Correlation of Mammography, Ultrasound and Sonoelastographic Findings With Histopathological Diagnosis in Breast Lesions.

Introduction Breast masses range from inflammatory and benign to malignant lesions, varying in different age groups and clinical presentations. Breast imaging techniques leading to prompt and specific diagnosis have been a lifesaver for millions around the globe saving them undue mental stress in inflammatory lesions and preventing early death in case of neoplasms. Here, we compare mammography, ultrasonography (US) and ultrasound elastography in the screening and diagnosis of breast lesions and the usefulness of strain ratio as a non-invasive tool in diagnosing breast malignancies.

Salmonella require the fatty acid regulator PPARδ for the establishment of a metabolic environment essential for long-term persistence.

Host-adapted Salmonella strains are responsible for a number of disease manifestations in mammals, including an asymptomatic chronic infection in which bacteria survive within macrophages located in systemic sites. However, the host cell physiology and metabolic requirements supporting bacterial persistence are poorly understood. In a mouse model of long-term infection, we found that S.

Caspase-11 increases susceptibility to Salmonella infection in the absence of caspase-1.

Inflammasomes are cytosolic multiprotein complexes assembled by intracellular nucleotide-binding oligomerization domain (NOD)-like receptors (NLRs) and they initiate innate immune responses to invading pathogens and danger signals by activating caspase-1 (ref. 1). Caspase-1 activation leads to the maturation and release of the pro-inflammatory cytokines interleukin (IL)-1β and IL-18, as well as lytic inflammatory cell death known as pyroptosis.

Salmonella's long-term relationship with its host.

Host-adapted strains of Salmonella enterica cause systemic infections and have the ability to persist systemically for long periods of time and pose significant public-health problems. Multidrug-resistant S. enterica serovar Typhi (S.

At home with hostility: How do pathogenic bacteria evade mammalian immune surveillance to establish persistent infection?

Bacterial persistence is of major concern as persistent bacterial infections involving bacteria such as Helicobacter pylori, Salmonella enterica serotype Typhi, and Mycobacterium tuberculosis pose significant public health problems worldwide. This report discusses the recent advances in understanding the strategies used by bacteria during persistent infection that allow them to colonize specific sites in the host and evade immune surveillance.

Type I IFN signaling constrains IL-17A/F secretion by gammadelta T cells during bacterial infections.

Recognition of intracellular bacteria by macrophages leads to secretion of type I IFNs. However, the role of type I IFN during bacterial infection is still poorly understood. Francisella tularensis, the causative agent of tularemia, is a pathogenic bacterium that replicates in the cytosol of macrophages leading to secretion of type I IFN.

Non-coding RNAs revealed during identification of genes involved in chicken immune responses.

Recent large-scale cDNA cloning studies have shown that a significant proportion of the transcripts expressed from vertebrate genomes do not appear to encode protein. Moreover, it was reported in mammals (human and mice) that these non-coding transcripts are expressed and regulated by mechanisms similar to those involved in the control of protein-coding genes. We have produced a collection of cDNA sequences from immunologically active tissues with the aim of discovering chicken genes involved in immune mechanisms, and we decided to explore the non-coding component of these immune-related libraries.

Transcriptional profiling reveals a possible role for the timing of the inflammatory response in determining susceptibility to a viral infection.

Using a novel cDNA microarray prepared from sources of actively responding immune system cells, we have investigated the changes in gene expression in the target tissue during the early stages of infection of neonatal chickens with infectious bursal disease virus. Infections of two lines of chickens previously documented as genetically resistant and sensitive to infection were compared in order to ascertain early differences in the response to infection that might provide clues to the mechanism of differential genetic resistance. In addition to major changes that could be explained by previously described changes in infected tissue, some differences in gene expression on infection, and differences between the two chicken lines, were observed that led to a model for resistance in which a more rapid inflammatory response and more-extensive p53-related induction of apoptosis in the target B cells might limit viral replication and consequent pathology.

Drebrin E2 is differentially expressed and phosphorylated in parietal cells in the gastric mucosa.

Developmentally regulated brain proteins (drebrins) are highly expressed in brain where they may regulate actin filament formation in dendritic spines. Recently, the drebrin E2 isoform was detected in certain epithelial cell types including the gastric parietal cell. In gastric parietal cells, activation of HCl secretion is correlated with actin filament formation and elongation within intracellular canaliculi, which are the sites of acid secretion.

Characterisation of a cluster of TRIM-B30.2 genes in the chicken MHC B locus.

We have identified and characterised a cluster of six TRIM-B30.2 genes flanking the chicken BF/BL region of the B complex. The TRIM-B30.