Clinimetric properties of a smartphone application to measure the craniovertebral angle in different age groups and positions.

Background: Craniovertebral angle (CVA) alteration is a causative factor for the neck, shoulder, and temporomandibular joints disorders. Therefore, as an outcome measure for therapeutic intervention, measuring the craniovertebral angle with the Surgimap smartphone app is a cost-effective, easily accessible, and reliable tool. This study's objective was to assess the clinimetric properties of the Surgimap smartphone application with Surgimap system software to measure the Craniovertebral Angle in different age groups and positions. Method: Ninety subjects with neck pain were randomly allocated to aged between 18 and 30 years (Group A; n = 45) and 45-60 years (Group B; n = 45). Using the Surgimap smartphone application and Surgimap system software, the craniovertebral angle was measured objectively in the sagittal plane. Intraclass correlation coefficients were used to determine validity and reliability. Receiver operating characteristic (ROC) curves and the area under the curves (AUC) were determined to distinguish participants with and without forward head posture. Result: The result of this study shows that Smartphone Surgimap Application and Surgimap System Software correlate 0.95 and have p-values of 0.01 for diverse positions and ages. CVA measurement in the sitting position was significantly lower than in the standing position, regardless of methodology or age. Both positions demonstrated high intra-rater reliability, as evidenced by Intraclass Correlation Coefficients (ICC) between 0.972 and 0.991. The minimum detectable change (MDC) values ranged from 1.3 to 1.733, indicating high measurement accuracy. The smartphone application demonstrated outstanding diagnostic sensitivity (100.00% for Group A standing) and specificity (93.55% for Group B standing). Conclusion: The Surgimap smartphone application is a reliable and accurate method for craniovertebral angle measurement and is useful for measuring outcomes. Also standing posture was found to be better than sitting posture while measuring the CVA.

c-Src Suppresses Dendritic Cell Antitumor Activity via T Cell Ig and Mucin Protein-3 Receptor.

The enhanced expression of T cell Ig and mucin protein-3 (TIM-3) on tumor-associated dendritic cells (DCs) attenuates antitumor effects of DNA vaccines. To identify a potential target (or targets) for reducing TIM-3 expression on tumor-associated DCs, we explored the molecular mechanisms regulating TIM-3 expression. In this study, we have identified a novel signaling pathway (c-Src→Bruton's tyrosine kinase→transcription factors Ets1, Ets2, USF1, and USF2) necessary for TIM-3 upregulation on DCs. Both IL-10 and TGF-ß, which are produced in the tumor microenvironment, upregulated TIM-3 expression on DCs via this pathway. Suppressed expression of c-Src or downstream Bruton's tyrosine kinase, Ets1, Ets2, USF1, or USF2 blocked IL-10- and TGF-ß-induced TIM-3 upregulation on DCs. Notably, in vivo knockdown of c-Src in mice reduced TIM-3 expression on tumor-associated DCs. Furthermore, adoptive transfer of c-Src-silenced DCs in mouse tumors enhanced the in vivo antitumor effects of immunostimulatory CpG DNA; however, TIM-3 overexpression in c-Src-silenced DCs blocked this effect. Collectively, our data reveal the molecular mechanism regulating TIM-3 expression in DCs and identify c-Src as a target for improving the efficacy of nucleic acid-mediated anticancer therapy.

Immunoregulation of dendritic cells by the receptor T cell Ig and mucin protein-3 via Bruton's tyrosine kinase and c-Src.

The receptor T cell Ig and mucin protein-3 (TIM-3) has emerged as an important regulator of innate immune responses. However, whether TIM-3-induced signaling promotes or inhibits the activation and maturation of dendritic cells (DCs) still remains uncertain. In addition, the TIM-3 signaling events involved in this immunoregulatory function are yet to be established. In this article, we report that TIM-3 crosslinking by anti-TIM-3 Ab inhibited DC activation and maturation by blocking the NF-κB pathway. After Ab-mediated crosslinking, TIM-3 became tyrosine phosphorylated, which then sequentially bound and activated the nonreceptor tyrosine kinases Bruton's tyrosine kinase (Btk) and c-Src. Activation of Btk-c-Src signaling in turn triggered the secretion of some inhibitory factor (or factors) from DCs that inhibited the NF-κB pathway and subsequent activation and maturation of DCs. Silencing of Btk or c-Src abrogated the inhibitory effects of TIM-3 on DCs. These results demonstrate an essential role for Btk-c-Src signaling in TIM-3-induced DC suppression. Thus, in addition to demonstrating an inhibitory role for TIM-3 signaling in DC activation, we define the molecular mechanism by which TIM-3 mediates this effect.