Mapping rare protein-coding variants on multi-organ imaging traits.

Human organ structure and function are important endophenotypes for clinical outcomes. Genome-wide association studies (GWAS) have identified numerous common variants associated with phenotypes derived from magnetic resonance imaging (MRI) of the brain and body. However, the role of rare protein-coding variations affecting organ size and function is largely unknown.

Identification of a novel porcine Teschovirus 2 strain as causative agent of encephalomyelitis in suckling piglets with high mortality in China.

Background: Porcine Teschovirus (PTV), also named Teschovirus A, is prevalent in pig populations, mainly causing neurological symptoms, diarrhea, pneumonia, and reproductive failure, however the morbidity and mortality are usually low in pig farms.

Case Presentation: In this study, we reported a PTV outbreak investigation in one large-scale pig farm in China with severe symptoms including diarrhea, lethargy, locomotor ataxia, nystagmus, paralysis of the hind limbs, and coma in piglets. More importantly, the mortality reached 38% in suckling pigs, which is remarkably high in PTV history.

Pre-treatment with phages achieved greater protection of mice against infection with Shiga toxin-producing Escherichia coli than post-treatment.

Shiga toxin-producing Escherichia coli (STEC) is a group of pathogen that can cause various diseases in both humans and animals, such as watery diarrhea, hemorrhagic colitis, and uremia syndrome. Due to the serious situation of antibiotic resistance, phage therapy is considered to have a great potential in combating bacterial diseases. In this study, three phages (NJ-10, NJ-20, and NJ-38) with strong abilities to lyse virulent STEC strain CVCC193 cells in vitro were isolated.

Microencapsulated phages show prolonged stability in gastrointestinal environments and high therapeutic efficiency to treat Escherichia coli O157:H7 infection.

Escherichia coli (E. coli) O157:H7 bacterial infection causes severe disease in mammals and results in substantial economic losses worldwide. Due to the development of antibiotic resistance, bacteriophage (phage) therapy has become an alternative to control O157:H7 infection.

Novel Host Recognition Mechanism of the K1 Capsule-Specific Phage of : Capsular Polysaccharide as the First Receptor and Lipopolysaccharide as the Secondary Receptor.

K1 capsule-specific phages of Escherichia coli have been reported in recent years, but the molecular mechanism involved in host recognition of these phages remains unknown. In this study, the interactions between PNJ1809-36, a new K1-specific phage, and its host bacterium, E. coli DE058, were investigated.

and in Prophage phiv142-3 Enhance the Iron-Acquisition Ability and Resistance of Avian Pathogenic Strain DE142 to Serum.

Avian pathogenic (APEC), an extraintestinal pathogenic (ExPEC), is the causative agent of avian colibacillosis, a disease that causes huge economic losses in the poultry industry and is characterized by infection through respiratory tract colonization followed by bacteraemia. A previous study in our lab demonstrated that phiv142-3 enhanced the survival ability of APEC strain DE142 in chickens serum. However, the mechanism of this affect has not been completely revealed.

Prophage phiv205-1 facilitates biofilm formation and pathogenicity of avian pathogenic Escherichia coli strain DE205B.

Avian colibacillosis caused by avian pathogenic Escherichia coli (APEC) causes significant economic losses to the poultry industry worldwide and is also a leading potential threat to human health. Bacteriophages integrate into the host bacterial chromosome, and are an important source of genetic variation and have a major impact on bacterial evolution. Previously, we predicted prophage phiv205-1 in APEC strain DE205B.

orf20 in prophage phiv142-3 contributes to the adhesion and colonization ability of avian pathogenic Escherichia coli strain DE142 by affecting the formation of flagella and I fimbriae.

We have previously demonstrated that prophage phiv142-3 enhances the colonization ability of avian pathogenic Escherichia coli (APEC) strain DE142. However, the mechanism of this action remains unknown. In this study, we demonstrate that deletion of phiv142-3 orf20 leads to a decrease in the survival ability in chicken serum, adhesion, and ability to invade DF-1 cells of mutant strain DE142Δorf20 compared with that of wild type (WT).