Cloning, sequencing, and identification of Phage 16, an unknown salmonella or EHEC (enterohemorrhagic E. coli) bacteriophage

Bacteriophage are viruses that infect, replicate and kill bacteria. Salmonella and EHEC food poisoning are caused by Salmonella and E. coli bacteria. Bacteriophage can be used to prevent food poisoning by application to food products or processing machinery. Bacteriophage P16 specifically infects Salmonella and E. coli bacteria. We cloned fragments of the P16 genome, sequence the DNA and used bioinformatics to identify P16. Phage P16 is a Salmonella phage similar to Stitch. A phylogenetic tree inferring relationships of P16 and other bacteriophage was created

Cloning and sequencing of the depolymerase-like gene from Bacteriophage J25

Bacteriophage are viruses that infect, replicate and kill bacteria. Salmonella and EHEC food poisoning are caused by Salmonella and E. coli bacteria. Bacteriophage can be used to prevent food poisoning by application to food products or processing machinery. Bacteriophage J25 specifically infects Salmonella and E. coli bacteria. We cloned fragments of the J25 genome, sequence the DNA and used bioinformatics to identify J25. We used genome data from similar bacteriophage in Genbank to design primers to amplify the depolymerase-like gene. We amplified and cloned this gene. When expressed, the gene product will be test with bacteriophage food treatment where it should augment bacteriophage killing

Near-field heat transfer in a scanning thermal microscope

We present measurements of the near-field heat transfer between the tip of a thermal profiler and planar material surfaces under ultrahigh vacuum conditions. For tip-sample distances below 10-8 m our results differ markedly from the prediction of fluctuating electrodynamics. We argue that these differences are due to the existence of a material-dependent small length scale below which the macroscopic description of the dielectric properties fails, and discuss a corresponding model which yields fair agreement with the available data. These results are of importance for the quantitative interpretation of signals obtained by scanning thermal microscopes capable of detecting local temperature variations on surfaces

Endosomal integrin signals for survival.

The mechanisms underlying integrin-dependent signalling are a topic of continued study. Endocytosed integrins are now shown to drive assembly of signalling complexes on the cytoplasmic face of endocytic membranes to promote cancer cell survival and increase metastatic capacity following cell detachment

Snipe taxonomy based on vocal and non-vocal sound displays: the South American Snipe is two species

We analysed breeding sounds of the two subspecies of South American Snipe Gallinago paraguaiae paraguaiae and Gallinago paraguaiae magellanica to determine whether they might be different species: loud vocalizations given on the ground, and the tail‐generated Winnow given in aerial display. Sounds of the two taxa differ qualitatively and quantitatively. Both taxa utter two types of ground call. In G. p. paraguaiae, the calls are bouts of identical sound elements repeated rhythmically and slowly (about five elements per second (Hz)) or rapidly (about 11 Hz). One call of G. p. magellanica is qualitatively similar to those of G. p. paraguaiae but sound elements are repeated more slowly (about 3 Hz). However, its other call type differs strikingly: it is a bout of rhythmically repeated sound couplets, each containing two kinds of sound element. The Winnow of G. p. paraguaiae is a series of sound elements that gradually increase in duration and energy; by contrast, that of G. p. magellanica has two or more kinds of sound element that roughly alternate and are repeated as sets, imparting a stuttering quality. Sounds of the related Puna Snipe (Gallinago andina) resemble but differ quantitatively from those of G. p. paraguaiae. Differences in breeding sounds of G. p. paraguaiae and G. p. magellanica are strong and hold throughout their geographical range. Therefore we suggest that the two taxa be considered different species: G. paraguaiae east of the Andes in much of South America except Patagonia, and G. magellanica in central and southern Chile, Argentina east of the Andes across Patagonia, and Falklands/Malvinas.Fil: Miller, Edward H.. Memorial University Of Newfoundland; CanadáFil: Areta, Juan Ignacio. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Salta. Instituto de Bio y Geociencias del NOA. Universidad Nacional de Salta. Facultad de Ciencias Naturales. Museo de Ciencias Naturales. Instituto de Bio y Geociencias del NOA; ArgentinaFil: Jaramillo, Alvaro. San Francisco Bay Bird Observatory; Estados UnidosFil: Imberti, Santiago. Asociación Ambiente Sur, Rio Gallegos; ArgentinaFil: Matus, Ricardo. Kilómetro 7 Sur; Chil

Colorectal Hyperplasia and Dysplasia Due to Human Carcinoembryonic Antigen (CEA) Family Member Expression in Transgenic Mice

CEA and CEACAM6 are immunoglobulin family intercellular adhesion molecules that are up-regulated without structural mutations in approximately 70% of human cancers. Results in in vitro systems showing tumorigenic effects for these molecules suggest that this correlation could indicate an instrumental role in tumorigenesis. To test whether this applies in vivo, transgenic mice harboring 187 kb of the human genome containing four CEA family member genes including the CEA and CEACAM6 genes were created and their copy numbers increased by mating until colonocyte expression levels reached levels seen in human colorectal carcinomas. The colonocyte surface level of integrin α5 and the activation of AKT increased progressively with the expression levels of CEA/CEACAM6. Colonic crypts showed a progressive increase in colonocyte proliferation, an increase in crypt fission, and a strong inhibition of both differentiation and anoikis/apoptosis. All transgenic mice showed massively enlarged colons comprising a continuous mosaic of severe hyperplasia, dysplasia and serrated adenomatous morphology. These results suggest that up-regulated non-mutated adhesion molecules could have a significant instrumental role in human cancer

A mutation in Nischarin causes otitis media via LIMK1 and NF-κB pathways

Otitis media (OM), inflammation of the middle ear (ME), is a common cause of conductive hearing impairment. Despite the importance of the disease, the aetiology of chronic and recurrent forms of middle ear inflammatory disease remains poorly understood. Studies of the human population suggest that there is a significant genetic component predisposing to the development of chronic OM, although the underlying genes are largely unknown. Using N-ethyl-N-nitrosourea mutagenesis we identified a recessive mouse mutant, edison, that spontaneously develops a conductive hearing loss due to chronic OM. The causal mutation was identified as a missense change, L972P, in the Nischarin (NISCH) gene. edison mice develop a serous or granulocytic effusion, increasingly macrophage and neutrophil rich with age, along with a thickened, inflamed mucoperiosteum. We also identified a second hypomorphic allele, V33A, with only modest increases in auditory thresholds and reduced incidence of OM. NISCH interacts with several proteins, including ITGA5 that is thought to have a role in modulating VEGF-induced angiogenesis and vascularization. We identified a significant genetic interaction between Nisch and Itga5; mice heterozygous for Itga5-null and homozygous for edison mutations display a significantly increased penetrance and severity of chronic OM. In order to understand the pathological mechanisms underlying the OM phenotype, we studied interacting partners to NISCH along with downstream signalling molecules in the middle ear epithelia of edison mouse. Our analysis implicates PAK1 and RAC1, and downstream signalling in LIMK1 and NF-κB pathways in the development of chronic OM

World War II Pearl Harbor Survivors Oral History Project

Interview with B. S. "Bud" Reddig, a United States Army veteran from Plumerville, Arkansas. Reddig explains his experiences as a member of K Company, 21st Infantry stationed at Schofield Barracks during the Japanese attack there and on Pearl Harbor on December 7, 1941