Hospital admissions for hypertensive crisis in the Emergency Departments: a large multicenter Italian study

Epidemiological data on the impact of hypertensive crises (emergencies and urgencies) on referral to the Emergency Departments (EDs) are lacking, in spite of the evidence that they may be life-threatening conditions. We performed a multicenter study to identify all patients aged 18 years and over who were admitted to 10 Italian EDs during 2009 for hypertensive crises (systolic blood pressure ≥220 mmHg and/or diastolic blood pressure ≥120 mmHg). We classified patients as affected by either hypertensive emergencies or hypertensive urgencies depending on the presence or the absence of progressive target organ damage, respectively. Logistic regression analysis was then performed to assess variables independently associated with hypertensive emergencies with respect to hypertensive urgencies. Of 333,407 patients admitted to the EDs over the one-year period, 1,546 had hypertensive crises (4.6/1,000, 95% CI 4.4-4.9), and 23% of them had unknown hypertension. Hypertensive emergencies (n = 391, 25.3% of hypertensive crises) were acute pulmonary edema (30.9%), stroke (22.0%,), myocardial infarction (17.9%), acute aortic dissection (7.9%), acute renal failure (5.9%) and hypertensive encephalopathy (4.9%). Men had higher frequency than women of unknown hypertension (27.9% vs 18.5%, p<0.001). Even among known hypertensive patients, a larger proportion of men than women reported not taking anti-hypertensive drug (12.6% among men and 9.4% among women (p<0.001). Compared to women of similar age, men had higher likelihood of having hypertensive emergencies than urgencies (OR = 1.34, 95% CI 1.06-1.70), independently of presenting symptoms, creatinine, smoking habit and known hypertension. This study shows that hypertensive crises involved almost 5 out of 1,000 patients-year admitted to EDs. Sex differences in frequencies of unknown hypertension, compliance to treatment and risk of hypertensive emergencies might have implications for public health programs

The toxic effect of fluoride on MG-63 osteoblast cells is also dependent on the production of nitric oxide

Some soda-lime-phospho-silicate glasses, such as Hench’s Bioglass® 45S5, form bone-like apatite ontheir surface when bound to living bone. To improve their osteointegration for clinical purposes, thefluoride insertion in their structure has been proposed, but we recently showed that fluoride causesoxidative damage in human MG-63 osteoblasts, via inhibition of pentose phosphate oxidative path-way (PPP) and its key enzyme glucose 6-phosphate dehydrogenase (G6PD). In the same cells we havenow investigated the role of nitric oxide (NO) in these effects. Fluoride-containing bioactive glasses andNaF caused, as expected, release of lactate dehydrogenase in the extracellular medium, accumulation ofintracellular malonyldialdehyde, inhibition of PPP and G6PD: we have now observed that these effectswere significantly reverted not only by superoxide dismutase (SOD) plus catalase (scavengers of reactiveoxygen species), but also by N-monomethyl l-arginine (l-NMMA, a NOS inhibitor) and 2-phenyl-4,4,5,5,-tetramethylimidazoline-1oxyl 3-oxide (PTIO, a NO scavenger). Moreover the two highest concentrationsof both fluoride-containing bioglasses and NaF caused increase of nitrite (a stable derivative of NO) levelsin the culture supernatant, which was inhibited by l-NMMA, erythrocytes, PTIO and SOD/catalase, andincrease of intracellular NO synthase (NOS) activity. The incubation with bioglasses or NaF increasedalso the phosphorylation of Ser1177 in the endothelial NOS isoform. Furthermore, the NO donor spermineNONOate was able to inhibit G6PD activity in vitro, and this effect was partly reverted by PTIO. Thereforeour results suggest that most cytotoxic effects of fluoride are mediated by the production of NO: reactiveoxygen species are important, causing NOS phosphorylation. We also observed, for the first time, thatTempol, but not SOD/catalase, besides inhibiting the oxidative stress induced by fluoride, also scavengesfluoride ions. For this reason it is not a selective inhibitor of the oxidative effects of fluoride

Fluoride-containing bioactive glasses inhibit pentose phosphate oxidative pathway and glucose 6-phosphate dehydrogenase activity in human osteoblasts

Bioactive glasses such as Hench's 45S5 (Bioglass\uae) have applications to tissue engineering aswell as bone repair, and the insertion of fluoride in their composition has been proposed to enhancetheir bioactivity. In view of a potential clinical application, we investigated whether fluoride-containingglasses exert toxic effects on human MG-63 osteoblasts, and whether and how fluoride, which isreleased in the cell culture medium, might play a role in such cytotoxicity. A 24 h incubation with 50\u3bcg/ml (12.5 \u3bcg /cm2) of fluoride-containing bioactive glasses termed HCaCaF2 (F content: 5, 10 and15% mol) caused the release of lactate dehydrogenase in the extracellular medium (index ofcytotoxicity), the accumulation of intracellular malonyldialdehyde (index of lipoperoxidation), and theincrease of glutathione consumption. Furthermore, fluoride-containing glasses inhibited the pentosephosphate oxidative pathway and the glucose 6-phosphate dehydrogenase activity. These effects areascribable to the fluoride content/release of glass powders, since they were mimicked by NaF solutionsand were prevented by dimethyl sulfoxide and tempol (two radical scavengers), by superoxidedismutase (a superoxide scavenger), and by glutathione (the most important intracellular antioxidantmolecule), but not by apocynin (an inhibitor of NADPH oxidase). The presence of fluoride-containingglasses and NaF caused also the generation of reactive oxygen species, which was prevented bysuperoxide dismutase and catalase. The data suggest that fluoride released from glasses is the cause ofMG-63 cell oxidative damage and is independent of NADPH oxidase activation. Our data provide a newmechanism to explain F \u305 ions toxicity: fluoride could trigger, at least in part, an oxidative stress viainhibition of the pentose phosphate oxidative pathway and, in particular, through the oxidativeinhibition of glucose 6-phosphate dehydrogenase

Variation of vascular and blood indicators of early endothelial dysfunction after root canal therapy: A clinical and biomolecular study

Aim: Apical periodontitis (AP) is correlated with a higher risk of developing cardiovascular disease (CVD). No data currently exist to suggest that endothelial dysfunction (ED) improves after endodontic treatment in patients who have AP, despite a link between chronic AP and ED. This study was designed to investigate the expression of early ED markers in young adults with chronic AP, before and after root canal treatment. Methodology: 41 subjects (20 controls and 21 patients with AP) were examined at enrolment. Patients with AP were also assessed 2 and 12 months after treatment. ENDO-PAT was used to measure endothelial flow reserve (EFR) and ELISAs were used to assess plasma levels of interleukin (IL)-1, IL-6 and TNF-alpha, vasoconstrictor ED endothelin (ET)-1, the circulating endothelial adhesion markers intercellular adhesion molecule-1 (ICAM)-1/ CD54 and soluble vascular cellular adhesion molecule-1 (sVCAM)-1/CD106, soluble CD14, and the endothelial leukocyte adhesion molecule E-selectin. Results: Baseline serum levels of ET-1, ICAM-1, E-selectin, IL-1, and sCD14 were elevated in patients with AP compared to the control group. There was no macroscopic evidence of reduced EFR in either group. Treatment for AP was associated with reduced inflammation and improved early ED, indicated by a lowering of IL-1, sCD14, ET-1, ICAM-1/ CD54 and E-selectin levels to resemble those of control subjects. Conclusions: Early vascular ED may be driven by AP but is reversible with effective endodontic treatment

Bioactive phospho-silicate glasses containing CaF2: bioactivity test in simulated body fluids and behaviour towards osteoblast cells

In this work it is reported a study, in vitro (DMEM), of some potentially bioactive glasses based on the composition of Bioglass® 45S5 bioactive glass, in which CaF2 substitutes alternatively CaO and Na2O. Using a multi-techniques investigation, it is possible to explain in detail the glasses degradatation and the mechanism of formation of an apatitic layer between inorganic material and biological medium. The behaviour of doped glasses is differs from that proposed by Hench for Bioglass® 45S5 bioactive glass, however, these doped glasses have capability of developing bio-activity.A preliminary cellular test is also performed in view of a potential clinical applicatio