Development of a Artificial Intelligence Dental Anxiety Scale (AI -CDAS) For Children: Validation And Reliability.

Assessing children's pain using patient-based pain scales can be challenging. Hence, there is a need of new version Artificial Intelligence Child Dental Anxiety Scale (AI-CDAS) to scale and test its psychometric properties (validity and reliability). This study was conducted to evaluate the validity and reliability of Artificial Intelligence version of the Child Dental Anxiety Scale (AI-CDAS) for anxiety detection scale in children using face as a response set from October 2022 to December 2023. Aim of this study was to examine the reliability and validity of Artificial Intelligence based Child Dental Anxiety Scale (AI-CDAS) using a wide range of age samples in dental clinics. A total of 100 outpatients (Age 03-09 years) from Bharati Vidyapeeth Deemed to be University Dental College and Hospital, Pune, India participated in this study. Dental anxiety was assessed using the Artificial Intelligence Child Dental Anxiety Scale (AI-CDAS) and comparing with a valid and reliable scale of Colored Version of Modified Facial Affective Scale. Reliability and validity was good and significant correlations were found between the AI-CDAS and the Colored Version of Modified Facial Affective Scale. This study suggests that the Artificial Intelligence based Child Dental Anxiety Scale (AI-CDAS) is a valid and reliable measure for assessing children's dental anxiety and may help encourage dentists to formally assess dental anxiety scale in day to day practice. Self-report measures are commonly employed in dental anxiety assessments. One advantage of self report measures is the ease of administration, taking relatively short period of time to complete. They can also assess the reaction to different aspects of the dental experience.

Pertussis toxin B-oligomer suppresses human immunodeficiency virus-1 Tat-induced neuronal apoptosis through feedback inhibition of phospholipase C-beta by protein kinase C.

Human immunodeficiency virus (HIV)-1 Tat is a multifunctional protein involved in viral replication, inflammation and apoptosis. Tat activates phospholipase C-beta (PLC-beta), presumably via a pertussis toxin (PTX) sensitive G(i) protein, which is critical for neuronal apoptosis. In this study, we show that Tat-mediated intracellular Ca(2+) release in rat pheochromocytoma (PC-12) cells and rat primary cortical neuronal cultures was abrogated by pretreatment with either pertussis toxin and/or its B-oligomer subunit (PTX-B), devoid of ADP ribosyltransferase activity. PTX-B pretreatment also inhibited intracellular Ca(2+) release by bradykinin and 2,4,6-trimethyl-N-(m-3-trifluoromethylphenyl) benzenesulfonamide (m-3M3FBS), a director activator of phospholipase C. Activation of protein kinase C (PKC) by phorbol 12,13-dibutyrate (PdBu) mimicked the PTX-B-mediated inhibition of m-3M3FBS-stimulated intracellular Ca(2+) increase, while inhibition of PKC by bisindolylmaleimide I hydrochloride (BIM) reversed the inhibitory action of PTX-B. Functionally, PTX-B reduced Tat-induced Bax and caspase-3 proteins and reduced cell apoptosis. We conclude that PTX inhibition of Tat-mediated intracellular Ca(2+) release is independent of ADP ribosylation of the G(i) protein via the A protomer, but mediated by the B-oligomer. Furthermore, PTX-B suppresses HIV-1 Tat-mediated apoptosis by reducing its activation of PLC-beta through a PKC activation pathway.

Short interfering RNA against STAT1 attenuates cisplatin-induced ototoxicity in the rat by suppressing inflammation.

Cisplatin is widely used for treating various solid tumors. However, this drug produces dose-limiting ototoxicity and nephrotoxicity, which significantly reduce the quality of life of cancer patients. While nephrotoxicity could be alleviated by diuresis, there is currently no approved treatment for hearing loss. Previous studies show that the ROS and inflammation are major contributors to cisplatin-induced hearing loss. In this study, we show that ROS trigger the inflammatory process in the cochlea by activating signal transducer and activator of transcription-1 (STAT1). Activation of STAT1 activation was dependent on ROS generation through NOX3 NADPH oxidase, knockdown of which by siRNA reduced STAT1 activation. Moreover, STAT1 siRNA protected against activation of p53, reduced apoptosis, reduced damage to OHCs and preserved hearing in rats. STAT1 siRNA attenuated the increase in inflammatory mediators, such as TNF-α, inhibition of which protected cells from cisplatin-mediated apoptosis. Finally, we showed that trans-tympanic administration of etanercept, a TNF-α antagonist, protected against OHC damage and cisplatin-induced hearing loss. These studies suggest that controlling inflammation by inhibition of STAT1-dependent pathways in the cochlea could serve as an effective approach to treat cisplatin ototoxicity and improve the overall quality of life for cancer patients.