ABSTRACT
Infective endocarditis (IE) is an uncommon, life-threatening systemic disorder with significant morbidity and persistently high mortality. The age of the peak incidence of IE has shifted from 45 years in the 1950s to 70 years at the present time, and elderly people have a five-fold higher risk of IE than the general adult population. Elderly IE patients demonstrate a higher prevalence of coagulase-negative staphylococci, enterococci and Streptococcus bovis, and lower rates of infection by viridans group streptococci. Methicillin resistance is more prevalent in elderly patients as a consequence of increased nosocomial acquisition. The elderly are a vulnerable group in whom diagnosis is often difficult on account of non-specific presenting features and where higher prevalence of comorbidities contributes to adverse outcomes. Treatment of older patients with IE presents specific challenges associated with prolonged antibiotic therapy, and access to surgery may be denied on account of advanced age and attendant comorbidities. This practical review covers all aspects of elderly IE, including clinical and microbiological diagnosis and appropriate diagnostic procedures, initial antibiotic selection, antibiotic prophylaxis, considerations about antibiotic therapy and surgery.
Subject(s)
Endocarditis, Bacterial/diagnosis , Endocarditis, Bacterial/therapy , Age Factors , Anti-Bacterial Agents/therapeutic use , Antibiotic Prophylaxis , Endocarditis, Bacterial/microbiology , Enterococcus/isolation & purification , Humans , Staphylococcus/isolation & purification , Streptococcus bovis/isolation & purificationABSTRACT
INTRODUCTION: We evaluated the congenital malformation rate in the progeny of the personnel of the Salto di Quirra military base in Sardinia. METHODS: During 2011, we gathered questionnaire information on the reproductive history of 389 employees, more then 99% of those eligible for routine health surveillance. RESULTS: the observed congenital malformation rate (20.1 x 10(-3), 95% CI 6.3 - 33.8) was lower than that reported by the Italian Registries of Congenital Malformations, and it did not vary by exposure to radiofrequency, elf electromagnetic fields, and solvents, and by jobs associated with alleged exposure to nanoparticles or alpha radiation. CONCLUSIONS: Our findings suggest that the documented or alleged occupational exposures among the PISQ workforce did not increase the congenital malformation rate in the progeny.
Subject(s)
Congenital Abnormalities/epidemiology , Congenital Abnormalities/genetics , Military Personnel , Adult , Humans , Italy , Military Facilities , Risk AssessmentABSTRACT
INTRODUCTION: We explored the association between use of mobile phones and lymphoma risk in a case-control study. METHODS: We conducted unconditional logistic regression analysis in 322 lymphoma cases and 446 population controls, adjusting by age, gender and education. RESULTS: Risk of lymphoma (all types; OR = 1.5; 95% CI 1.0 - 2.1), and chronic lymphocytic leukaemia (OR = 1.8; 95% CI 1.0 - 3.4) was elevated in subjects reporting use of mobile phones, but it decreased with duration of use, and years from first purchase. CONCLUSIONS: Our contradictory findings would not support the aetiological nature of the observed associations.
Subject(s)
Cell Phone/statistics & numerical data , Lymphoma/classification , Lymphoma/epidemiology , Adult , Aged , Case-Control Studies , Humans , Middle Aged , Risk FactorsABSTRACT
BACKGROUND: Angiotensin II (Ang II) has been shown to be implicated in the development of renal fibrosis in several forms of chronic glomerulonephritides, but the precise mechanisms of its effects remain unclear. It has recently been reported that Ang II stimulates the expression of plasminogen activator inhibitor-1 (PAI-1) in several cell lines. PAI-1 is a major physiological inhibitor of the plasminogen activator/plasmin system, a key regulator of fibrinolysis and extracellular matrix (ECM) turnover. PAI-1 induction by Ang II in endothelial cells seems to be mediated by Ang IV via a receptor that is different from Ang II type 1 and 2 receptors (AT1 and AT2). METHODS: In this study, we sought to evaluate the effects of Ang IV on PAI-1 gene and protein expression in a well-characterized and immortalized human proximal tubular cell line (HK2) by Northern blot and enzyme-linked immunosorbent assay. RESULTS: Ang IV stimulated PAI-1 mRNA expression, whereas it did not induce a significant increase in tritiated thymidine uptake after 24 hours of incubation. This effect was dose and time dependent. Ang IV (10 nM) induced a 7.8 +/- 3.3-fold increase in PAI-1 mRNA expression. The PAI-1 antigen level was significantly higher in conditioned media and the ECM of cells treated with Ang II and Ang IV than in control cells (both P < 0.02). Although Ang II induced a 4.2 +/- 2. 1-fold increase in PAI-1 mRNA expression, its effect underwent a dose-dependent reduction when amastatin, a potent inhibitor of the endopeptidases that catalyzes the conversion of Ang II to Ang IV, was added. In contrast, amastatin was not able to prevent the expression of PAI-1 mRNA induced by Ang IV. Finally, pretreatment of HK2 cells with losartan and N-Nicotinoyl-Tyr-N3-(Nalpha-CBZ-Arg)-Lys-His-Pro-Ile, the specific antagonists of AT1 and AT2 receptors, failed to modify PAI-1 mRNA expression as induced by Ang II. CONCLUSIONS: Our results demonstrate that Ang II stimulates PAI-1 mRNA expression and the production of its protein in human proximal tubular cells. This is mainly-if not exclusively-due to Ang IV, which acts on a receptor that is different than AT1 or AT2. Therefore, it can be hypothesized that the induction of PAI-1 by Ang IV may be implicated in the pathogenesis of renal interstitial fibrosis in several forms of chronic glomerulonephritides.
