Infective endocarditis caused by methicillin-resistant Staphylococcus aureus in a young woman after ear piercing: a case report

<p>Abstract</p> <p>Introduction</p> <p>Ear piercing is a common practice among Korean adolescents and young women and usually is performed by nonmedical personnel, sometimes under suboptimal hygienic conditions. Consequently, ear piercing has been associated with various infectious complications, including fatal infective endocarditis. We report a case of infective endocarditis that was caused by community-associated methicillin-resistant <it>Staphylococcus aureus </it>after ear piercing and that was accompanied by a noticeable facial rash.</p> <p>Case presentation</p> <p>A 29-year-old Korean woman underwent ear piercing six days before hospitalization. On admission, she had fever, erythematous maculopapular rashes on her face, signs of generalized emboli, vegetation in her mitral valve, and methicillin-resistant <it>S. aureus </it>bacteremia. On the basis of the blood culture results, she was treated with vancomycin in combination with gentamicin. On day six of hospitalization, a rupture of the papillary muscle of her mitral valve developed, and emergency cardiac surgery replacing her mitral valve with a prosthetic valve was performed. After eight weeks of antibiotic therapy, she was treated successfully and discharged without significant sequelae.</p> <p>Conclusions</p> <p>Numerable cases of body piercing-related infective endocarditis have been reported, and since ear piercing is commonplace nowadays, the importance of risk recognition cannot be overemphasized. In our report, a patient developed infective endocarditis that was caused by methicillin-resistant <it>S. aureus </it>after ear piercing and that was accompanied by an interesting feature, namely facial rash.</p

Confounding and exposure measurement error in air pollution epidemiology

Studies in air pollution epidemiology may suffer from some specific forms of confounding and exposure measurement error. This contribution discusses these, mostly in the framework of cohort studies. Evaluation of potential confounding is critical in studies of the health effects of air pollution. The association between long-term exposure to ambient air pollution and mortality has been investigated using cohort studies in which subjects are followed over time with respect to their vital status. In such studies, control for individual-level confounders such as smoking is important, as is control for area-level confounders such as neighborhood socio-economic status. In addition, there may be spatial dependencies in the survival data that need to be addressed. These issues are illustrated using the American Cancer Society Cancer Prevention II cohort. Exposure measurement error is a challenge in epidemiology because inference about health effects can be incorrect when the measured or predicted exposure used in the analysis is different from the underlying true exposure. Air pollution epidemiology rarely if ever uses personal measurements of exposure for reasons of cost and feasibility. Exposure measurement error in air pollution epidemiology comes in various dominant forms, which are different for time-series and cohort studies. The challenges are reviewed and a number of suggested solutions are discussed for both study domains

Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)1.

In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field

Investigating the cell biological mechanisms regulated by the cellular prion protein

Transmissible spongiform encephalopathies (TSEs) are rare, uniformly fatal neurodegenerative disorders that can affect many mammalian species, including humans. A hallmark of these diseases is the conversion of cellular prion protein (PrPC) into an abnormally folded form. This misfolded PrPC is infectious, since it can provide a template for pathogenic conversion of PrPC in a new host. In addition to any toxicity of the misfolded protein, loss of normal PrPC function could be involved in the neurodegenerative processes. However, the physiological role of PrPC is still poorly understood and this project has aimed to address that lack of knowledge. Out of the many putative functions ascribed to PrPC, the most commonly proposed is that it protects cells from stress. In contrast, I have found that stable transfection of the prion protein gene into SH-SY5Y neuroblastoma cells increases cell death in response to serum removal from the culture medium. Following treatment with several chemical toxins, two out of four stably transfected clones did, generally, display greater viability than untransfected cells that do not express detectable levels of PrPC. However, knockdown of PrPC expression by RNA interference had no effect on this stress resistance, indicating that it may not have been mediated directly by PrPC. Given the lack of robust stress protection afforded by PrPC transfection, proteomic analyses of the cells were carried out to identify alternative processes that were perturbed as a result of PrPC expression. The results obtained suggested roles for PrPC in cytoskeletal organisation and cell cycle regulation. Various proteins involved in cytoskeletal organisation were confirmed by western blotting to be differentially expressed in some or all of the stably transfected clones. Additionally, the expression changes to proteins involved in cell cycle regulation resulted in slower proliferation of the clones compared with untransfected cells, a difference that was reduced following RNA interference-mediated knockdown of PrPC. Taken together, these data suggested that specific growth factor-activated pathways were differentially regulated in the stably transfected clones. One candidate pathway was nerve growth factor (NGF) signalling, which promotes neuronal survival and differentiation as well as regulating various processes outside of the nervous system. PrPC-transfection resulted in altered expression of receptors for NGF, suggesting that the stably transfected clones were, indeed, responding differently to NGF stimulation. However, the molecular mechanism responsible for these expression changes remains to be determined, since co-immunoprecipitation experiments did not identify any physical interactions between PrPC and the NGF receptors. Nonetheless, a role for PrPC in modulating NGF signalling has the potential to explain many of the diverse phenotypic observations in PrPC-null mice and might indicate that loss of PrPC function is an important part of TSE pathogenesis

Testicular atrophy: A complication of non-mumps orchitis after scrotal exploration for presumed testicular torsion

An acute illness related to the scrotum is a common paediatric surgical emergency. Difficulty in ruling out testicular torsion means that scrotal exploration is often performed for other scrotal pathologies, including orchitis. The clinical course of orchitis is usually benign and long-term sequelae are rare. We describe two adolescent boys, previously vaccinated for mumps, whom had scrotal exploration for presumed testicular torsion. Both were found intraoperatively to have orchitis, and both subsequently developed testicular atrophy, within 2 months post-surgery. These cases demonstrate the rare, but potentially devastating, complication of testicular atrophy that may arise in non-mumps orchitis. The causative pathophysiology may involve some degree of testicular compartment syndrome and subsequent ischaemia. Patients must be made aware of the potential for this outcome and be advised on testicular self-examination after surgery

Effects of Panax ginseng on Tumor Necrosis Factor-α-Mediated Inflammation: A Mini-Review

Panax ginseng is one of the most commonly used Chinese medicines in China, Asia and Western countries. The beneficial effects of ginseng have been attributed to the biological activities of its constituents, the ginsenosides. In this review, we summarize recent publications on the anti-inflammatory effects of ginseng extracts and ginsenosides on cellular responses triggered by different inducers including endotoxin, tumor necrosis factor-alpha (TNF-α), interferon-gamma and other stimuli. Proinflammatory cytokines, chemokines, adhesion molecules and mediators of inflammation including inducible nitric oxide synthase, cyclooxygenase-2 and nitric oxide orchestrate the inflammatory response. Ginseng extracts and ginsenosides including Rb1, Rd, Rg1, Rg3, Rh1, Rh2, Rh3 and Rp1 have been reported to have anti-inflammatory properties in different studies related to inflammation. Ginsenosides inhibit different inducers-activated signaling protein kinases and transcription factor nuclear factor-kappaB leading to decreases in the production of cytokines and mediators of inflammation. The therapeutic potential of ginseng on TNF-α-mediated inflammatory diseases is also discussed. Taken together, this summary provides evidences for the anti-inflammatory effects of ginseng extracts and ginsenosides as well as the underlying mechanisms of their effects on inflammatory diseases

New main-group and early transition-metal complexes of mono-pendant arm triazacyclononane ligands

A family of new Group 3, Group 13 and early transition metal complexes of the previously described monoanionic, pendant arm macrocyclic ligands L a, L b and L c are described where HL a = (3,5-dimethyl-2-hydroxybenzyl)-4,7-diisopropyl-1,4,7-triazacyclononane 1a, HL b = (3,5-di-tert-butyl-2-hydroxybenzyl)-4,7-diisopropyl-1,4,7-triazacyclonon ane 1b, and HL c = (3,5-di-tert-butyl-2-hydroxybenzyl)-4,7-dimethyl-1,4,7-triazacyclononane 1c. The ligand precusors 1a-c are quantitatively converted to the corresponding new potassium salts KL a, KL b and KL c 2a-c by reaction with potassium hydride in tetrahydrofuran (THF). An improved synthesis of HL c 1c is also reported. Reaction of KL a-c with Group 13 metal salts MCl 3 (M = Al, Ga or In) gives monomeric derivatives [M(κ 4-L a-c)Cl 2] 3-5 in good yields. The crystal structure of [In(κ 4-L b)Cl 2] 5b has been determined and confirms the six-coordinate, cis-dichloride structures proposed for these complexes. Reaction of KL a-c with TlCl 3 gives the asymmetric, binuclear analogues [Tl(κ 4-L a-c)Cl 2] 2 6a-c. Reaction of [Al(κ 4-L c)Cl 2] 3c with AlCl 3 gives the unstable, five-coordinate cation [Al(κ 4-L c)Cl] + as its AlCl 4- salt 8c. Reaction of KL a-c with MCl 3, (M = Sc or Y) or [MCl 3(THF) 3] (M = Ti, V, Cr) in THF gives generally good yields of the Group 3 cis-dichloride derivatives [M(κ 4-L 1a-c)Cl 2] (M = Sc 8a-c or Y 9b,c) and the early transition metal analogues [M(κ 4-L b,c)Cl 2] (M = Ti 10b,c, V 11b,c or Cr 12b,c). Reaction of HL 1a-c with TlOEt yields the monomeric, four-coordinate thallium(I) derivatives [Tl(κ 4-L 1a-c)] 13a-c as confirmed by the X-ray crystal structures of 13b and 13c. © The Royal Society of Chemistry 2001