Feeding of Most Abundant Fish Species in Flemish Cap in Summer 1993

The stomach contents of 4320 fishes comprising 14 species were collected from Flemish Cap Bank (NW Newfoundland) at depths ranging from 130 to 730 m, during summer 1993. The general feeding intensity was high in all species. Three main feeding patterns were evident: the genus Sebastes consume primarily pelagic species, although they also feed on preys which migrate vertically such as shrimps, Euphausids and mysids. The benthic group is made up of American plaice (Hippoglossoides platessoides), witch flounder (Glyptocephalus cygnoglossus), arctic eelpout (Lycodes reticulatus), wolffishes (Anarhichas lupus and Anarhichas minor) and thorny skate (Raja radiata). Lastly, the group of benthopelagic fish remains, longf in hake (Urophycis chesteri), cod (Gadus morhua), grenadiers (Nezumia bairdi and Macrourus berglax) and Greenland halibut (Reinhardtius hippoglossoides). Pelagic and benthopelagic preys are an important food resource for all fish considered, the abundance of Hyperids, P. borealis and Sebastes sp. in summer makes them an important food resource in the diet of fish in Flemish Cap

Is juvenile anchovy a feeding resource for the demersal community in the Bay of Biscay? On the availability of pelagic prey to demersal predators

The role that juvenile anchovy (Engraulis encrasicolus) play as a food resource for the demersal community in the southern Bay of Biscay is assessed using 21 years of anchovy abundance data and demersal predator diets. During the study period, a total of 26 fish and elasmobranch species preyed on anchovy either frequently or occasionally. Predators with a crustacean-based diet targeted the smaller anchovy individuals. The size range of anchovy juveniles (centred at 7.5–8.9 cm) was comparable to that of the largest nektonic–benthic crustaceans, but generally smaller than other demersal and pelagic fish prey. Hake (Merluccius merluccius) and megrim (Lepidorhombus whiffiagonis) were the predators that consumed the highest number of anchovy, one of the main prey items driving the variability of their diets. Anchovy consumption conformed only partially to the abundance of anchovy in the southern Bay of Biscay, suggesting that factors other than abundance might condition its availability to demersal predators. Prey size could be one of them, as the size of the anchovy preyed on proved to be significantly smaller than the individuals collected with bottom trawls. However, other factors, such as the vertical position of the shoals of anchovy juveniles, could also constrain anchovy availability to demersal predators

Impaired dermal wound healing in discoidin domain receptor 2-deficient mice associated with defective extracellular matrix remodeling

Background The wounding response relies on tightly regulated crosstalk between recruited fibroblasts and the collagenous extracellular matrix (ECM). Discoidin domain receptor 2 (DDR2) is a tyrosine kinase receptor for fibrillar collagen expressed during pathologic scarring, for example wound healing, arthritis and cancer. We have previously shown that DDR2 phosphorylation drives key wounding responses in skin fibroblasts including proliferation, chemotactic migration and secretion of both metalloproteinases and fibrillar collagen. In this study we compared healing of cutaneous wounds in DDR2+/+ and DDR2-/- mice and analyzed specific fibroblast responses. Results Cutaneous wound healing was significantly delayed in DDR2-/- mice compared with DDR2+/+ animals. Reduced α-smooth muscle actin (αSMA) expression and matrix metalloproteinase 2 (MMP2) activity in the DDR2-/- wound extracts indicated defective recruitment of skin fibroblasts. DDR2-/- wounds showed decreased tensile strength during healing, which correlated with a significant reduction in collagen content and defective collagen crosslinking. Non-wounded skin in DDR2-/- mice expressed less mRNA of the crosslinking enzymes lysyl oxidase (LOX), lysyl hydroxylase1 (LH1) and matricellular 'secreted protein, acidic and rich in cysteine' (SPARC; also known as osteonectin). Skin fibroblasts isolated from DDR2-/- mice displayed altered mRNA expression of a cluster of collagens, proteoglycans, integrins and MMPs that have been previously correlated with DDR2 expression, and reduced LOX, LH1 and SPARC mRNA levels and proteins. Stable reconstitution of wild-type DDR2 by retroviral infection restored LOX, LH1 and SPARC mRNA and protein levels in DDR2-/- fibroblasts. Contraction of collagen gels was reduced in DDR2-/- fibroblasts, accompanied by significantly reduced phosphorylated SrcY418. Inhibition of either LOX activity by β-aminoproprionitrile or MMP activity by N-[(2R)-2-(hydroxamido carbonylmethyl)-4-methylpentanoyl]-l-tryptophan methylamide (GM6001) reduced collagen gel contraction by skin fibroblasts after DDR2 induction with soluble collagen type I. Conclusions DDR2 contributes to skin fibroblast responses during tissue injury. Defective synthesis of collagen type I, crosslinking molecules and MMP2 predispose DDR2-/- mice to defective dermal wounding

Consumption of fruits and vegetables in a group of valencian children of school age.

Introducción: En los últimos 25 años ha habido un gran cambio en los hábitos alimentarios en España. Objetivos: Calcular y valorar el consumo de frutas, verduras y hortalizas en niños de edad escolar e identificar el tipo de postre que toman analizando la influencia de los niños en la compra de fruta y verdura que realizan los padres. Material y métodos: Se realizó un cuestionario dirigido a los padres de niños y niñas en edad escolar que estaban cursando primaria. De 155 cuestionarios entregados en el colegio, se obtuvo una muestra de 116. Resultados: Solo el 5,17% de los niños consumen 3 ó más raciones de frutas al día. El 30,17% consumen 1 ó 2 raciones de verduras y hortalizas al día. El 18,97% toman fruta como postre de forma habitual. El 25% de los padres compran fruta la mayoría de los días porque sus hijos se la piden y el 12,93% compran verdura. Discusión: No hay un consumo suficiente de frutas, verduras y hortalizas entre los escolares estudiados. Los niños influyen en la compra de frutas, verduras y hortalizas que realizan sus padres. Conclusiones: El consumo de frutas, verduras y hortalizas en la mayoría de estos niños, no sigue las recomendaciones de las Guías Dietéticas. El consumo de fruta como postre de forma habitual es bajo. Los niños tienen más influencia en la compra de frutas que en las de verduras.Introduction: In the last 25 years there has been a great change in the food habits in Spain. Objectives: To calculate and assess the consumption of fruits and vegetables in school children. To identify the type of desserts eaten and analyze the influence children have on the purchase of fruit and vegetables made by parents. Materials and methods: A survey was carried out on parents of primary school children. A total of 155 questionnaires were handed into the school, obtaining a sample of 116 completed questionnaires. Results: Only 5.17% eat 3 or more portions of fruit per day. Regarding vegetables, 30.17% consume 1 or 2 portions. 18.97% have fruit as a dessert. 25% of the parents purchase fruit most days as a result of the children request and 12.93% purchase vegetables. Discussion: Children do not consume enough fruit and vegetables. Children have an influence on fruit and vegetable purchases. Conclusions: The majority of the studied children do not follow the dietary recommendations regarding consumption of fruit and vegetables. Consumption of fruit for dessert is low. Children have a bigger influence on fruit purchases than in vegetables purchases.Nutrición humana y dietétic

The Prometastatic Microenvironment of the Liver

The liver is a major metastasis-susceptible site and majority of patients with hepatic metastasis die from the disease in the absence of efficient treatments. The intrahepatic circulation and microvascular arrest of cancer cells trigger a local inflammatory reaction leading to cancer cell apoptosis and cytotoxicity via oxidative stress mediators (mainly nitric oxide and hydrogen peroxide) and hepatic natural killer cells. However, certain cancer cells that resist or even deactivate these anti-tumoral defense mechanisms still can adhere to endothelial cells of the hepatic microvasculature through proinflammatory cytokine-mediated mechanisms. During their temporary residence, some of these cancer cells ignore growth-inhibitory factors while respond to proliferation-stimulating factors released from tumor-activated hepatocytes and sinusoidal cells. This leads to avascular micrometastasis generation in periportal areas of hepatic lobules. Hepatocytes and myofibroblasts derived from portal tracts and activated hepatic stellate cells are next recruited into some of these avascular micrometastases. These create a private microenvironment that supports their development through the specific release of both proangiogenic factors and cancer cell invasion- and proliferation-stimulating factors. Moreover, both soluble factors from tumor-activated hepatocytes and myofibroblasts also contribute to the regulation of metastatic cancer cell genes. Therefore, the liver offers a prometastatic microenvironment to circulating cancer cells that supports metastasis development. The ability to resist anti-tumor hepatic defense and to take advantage of hepatic cell-derived factors are key phenotypic properties of liver-metastasizing cancer cells. Knowledge on hepatic metastasis regulation by microenvironment opens multiple opportunities for metastasis inhibition at both subclinical and advanced stages. In addition, together with metastasis-related gene profiles revealing the existence of liver metastasis potential in primary tumors, new biomarkers on the prometastatic microenvironment of the liver may be helpful for the individual assessment of hepatic metastasis risk in cancer patients

Hernia fibroblasts lack β-estradiol induced alterations of collagen gene expression

BACKGROUND: Estrogens are reported to increase type I and type III collagen deposition and to regulate Metalloproteinase 2 (MMP-2) expression. These proteins are reported to be dysregulated in incisional hernia formation resulting in a significantly decreased type I to III ratio. We aimed to evaluate the β-estradiol mediated regulation of type I and type III collagen genes as well as MMP-2 gene expression in fibroblasts derived from patients with or without history of recurrent incisional hernia disease. We compared primary fibroblast cultures from male/female subjects without/without incisional hernia disease. RESULTS: Incisional hernia fibroblasts (IHFs) revealed a decreased type I/III collagen mRNA ratio. Whereas fibroblasts from healthy female donors responded to β-estradiol, type I and type III gene transcription is not affected in fibroblasts from males or affected females. Furthermore β-estradiol had no influence on the impaired type I to III collagen ratio in fibroblasts from recurrent hernia patients. CONCLUSION: Our results suggest that β-estradiol does not restore the imbaired balance of type I/III collagen in incisional hernia fibroblasts. Furthermore, the individual was identified as an independent factor for the β-estradiol induced alterations of collagen gene expression. The observation of gender specific β-estradiol-dependent changes of collagen gene expression in vitro is of significance for future studies of cellular response

Reversibility of liver fibrosis

Liver fibrosis, and its end stage cirrhosis are a major cause of morbidity and mortality and therapeutic options are limited. However, the traditional view of liver disease as an irreversible process is obsolete and it is now evident that the development of liver fibrosis is a dynamic and potentially bidirectional process. Spontaneous resolution of scarring is seen in animal models of liver fibrosis and in human trials in which the stimuli responsible for chronic or repeated hepatic inflammation is successfully removed. Key players in the process are hepatic stellate cells, macrophages, MMPs and their inhibitors Timps. It is also evident that in advanced fibrotic liver disease, specific histological features define what is currently described as "irreversible" fibrosis. This includes the development of paucicellular scars enriched in extensively cross-linked matrix components, such as fibrillar collagen and elastin. Our recent work has focused on the role of macrophage metalloelastase (MMP-12) in the turnover of elastin in reversible and irreversible models of fibrosis. We have shown that elastin turnover in liver injury and fibrosis is regulated by macrophages via Mmp-12 expression, activity and ratio to its inhibitor Timp-1. Failure of elastin degradation, together with increased deposition leads to accumulation of elastin in the fibrotic scars

Endothelin-1 enhances fibrogenic gene expression, but does not promote DNA synthesis or apoptosis in hepatic stellate cells

BACKGROUND: In liver injury, the pool of hepatic stellate cell (HSC) increases and produces extracellular matrix proteins, decreasing during the resolution of fibrosis. The profibrogenic role of endothelin-1 (ET-1) in liver fibrosis remains disputed. We therefore studied the effect of ET-1 on proliferation, apoptosis and profibrogenic gene expression of HSCs. RESULTS: First passage HSC predominantly expressed endothelin A receptor (ETAR) mRNA and 4th passage HSC predominantly expressed the endothelin B receptor (ETBR) mRNA. ET-1 had no effect on DNA synthesis in 1st passage HSC, but reduced DNA synthesis in 4th passage HSC by more than 50%. Inhibition of proliferation by endothelin-1 was abrogated by ETBR specific antagonist BQ788, indicating a prominent role of ETBR in growth inhibition. ET-1 did not prevent apoptosis induced by serum deprivation or Fas ligand in 1st or 4th passage HSC. However, ET-1 increased procollagen α1(I), transforming growth factor β-1 and matrix metalloproteinase (MMP)-2 mRNA transcripts in a concentration-dependent manner in 1st, but not in 4th passage HSC. Profibrogenic gene expression was abrogated by ETAR antagonist BQ123. Both BQ123 and BQ788 attenuated the increase of MMP-2 expression by ET-1. CONCLUSION: We show that ET-1 stimulates fibrogenic gene expression for 1st passage HSC and it inhibits HSC proliferation for 4th passage HSC. These data indicate the profibrogenic and antifibrogenic action of ET-1 for HSC are involved in the process of liver fibrosis

Broad-Spectrum Matrix Metalloproteinase Inhibition Curbs Inflammation and Liver Injury but Aggravates Experimental Liver Fibrosis in Mice

Background Liver fibrosis is characterized by excessive synthesis of extracellular matrix proteins, which prevails over their enzymatic degradation, primarily by matrix metalloproteinases (MMPs). The effect of pharmacological MMP inhibition on fibrogenesis, however, is largely unexplored. Inflammation is considered a prerequisite and important co-contributor to fibrosis and is, in part, mediated by tumor necrosis factor (TNF)-α-converting enzyme (TACE). We hypothesized that treatment with a broad-spectrum MMP and TACE-inhibitor (Marimastat) would ameliorate injury and inflammation, leading to decreased fibrogenesis during repeated hepatotoxin-induced liver injury.Methodology/Principal Findings Liver fibrosis was induced in mice by repeated carbon tetrachloride (CCl4) administration, during which the mice received either Marimastat or vehicle twice daily. A single dose of CCl4was administered to investigate acute liver injury in mice pretreated with Marimastat, mice deficient in Mmp9, or mice deficient in both TNF-α receptors. Liver injury was quantified by alanine aminotransferase (ALT) levels and confirmed by histology. Hepatic collagen was determined as hydroxyproline, and expression of fibrogenesis and fibrolysis-related transcripts was determined by quantitative reverse-transcription polymerase chain reaction. Marimastat-treated animals demonstrated significantly attenuated liver injury and inflammation but a 25% increase in collagen deposition. Transcripts related to fibrogenesis were significantly less upregulated compared to vehicle-treated animals, while MMP expression and activity analysis revealed efficient pharmacologic MMP-inhibition and decreased fibrolysis following Marimastat treatment. Marimastat pre-treatment significantly attenuated liver injury following acute CCl4-administration, whereas Mmp9 deficient animals demonstrated no protection. Mice deficient in both TNF-α receptors exhibited an 80% reduction of serum ALT, confirming the hepatoprotective effects of Marimastat via the TNF-signaling pathway.Conclusions/Significance Inhibition of MMP and TACE activity with Marimastat during chronic CCl4administration counterbalanced any beneficial anti-inflammatory effect, resulting in a positive balance of collagen deposition. Since effective inhibition of MMPs accelerates fibrosis progression, MMP inhibitors should be used with caution in patients with chronic liver diseases