Transition rates and nuclear structure changes in mirror nuclei 47Cr and 47V

Lifetime measurements in the mirror nuclei 47Cr and 47V were performed by means of the Doppler-shift attenuation method using the multidetector array EUROBALL, in conjunction with the ancillary detectors ISIS and the Neutron Wall. The determined transition strengths in the yrast cascades are well described by full pf shell model calculations.Comment: Latex2e, 11 pages, 3 figure

Transition probabilities in the X(5) candidate 122^{122}Ba

To investigate the possible X(5) character of 122Ba, suggested by the ground state band energy pattern, the lifetimes of the lowest yrast states of 122Ba have been measured, via the Recoil Distance Doppler-Shift method. The relevant levels have been populated by using the 108Cd(16O,2n)122Ba and the 112Sn(13C,3n)122Ba reactions. The B(E2) values deduced in the present work are compared to the predictions of the X(5) model and to calculations performed in the framework of the IBA-1 and IBA-2 models

Helicobacter species in cancers of the gallbladder and extrahepatic biliary tract

Helicobacter species have been found in human bile and biliary tract (BT) tissue and are suspected to cause BT diseases, including gallbladder and extrahepatic cancers, collectively referred to in this work as BT cancers. We conducted a literature review of the epidemiological evidence linking the presence of Helicobacter species in bile or BT biopsies to BT cancers and benign diseases. Reports showed great variability with respect to study methods. Nine studies of BT cancers were identified, all with 30 or fewer BT cancers; eight included cancer-free control subjects and used polymerase chain reaction (PCR) as a means of Helicobacter species detection. In four of these studies, Helicobacter species were detected in patients with BT cancer significantly more frequently than in controls, at least when controls without BT diseases were used. In two studies, no Helicobacter species were detected in either cases or controls. Helicobacter species were also often detected in benign BT diseases such as gallstone disease or chronic cholecystitis. As our current knowledge relies on a few small studies that showed substantial differences, larger studies and more standardised protocols for detecting DNA and antibodies against Helicobacter species are needed to investigate a potential association with BT cancer

Verifying and Quantifying Helicobacter pylori Infection Status of Research Mice [Chapter 19]

available in PMC 2013 January 15Mice used to model helicobacter gastritis should be screened by PCR prior to experimental dosing to confirm the absence of enterohepatic Helicobacter species (EHS) that colonize the cecum and colon of mice. Natural infections with EHS are common and impact of concurrent EHS infection on Helicobacter pylori-induced gastric pathology has been demonstrated. PCR of DNA isolated from gastric tissue is the most sensitive and efficient technique to confirm the H. pylori infection status of research mice after experimental dosing. To determine the level of colonization, quantitative PCR to estimate the equivalent colony-forming units of H. pylori per μg of mouse DNA is less labor-intensive than limiting dilution culture methods. Culture recovery of H. pylori is a less sensitive technique due to its fastidious in vitro culture requirements; however, recovery of viable organisms confirms persistent colonization and allows for further molecular characterization of wild-type or mutant H. pylori strains. ELISA is useful to confirm PCR and culture results and to correlate pro- and anti-inflammatory host immune responses with lesion severity and cytokine gene or protein expression. Histologic assessment with a silver stain has a role in identifying gastric bacteria with spiral morphology consistent with H. pylori but is a relatively insensitive technique and lacks specificity. A variety of spiral bacteria colonizing the lower bowel of mice can be observed in the stomach, particularly if gastric atrophy develops, and these species are not morphologically distinct at the level of light microscopy either in the stomach or lower bowel. Other less commonly used techniques to localize H. pylori in tissues include immunohistochemistry using labeled polyclonal antisera or in situ hybridization for H. pylori rRNA. In this chapter, we will summarize strategies to allow initiation of experiments with helicobacter-free mice and then focus on PCR and ELISA techniques to verify and quantify H. pylori infection of research mice

Loss of integrin αvβ8 on dendritic cells causes autoimmunity and colitis in mice

The cytokine transforming growth factor-β (TGF-β) is an important negative regulator of adaptive immunity1–3. TGF-β is secreted by cells as an inactive precursor that must be activated to exert biological effects4, but the mechanisms that regulate TGF-β activation and function in the immune system are poorly understood. Here we show that conditional loss of the TGF-β-activating integrin α(v)β(8) on leukocytes causes severe inflammatory bowel disease and age-related autoimmunity in mice. This autoimmune phenol-type is largely due to lack of α(v)β(8) on dendritic cells, as mice lacking α(v)β(8) principally on dendritic cells develop identical immunological abnormalities as mice lacking α(v)β(8) on all leukocytes, whereas mice lacking α(v)β(8) on T cells alone are phenotypically normal. We further show that dendritic cells lacking α(v)β(8) fail to induce regulatory T cells (T(R) cells) in vitro, an effect that depends on TGF-β activity. Furthermore, mice lacking α(v)β(8) on dendritic cells have reduced proportions of T(R) cells in colonic tissue. These results suggest that α(v)β(8)-mediated TGF-β activation by dendritic cells is essential for preventing immune dysfunction that results in inflammatory bowel disease and autoimmunity, effects that are due, at least in part, to the ability of α(v)β(8) on dendritic cells to induce and/or maintain tissue T(R) cells