Background
Oral lichen planus (OLP) is a chronic, inflammatory disease with uncertain etiology. The aim of this study was to assess Interleukin‐18 (IL‐18) gene polymorphism and serum levels in OLP cases of Indian origin and to compare them with a control population of similar background.
Methods
The assessment of single‐nucleotide polymorphisms (SNPs) of IL‐18 gene at promoter regions −137(G/C) and −607(C/A) was done in 70 OLP cases and 70 healthy controls using sequence‐specific primer‐polymerase chain reaction (SSP‐PCR). In a subset of this cohort, comprising of 41 OLP cases and 41 controls, serum IL‐18 levels were assessed using enzyme‐linked immunosorbent assay (ELISA).
Results
Mean serum levels of IL‐18 among OLP cases were significantly higher when compared to controls. Genotypic and allelic frequencies of IL‐18 at position −137(G/C) showed that GG genotype and allele G was significantly higher in OLP cases, whereas, GC genotype and C allele was high in the control group. Polymorphism of IL‐18 at position −607(C/A) showed no significant differences.
Conclusions
Gene polymorphism at −137GG genotype and allele G seems to be associated with genetic susceptibility to OLP whereas −137GC and allele C may have a protective role against its development. However, our study lacks clear statistical correlation, the differences observed could be caused by sampling problems and the results could not be fully representative of Indian patients with OLP. Further studies are warranted to explore the role of IL‐18 genetic polymorphisms in OLP development.
In neurodegenerative diseases, changes in neuronal proteins in the cerebrospinal fluid and blood are viewed as potential biomarkers of the primary pathology in the central nervous system (CNS). Recent reports suggest, however, that level of neuronal proteins in fluids also alters in several types of epilepsy in various age groups, including children. With increasing evidence supporting clinical and sub-clinical seizures in Alzheimer’s disease, Lewy body dementia, Parkinson’s disease, and in other less common neurodegenerative conditions, these findings call into question the specificity of neuronal protein response to neurodegenerative process and urge analysis of the effects of concomitant epilepsy and other comorbidities. In this article, we revisit the evidence for alterations in neuronal proteins in the blood and cerebrospinal fluid associated with epilepsy with and without neurodegenerative diseases. We discuss shared and distinctive characteristics of changes in neuronal markers, review their neurobiological mechanisms, and consider the emerging opportunities and challenges for their future research and diagnostic use.
Objective
To evaluate trappin‐2 levels in cervicovaginal secretions for prediction of spontaneous preterm birth (sPTB) and compare it with transvaginal sonography (TVS) cervical length in asymptomatic women at risk of PTB.
Methods
Trappin‐2 levels assessed in cervicovaginal secretions collected from 80 asymptomatic pregnant women at high risk for preterm delivery and cervical length measured by TVS, first at 14–20 weeks of pregnancy and repeated 8 weeks later. On the basis of delivery outcomes, participants were divided into cases (delivery <37 weeks) and controls (delivery at 37–41 weeks).
Results
The mean value of cervicovaginal trappin‐2 was significantly higher in women who delivered preterm (n = 40), compared with the term group (n = 40: P < 0.001) both at 14–20 weeks and at 22–28 weeks. The critical cut‐off value for cervicovaginal trappin‐2 at 14–20 weeks was 4620 pg/mL, above which participants delivered prematurely with sensitivity, specificity, and positive and negative predictive values of 82.5%, 71.0%, 78.5%, and 81.5% respectively, whereas TVS cervical length in this window period was not significantly associated with preterm birth. At 22–28 weeks a trappin‐2 value of 6900 pg/mL had similar predictive accuracy.
Conclusion
Raised cervicovaginal trappin‐2 levels can be used as an early tool for prediction of PTB as early as 14–20 weeks (earlier than TVS) in asymptomatic high‐risk women.
Pleomorphic Adenoma (PA) is the most common salivary gland tumor and accounts for about 60% of all salivary gland neoplasms. Intraorally, the hard palate is the most common presenting site (50-60%) followed by upper lip (15-20%) and rarely buccal mucosa (8-10%). Histopathologically, PA shows diverse morphology resulting from amalgamation of cellular and stromal components. The PA may show changes in the stromal and epithelial components, such as sebaceous, lipocytic and oncocytic metaplasia. A rare characteristic of PA is to show extensive squamous and mucous differentiation which poses diagnostic dilemma to the pathologist. Here, we present an unusual case of PA of buccal minor salivary gland with squamous and mucous metaplasia. The localization, gender and microscopic features of the presented case are unusual.
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