The renin-angiotensin system (RAS) is classically considered to be a protective system for volume balance and is activated during states of volume depletion. Interestingly, one of the major pathways activating the system is the sympathetic nervous system, also the primary mediator of the acute stress response. When one further examines the cells mediating the immune site of the response, which is primarily an inflammatory response leading to defense at a locally injured area, these cells all express the ANG II type 1 receptor (AGTR1). Scattered throughout the literature are reports indicating that acute and chronic stress can activate renin and increase plasma levels of components of the RAS. Moreover, there are reports describing that ANG II can modulate the distribution and function of immune cells. Since the inflammatory response is also implicated to be central in the initiation and progression of vascular damage, we propose in this review that recurrent acute stress and chronic stress can induce a state with inflammation, due to ANG II-mediated activation of inflammatory cells, specifically monocytes and lymphocytes. Such a proposal would explain a lot of the observations regarding RAS components in inflammatory cells. Despite its attractiveness, substantial research in this area would be required to substantiate this hypothesis.

BackgroundErysipelothrix rhusiopathiae is a zoonotic pathogen that causes erysipeloid and is most frequently associated with exposure to domestic swine. Infection of native and prosthetic joints is a rarely reported manifestation.Case presentationWe describe a case of E. rhusiopathiae prosthetic joint infection in a woman with a history of exposure to wild animals in the Canadian Arctic. Patient management involved a 1-stage surgical revision exchange with an antibiotic impregnated cement spacer and 6 weeks of intravenous penicillin G followed by 6 weeks of oral amoxicillin. Ten previously reported cases of E. rhusiopathiae joint infection are reviewed. Recent increases in mortality due to infection with this organism among host animal populations in the Canadian Arctic have generated concern regarding a potential increase in human infections. However, whole genome sequencing (WGS) of the organism was unable to identify a zoonotic origin for this case.ConclusionsConsideration should be given to E. rhusiopathiae as a cause of joint infections if the appropriate epidemiologic and host risk factors exist. Expanded use of WGS in other potential animal hosts and environmental sources may provide important epidemiologic information in determining the source of human infections.

ExtractThis paper reports the cytogenetic investigation of nine children exposed to LSD-25 ,in utero, four children of'other LSD users not exposed in utero, the mothers of these children, and six additional adults taking the drug. In comparison with matched controls, significantly elevated frequencies of chromosomal damage were observed in all the individuals exposed. The frequencies of aberrations, however, were markedly reduced in those children not exposed in utero. Eight structural rearrangements were observed, six dicentric chromosomes and two quadriradial formations, among those individuals exposed to the drug, but none was observed in the controls. In spite of obvious chromosomal aberrations, all of the individuals in this study were apparently healthy and showed no obvious birth defects. Speculation