PIM1 controls GBP1 activity to limit self-damage and to guard against pathogen infection.

Disruption of cellular activities by pathogen virulence factors can trigger innate immune responses. Interferon-γ (IFN-γ)-inducible antimicrobial factors, such as the guanylate binding proteins (GBPs), promote cell-intrinsic defense by attacking intracellular pathogens and by inducing programmed cell death. Working in human macrophages, we discovered that GBP1 expression in the absence of IFN-γ killed the cells and induced Golgi fragmentation.

Conserved Pseudoknots in lncRNA MEG3 Are Essential for Stimulation of the p53 Pathway.

Long non-coding RNAs (lncRNAs) are key regulatory molecules, but unlike with other RNAs, the direct link between their tertiary structure motifs and their function has proven elusive. Here we report structural and functional studies of human maternally expressed gene 3 (MEG3), a tumor suppressor lncRNA that modulates the p53 response. We found that, in an evolutionary conserved region of MEG3, two distal motifs interact by base complementarity to form alternative, mutually exclusive pseudoknot structures ("kissing loops").

Serological evidence of Mycoplasma pneumoniae infection in patients with acute exacerbation of COPD: analysis of 100 hospitalizations.

Purpose: A prospective study was conducted in order to investigate the serologic evidence of Mycoplasma pneumoniae infection in Greek hospitalized patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD). Furthermore, we have assessed the frequency of a number of variables in the group of patients with a serological diagnosis of an acute M. pneumoniae infection compared to patients in whom M.

Chlamydophila pneumoniae infection and COPD: more evidence for lack of evidence?

Chlamydophila pneumoniae has been recognized as a common cause of respiratory tract infections affecting all age groups. The organism has been implicated as an infectious trigger for acute exacerbations of COPD. Moreover, the intracellular existence of this pathogen and the ability to cause chronic respiratory infections have led to a number of studies that investigated its possible association with disease development.

Do proton pump inhibitors attenuate the effect of aspirin on platelet aggregation? A randomized crossover study.

It is common practice to coadminister proton pump inhibitors with aspirin to diminish the risk of upper gastrointestinal bleeding. This is the first study that investigated the potential impact of a proton pump inhibitor on aspirin effects on platelet aggregation. Twenty-four hypertensive subjects eligible for treatment with low-dose enteric-coated aspirin (LDECA) for primary prevention of cardiovascular disease were randomized to receive 100 mg LDECA or 100 mg LDECA plus 30 mg lansoprazole for 4 weeks.