58 research outputs found
A quality-adjusted survival analysis (Q-TWiST) of rituximab plus CVP vs CVP alone in first-line treatment of advanced follicular non-Hodgkin's lymphoma
Expression of αvβ6integrin in oral leukoplakia
The distribution of αvβ6integrin was examined in oral leukoplakia, lichen planus and squamous cell carcinomas using immunohistochemistry. Controls included oral mucosal wounds, chronically inflamed and normal oral mucosa. Integrins β1, β3, β4, β5, fibronectin and tenascin were also studied. The integrin αvβ6was highly expressed throughout the whole lesion of 90% of the squamous cell carcinomas but was not present in any of the normal specimens. αvβ6integrin was also expressed in 41% of the leukoplakia specimens, and 85% of the lichen planus samples, but in none of the tissues with inflammatory hyperplasia or chronic inflammation. The expression of β1 integrins was localized in the basal layer, and that of the β4at the cell surface facing the basement membrane of all specimens. The integrins β3and β5were absent from all normal and leukoplakia specimens. Fibronectin and tenascin were present in the connective tissue underneath the epithelium of all the sections, and their expression was similar in both αvβ6-positive and αvβ6-negative tissues. A group of 28 leukoplakia patients were followed 1–4 years after first diagnosis. In this group, initially αvβ6integrin-positive leukoplakia specimens had high tendency for disease progression while αvβ6-negative specimens did not progress. These results suggest that the expression of αvβ6integrin could be associated in the malignant transformation of oral leukoplakias. © 2000 Cancer Research Campaig
Activation of the NLRP3/caspase-1 inflammasome in human dental pulp tissue and human dental pulp fibroblasts
sodC-Based Real-Time PCR for Detection of Neisseria meningitidis
Real-time PCR (rt-PCR) is a widely used molecular method for detection of
Neisseria meningitidis (Nm). Several rt-PCR assays for Nm
target the capsule transport gene, ctrA. However, over
16% of meningococcal carriage isolates lack ctrA,
rendering this target gene ineffective at identification of this sub-population
of meningococcal isolates. The Cu-Zn superoxide dismutase gene,
sodC, is found in Nm but not in other
Neisseria species. To better identify Nm, regardless of
capsule genotype or expression status, a sodC-based TaqMan
rt-PCR assay was developed and validated. Standard curves revealed an average
lower limit of detection of 73 genomes per reaction at cycle threshold
(Ct) value of 35, with 100% average reaction efficiency
and an average R2 of 0.9925. 99.7% (624/626) of Nm isolates
tested were sodC-positive, with a range of average
Ct values from 13.0 to 29.5. The mean sodC
Ct value of these Nm isolates was 17.6±2.2 (±SD).
Of the 626 Nm tested, 178 were nongroupable (NG) ctrA-negative
Nm isolates, and 98.9% (176/178) of these were detected by
sodC rt-PCR. The assay was 100% specific, with all
244 non-Nm isolates testing negative. Of 157 clinical specimens tested,
sodC detected 25/157 Nm or 4 additional specimens compared
to ctrA and 24 more than culture. Among 582 carriage specimens,
sodC detected Nm in 1 more than ctrA and
in 4 more than culture. This sodC rt-PCR assay is a highly
sensitive and specific method for detection of Nm, especially in carriage
studies where many meningococcal isolates lack capsule genes
A New Method To Evaluate the Germinative and Differentiating Compartments of Normal Human-epidermis
Dermatoses auto-immunes alt\ue9ration de la molecule a6b4 dans des lesions de pemphigoides bulleuses.
Reverse-Bayes analysis of two common misinterpretations of significance tests
BACKGROUND: Misunderstanding of significance tests and P values is widespread in clinical research and elsewhere.
PURPOSE: To assess the implications of two common mistakes in the interpretation of statistical significance tests. The first one is the misinterpretation of the type I error rate as the expected proportion of false-positive results among all those called significant, also known as the false-positive report probability (FPRP). The second is the misinterpretation of a P value as (posterior) probability of the null hypothesis.
METHODS: A reverse-Bayes approach is used to calculate a lower bound on the proportion of truly effective treatments that would ensure the FPRP to be equal or below the type I error rate. A reverse-Bayes approach using minimum Bayes factors (BFs) yields upper bounds on the prior probability of the null hypothesis that would justify the interpretation of the P value as the posterior probability of the null hypothesis.
RESULTS: In a typical clinical trials setting, more than 50% of the treatments need to be truly effective to justify equality of the type I error rate and the FPRP. To interpret the P value as posterior probability, the difference between the corresponding prior probability and the P value cannot exceed 12.4 percentage points.
LIMITATIONS: The first analysis requires that the (one-sided) type I error rate is smaller than the type II error rate. The second result is valid under different scenarios describing how to transform P values to minimum BFs.
CONCLUSIONS: The two misinterpretations imply strong and often unrealistic assumptions on the prior proportion or probability of truly effective treatments
Applying a coping with stress questionnaire for cancer patients to patients with non-cancer chronic illnesses
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