Data on vegetation across forest edges from the FERN (Forest Edge Research Network).

Many studies have focused on vegetation across forest edges to study impacts of edges created by human activities on forest structure and composition, or patterns of vegetation at inherent natural edges. Our objective was to create a database of plant-related variables across different types of edges from various studies (mainly from across Canada, but also in Brazil and Belize) to facilitate edge research. We compiled data on vegetation along more than 300 transects perpendicular to forest edges adjacent to clear-cuts, burned areas, bogs, lakes, barrens, insect disturbances, and riparian areas from 24 studies conducted over the past three decades. Data were compiled for more than 400 plant species and forest structure variables (e.g., trees, logs, canopy cover). All data were collected with a similar sampling design of quadrats along transects perpendicular to forest edges, but with varying numbers of transects and quadrats, and distances from the edge. The purpose for most of the studies was either to determine the distance of edge influence (edge width) or to explore the pattern of vegetation along the edge to interior gradient. We provide data tables for the cover of plant species and functional groups, the species and size of live and dead trees, the density of saplings, maximum height of functional groups and shrub species, and the cover of functional groups at different heights (vertical distribution of vegetation). The Forest Edge Research Network (FERN) database provides extensive data on many variables that can be used for further study including meta-analyses and can assist in answering questions important to conservation efforts (e.g., how is distance of edge influence from created edges affected by different factors?). We plan to expand this database with subsequent studies from the authors and we invite others to contribute to make this a more global database. The data are released under a CC0 license. When using these data, we ask that you cite this data paper and any relevant publications listed in our metadata file. We also encourage you to contact the first author if you are planning to use or contribute to this database.

Knockout of secretin receptor reduces large cholangiocyte hyperplasia in mice with extrahepatic cholestasis induced by bile duct ligation.

UNLABELLED: During bile duct ligation (BDL), the growth of large cholangiocytes is regulated by the cyclic adenosine monophosphate (cAMP)/extracellular signal-regulated kinase 1/2 (ERK1/2) pathway and is closely associated with increased secretin receptor (SR) expression. Although it has been suggested that SR modulates cholangiocyte growth, direct evidence for secretin-dependent proliferation is lacking. SR wild-type (WT) (SR(+/+)) or SR knockout (SR(-/-)) mice underwent sham surgery or BDL for 3 or 7 days. We evaluated SR expression, cholangiocyte proliferation, and apoptosis in liver sections and proliferating cell nuclear antigen (PCNA) protein expression and ERK1/2 phosphorylation in purified large cholangiocytes from WT and SR(-/-) BDL mice. Normal WT mice were treated with secretin (2.5 nmoles/kg/day by way of osmotic minipumps for 1 week), and biliary mass was evaluated. Small and large cholangiocytes were used to evaluate the in vitro effect of secretin (100 nM) on proliferation, protein kinase A (PKA) activity, and ERK1/2 phosphorylation. SR expression was also stably knocked down by short hairpin RNA, and basal and secretin-stimulated cAMP levels (a functional index of biliary growth) and proliferation were determined. SR was expressed by large cholangiocytes. Knockout of SR significantly decreased large cholangiocyte growth induced by BDL, which was associated with enhanced apoptosis. PCNA expression and ERK1/2 phosphorylation were decreased in large cholangiocytes from SR(-/-) BDL compared with WT BDL mice. In vivo administration of secretin to normal WT mice increased ductal mass. In vitro, secretin increased proliferation, PKA activity, and ERK1/2 phosphorylation of large cholangiocytes that was blocked by PKA and mitogen-activated protein kinase kinase inhibitors. Stable knockdown of SR expression reduced basal cholangiocyte proliferation. SR is an important trophic regulator sustaining biliary growth. CONCLUSION: The current study provides strong support for the potential use of secretin as a therapy for ductopenic liver diseases.

Polymorphism in alcohol-metabolizing enzymes, glutathione S-transferases and apolipoprotein E and susceptibility to alcohol-induced cirrhosis and chronic pancreatitis.

BACKGROUND AND AIM: Susceptibility to organ damage induced by alcohol may be due to inherited variation (polymorphism) in ethanol-metabolizing enzymes, or to polymorphisms affecting free radical or lipid metabolism mediated by enzymes such as glutathione S-transferases and apolipoprotein E. The aim was to compare the genotype frequencies of alcohol dehydrogenase-2 (ADH2), ADH3, aldehyde dehydrogenase-2 (ALDH2), cytochrome P450-2E1 (CYP2E1), glutathione S-transferase-M1 (GSTM1), GSTT1, and apolipoprotein E in patients with alcoholic cirrhosis and alcoholic chronic pancreatitis to those in control groups. PATIENTS AND METHODS: The case-control study was restricted to Caucasian adults: 57 with alcoholic cirrhosis, 71 with alcoholic chronic pancreatitis, 57 alcoholics without apparent organ damage and 200 healthy blood donors. Genotypes were determined by restriction fragment length polymorphism after amplification of genomic DNA by polymerase chain reaction. RESULTS: The genotype ADH3*2/*2 was more frequent in patients with cirrhosis (40%) than blood donors (12%; OR 4.92, 95% CI 2.36-10.31) and patients with chronic pancreatitis (8%; OR 7.33, 95% CI 2.54-23.78) but was not significantly different from alcoholic controls (23%; OR 2.27, 95% CI 0.95-5.66). Patients with cirrhosis also had a higher frequency (P < 0.05) of ADH2*1/*1 (100%) than blood donors (92%) and those with chronic pancreatitis (93%). The frequencies of genotypes of ALDH2, CYP2E1, GSTM1, GSTT1 and apolipoprotein E were similar in all groups. CONCLUSION: Alcoholic cirrhosis but not alcoholic chronic pancreatitis is associated with ADH3*2/*2 and perhaps with ADH2*1/*1. Both genes encode less active alcohol-metabolizing enzymes that may be associated with cirrhosis because of delayed formation of acetaldehyde (with higher intakes of alcohol), or diversion of alcohol metabolism through pathways other than ADH.