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Wegener's granulomatosis (WG) is a unique clinicopathological disease characterized by necrotizing granulomatous vasculitis of the respiratory tract, pauci-immune necrotizing glomerulonephritis and small-vessel vasculitis. Owing to its wide range of clinical manifestations, WG has a broad spectrum of severity that includes the potential for alveolar hemorrhage or rapidly progressive glomerulonephritis, which are immediately life threatening. WG is associated with the presence of circulating antineutrophil cytoplasm antibodies (c-ANCAs). The most widely accepted pathogenetic model suggests that c-ANCA-activated cytokine-primed neutrophils induce microvascular damage and a rapid escalation of inflammation with recruitment of mononuclear cells. The diagnosis of WG is made on the basis of typical clinical and radiologic findings, by biopsy of involved organ, the presence of c-ANCA and exclusion of all other small-vessel vasculitis. Currently, a regimen consisting of daily cyclophosphamide and corticosteroids is considered standard therapy. A number of trials have evaluated the efficacy of less-toxic immunosuppressants and antibacterials for treating patients with WG, resulting in the identification of effective alternative regimens to induce or maintain remission in certain subpopulations of patients. Recent investigation has focused on other immunomodulatory agents (e.g., TNF-α inhibitors and anti-CD20 antibodies), intravenous immunoglobulins and antithymocyte globulins for treating patients with resistant WG. [ABSTRACT FROM AUTHOR]

Objective-To quantitatively analyze modifications of the paratubal muscles in developing Wistar rats following nasal obstruction. Material and Methods-Twenty-four Wistar rats were used. Twelve were examined at 6, 8 and 12 weeks after birth and were considered normal controls. The nostrils of the remaining 12 rats were bilaterally obstructed by means of a synthetic resin 28 days after birth. The animals were sacrificed at either 2, 4 or 8 weeks after nostril occlusion. Serial sections were made in the dorsoventral plane and stained with hematoxylin-eosin. Four 5×5 μm[SUP2] areas, selected within the paratubal muscles, were histologically analyzed and the number of muscular fibers was counted manually. Results-The number of tensor veli palatini muscle fibers progressively decreased in the obstructed rats compared with age-matched normal controls and in those that had been obstructed for 4 and 8 weeks these reductions were statistically significant. Conclusion-The correct development of the paratubal muscles seems to be linked to physiological nasal breathing and is negatively affected by oral breathing. [ABSTRACT FROM AUTHOR]

Summary: Multiple sclerosis (MS), a chronic inflammatory disorder of the central nervous system results in damage to axons and their surrounding myelin sheath. Sensorineural hearing loss (SNHL) is an uncommon symptom of MS. We describe the case of a 15-year-old girl with unilateral sudden hearing loss as presenting symptom of multiple sclerosis. [Copyright &y& Elsevier]

Background The purpose of this study is to evaluate whether demographics, lifestyle habits, clinical data and alcohol dehydrogenase rs1229984 and rs1573496 associated with first primary head and neck (HNC) are associated with overall survival, recurrence, and second primary cancer (SPC). Methods We conducted a follow-up study in five centres including 801 cases. Hazard Ratios (HRs) and 95% confidence intervals (CIs) were estimated for overall survival, recurrence and SPC. Results Five-years overall survival was 62% for HNC cases, 55% for oral cavity, 53% for oropharynx, 41% for hypopharynx, and 71% for larynx. Predictors of survival were older ages (HR = 1.18 for 5 years increase; CI: 1.09–1.29), higher tumour stage (HR = 3.70; CI: 2.44–5.60), and high alcohol consumption (HR = 3.49; CI: 1.09–11.13). A combined therapy (HR = 3.05; CI: 1.22–7.66), and smoking (HR = 2.35; CI: 1.09–5.04), were associated with a worst prognosis for oral cavity cancer. The only predictor was higher tumour stage (HR = 2.25; CI:1.26–4.03) for recurrence, and duration of smoking (HR = 1.91; CI: 1.00–3.68) for SPC. Conclusions The survival expectation differs among HNC sites. Increasing age and stage, and high alcohol consumption were unfavourable predictors of HNC survival overall, while smoking status was a negative prognostic factor for oral cavity cancer. Duration of tobacco consumption before the first primary tumour was a risk factor for SPC. [ABSTRACT FROM AUTHOR]

Abstract Background The purpose of this study is to analyze the combined effects of selected p53 and p73 polymorphisms and their interaction with lifestyle habits on squamous cell carcinoma of the head and neck (SCCHN) risk and progression in an Italian population. Methods Two hundred and eighty-three cases and 295 hospital controls were genotyped for p53 polymorphisms on exon 4 (Arg72Pro), intron 3 and 6, and p73 G4C14-to-A4T14. Their association with SCCHN was estimated using a logistic regression analysis, while a multinomial logistic regression approach was applied to calculate the effect of the selected polymorphisms on SCCHN different sites (oral cavity, oropharynx, hypopharynx and larynx). We performed an haplotype analysis of the p53 polymorphisms, and a gene-gene interaction analysis for the combined effects of p73 G4C14-to-A4T14 and p53 polymorphisms. Results We found a significant increased risk of SCCHN among individuals with combined p73 exon 2 G4A and p53 intron 3 variant alleles (OR = 2.22, 95% CI: 1.08–4.56), and a protective effect for those carrying the p53 exon 4-p53 intron 6 diplotype combination (OR = 0.67; 95% CI: 0.47–0.92). From the gene-environment interaction analysis we found that individuals aged < 45 years carrying p73 exon 2 G4A variant allele have a 12.85-increased risk of SCCHN (95% CI: 2.10–78.74) compared with persons of the same age with the homozygous wild type genotype. Improved survival rate was observed among p53 intron 6 variant allele carriers (Hazard Ratio = 0.51 (95% CI: 0.23–1.16). Conclusion Our study provides for the first time evidence that individuals carrying p53 exon 4 and p53 intron 6 variant alleles are significantly protected against SCCHN, and also shows that an additional risk is conferred by the combination of p73 exon 2 G4C14-to-A4T14 and p53 intron 3 variant allele. Larger studies are required to confirm these findings.