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Alcohol is a major cause of both acute and chronic pancreatitis. Activated pancreatic stellate cells (PSCs) have recently been implicated in the pathogenesis of pancreatic inflammation and fibrosis. Herein, we examined the effect of ethanol and acetaldehyde on the activation of transcription factors and mitogenactivated protein (MAP) kinases in PSCs. PSCs were isolated from rat pancreas tissue and used in their culture-activated, myofibroblast-like phenotype. PSCs were treated with ethanol and acetaldehyde at clinically relevant concentrations (50 mM and 200 M, respectively). Ethanol and acetaldehyde activated activator protein-1 but not nuclear factor-B. In addition, they activated three classes of MAP kinases: extracellular signalregulated kinase 1/2, c-Jun N-terminal kinase/stress-activated protein kinase, and p38 MAP kinase. Ethanol-and acetaldehyde-induced activation of activator protein-1 and MAP kinases was blocked by the antioxidant N-acetyl-cysteine, suggesting a role of oxidative stress in the signal transduction. Ethanol and acetaldehyde induced ␣1(I) procollagen gene expression but did not induce intercellular adhesion molecule-1 and monocyte chemoattractant protein-1. The acetaldehydeinduced increase of ␣1(I) procollagen gene expression was inhibited by the p38 MAP kinase inhibitor 4-(4-fluorophenyl)-2-(4-methylsulfinylphenyl)-5-(4-pyridyl)imidazole (SB203580) but not by the MAP kinase inhibitor 2Ј-amino-

Genetic parameters were estimated for six reproductive traits related to farrowing events in Landrace and Large White pigs; total number born (TNB), number born alive (NBA), number stillborn (NSB), total litter weight at birth (LWB), mean litter weight at birth (MWB), and gestation length (GL). We analyzed 62,534 farrowing records for 10,637 Landrace dams and 49,817 farrowing records for 8,649 Large White dams. Estimated heritabilities of TNB, NBA, NSB, LWB, MWB, and GL by single‐trait repeatability model analyses were 0.12, 0.12, 0.08, 0.18, 0.19, and 0.29, respectively, in Landrace, and 0.12, 0.10, 0.08, 0.18, 0.16, and 0.34, respectively, in Large White. Genetic correlation between NBA and NSB was unfavorable: 0.20 in Landrace and 0.33 in Large White. Genetic correlations of GL with the other five traits were weak: from −0.18 with NSB to −0.03 with NBA in Landrace, and from −0.22 with NSB to −0.07 with NBA in Large White. LWB had a highly favorable genetic correlation with NBA (0.74 in both breeds), indicating the possibility of using LWB for the genetic improvement of NBA.

Galectin-1 is a β-galactoside-binding lectin. Previous studies have shown that galectin-1 was expressed in fibroblasts of chronic pancreatitis and of desmoplastic reaction associated with pancreatic cancer. These fibroblasts are now recognized as activated pancreatic stellate cells (PSCs). Here, we examined the role of galectin-1 in cell functions of PSCs. PSCs were isolated from rat pancreatic tissue and used in their culture-activated phenotype unless otherwise stated. Expression of galectin-1 was assessed by Western blot analysis, RT-PCR, and immunofluorescent staining. The effects of recombinant galectin-1 on chemokine production and proliferation were evaluated. Activation of transcription factors was assessed by EMSA. Activation of MAPKs was examined by Western blot analysis using anti-phosphospecific antibodies. Galectin-1 was strongly expressed in culture-activated but not freshly isolated PSCs. Recombinant galectin-1 increased proliferation and production of monocyte chemoattractant protein-1 and cytokine-induced neutrophil chemoattractant-1. Galectin-1 activated ERK, JNK, activator protein-1, and NF-κB, but not p38 MAPK or Akt. Galectin-1 induced proliferation through ERK and chemokine production mainly through the activation of NF-κB and in part by JNK and ERK pathways. These effects of galectin-1 were abolished in the presence of thiodigalactosie, an inhibitor of β-galactoside binding. In conclusion, our results suggest a role of galectin-1 in chemokine production and proliferation through its β-galactoside binding activity in activated PSCs.

We evaluated the performance of GBLUP including dominance genetic effect (GBLUP-D) by estimating variances and predicting genetic merits in a computer simulation and 2 actual traits (T4 and T5) in pigs. In simulation data, GBLUP-D explained more than 50% of dominance genetic variance. Moreover, GBLUP-D yielded estimated total genetic effects over 1.2% more accurate than those yielded by GBLUP. In particular, when the dominance genetic variance was large, the accuracy could be substantially improved by increasing the number of markers. The dominance genetic variances in T4 and T5 accounted for 9.6% and 6.3% of the phenotypic variances, respectively. Estimates of such small dominance genetic variances contributed little to the improvement of the accuracies of estimated total genetic effects. In both simulation and pig data, there were nearly no differences in the estimates of additive genetic effects or their variance between GBLUP-D and GBLUP. Therefore, we conclude GBLUP-D is a feasible approach to improve genetic performance in crossbred populations with large dominance genetic variation and identify mating systems with good combining ability.

Activated pancreatic stellate cells (PSCs) play a pivotal role in