[Footbath as treatment of footrot in sheep. Current -situation on Swiss sheep farms]. / Klauenbad zur Bekämpfung der ­Moderhinke bei Schafen. Eine Bestandes­aufnahme bei Schweizer Schafhaltern.

INTRODUCTION: Footrot in sheep should be eradicated in Switzerland in the future. Based on scientific findings, this can be achieved with disinfectant footbaths. It is unknown how many sheep farmers are already using this means and how it is used. The current study evaluated the farm operation, the design of the footbath, the use of disinfectants and footbath with a written survey of a representative sample of all sheep farmers. The sample population was selected randomly, however stratified by language region and herdsize to control for differences between these groups. 45.3% (n=1134) of the distributed questionnaires were received for evaluation. On average 32.8% of the respondents used a footbath. Even on large farms (> 50 animals), which were more frequently affected by footrot, a footbath was available only in 52.6% of the farms in the French-speaking part and 67.7% in the German/Italian speaking part of Switzerland. The footbaths were correctly applied in most respects (e.g., pre-claw cleaning, liquid level and concentration of disinfectants, time in the footbath, post-bath drying phase) in the current study. Most commonly mobile plastic baths were in use. The disinfectants used were mainly formalin, copper and zinc sulfate. The incorrect disposal of the heavy-metal containing copper and zinc sulfate solutions was identified as an important problem: In 59% of the sheep farms the remaining footbath solutions were disposed in the slurry pit or manure storage. In summary the current study recommends (i) to motivate sheep farmers to use a footbath for the treatment and prevention of footrot, and (ii) to replace the currently used disinfectants with substances that are non-toxic to humans, animals and the environment.

INTRODUCTION: Le piétin du mouton doit être, à l'avenir, combattu sur l'ensemble du territoire suisse. Sur la base des connaissances scientifiques, cela peut être fait avec un bain désinfectant pour les onglons. On ignore combien d'éleveurs utilisent déjà cette mesure et comment elle est utilisée. On a cherché, au moyen d'un sondage d'un échantillon représentatif d'éleveurs de moutons, à obtenir la réponse à quatre groupes de questions sur l'exploitation, la construction du pédiluve, l'utilisation de désinfectants et l'usage du bain des onglons. La stratification concernant la région linguistique d'une part et la taille du troupeau d'autre part, permettait de donner la meilleure image possible dans l'échantillon. Avec l'évaluation de 1134 des questionnaires évaluables (45,3% de ceux initialement envoyés) ont a constaté qu'en moyenne 32,8% seulement des exploitants utilisaient un bain des onglons. Même avec les grands troupeaux avec > 50 animaux, qui sont donc plus fréquemment touchés par le piétain, seuls 52,6% des exploitants francophones respectivement 67,7% des germanophones ou des italophones disposent d'un bain. D'autre part, les utilisateurs de bain des onglons appliquent dans la plupart des cas correctement les aspects principaux (par ex.: prélavage des onglons, niveau de liquide et concentration des désinfectants, temps passé dans le bain, phase de séchage après le bain). Les installations les plus communément utilisées étaient les bains mobiles en plastique. La formaline, le sulfate de cuivre et de zinc étaient principalement utilisés comme désinfectants. On constatait un grand manque quant à l'élimination des désinfectants, en particulier des solutions contenant des métaux lourds comme le cuivre ou le zinc. Ainsi, 59,4% des éleveurs ont déclaré jeter les liquides dans la fosse à lisier ou sur le tas de fumier. Les constatations principales sont donc: (i) que les éleveurs de moutons devraient être motivés à utiliser un bain des onglons pour le traitement et la prévention du piétain, et (ii) que le remplacement des désinfectants actuellement utilisés par des substances non toxiques pour l'homme, l'animal et l'environnement est absolument nécessaire.

Molecular cytogenetic characterization of head and neck squamous cell carcinoma and refinement of 3q amplification.

We applied a combination of molecular cytogenetic methods, including comparative genomic hybridization (CGH), spectral karyotyping (SKY), and fluorescence in situ hybridization, to characterize the genetic aberrations in a panel of 11 cell lines derived from head and neck squamous cell carcinoma and 1 cell line derived from premalignant oral epithelium. CGH identified recurrent chromosomal losses at 1p, 3p, 4, 8p, 10p, and 18q; gains at 3q, 5p, 8q, 9q, and 14q; and high-level amplification at 3q13, 3q25-q26, 5q22-q23, 7q21, 8q24, 11q13-q14, 12p13, 14q24, and 20q13.1. Several recurrent translocations including t(1;13)(q10;q10), t(13;13)(q10;q10), t(14;14)(q10;q10), i(8)(q10), and i(9)(q10) and breakpoint clusters at 1p11, 1q21, 3p11, 5q11, 5q13, 6q23, 8p11, 8q11, 9p13, 9q13, 10q11, 11q13, 13q10, 14q10, and 15q10 were identified by SKY. There was a good correlation between the number of aberrations identified by CGH and SKY (r = 0.69), and the analyses were both confirmatory and complementary in their assessment of genetic aberrations. Amplification at 3q26-q27 was identified in 42% of cases. Although SKY defined the derivation of 3q gain, the precise breakpoint remained unassigned. Positional cloning efforts directed at the amplified region at 3q26-q27 identified three highly overlapping nonchimeric yeast artificial chromosome clones containing the apex of amplification. The use of these yeast artificial chromosome clones as a probe for fluorescence in situ hybridization analysis allowed a detailed characterization and quantification of the 3q amplification and refinement of unassigned SKY breakpoints.

The API2/MALT1 fusion product may lead to germinal center B cell lymphomas by suppression of apoptosis.

Low-grade B cell lymphomas of mucosa-associated lymphoid tissue (MALT) represent a distinct clinicopathological entity that arises in a wide variety of extranodal sites. Genetically, MALT lymphomas are characterized by the t(11;18)(q21;q21). The genes involved in this translocation have been identified to be API2 on chromosome 11, which encodes an apoptotic inhibitor, and MALT1, a novel gene on chromosome 18. We identified the t(11;18)(q21;q21) by Southern blot analysis and reverse transcriptase PCR in 42% of a panel of extranodal MALT lymphomas. We also identified the breakpoints within the API2 and MALT1 genes in 7 patients, which revealed a consistent breakpoint after the third baculoviral inhibitor of apoptosis repeat domain within API2, and variable breakpoints in MALT1. We determined the API2/MALT1 fusion transcript in 2 cases by Northern blot analysis and also showed that MALT1 mRNA is constitutively expressed in a variety of human tissues. To understand the functional consequence of the translocation, we determined the pattern of expression of API2 and MALT1 through B lineage differentiation. API2 was expressed only in cell lines which correspond to mature B cells, whereas MALT1 mRNA was detectable in pre-B cells, mature B cells and plasma cells. These results suggest that fusion of MALT1 to API2 mediated by the t(11;18)(q21;q21) may result in an increased inhibition of germinal center B cell apoptosis and subsequent development of MALT lymphomas.

Chromosome 18 breakpoint in t(11;18)(q21;q21) translocation associated with MALT lymphoma is proximal to BCL2 and distal to DCC.

The t(11;18)(q21;q21) translocation has recently been identified as a recurring chromosomal abnormality in a subset of extranodal marginal zone B-cell lymphoma, a low-grade lymphoma of mucosa-associated lymphoid tissue (MALT). Neither the 11q21 nor the 18q21 breakpoints have been characterized by molecular genetic analysis. As a prelude to isolation of the gene(s) involved in this translocation, we have mapped the 18q21 breakpoint region by fluorescence in situ hybridization (FISH) of YAC and PAC clones. We mapped 37 YACs assigned to a 29-cM region within the chromosomal band 18q21. Using nine of these YACs in single- and/or dual-color FISH to analyze three cases of MALT lymphomas with the t(11;18)(q21;q21) translocation, we localized the breakpoints within a 1.6-Mb nonchimeric YAC (938E1). This YAC is useful for the detection of the translocation in metaphase and in interphase cells. A nonchimeric YAC contig of an 8-cM region around the breakpoint comprising nine YACs and a PAC contig of YAC 938E1 were constructed, which enabled the refinement of the breakpoint region in the proximal region of the YAC within a <820-kb segment. This breakpoint is proximal to the BCL2 locus and distal to DCC and DPC4 loci in chromosomal band 18q21.

Molecular delineation of the smallest commonly deleted region of chromosome 5 in malignant myeloid diseases to 1-1.5 Mb and preparation of a PAC-based physical map.

Loss of a whole chromosome 5 or a deletion of the long arm, del(5q), is a recurring abnormality in malignant myeloid diseases. In previous studies, we delineated a commonly deleted segment of approximately 4 Mb within band 5q31 that was flanked by IL9 on the proximal side and D5S166 on the distal side. We have generated a physical map of P1 (PAC), bacterial (BAC), and yeast artificial chromosome (YAC) clones of this interval. The contig consists of 108 clones (78 PACs, 2 BACs, and 28 YACs) to which 125 markers (5 genes, 11 expressed sequence tags, 12 polymorphisms, and 97 sequence-tagged sites) have been mapped. Using PAC clones for fluorescence in situ hybridization analysis of leukemia cells with a del(5q), we have narrowed the commonly deleted segment to 1-1.5 Mb between D5S479 and D5S500. To search for allele loss, we used 7 microsatellite markers within and flanking the commonly deleted segment to examine leukemia cells from 28 patients with loss of 5q, and 14 patients without cytogenetically detectable loss of 5q. In the first group of patients, we detected hemizygous deletions, consistent with the cytogenetically visible loss; no homozygous deletions were detected. No allele loss was detected in patients without abnormalities of chromosome 5, suggesting that allele loss on 5q is the result of visible chromosomal abnormalities. The development of a stable PAC contig and the identification of the smallest commonly deleted segment will facilitate the molecular cloning of a myeloid leukemia suppressor gene on 5q.

Monoclonal, anti-domain and anti-peptide antibodies assign the molecular weight 160,000 granulocyte membrane antigen of the CD66 cluster to a mRNA species encoded by the biliary glycoprotein gene, a member of the carcinoembryonic antigen gene family.

mAb directed against the CD66 cluster of granulocyte differentiation Ag recognize Ag of the carcinoembryonic Ag family. A major Ag in extracts from granulocyte membranes bound by CD66 antibodies exhibits a relative molecular mass of 160,000. According to recent data, this Ag may be a product of the biliary glycoprotein (BGP) gene that belongs to the CEA gene family. As a result of alternative splicing, the BGP gene is transcribed into at least seven distinct mRNA species. To identify splice variants of BGP, antisera were raised against the A2 domain expressed in bacteria and to a peptide comprising the C-terminal 23 amino acids encoded by the 3' exon of the BGP gene. The antisera and an mAb specific for members of the BGP family were used to identify potential BGP splice variants in granulocyte membranes. For comparison, the binding of antibodies to Ag purified from human bile was investigated. In the membrane preparation from granulocytes, the only Ag identified by the mAb, the domain antiserum and the peptide antiserum, was the Ag of M(r) 160,000 recognized by a CD66 antibody. These results indicate that the M(r) 160,000 granulocyte membrane Ag of the CD66 cluster is the product of the BGP-specific mRNA containing all coding sequences of the BGP gene. Among two major biliary glycoproteins present in human bile, the M(r) 115,000 Ag contains the A2 domain, whereas the domain is lacking in the "classical" biliary glycoprotein of M(r) 85,000. None of the bile Ag bound the peptide antiserum.