Effects of the combined action of a desensitizing gel and toothpaste on dentin hypersensitivity due to dental bleaching

Objectives: The present study is aimed at evaluating the effectiveness of a fluoride- and potassium nitrate-containing gel and toothpaste in reducing dentinal hypersensitivity due to dental bleaching. Materials and methods: Specific inclusion and exclusion criteria were used to recruit patients for the study. They were randomly allocated to a test or a placebo control group. Patients underwent a treatment of home dental bleaching with 10% carbamide peroxide. Dental shades were evaluated in a standardized environment and dentinal hypersensitivity was valuated by means of evaporation stimuli. A nominal scale was used to score the painful reaction. The patients were recalled 8, 15 and 28 days after the baseline for both shade and sensitivity assessment. Statistical analysis was performed using the Student’s T-test. Results: The patients recall rate was 96.9%. The statistical analysis demonstrated a significant reduction of the painful symptoms in the experimental group (p=0.031) while no statistically significant differences were evidenced in the control group at any follow-up recall (p>0.05). Discussion: The tested agents proved to be safe and effective in the short term. Neither pigmentations nor interferences with the bleaching action of peroxides due to the desensitizing agents were observed. The compliance of the patients to the proposed protocol as well as the motivation to maintain good oral hygiene were paramount in the achievement of the reported results. Conclusions: The use of a desensitizing gel and toothpaste containing fluoride and potassium nitrate was effective in reducing dentinal hypersensitivity due to dental bleaching and did not interfere with the bleaching action of peroxides. Clinical significance: Desensitizing gels and toothpastes containing fluoride and potassium nitrate can be considered safe and effective in the control of tooth sensitivity after dental bleaching

Long term evaluation of mental fatigue by Maastricht Questionnaire in patients with OSAS treated with CPAP

Background. Patients with obstructive sleep apnoea syndrome (OSAS) suffer from disrupted sleep. Impaired nightly sleep leads to increase physical and mental fatigue. The effect of long term continuous positive airway pressure (CPAP) on mental fatigue in OSAS patients, assessed by Maastricht Questionnaire (MQ), has not been investigated yet. Methods. In order to evaluate the role of CPAP in improving mental fatigue of patients with OSAS, we studied 35 patients (26 males, age <65 years at the time of the diagnosis) affected by OSAS, established by polysomnography (PSG). Patients were divided into two groups; 19 subjects (15 males), who refused CPAP therapy, and 16 patients (11 males) well matched for sex, age, body mass index (BMI), neck circumference, duration of follow up, and severity of disease, who had been treated with CPAP for at least two years. Results. All patients had severe OSAS with Respiratory Disturbance Index (RDI), of 48±20.9 (range 22-90) and 61.48±18.6 (range 34-101) respectively, for group one (untreated patients) and group two (CPAP treatment). In addition, all patients had severe impairment of mental fatigue and of daytime sleepiness, demonstrated by high values of MQ score (32.17±15.33 and 37.36±12.4, respectively) and Epworth Sleepiness Scale (ESS) (14.21±4.77 and 15.06±6.07 respectively). There was no statistical significant difference in the group one at baseline and after follow- up, in terms of BMI, MQ score, ESS, and RDI. In the CPAP group (group two), the patients reported a significant improvement of the quality of their mental health (MQ 37.36±12.4 vs. 16.41±9.02; p<0.0001) and sleepiness (ESS 15.06±6.07 vs. 4.13±3.93; p<0.0001) with a stable BMI. There was significant correlation between the severity of sleep apnoea, expressed as RDI, and MQ at admission compared to at the end of follow-up (r=0.4, p<0.05). Conclusions. This study demonstrates an evident deterioration of mental fatigue in patients with OSAS, directly correlated to the severity of nocturnal disorder breathing; however supports the hypothesis that long term CPAP therapy significantly improves sleepiness and mental fatigue

Increased IL-6 and IL-4 in exhaled breath condensate of patients with nasal polyposis

Background and Aim. Nasal polyposis (NP) occurs in about 1-4% of the worldwide population. Increased plasma concentrations of different pro-inflammatory cytokines have been observed in NP, and might be related to the pathogenesis of this syndrome.The present study was designed to investigate IL-6 and IL-4 concentrations in nasal and oral exhaled breath condensate of patients with early and advanced NP, and following polypectomy. Methods. Ten individuals with polyposis in early status, twenty-three patients affected by advanced status of NP and ten healthy controls were enrolled into the study. Exhaled breath condensate was collected by all individuals, according to a previous standardised method. An immunoassay kit was used to measure IL-6 and IL-4 levels. Results. Concentrations of oral and nasal exhaled IL- 6 and IL-4 were significantly higher in patients with early nasal polyposis and advanced nasal polyposis, compared to healthy controls. A statistically significant decrease of nasally but not of orally exhaled IL-6 (p<0.001) and IL-4 (p<0.05) was observed after polypectomy. Conclusions. We consider oral and nasal exhaled condensate of IL-6 and IL-4 as valid inflammatory and oxidative stress marker in patients with nasal polyposis

NADPH oxidase elevations in pyramidal neurons drive psychosocial stress-induced neuropathology

Oxidative stress is thought to be involved in the development of behavioral and histopathological alterations in animal models of psychosis. Here we investigate the causal contribution of reactive oxygen species generation by the phagocyte NADPH oxidase NOX2 to neuropathological alterations in a rat model of chronic psychosocial stress. In rats exposed to social isolation, the earliest neuropathological alterations were signs of oxidative stress and appearance of NOX2. Alterations in behavior, increase in glutamate levels and loss of parvalbumin were detectable after 4 weeks of social isolation. The expression of the NOX2 subunit p47phox was markedly increased in pyramidal neurons of isolated rats, but below detection threshold in GABAergic neurons, astrocytes and microglia. Rats with a loss of function mutation in the NOX2 subunit p47phox were protected from behavioral and neuropathological alterations induced by social isolation. To test reversibility, we applied the antioxidant/NOX inhibitor apocynin after initiation of social isolation for a time period of 3 weeks. Apocynin reversed behavioral alterations fully when applied after 4 weeks of social isolation, but only partially after 7 weeks. Our results demonstrate that social isolation induces rapid elevations of the NOX2 complex in the brain. Expression of the enzyme complex was strongest in pyramidal neurons and a loss of function mutation prevented neuropathology induced by social isolation. Finally, at least at early stages, pharmacological targeting of NOX2 activity might reverse behavioral alterations

Supportive and symptomatic management of amyotrophic lateral sclerosis

The main aims in the care of individuals with amyotrophic lateral sclerosis (ALS) are to minimize morbidity and maximize quality of life. Although no cure exists for ALS, supportive and symptomatic care provided by a specialist multidisciplinary team can improve survival. The basis for supportive management is shifting from expert consensus guidelines towards an evidence-based approach, which encourages the use of effective treatments and could reduce the risk of harm caused by ineffective or unsafe interventions. For example, respiratory support using noninvasive ventilation has been demonstrated to improve survival and quality of life, whereas evidence supporting other respiratory interventions is insufficient. Increasing evidence implicates a causal role for metabolic dysfunction in ALS, suggesting that optimizing nutrition could improve quality of life and survival. The high incidence of cognitive dysfunction and its impact on prognosis is increasingly recognized, although evidence for effective treatments is lacking. A variety of strategies are used to manage the other physical and psychological symptoms, the majority of which have yet to be thoroughly evaluated. The need for specialist palliative care throughout the disease is increasingly recognized. This Review describes the current approaches to symptomatic and supportive care in ALS and outlines the current guidance and evidence for these strategies

HPV16 E7-Dependent Transformation Activates NHE1 through a PKA-RhoA-Iinduced Inhibition of p38alpha

Background: Neoplastic transformation originates from a large number of different genetic alterations. Despite this genetic variability, a common phenotype to transformed cells is cellular alkalinization. We have previously shown in human keratinocytes and a cell line in which transformation can be turned on and followed by the inducible expression of the E7 oncogene of human papillomavirus type 16 (HPV16), that intracellular alkalinization is an early and essential physiological event driven by the up-regulation of the Na/H-+(+) exchanger isoform 1 (NHE1) and is necessary for the development of other transformed phenotypes and the in vivo tumor formation in nude mice.Methodology: Here, we utilize these model systems to elucidate the dynamic sequence of alterations of the upstream signal transduction systems leading to the transformation-dependent activation of NHE1.Principal Findings: We observe that a down-regulation of p38 MAPK activity is a fundamental step in the ability of the oncogene to transform the cell. Further, using pharmacological agents and transient transfections with dominant interfering, constitutively active, phosphorylation negative mutants and siRNA strategy to modify specific upstream signal transduction components that link HPV16 E7 oncogenic signals to up-regulation of the NHE1, we demonstrate that the stimulation of NHE1 activity is driven by an early rise in cellular cAMP resulting in the down-stream inhibition of p38 MAPK via the PKA-dependent phosphorylation of the small G-protein, RhoA, and its subsequent inhibition.Conclusions: All together these data significantly improve our knowledge concerning the basic cellular alterations involved in oncogene-driven neoplastic transformation

Endothelin-1 excretion in urine in active Pulmonary Sarcoidosis and in other Interstitial Lung Disease

Endothelin-1 (ET-1) is a vasoactive, mitogenic peptide that is variably increased in Bronchoalveolar Lavage Fluid (BALF) and immunohistochemically found in lung tissue of patients with Interstitial Lung Disease (ILD). To assess if endogenous ET-1 production is increased in ILD we evaluated 24 hour (24h) urine excretion of ET-1 in 20 patients with ILD and 10 healthy age-matched controls (HC). Eight patients with active pulmonary sarcoidosis (S), 6 with idiopathic pulmonary fibrosis (IPF) and 6 with focal lung fibrosis due to inactive pulmonary tuberculosis (hTB) were studied. Plasma ET-1 levels (ET-1pl, pg/ml) and 24h ET-1 levels in urine (ET-1ur, ng/24h) were measured by a specific radio-immunoassay. Determinations of ET-1p1 and ET-1ur were repeated in S and IPF patients after 30 days of prednisone (0.75 mg/kg/day) treatment. ET-1p1 concentrations were not different between HC (5.34 +/- 0.48), S (5.95 +/- 0.96), IPF (4.75 +/- 1.37) and hTB (5.97 +/- 1.05) groups. ET-1ur was significantly higher in S (189.50 +/- 60.57) than in HC (69.00 +/- 10.76), IPF (62.17 +/- 19.07) and hTB (82.00 +/- 24.97). After prednisone, ET-1ur in the S group decreased significantly (189.50 +/- 60.57 to 94.00 +/- 13.60), and the decrease paralleled the improved clinical status. In S patients, ET-1ur was not significantly correlated to the degree of respiratory impairment, but it was significantly correlated to the intensity of lymphocytic alveolitis (r = 0.80)