natural and social systems. These abrupt transitions produce dramatic shifts in the composition and functioning of socioecological systems. Existing theory on ecosystem resilience has only considered regime shifts to be caused by changes in external conditions beyond a tipping point and therefore lacks an evolutionary perspective. In this study, we show how a change in external conditions has little ecological effect and does not push the system beyond a tipping point. The change therefore does not cause an immediate regime shift but instead triggers an evolutionary process that drives a phenotypic trait beyond a tipping point, thereby resulting (after a substantial delay) in a selection-induced regime shift. Our finding draws attention to the fact that regime shifts observed in the present may result from changes in the distant past, and highlights the need for integrating evolutionary dynamics into the theoretical foundation for ecosystem resilience.

Environmental change effects on life-history traits and population dynamics of anadromous fishes.

Migration, the recurring movement of individuals between a breeding and a non-breeding habitat, is a widespread phenomenon in the animal kingdom. Since the life cycle of migratory species involves two habitats, they are particularly vulnerable to environmental change, which may affect either of these habitats as well as the travel between them. In this study, we aim to reveal the consequences of environmental change affecting older life-history stages for the population dynamics and the individual life history of a migratory population. We formulate a population model based on the individual energetics and life history to study how increased energetic cost of the breeding travel and reduced survival and food availability in the non-breeding habitat affect an anadromous fish population. These unfavourable conditions have impacts at the individual and the population level. First, when conditions deteriorate individuals in the breeding habitat have a higher body growth rate as a consequence of reductions in spawning that reduce competition. Second, population abundance decreases, and its dynamics change from a regular annual cycle to oscillations with a period of four years. The oscillations are caused by the density-dependent feedback between individuals within a cohort through the food abundance in the breeding habitat, which results in alternation of a strong and a weak cohort. Our results explain how environmental change, by affecting older life-history stages, has multiple consequences for other life stages and for the entire population. We discuss these results in the context of empirical data and highlight the need for mechanistic understanding of the interactions between life-history and population dynamics in response to environmental change.

Calidad de vida en los pacientes con parálisis cerebral en proceso de envejecimiento / Quality of life in patients with cerebral palsy during aging process

Objetivo: Determinar la calidad de vida (CV) de los pacientes adultos con parálisis cerebral (PC) en proceso de envejecimiento, y analizar el efecto de la función motora, los trastornos de la comunicación y la discapacidad intelectual (DI) sobre la CV. Material y método: Estudio transversal en personas adultas con PC. Se administró un cuestionario para recoger las características sociodemográficas relacionadas con la discapacidad, y 2 escalas para evaluar el nivel de la función motora Gross Motor Function Classification System (GMFCS) y de la CV (escala GENCAT). Análisis estadístico: se realizaron la prueba de la t de Student para comparar con las puntuaciones estándar, y el análisis ANOVA para analizar la incidencia del nivel de función motora, la DI y los trastornos de comunicación . Resultados: Participaron 46 pacientes (27 varones y 19 mujeres; edad: M ± DE = 50 ± 7,9). Presentaron niveles inferiores de CV en relaciones interpersonales, autodeterminación, inclusión social y derechos, y buenos niveles en bienestar emocional. No se obtuvieron efectos significativos del nivel de función motora, pero sí del grado de DI y de los trastornos de comunicación, y fueron significativas las interacciones con las dimensiones de CV. Conclusiones: La CV de los adultos con PC es buena en bienestar emocional, no tanto en autodeterminación y derechos. El grado de afectación motora incide sobre el bienestar material y físico; el grado de DI, sobre el desarrollo personal y la autodeterminación; y los problemas de comunicación, sobre las diferentes dimensiones de CV, aunque en menor medida sobre el bienestar físico (AU)

Objective: To determine quality of life (QoL) of adult patients with cerebral palsy (CP) during the ageing process and to analyze the effect of motor function, communication disorders, and intellectual disability (ID) on QoL. Material and method: A cross-sectional study on adults with CP was performed. A questionnaire to collect sociodemographic characteristics related to the disability, and two scales to assess the level of motor function Gross Motor Function Classification System (GMFCS) and a scale to measure QoL (GENCAT Scale) were used. Statistical analysis: T tests were performed to make a comparison with standard scores, and ANOVAS to analyze the incidence of motor function level, ID, and communication disorders. Results: Participants were 46 patients (27 males, 19 females; age: M±SD, 50±7.9). They presented low levels of QoL in interpersonal relations, self-determination, and social inclusion, and rights, and good levels of emotional well-being. No significant effects were found for motor function level, but ID and communication disorders produced significant effects, and interactions with QoL dimensions were also significant. Conclusions: QoL of adults with CP is satisfactory in emotional well-being and lower in selfdetermination and rights. Degree of motor impairment has an impact on material and physical well-being; degree of ID affects personal development and self-determination; and communication problems influence diverse dimensions of QoL, although physical well-being to a lesser degree (AU)

Renal protective effect of chronic inhibition of COX-2 with SC-58236 in streptozotocin-diabetic rats.

The induction of renal cyclooxygenase-2 (COX-2) in diabetes has been implicated in the renal functional and structural changes in models where hypertension or uninephrectomy was superimposed. We examined the protective effects of 3 mo treatment of streptozotocin-diabetic rats with a highly selective COX-2 inhibitor (SC-58236) in terms of albuminuria, renal hypertrophy, and the excretion of TNF-α and TGF-ß, which have also been implicated in the detrimental renal effects of diabetes. SC-58236 treatment (3 mg·kg(-1)·day(-1)) of diabetic rats resulted in reduced urinary excretion of PGE(2), 6-ketoPGF(1α), and thromboxane B(2), all of which were increased in the diabetic rat compared with age-matched nondiabetic rats. However, serum thromboxane B(2) levels were unchanged, confirming the selectivity of SC-58236 for COX-2. The renal protective effects of treatment of diabetic rats with the COX-2 inhibitor were reflected by a marked reduction in albuminuria, a reduction in kidney weight-to-body weight ratio, and TGF-ß excretion and a marked decrease in the urinary excretion of TNF-α. The protective effects of SC-58236 were independent of changes in plasma glucose levels or serum advanced glycation end-product levels, which were not different from those of untreated diabetic rats. In an additional study, the inhibition of COX-2 with SC-58236 for 4 wk in diabetic rats resulted in creatinine clearance rates not different from those of control rats. These results confirm that the inhibition of COX-2 in the streptozotocin-diabetic rat confers renal protection and suggest that the induction of COX-2 precedes the increases in cytokines, TNF-α, and TGF-ß.

Desarrollo de la comunicación y del lenguaje: indicadores de preocupación / No disponible

El lenguaje oral es un sistema reglado, muy complejo. Permite un intercambio de informaciones a través de un determinado sistema de codificación. No es el único, pero con él se estructura, inventa y recrea el pensamiento; regula las relaciones interpersonales, la propia conducta del sujeto y permeabiliza al niño en el medio sociocultural en el que está inmerso. Su desarrollo es el resultado de la interacción entre las bases biológicas y el entorno físico y social que rodea al niño. Nuestro objetivo al escribir este artículo es el abordaje del lenguaje oral desde su nacimiento hasta la edad de 6 años, atendiendo a la evolutiva normalizada desde sus diferentes dimensiones (forma, contenido y uso) con el fin de detectar lo más tempranamente posible las dificultades y atajarlas con las medidas educativas y terapéuticas adecuadas (AU)

The oral language is a ruled and complex system. It allows an exchange of information through a determined system of codification. It is not the only system, but with it, the thinking is constructed, invented and recreated, it regulates the interpersonal relationships, the behaviour of the individual itself and promotes the relationship between the child and his/her sociocultural atmosphere. The development of the oral language is the result of the interaction between the biological basis and the physical and social environment that surrounds the child. Our aim at writing this article is to approach the oral language from birth up to the age of 6 years, attending to the normalized evolution from its different dimensions (form, content and use) in order to detect as soon as possible the hypothetic problems and to put a stop to them with the educational and therapeutic suitable measures (AU)

Audiogenic seizure susceptibility in thyroid hormone receptor beta-deficient mice.

As early-onset hypothyroidism produces audiogenic seizure susceptibility (AGS) in rodents, the role of TR alpha 1 and TR beta thyroid hormone receptors in AGS was investigated. AGS occurs in mice lacking specifically TR beta (Thrb(tm1/tm1)) and is marked by early onset and persistence, thereby differing from mouse strains where AGS is age-restricted. Thrb(tm1/tm1) mice display AGS whether on a mixed 129/Sv x C57BL/6J or congenic C57BL/6J background. 27% of wild-type mice on the mixed and 0% on the congenic background exhibited AGS. The inability of Thrb(tm1/tm1) mice to downregulate the response to sustained acoustic stimulation may reside in the brain or in the auditory system itself as Thrb(tm1/tm1) mice also display auditory deficits. The AGS phenotype identifies a novel neurological role for TR beta.

Myelin basic protein immunoreactivity in the internal capsule of neonates from rats on a low iodine intake or on methylmercaptoimidazole (MMI).

Rats fed on low iodine diets (LIDs) result in a normal circulating level of triiodothyronine (T3), a low level of thyroxine (T4) and an elevated thyroid-stimulating hormone (TSH). These changes are similar to those observed in habitants who live in iodine-deficient areas and different from those observed when the hypothyroidism is produced by goitrogens. To study the effects of LID or goitrogens on the myelin basic protein (MBP) immunoreactivity (MBP-ir) during the myelination of the internal capsule, one group of experimental female rats was fed on an LID, and another group received a standard laboratory diet with methylmercaptoimidazole (MMI) added in the drinking water. Animals fed on a standard laboratory diet and animals fed on an LID supplemented with KI were used as controls. At P10, the MMI treatment has produced a more marked decrease in the surface density of MBP-ir processes with respect to controls than that produced in the LID animals. This decrease was correlated with the cerebral concentrations of triiodothyronine (T3) we found. During the postnatal development, a recovery in the levels of the surface density with respect to controls was observed in both experimental groups. The recovery occurred by P20 in the LID group and by P32 in the MMI rats.

Early effects of iodine deficiency on radial glial cells of the hippocampus of the rat fetus. A model of neurological cretinism.

The most severe brain damage associated with thyroid dysfunction during development is observed in neurological cretins from areas with marked iodine deficiency. The damage is irreversible by birth and related to maternal hypothyroxinemia before mid gestation. However, direct evidence of this etiopathogenic mechanism is lacking. Rats were fed diets with a very low iodine content (LID), or LID supplemented with KI. Other rats were fed the breeding diet with a normal iodine content plus a goitrogen, methimazole (MMI). The concentrations of -thyroxine (T4) and 3,5,3'triiodo--thyronine (T3) were determined in the brain of 21-d-old fetuses. The proportion of radial glial cell fibers expressing nestin and glial fibrillary acidic protein was determined in the CA1 region of the hippocampus. T4 and T3 were decreased in the brain of the LID and MMI fetuses, as compared to their respective controls. The number of immature glial cell fibers, expressing nestin, was not affected, but the proportion of mature glial cell fibers, expressing glial fibrillary acidic protein, was significantly decreased by both LID and MMI treatment of the dams. These results show impaired maturation of cells involved in neuronal migration in the hippocampus, a region known to be affected in cretinism, at a stage of development equivalent to mid gestation in humans. The impairment is related to fetal cerebral thyroid hormone deficiency during a period of development when maternal thyroxinemia is believed to play an important role.

Displacement of T4 from transthyretin by the synthetic flavonoid EMD 21388 results in increased production of T3 from T4 in rat dams and fetuses.

EMD 21388 displaces T4 from circulating transthyretin, is a potent in vitro inhibitor of outer-ring deiodination (5'D) of T4 and affects thyroid hormone secretion. To study its extrathyroidal effects on the thyroid hormone status of pregnant dams and their fetuses, we treated the dams with methimazole and infused them with T4 and with either 2.5 mg EMD 21388/rat per day [(EMD(+)], or placebo solution [EMD(-)]. EMD reduced total T4 and T3 in the maternal circulation, but free T4 increased and free T3 decreased. The total amount of T3 generated from T4 in the maternal compartment increased. Placental T3 also increased in EMD(+) animals, T4 remaining the same. EMD also reached the fetal circulation. The total fetal extrathyroidal T4 pool decreased to half that of EMD(-) fetuses, whereas T3 increased 1.8-fold, thus mitigating fetal T3 deficiency, especially in the lung. Thus, if the maternal supply of T4 is kept constant, EMD mitigates the T3 deficiency of many tissues of the hypothyroid fetus. Most of the effects of this dose of EMD could result from the displacement of T4 from circulating transthyretin. Liver 5'D-I activity did not decrease, but actually increased by 40% in dams and fetuses. The enhanced transfer of T4 into tissues would also increase the amount of substrate available to 5'D-I, leading to an increased amount of T3 in maternal and fetal pools. This had not been anticipated from the changes in circulating T4 and T3, whether maternal or fetal, total or free.

Archival and wide exposure latitude process for holography.

A high diffraction efficiency and wide exposure latitude holographic processing method, capable of producing archival quality holograms is presented. It consists of a solution stage physical development on CPA-1, followed by a fixing stage. Holograms thus obtained have a wide exposure latitude and high diffraction efficiency. The method has been tried on 875-HD and 10E75-HD Agfa-Gevaert emulsions.

Combined valve replacement and coronary bypass surgery. Results in 127 operations stratified by surgical risk factors.

The results of 127 operations with both valve replacement and coronary bypass were compared with all 5,053 operations involving coronary bypass performed from August 1972 through June 1985. Both groups were stratified by the number of risk factors (age over 70 years, bad ventricle, extensive endarterectomy, and reoperation). Compared with all bypass operations, valve replacement had no effect on surgical mortality except in the group at highest risk. Conversely, valve replacement was associated with reduced late survival in all but those at highest risk. Results with tissue valves were better than with mechanical, but statistical significance was lacking. Relief of angina was equal. Ischemic mitral insufficiency continues to be the greatest challenge, with 46 percent five-year survival. We conclude that combined valve replacement and bypass surgery can be performed successfully, even in the patients at higher risk; however, this operation should be performed only by teams with demonstrated success in surgically treating advanced coronary artery disease.

Angina pectoris and coronary bypass surgery: patterns of prevalence and recurrence in 3105 consecutive patients followed up to 11 years.

Many studies document the effectiveness of bypass surgery in relieving angina pectoris. Few, however, have described patterns of prevalence preoperatively and recurrence postoperatively. After excluding those known to be dead and those residing outside the continental United States, we attempted to contact all patients who had undergone first bypass surgery by us. Follow-up was 94.4% complete. Women had a higher prevalence of preoperative angina and lesser relief after surgery (p less than 0.01). Because of this difference, only men presenting with angina preoperatively were analyzed in detail. In this subgroup, the cumulative percentage of patients with total relief of angina was 87% after the first year; thereafter, the percentage decreased 6%/year. The cumulative percentage of patients improved (those with no angina plus those with less angina than before surgery) was 97% after the first year; thereafter the percentage decreased 0.9%/year. Duration of angina preoperatively had no effect on recurrence unless preoperative duration was less than 6 months. Preoperative left ventricular function had little effect on relief of angina postoperatively. In a short follow-up, 1.5 to 2 years after the original study, we found that patients with postoperative angina had twice the mortality rate of those totally free of angina (p = 0.000004). Furthermore, those with angina at rest had twice the mortality rate of those who had angina but never at rest (p = 0.009).

Coronary artery surgery in diabetics: 261 consecutive patients followed four to seven years.

Diabetes mellitus is a well established risk factor for coronary artery disease, but its effect on the conduct and results of bypass surgery (CABG) are not well documented. We identified 261 (11.9%) diabetics among 2192 patients operated August, 1972, through December, 1977. All patients were surveyed, in identical manner, during January, 1981. There were 51 (19.5%) dead, seven (3.3%) lost, and seven (3.3%) residing in foreign countries whom we did not attempt to follow. We divided the 261 patients into three groups by severity of diabetes: drug therapy 106 (40.6%), diet therapy 60 (23.0%), and borderline 95 (36.4%). Severity of diabetes had no effect on any of the factors we investigated. Compared with nondiabetics, diabetics had the same average age, a higher proportion of women, the same number of grafts per patient, slightly more bad ventricles, and a higher surgical and late mortality. Frequency of preoperative angina was slightly higher in diabetics. Relief of angina was essentially the same in both groups. There were 54 serious complications which occurred in 45 (17.2%) patients; of these, 20 (7.7%) were hospital mortalities. The only factors reaching statistical significance were the proportion of women and the surgical mortality in good ventricles. We conclude that the presence of diabetes does increase the morbidity and mortality associated with bypass surgery, but only to a relatively small degree and that controlled diabetes is not sufficient reason to avoid bypass surgery.