Bifid mandibular canals and their cortex thicknesses: A comparison study on images obtained from cone-beam and multislice computed tomography

AbstractBackground/purposeHigh prevalence of bifid mandibular canals has been visualized with various types of computerized tomography (CT). Along the canals, a various ranged corticalization was recently reported. The depiction of the fine anatomic structures on multislice and cone-beam CT images was compared.Material and methodsThe presence or absence of the bifid canal was assessed on 327 images obtained by multislice CT (MSCT; n = 173) or by cone-beam CT (CBCT; n = 154), according to the configuration. The cortex thickness and distribution were also assessed.ResultsThe prevalence of bifid canal detected by CBCT was significantly greater than that detected by MSCT (42.2% vs. 18.7% for hemi-mandibles and 58.4% vs. 30.6% for patients). Cortical thickness recorded by CBCT was significantly thinner than that recorded by MSCT (0.48 mm vs. 0.65 mm, P < 0.001); however, the distributions of corticalization detected by the two tomography methods were similar. There was a significant association of cortex thickness with CT type and corticalization degree (R2 = 0.530, P < 0.001).ConclusionThinner cortices, but greater prevalence of bifid canals recorded by CBCT, compared to MSCT, suggests that clinicians should be cautious when using CT to interpret this fine anatomic structure

Rapid Diagnosis of Bacterial Meningitis Using a Microarray

Microarrays, or biochips, are a new technology that can allow rapid detection of bacterial genetic materials. To explore their practical applications, we compared use of a microarray for the diagnosis of bacterial meningitis with the traditional blood and cerebrospinal fluid (CSF) culture methods. Methods: Samples from 50 patients with suspected bacterial meningitis were analyzed by microarray and by traditional blood and CSF cultures. Results: Among all samples, 11 were positive by microarray analysis, seven were positive by CSF bacterial culture and six were positive by blood culture. CSF pleocytosis was found in 26 patients. Of these, eight were positive by microarray analysis, seven were positive by CSF culture and five were positive by blood culture. The percentage of positive results from microarray analysis was 22%, compared to 14% by CSF culture and 12% by blood culture. The CSF bacterial culture method had the highest positive predictive value and specificity (both 100%). The sensitivity of microarray analysis was higher (30.8%) than that of CSF and blood cultures (26.9% and 19.2%). All three methods had a similar negative predictive value in the range of 52.3–55.8%. Of the 11 microarray positive samples, four were identified successfully in CSF culture (36.4%) and three samples were identified in blood culture (27.2%). One of the microarray positive samples was diagnosed as a polymicrobial infection (9%), and the rest were monomicrobial infections. Conclusion: The microarray method provides a more accurate and rapid diagnostic tool for bacterial meningitis compared to traditional culture methods. Clinical application of this new technique may reduce the potential risk of delay in treatment

Effect of m-3m3FBS on Ca2+ handling and viability in OC2 human oral cancer cells

The effect of 2,4,6-trimethyl-N-(meta-3-trifluoromethyl-phenyl)-benzenesulfonamide (m-3M3FBS), a presumed phospholipase C activator, on cytosolic free Ca2+ concentrations ([Ca2+]i) in OC2 human oral cancer cells is unclear. This study explored whether m-3M3FBS changed basal [Ca2+]i levels in suspended OC2 cells by using fura-2 as a Ca2+-sensitive fluorescent dye. M-3M3FBS at concentrations between 10–60 μM increased [Ca2+]i in a concentration-dependent manner. The Ca2+ signal was reduced partly by removing extracellular Ca2+. M-3M3FBS-induced Ca2+ influx was inhibited by the store-operated Ca2+ channel blockers nifedipine, econazole and SK&amp;F96365, and by the phospholipase A2 inhibitor aristolochic acid. In Ca2+-free medium, 30 μM m-3M3FBS pretreatment inhibited the [Ca2+]i rise induced by the endoplasmic reticulum Ca2+ pump inhibitors thapsigargin and 2,5-di-tert-butylhydroquinone (BHQ). Conversely, pretreatment with thapsigargin, BHQ or cyclopiazonic acid partly reduced m-3M3FBS-induced [Ca2+]i rise. Inhibition of inositol 1,4,5-trisphosphate formation with U73122 did not alter m-3M3FBS-induced [Ca2+]i rise. At concentrations between 5 and 100 μM m-3M3FBS killed cells in a concentration-dependent manner. The cytotoxic effect of m-3M3FBS was not reversed by prechelating cytosolic Ca2+ with 1,2-bis(2-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid (BAPTA). Propidium iodide staining data suggest that m-3M3FBS (20 or 50 μM) induced apoptosis in a Ca2+-independent manner. Collectively, in OC2 cells, m-3M3FBS induced [Ca2+]i rise by causing inositol 1,4,5-trisphosphate-independent Ca2+ release from the endoplasmic reticulum and Ca2+ influx via phospholipase A2-sensitive store-operated Ca2+ channels. M-3M3FBS also induced Ca2+-independent cell death and apoptosis

RelA-Mediated BECN1 Expression Is Required for Reactive Oxygen Species-Induced Autophagy in Oral Cancer Cells Exposed to Low-Power Laser Irradiation

<div><p>Low-power laser irradiation (LPLI) is a non-invasive and safe method for cancer treatment that alters a variety of physiological processes in the cells. Autophagy can play either a cytoprotective role or a detrimental role in cancer cells exposed to stress. The detailed mechanisms of autophagy and its role on cytotoxicity in oral cancer cells exposed to LPLI remain unclear. In this study, we showed that LPLI at 810 nm with energy density 60 J/cm² increased the number of microtubule associated protein 1 light chain 3 (MAP1LC3) puncta and increased autophagic flux in oral cancer cells. Moreover, reactive oxygen species (ROS) production was induced, which increased RelA transcriptional activity and beclin 1 (BECN1) expression in oral cancer cells irradiated with LPLI. Furthermore, ROS scavenger or knockdown of RelA diminished LPLI-induced BECN1 expression and MAP1LC3-II conversion. In addition, pharmacological and genetic ablation of autophagy significantly enhanced the effects of LPLI-induced apoptosis in oral cancer cells. These results suggest that autophagy may be a resistant mechanism for LPLI-induced apoptosis in oral cancer cells.</p></div

LPLI reduced tumor viability in spheroid culture.

<p>(A) OECM-1 or Ca9-22 cells were sphere cultured and then exposed to LPLI (810 nm, 60 J/cm²) in the presence or absence of CQ (20 μM) for 48 h. The spheres were lysed to measure ATP level for cell viability. (B) The viable and dead spheres as cultured and treated as (A) were imaged with LIVE (green)/DEAD (red) staining kit. Representative data are shown. Scale bar: 400 μm. (C) The green and (D) red fluorescence of the spheres as (B) was quantitated with a reader for the viable and dead cell population, respectively (n = 6). The quantified results are expressed as the mean ± SEM from 3 individual experiments. n.s., p > 0.05; *p < 0.05; **p < 0.01; ***p < 0.001.</p

LPLI-induced apoptosis is elevated in autophagy-deficient oral cancer cells.

<p>(A) OECM-1 cells stably harboring shRNA against ATG7 or SQSTM1 were treated without (-) or with (+) 20 μM CQ prior to harvest. The harvested cells were used for immunoblotting to determine the protein levels of ATG7, SQSTM1 and MAP1LC3-II. (B) The knockdown efficiency of ATG7 and SQSTM1 in the cells was quantified using ACTB as a normalization control (left panel). The net protein levels of MAP1LC3-II between cells treated with or without CQ were used to determine autophagic flux as quantitated results in the right panel. (C) The recovered cells were accessed for cell viability with CellTiter-Glo. (D) The LPLI-treated cells were irradiated with LPLI and cultured for 14 days. Colony formation was accessed by staining with crystal violet. (E) The irradiated cells were fixed and stained with Hoechst 33342 to determine the number of apoptotic cells. Scale bar: 100 μm. The number of apoptotic cells is shown in the right panel. (F) The cells treated as panel E were lysed to measured caspase-3/7 activity with Caspase-Glo 3/7 luminescent assay. The results are expressed as the mean ± SEM from three independent experiments.</p