Atlantic Salmon (Salmo salar) Performance Fed Low Trophic Ingredients in a Fish Meal and Fish Oil Free Diet.

To evolve fish farming in an eco-efficient way, feed production must become less dependent on forage fish-based ingredients and make more use of low trophic level organisms, including microalgae, higher plants, as filter feeding organisms and other ingredients with low competition to established food value chains. Diets nearly free of fish meal and fish oil are not a novelty but are often composed of complex mixtures, containing supplements to meet the farmed animal's nutritional requirements. Sustaining a growing aquaculture production, maintaining at the same time fish health, welfare, and profitability, and meeting strict environmental and food safety demands, is challenging and requires new technologies, great investments, and more knowledge. A benchmarking feeding trial was performed to demonstrate the main effects of four low trophic raw materials on Atlantic salmon (Salmo salar) growth, metabolism, skin health and fillet quality. To this end, a diet was produced to contain commercially relevant levels of fresh high quality organic FM and FO and was used as a control in the trial (FMFO). Heterotrophically produced Schizochytrium limacinum biomass was used to replace organic FO (HM diet). Spray dried cell wall disrupted biomass of the phototrophically cultured diatom Phaeodactylum tricornutum replaced partly FM and FO (PM diet). Black soldier fly (Hermetia illucens) larvae meal and tunicate (Ciona intestinalis) meal, were used to produce the diets BSFL and TM, respectively, replacing large parts of FM as compared to the FMFO. A fifth test diet was produced combining all test raw materials and removing all FM and FO (0FM0FO diet). All test ingredients were well accepted sustaining high growth rates (TGC values near 4) and feed efficiency (FCR values below 0.9) in salmon showing good gut health and normal metabolic responses. However, none of the treatments reached the growth performance of FMFO. Additional differences between test and control treatments were identified in dietary nutrient apparent digestibility, fish biometrics, blood metabolites and fillet and skin composition. Extensive raw material and dietary chemical characterisation was performed to provide insight on potential shortcomings in the novel low trophic level ingredients which can possibly be overcome combining complementary raw materials.

Prevalence of BRCA1 and BRCA2 mutations among clinic-based African American families with breast cancer.

To define the prevalence and relative contributions of BRCA1 and BRCA2 mutations among African American families with breast cancer, we analyzed 28 DNA samples from patients identified through two oncology clinics. The entire coding regions of BRCA1 and BRCA2 were screened by protein truncation test, heteroduplex analysis, or single-stranded conformation polymorphism followed by DNA sequencing of variant bands. Deleterious protein-truncating BRCA1 and BRCA2 mutations were identified in five patients or 18% of the entire cohort. Only 8% (1 of 13) of women with a family history of breast cancer, but no ovarian cancer, had mutations. The mutation rates were higher for women from families with a history of breast cancer and at least one ovarian cancer (three of six, 50%). One woman with a family history of undocumented cancers was also found to carry a deleterious mutation in BRCA2. The spectrum of mutations was unique in that one novel BRCA1 mutation (1625del5) and three novel BRCA2 mutations (1536del4, 6696delTC, and 7795delCT) were identified. No recurrent mutations were identified in this cohort, although one BRCA2 (2816insA) mutation had been previously reported. In addition, two BRCA1 and four BRCA2 missense mutations of unknown significance were identified, one of which was novel. Taken together with our previous report on recurrent mutations seen in unrelated families, we conclude that African Americans have a unique mutation spectrum in BRCA1 and BRCA2 genes, but recurrent mutations are likely to be more widely dispersed and therefore not readily identifiable in this population.

Construction of a 2.8-megabase yeast artificial chromosome contig and cloning of the human methylthioadenosine phosphorylase gene from the tumor suppressor region on 9p21.

Many human malignant cells lack methylthioadenosine phosphorylase (MTAP) enzyme activity. The gene (MTAP) encoding this enzyme was previously mapped to the short arm of chromosome 9, band p21-22, a region that is frequently deleted in multiple tumor types. To clone candidate tumor suppressor genes from the deleted region on 9p21-22, we have constructed a long-range physical map of 2.8 megabases for 9p21 by using overlapping yeast artificial chromosome and cosmid clones. This map includes the type IIFN gene cluster, the recently identified candidate tumor suppressor genes CDKN2 (p16INK4A) and CDKN2B (p15INK4B), and several CpG islands. In addition, we have identified other transcription units within the yeast artificial chromosome contig. Sequence analysis of a 2.5-kb cDNA clone isolated from a CpG island that maps between the IFN genes and CDKN2 reveals a predicted open reading frame of 283 amino acids followed by 1302 nucleotides of 3' untranslated sequence. This gene is evolutionarily conserved and shows significant amino acid homologies to mouse and human purine nucleoside phosphorylases and to a hypothetical 25.8-kDa protein in the pet gene (coding for cytochrome bc1 complex) region of Rhodospirillum rubrum. The location, expression pattern, and nucleotide sequence of this gene suggest that it codes for the MTAP enzyme.

Mapping a putative tumor suppressor gene on chromosome 9 bands p21-p22 with microdissection probes.

Deletions of the short arm of chromosome 9 have been observed in a number of malignant cell lines and primary tumor samples using cytogenetic and molecular techniques. These tumors include acute lymphoblastic leukemias, lymphomas, gliomas, melanomas, mesotheliomas, bladder cancer, and lung cancer. The smallest region of overlap (SRO) of these deletions is thought to contain a tumor suppressor gene. A microdissection library was constructed from bands 9p21-p23 to obtain DNA probes that would be useful in further defining the limits of the deletions. Eight single-copy probes were found to be homozygously deleted in at least 1 of the 10 cell lines examined. The mapping of these 8 clones using a panel of cell lines with deletions revealed that 3 probes mapped telomeric to the SRO and 5 clones mapped centromeric to the SRO.