Source:Annals of Allergy, Asthma & Immunology
Author(s): Philip Hei Li, Annette Wagner, Ryszard Rutkowski, Krzysztof Rutkowski
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Publication date: Available online 27 April 2017
Source:Annals of Allergy, Asthma & Immunology
Author(s): Jessica W. Hui, Jason Ong, James J. Herdegen, Hajwa Kim, Christopher D. Codispoti, Vahid Kalantari, Mary C. Tobin, Robert P. Schleimer, Pete S. Batra, Phillip S. LoSavio, Mahboobeh Mahdavinia
BackgroundIt is widely known that patients with chronic rhinosinusitis (CRS) commonly experience sleep disruption. Many of these patients have the associated diagnosis of obstructive sleep apnea (OSA). However, little is known about the risk factors for developing OSA in the CRS population.ObjectiveTo identify the risk factors for OSA in CRS to determine who should be screened for OSA among patients with CRS.MethodsWe evaluated a large cohort of patients with confirmed diagnostic criteria for CRS. Patient medical records were reviewed to identify those with OSA confirmed by overnight polysomnography. Records were further reviewed for demographic information (age, sex, race, and ethnicity), body mass index, and medical history, including the presence of nasal polyps, asthma, aspirin-exacerbated respiratory disease, allergic rhinitis, and eczema. The number of endoscopic sinus operations, duration of CRS, presence of subjective smell loss, and computed tomography Lund-Mackay score were also ascertained.ResultsA total of 916 patients with CRS were included in the study. Implementation of a multivariable regression model for identifying adjusted risk factors revealed that African American patients had a significantly higher risk for OSA than white patients, with an adjusted odds ratio of 1.98 (95% confidence interval, 1.19–3.29). Furthermore, patients with CRS without nasal polyps were at higher risk for OSA, with an odds ratio of 1.63 (95% confidence interval, 1.02–2.61) compared with patients with CRS with nasal polyps.ConclusionAfrican American patients with CRS were at higher risk for OSA compared with white patients, and this patient group needs to be screened for OSA.
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Publication date: August 2017
Source:Archives of Oral Biology, Volume 80
Author(s): Frank Lippert
ObjectiveThe aim was to investigate the effects of fluoride, strontium, theobromine and their combinations on caries lesion rehardening and fluoridation (EFU) under pH cycling conditions.DesignHuman enamel specimens were demineralized at 37°C for 24h using a pH 5.0 solution containing 50mM lactic acid and 0.2% Carbopol 907 which was 50% saturated with respect to hydroxyapatite. Lesions were assigned to nine treatment groups (n=16) based on Knoop surface microhardness indentation length.Treatmentaqueous solutions were: placebo, 11.9mM sodium fluoride (F), 23.8mM sodium fluoride (2×F), 1.1mM strontium chloride hexahydrate (Sr), 1.1mM F theobromine, Sr+theobromine, F+Sr, F+theobromine, F+Sr+theobromine. Lesions were pH cycled for 5d (daily protocol: 3×1min-treatment; 2×60min-demineralization; 4×60min & overnight-artificial saliva). Knoop indentation length was measured again and%surface microhardness recovery (%SMHr) calculated. EFU was determined using the acid-etch technique. Data were analysed using ANOVA.ResultsModel showed fluoride dose-response for both variables (2×F>F>placebo). For%SMHr, F+Sr+/−theobromine resulted in more rehardening than F, however less than 2×F. F+theobromine was similar to F. For EFU, F+Sr was inferior to F, F+theobromine and F+Sr+theobromine which were similar and inferior to 2×F. In absence of fluoride, Sr, theobromine or Sr+theobromine were virtually indistinguishable from placebo and inferior to F.ConclusionsIt can be concluded that a) strontium aids rehardening but not EFU and only in presence of fluoride; b) theobromine does not appear to offer any anti-caries benefits in this model; c) there are no synergistic effects between strontium and theobromine in the presence or absence of fluoride.
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In this report, we summarized the clinicopathologic features of ten cases of lymphoepithelioma-like carcinoma (LELC) of the upper urinary tract (ureter n = 6; renal pelvis n = 4), a rare variant of urothelial cancer characterized by a malignant epithelial component densely infiltrated by lymphoid cells. The initial diagnosis was made on radical nephrectomy in five cases, nephroureterectomy in three cases, and ureterectomy in two others. Four patients had pathologic stage T1 (n = 2) or T2 (n = 2) tumors, and six patients had stage pT3 disease. Microscopically, all tumors contained pure (n = 3) or predominant (n = 7) LELC, which composed 60 to 80% of the entire tumor. Non-LELC tumor component was adenocarcinoma (n = 2), spindle cell carcinoma (n = 1), or high-grade conventional urothelial carcinoma (n = 4). The LELC component was characterized by indistinct cytoplasmic borders and a syncytial growth pattern. Immunohistochemical staining showed LELC to be positive for cytokeratin AE1/AE3, CK7, CK34ßE12 (rare cells), CK5/6 (rare cells), and CK20 (rare cells); rare cells were p40 positive. GATA 3 was positive in all cases in a variable proportion of cells (20–80%). Lymphoid markers showed a polyclonal proliferation of predominant T cells admixed with B cells. In situ hybridization for the HPV genome was negative in all ten cases. Survival analysis showed no differences between LELC and conventional upper urinary tract urothelial carcinoma, pT classification being the only significant prognostic parameter. Morphologic recognition and distinction from other (non-)neoplastic lesions with prominent lymphoid stroma are critical for its clinical management.