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The Dutch policy objective of a fully sustainable livestock sector without mutilations by 2023 is not compatible with the routine practice of tail docking to minimize the risk of tail biting. To examine farmer attitudes towards docking, a telephone survey was conducted among 487 conventional and 33 organic Dutch pig farmers. 'Biting' (of tails, ears, or limbs) was identified by the farmers as a main welfare problem in pig farming. About half of the farmers reported to have no tail biting problems in their own herd. When farmers did report problems, they most often reported figures between 1 and 5 % of the animals. High incidences of tail biting were anticipated when trying to keep undocked pigs. Enrichment materials used in the conventional sector included mainly chains (52-63 % of the farms) and hanging rubber or plastic balls (22-30 %). Straw, sawdust, or wood shavings was hardly provided in conventional pig farming (2-3 %), in contrast to organic farming (88-100 % of farms). Conventional pig farmers feel a curly tail is not very important for sustainable pig farming. They consider enrichment to be less effective and tail docking to be less stressful for them and their piglets than their organic colleagues do. Pig farmers identified climate as a main risk factor for tail biting as opposed to enrichment. The objective of reducing routine tail docking requires solutions for dealing with tail biting problems at the farm level. In this process, transfer of scientific knowledge about enrichment materials and other measures to prevent and cure tail biting is critical, as is a change in farmer attitudes and awareness of the moral issues involved. [ABSTRACT FROM AUTHOR]

Background: Four-and-a-half LIM domains protein 2 (FHL2) is a component of the focal adhesion structures and has been suggested to have a role in cancer progression. It has been shown to be overexpressed in the colorectal cancer (CRC).Methods: Here, we examined a possible prognostic value of FHL2 in CRC. Immunohistochemistry for FHL2 was performed on 296 CRCs without distant metastases at the time of surgery. Staining in the epithelial compartment was quantitatively evaluated using image analysis, and results were related to clinical variables. Antibody specificity was tested using small-interfering RNA transfection in hTERT-immortalised myofibroblasts.Results: Varying degrees of cytoplasmic FHL2 expression by neoplastic epithelial cells were detectable in all cases. Higher FHL2 expression in the epithelial compartment was an independent adverse prognostic factor. Multivariate Cox analysis shows that expression in the tumour invasion front (P<0.001) as well as in the centre of the tumour (P<0.001) was associated with metachronous metastases independently of the clinicopathological variables; expression in the tumour invasion front was also associated with overall survival independently of the clinicopathological variables (P<0.01).Conclusion: Higher FHL2 expression is involved in CRC progression and correlates with the development of metachronous metastases and overall survival, suggesting that FHL2 is an independent adverse prognostic indicator for CRC. [ABSTRACT FROM AUTHOR]

Background: Persistent subretinal fluid after rhegmatogenous retinal detachment (RRD) surgery is responsible for delayed recovery, and may affect the final visual outcome. Cause, consequences, and treatment remain elusive. Design: Literature review and case series. Methods: We reviewed the pathophysiological principles and therapeutic options from the literature, and we report the results from a subretinal fluid cytology study. Nine eyes from nine patients with macula-involving RRD underwent surgical repair. The cellular content of subretinal fluid (SRF) was studied by electron microscopy and anti-rhodopsin immunostaining. All eyes were assessed postoperatively with optical coherence tomography for the detection of persistent submacular fluid (PSF) (Ethics Committee Ghent University Hospital, registration number B6702006169). Results: Certain patient characteristics as well as surgical methods were implicated. PSF appears to occur more frequently in patients with longstanding detachments treated with buckling surgery. Several therapeutic options have been suggested but safety and efficacy remain unclear. We found PSF in three eyes on postoperative OCT scans, which corresponded to the three cell-rich subretinal samples. Conclusions: PSF after successful RRD repair seems to be related to fluid composition. We hypothesize, in the absence of an effective treatment, that a modified surgical drainage, including a washout of the subretinal space, could evacuate the subretinal fluid more completely, and may prevent this complication. [ABSTRACT FROM AUTHOR]

Cell–cell adhesion is an elementary process in normal epithelial cellular architecture. Several studies have shown the role mediated by cadherins in this process, besides their role in the maintenance of cell polarity, differentiation and cell growth. However, during tumour progression, these molecules are frequently altered. In breast cancer, tumours that overexpress P-cadherin usually present a high histological grade, show decreased cell polarity and are associated with worse patient survival. However, little is known about how this protein dictates the very aggressive behaviour of these tumours. To achieve this goal, we set up two breast cancer cell models, where P-cadherin expression was differently modulated and analysed in terms of cell invasion, motility and migration. We show that P-cadherin overexpression, in breast cancer cells with wild-type E-cadherin, promotes cell invasion, motility and migration. Moreover, we found that the overexpression of P-cadherin induces the secretion of matrix metalloproteases, specifically MMP-1 and MMP-2, which then lead to P-cadherin ectodomain cleavage. Further, we showed that soluble P-cadherin fragment is able to induce in vitro invasion of breast cancer cells. Overall, our results contribute to elucidate the mechanism underlying the invasive behaviour of P-cadherin expressing breast tumours. [ABSTRACT FROM AUTHOR]

From the conditioned medium of the human colon carcinoma cells, HT-29 5M21 (CM-5M21), expressing a spontaneous invasive phenotype, tumor-associated trypsin inhibitor (TATI) was identified and characterized by proteomics, cDNA microarray approaches and functional analyses. Both CM-5M21 and recombinant TATI, but not the K18Y-TATI mutant at the protease inhibitor site, trigger collagen type I invasion by several human adenoma and carcinoma cells of the colon and breast, through phosphoinositide-3-kinase, protein kinase C and Rho-GTPases/Rho kinase-dependent pathways. Conversely, the proinvasive action of TATI in parental HT29 cells was alleviated by the TATI antibody PSKAN2 and the K18Y-TATI mutant. Stable expression of K18Y-TATI in HT-29 5M21 cells downregulated tumor growth, angiogenesis and the expression of several metastasis-related genes, including CSPG4 (13.8-fold), BMP-7 (9.7-fold), the BMP antagonist CHORDIN (5.2-fold), IGFBP-2 and IGF2 (9.6- and 4.6-fold). Accordingly, ectopic expression of KY-TATI inhibited the development of lung metastases from HT-29 5M21 tumor xenografts in immunodeficient mice. These findings identify TATI as an autocrine transforming factor potentially involved in early and late events of colon cancer progression, including local invasion of the primary tumor and its metastatic spread. Targeting TATI, its molecular partners and effectors may bring novel therapeutic applications for high-grade human solid tumors in the digestive and urogenital systems.Oncogene (2008) 27, 4024–4033; doi:10.1038/onc.2008.42; published online 3 March 2008 [ABSTRACT FROM AUTHOR]

TFF1 is overexpressed in inflammatory diseases and human cancers of the digestive and urogenital systems. To examine the transforming potential of TFF1 in human colon epithelial cells, premalignant PC/AA/C1 adenoma cells (PC) derived from a patient with familial adenomatous polyposis (FAP) were transformed by the TFF1 cDNA and used as a model of the adenoma–carcinoma transition. Constitutive expression of TFF1 increased anchorage-independent cell growth in soft agar, and induced or potentiated the growth of colon PC-TFF1 and kidney MDCKts.src-TFF1 tumor xenografts in athymic mice. This resulted in reduction of thapsigargin-induced apoptosis and promotion of collagen type I invasion through several oncogenic pathways. Using the differential display approach to identify TFF1 target genes, we found that the dual specific phosphatases Cdc25A and B implicated in cell cycle transitions are strongly upregulated under active forms in both PC-TFF1 and HCT8/S11-TFF1 colon cancer cells. Accordingly, TFF1 expression is absent in normal human colon crypts but is induced in correlation with Cdc25a and b transcript levels and tumor grade in familial and sporadic colon adenomas and carcinomas. We propose that TFF1 and Cdc25A-B cooperate with other dominant oncogenic pathways to induce the adenoma and adenocarcinoma transitions. Agents that target TFF1/Cdc25 signaling pathways may be useful for treating patients with TFF1-positive solid tumors.Oncogene (2006) 25, 6628–6636. doi:10.1038/sj.onc.1209665; published online 22 May 2006 [ABSTRACT FROM AUTHOR]

Endothelial cells express two dependent intercellular adhesion molecules: vascular endothelial (VE)-cadherin, specific for endothelial cells, and N-cadherin, also present in neuronal, lens, skeletal and heart muscle cells, osteoblasts, pericytes and fibroblasts. While there exists a vast amount of evidence that VE-cadherin promotes angiogenesis, the role of N-cadherin still remains to be elucidated. We found that a soluble 90-kDa fragment N-cadherin promotes angiogenesis in the rabbit cornea assay and in the chorioallantoic assay when cleaved enzymatically from the extracellular domain of N-cadherin. Soluble N-cadherin stimulates migration of endothelial cells in the wound healing assay and stimulates phosphorylation of extracellular regulated kinase. In vitro experiments with PD173074 and knock-down of N-cadherin and fibroblast growth factor (FGF)-receptor, showed that the pro-angiogenic effect of soluble N-cadherin is N-cadherin- and FGF-receptor-dependent. Our results suggest that soluble N-cadherin stimulates migration of endothelial cells through the FGF-receptor. [ABSTRACT FROM AUTHOR]

The concept of natural behavior is a key element in current Dutch policy-making on animal welfare. It emphasizes that animals need positive experiences, in addition to minimized suffering. This paper interprets the concept of natural behavior in the context of the scientific framework for welfare assessment. Natural behavior may be defined as behavior that animals have a tendency to exhibit under natural conditions, because these behaviors are pleasurable and promote biological functioning. Animal welfare is the quality of life as perceived by the animal. Animals have evolved cognitive-emotional systems (''welfare needs'') to deal with a variable environment. Animals do not only have so-called physiological needs such as the need for food, water, and thermal comfort. They also need to exercise certain natural behaviors such as rooting or nest-building in pigs, and scratching or dust-bathing in poultry. All needs must be taken into account in order to assess overall welfare. The degree of need satisfaction and frustration can be assessed from scientific information about the intensity, duration, and incidence of (welfare) performance criteria such as measurements of behavior and/or (patho)physiology. Positive welfare value relates to how animals are inclined to behave under natural conditions, in preference tests, and in consumer-demand studies. Negative welfare value relates to stress, frustration, abnormal behavior, aggression, and reduced fitness. Examples are given to illustrate how the need to perform natural behaviors can be assessed following the general principles for welfare assessment, providing a first approximation of how different natural behaviors affect animal welfare. [ABSTRACT FROM AUTHOR]

Investigating three somatostatin receptor (SSTR)-positive (+) human breast cancer cell lines, Xu et al. found a time- and dose-dependent up- or down-regulation of SSTR2 mRNA expression by 17β-oestradiol (E2) or the anti-oestrogen tamoxifen, respectively, in the two oestrogen receptor-positive (ER+) cell lines but not in the oestrogen receptor-negative (ER-) cell line. This study aimed to confirm the findings of Xu et al. at the protein level by means of western blotting and saturation binding studies using 99mTc-depreotide (NeoSpect). The ER+/SSTR+ ZR75-1 and T47D and SSTR+/ER- MDA MB231 breast cancer cell lines were exposed to 1 nM E2 or a combination of 1 nM E2 plus 100 nM tamoxifen or ICI 182 780 (Faslodex) for 48 h. Exposed and non-exposed controls were incubated with increasing concentrations of 99mTc-depreotide (0.5 nM–15 nM) in the absence and the presence of 20 μM of octreotide. Scatchard-Rosenthal plots were derived using commercially available software. SSTR subtypes responsible for E2-induced changes in 99mTc-depreotide binding were identified by means of western blotting. Mean Kd values for 99mTc-depreotide were 13 nM, 7 nM and 4 nM for T47D, ZR75-1 and MDA MB231 cells, respectively. After stimulation with E2, the ER+ cell line T47D demonstrated a mean increase of 81% (P<0.05) in 99mTc-depreotide binding. Adding the partial agonist tamoxifen and full antagonist ICI 182 780 to E2 blocked the induced increase in T47D cells, either reducing SSTR expression or restoring it to control levels. ZR75-1 cells stimulated with E2 showed a mean decrease in 99mTc-depreotide binding of 36% as compared to control cells; this difference, however, proved to be not statistically significant. Similarly, Bmax values did not change in ZR75-1 cells exposed to E2 in combination with an ER antagonist as compared to control cells. Finally, no influence of E2 on 99mTc-depreotide binding was observed in the ER- cell line MDA MB231. Both SSTR2 and SSTR5 were expressed at high levels in T47D cells and ZR75-1 cells. SSTR5 drastically increased in the absence of E2 and was restored to the original detection level after E2 treatment. The presented findings support an oestrogen-dependent regulation of SSTR expression in breast cancer cell lines. [ABSTRACT FROM AUTHOR]

MCF-7 human breast cancer cells express E-cadherin and show, at least in some circumstances, E-cadherin-dependent cell-cell adhesion (Bracke et al., 1993). The MCF-7/AZ variant spontaneously displays E-cadherin-dependent fast aggregation; in the MCF-7/6 variant, E-cadherin appeared not to be spontaneously functional in the conditions of the fast aggregation assay, but function could be induced by incubation of the suspended cells in the presence of insulinlike growth factor I (IGF-I) (Bracke et al., 1993). E-cadherin from MCF-7 cells was shown to contain sialic acid. Treatment with neuraminidase was shown to remove this sialic acid, as well as most of the sialic acid present at the cell surface. Applied to MCF-7/AZ, and MCF-7/6 cells, pretreatment with neuraminidase abolished spontaneous as well as IGF-I induced, E-cadherin-dependent fast cell-cell adhesion of cells in suspension, as measured in the fast aggregation assay. Treatment with neuraminidase did not, however, inhibit the possibly different, but equally E-cadherin-mediated, process of cell-cell adhesion of MCF-7 cells on a flat plastic substrate as assessed by determining the percentage of cells remaining isolated (without contact with other cells) 24 h after plating. [ABSTRACT FROM AUTHOR]

A letter to the editor is presented in response to the articles, "Peritoneal pH during laparoscopy is dependent on ambient gas environment: helium and nitrous oxide do not cause peritoneal acidosis" and "Carbon dioxide pneumoperitoneum causes severe peritoneal acidosis, unaltered by heating, humidification, or bicarbonate in a porcine model," both by Y.T. Wong and colleagues.