Season-specific genetic variation underlies early-life migration in a partially migratory bird.

Eco-evolutionary responses to environmentally induced selection fundamentally depend on magnitudes of genetic variation underlying traits that facilitate population persistence. Additive genetic variances and associated heritabilities can vary across environmental conditions, especially for labile phenotypic traits expressed through early life. However, short-term seasonal dynamics of genetic variances are rarely quantified in wild populations, precluding inference on eco-evolutionary outcomes in seasonally dynamic systems.

Early-life variation in migration is subject to strong fluctuating survival selection in a partially migratory bird.

Population dynamic and eco-evolutionary responses to environmental variation and change fundamentally depend on combinations of within- and among-cohort variation in the phenotypic expression of key life-history traits, and on corresponding variation in selection on those traits. Specifically, in partially migratory populations, spatio-seasonal dynamics depend on the degree of adaptive phenotypic expression of seasonal migration versus residence, where more individuals migrate when selection favours migration. Opportunity for adaptive (or, conversely, maladaptive) expression could be particularly substantial in early life, through the initial development of migration versus residence.

Seasonality and competition select for variable germination behavior in perennials.

The occurrence of within-population variation in germination behavior and associated traits such as seed size has long fascinated evolutionary ecologists. In annuals, unpredictable environments are known to select for bet-hedging strategies causing variation in dormancy duration and germination strategies. Variation in germination timing and associated traits is also commonly observed in perennials and often tracks gradients of environmental predictability.

A reaction norm framework for the evolution of learning: how cumulative experience shapes phenotypic plasticity.

Learning is a familiar process to most people, but it currently lacks a fully developed theoretical position within evolutionary biology. Learning (memory and forgetting) involves adjustments in behaviour in response to cumulative sequences of prior experiences or exposures to environmental cues. We therefore suggest that all forms of learning (and some similar biological phenomena in development, aging, acquired immunity and acclimation) can usefully be viewed as special cases of phenotypic plasticity, and formally modelled by expanding the concept of reaction norms to include additional environmental dimensions quantifying sequences of cumulative experience (learning) and the time delays between events (forgetting).

Digest: What keeps sexual signals honest? A general new explanation.

One of the most tantalizing phenomena in evolutionary biology has just received a new, elegant mathematical explanation. Rather than relying on the much-contested handicap principle, Fromhage and Henshaw's simple new model is based on resource trade-offs and explains why keeping costly sexual signals honest is evolutionarily optimal. Complications such as the supposed inherent wastefulness of the handicap principle, or social punishment of dishonest cheaters, are no longer needed to explain honesty in sexual signaling.

Individual reversible plasticity as a genotype-level bet-hedging strategy.

Reversible plasticity in phenotypic traits allows organisms to cope with environmental variation within lifetimes, but costs of plasticity may limit just how well the phenotype matches the environmental optimum. An additional adaptive advantage of plasticity might be to reduce fitness variance, in other words: bet-hedging to maximize geometric (rather than simply arithmetic) mean fitness. Here, we model the evolution of plasticity in the form of reaction norm slopes, with increasing costs as the slope or degree of plasticity increases.

Bet-hedging across generations can affect the evolution of variance-sensitive strategies within generations.

In order to understand how organisms cope with ongoing changes in environmental variability, it is necessary to consider multiple adaptations to environmental uncertainty on different time scales. Conservative bet-hedging (CBH) represents a long-term genotype-level strategy maximizing lineage geometric mean fitness in stochastic environments by decreasing individual fitness variance, despite also lowering arithmetic mean fitness. Meanwhile, variance-prone (aka risk-prone) strategies produce greater variance in short-term payoffs, because this increases expected arithmetic mean fitness if the relationship between payoffs and fitness is accelerating.

Alternative responses to rare selection events are differentially vulnerable to changes in the frequency, scope, and intensity of environmental extremes.

Extreme weather events are becoming more frequent, severe, and/or widespread as a consequence of anthropogenic climate change. While the economic and ecological implications of these changes have received considerable attention, the role of evolutionary processes in determining organismal responses to these critical challenges is currently unknown. Here we develop a novel theoretical framework that explores how alternative pathways for adaptation to rare selection events can influence population-level vulnerabilities to future changes in the frequency, scope, and intensity of environmental extremes.

Short-term insurance versus long-term bet-hedging strategies as adaptations to variable environments.

Understanding how organisms adapt to environmental variation is a key challenge of biology. Central to this are bet-hedging strategies that maximize geometric mean fitness across generations, either by being conservative or diversifying phenotypes. Theoretical models have identified environmental variation across generations with multiplicative fitness effects as driving the evolution of bet-hedging.

Differential allocation of parental investment and the trade-off between size and number of offspring.

When parents decide how much to invest in current versus future offspring and how many offspring to divide their current investments between, the optimal decision can be affected by the quality of their partner. This differential allocation (DA) is highly dependent on exactly how partner quality affects reproductive costs and offspring benefits. We present a stochastic dynamic model of DA in which females care for a series of clutches when mated with males of different quality.

Differential Allocation Revisited: When Should Mate Quality Affect Parental Investment?

Differential allocation (DA) is the adaptive adjustment of reproductive investment (up or down) according to partner quality. A lack of theoretical treatments has led to some confusion in the interpretation of DA in the empirical literature. We present a formal framework for DA that highlights the nature of reproductive benefits versus costs for females mated to males of different quality.

Molecular signatures of mRNAs and miRNAs as prognostic biomarkers in pancreatobiliary and intestinal types of periampullary adenocarcinomas.

Periampullary adenocarcinomas include four anatomical sites of origin (the pancreatic duct, bile duct, ampulla and duodenum) and most of them fall into two histological subgroups (pancreatobiliary and intestinal). Determining the exact origin of the tumor is sometimes difficult, due to overlapping histopathological characteristics. The prognosis depends on the histological subtype, as well as on the anatomical site of origin, the former being the more important.

Quantitative measurement of ultrasound attenuation and Hepato-Renal Index in Non-Alcoholic Fatty Liver Disease.

Objective: The aim of this study was to non-invasively explore new methods of ultrasound attenuation measurements in livers of patients with Non-Alcoholic-Fatty-Liver-Disease (NAFLD) and to measure the liver tissue elasticity.

Material And Method: Sixteen patients with NAFLD, twelve patients with liver fibrosis and fifteen healthy subjects were included. Echo Levels (ELs) in dB were measured at 2 and 7 cm depths in the right liver to calculate the attenuation.

Combining transient elastography with FIB4 enhances sensitivity in detecting advanced fibrosis of the liver.

Objective: To evaluate the predictive value of transient elastography (TE), easy available biochemical scores and a combination of these to detect advanced liver fibrosis (i.e. fibrosis stage ≥F3) in patients with chronic liver disease of different etiologies.

Fetuin A in nonalcoholic fatty liver disease: in vivo and in vitro studies.

Objective: Fetuin A has been associated with insulin resistance and the metabolic syndrome. We therefore explored the role of fetuin A in nonalcoholic fatty liver disease (NAFLD).

Design: Cross-sectional and intervention studies.

Intracellular nicotinamide phosphoribosyltransferase protects against hepatocyte apoptosis and is down-regulated in nonalcoholic fatty liver disease.

Context: Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease in Western and non-Western countries, but its pathogenesis is not fully understood.

Objective: Based on the role of nicotinamide phosphoribosyltransferase (NAMPT) in fat and glucose metabolism and cell survival, we hypothesized a role for NAMPT/visfatin in the pathogenesis of NAFLD-related disease.

Design And Setting: We conducted clinical studies at a referral medical center in well-characterized NAFLD patients (n = 58) and healthy controls (n = 27).

Metformin in patients with non-alcoholic fatty liver disease: a randomized, controlled trial.

Objective: The antidiabetic agent metformin is regularly discussed as a promising treatment for non-alcoholic fatty liver disease (NAFLD), which is characterized by insulin resistance. However, the evidence for its beneficial effects is limited, and conflicting reports have been published. The purpose of this study was to conduct a randomized, double-blind, placebo-controlled trial to test whether metformin improves liver histology in patients with non-alcoholic fatty liver disease.

A complex role of activin A in non-alcoholic fatty liver disease.

Objectives: Recent studies suggest that activin A, a member of the transforming growth factor (TGF) superfamily, is involved in the pathogenesis of liver disorders. We sought to explore its possible role in non-alcoholic fatty liver disease (NAFLD).

Methods: Serum levels of activin A and its natural inhibitor, follistatin, were measured in patients with NAFLD (n=70) and in control subjects (n=30).

Gene expression profiles reflect sclerosing cholangitis activity in abcb4 (-/-) mice.

Objective: Abcb4 (-/-) mice secrete phosphatidylcholine-deficient bile and develop sclerosing cholangitis (SC), a condition that involves differential hepatic transcription of genes governing inflammation, tissue remodelling and fibrosis. The objective of this study was to test the hypothesis that genes involved in the regulation of tissue inflammation and fibrosis display transcription rates that parallel differences in abcb4 (-/-) SC activity. The activity of abcb4 (-/-) SC can be altered through dietary intervention: abcb4 (-/-) mice fed cholic acid (CA) display high SC activity, whereas ursodeoxycholic acid (UDCA)-fed mice display low SC activity.

Multiple inflammatory-, tissue remodelling- and fibrosis genes are differentially transcribed in the livers of Abcb4 (-/ - ) mice harbouring chronic cholangitis.

Objective: Abcb4 (-/-) mice secrete phosphatidylcholine-free, cytotoxic bile and develop chronic cholangitis. The aim of this study was to identify differentially transcribed genes whose products contribute to the liver tissue pathology during this disease.

Material And Methods: Hepatic gene transcription was measured in 3-, 6-, 9- and 20-week-old Abcb4 (-/-) mice (FVB.

Systemic inflammation in nonalcoholic fatty liver disease is characterized by elevated levels of CCL2.

Background/aims: To elucidate the role of systemic inflammation in nonalcoholic fatty liver disease (NAFLD).

Methods: Serum samples in 47 patients with histologically verified NAFLD (22 with simple steatosis and 25 with nonalcoholic steatohepatitis [NASH]), and in 30 age-, sex- and ethnicity-matched healthy controls, were assessed for (i) general markers of inflammation (C-reactive protein [CRP], tumor necrosis factor [TNF]-alpha, and interleukin [IL]-6), (ii) chemokines (CC-chemokine ligand [CCL] 2/monocyte chemoattractant protein [MCP]-1, CCL19 and CCL21), (iii) adipocytokines related to insulin resistance and inflammation (adiponectin and leptin) and (iv) a marker of oxidative stress (8-isoprostane-F2alpha).

Results: Serum levels of several inflammatory cytokines were increased in NAFLD as compared to controls, and IL-6 (P=0.

Abnormal glucose tolerance is a predictor of steatohepatitis and fibrosis in patients with non-alcoholic fatty liver disease.

Objective: The majority of patients with non-alcoholic fatty liver disease (NAFLD) have simple steatosis. A minority, however, present with non-alcoholic steatohepatitis (NASH), a condition that can lead to advanced fibrosis and cirrhosis. The frequencies of NASH and fibrosis among patients with NAFLD and sustained elevation of liver function tests (LFT) are uncertain.

Long-term outcome of chronic hepatitis C virus infection in primary hypogammaglobulinaemia.

The clinical course of HCV infection in patients with primary hypogammaglobulinaemia appears to be more severe than in immunocompetent patients. We studied the long-term course of chronic HCV infection in 20 Norwegian hypogammaglobulinaemia patients with a 13-15 year known history of HCV infection. Twelve of 20 patients developed cirrhosis during the observation period (1984-1999), and the remaining eight also had chronic liver disease verified by liver biopsy in the majority of the cases.

The spectrum of hepatobiliary disease in primary hypogammaglobulinaemia.

Objective: To study the prevalence of hepatobiliary disease in a clinically and immunologically well-characterized group of 88 adult Norwegian patients with primary hypogammaglobulinaemia.

Subjects: Eighty-eight patients with primary hypogammaglobulinaemia were followed and signs and symptoms of liver disease were recorded. The patients were examined clinically and radiologically on a regular basis with liver biopsies performed when indicated.