We present a comprehensive analysis of the potential sensitivity of the Electron-Ion Collider (EIC) to charged lepton flavor violation (CLFV) in the channel ep→τX, within the model-independent framework of the Standard Model Effective Field Theory (SMEFT). We compute the relevant cross sections to leading order in QCD and electroweak corrections and perform simulations of signal and SM background events in various τ decay channels, suggesting simple cuts to enhance the associated estimated efficiencies. To assess the discovery potential of the EIC in τ-e transitions, we study the sensitivity of other probes of this physics across a broad range of energy scales, from pp→eτX at the Large Hadron Collider to decays of B mesons and τ leptons, such as τ→eγ, τ→eℓ⁺ℓ⁻, and crucially the hadronic modes τ→eY with Y∈π, K, ππ, Kπ, …. We find that electroweak dipole and four-fermion semi-leptonic operators involving light quarks are already strongly constrained by τ decays, while operators involving the c and b quarks present more promising discovery potential for the EIC. An analysis of three models of leptoquarks confirms the expectations based on the SMEFT results. We also identify future directions needed to maximize the reach of the EIC in CLFV searches: these include an optimization of the τ tagger in hadronic channels, an exploration of background suppression through tagging b and c jets in the final state, and a global fit by turning on all SMEFT couplings, which will likely reveal new discovery windows for the EIC.

The Higgs boson production can be affected by several anomalous couplings, e.g. $c_t$ and $c_g$ anomalous couplings. Precise measurement of $gg\to h$ production yields two degenerate parameter spaces of $c_t$ and $c_g$; one parameter space exhibits the SM limit while the other does not. Such a degeneracy could be resolved by Higgs boson pair production. In this work we adapt the strategy suggested by the ATLAS collaboration to explore the potential of distinguishing the degeneracy at the 14 TeV LHC. If the $c_t$ anomalous coupling is induced only by the operator $H^\dag H \bar Q_L \tilde{H} t_R$, then the non-SM-like band could be excluded with an integrated luminosity of $\sim 235~{\rm fb}^{-1}$. Making use of the fact that the Higgs boson pair is mainly produced through an $s$-wave scattering, we propose an analytical function to describe the fraction of signal events surviving a series of experimental cuts for a given invariant mass of Higgs boson pair. The function is model independent and can be applied to estimate the discovery potential of various NP models

We consider effective Higgs boson couplings, including both $CP$-even and $CP$-odd couplings, which affect Higgs boson pair production. Through partial wave analysis, we find that the process $gg\to hh$ is dominated by the $s$-wave component even at a 100 TeV $pp$ collider. Making use of $s$-wave kinematics, we propose a cut efficiency function to mimic the collider simulation and obtain the potential of measuring Higgs effective couplings at the 14 TeV LHC with an integrated luminosity of $3000{\mathrm{fb}}^{-1}$ and at a 100 TeV $pp$ collider. Analytical expressions of 2σ exclusion limits at the LHC and $5\sigma$ discovery bands at the 100 TeV machine are given.

Background: The purpose of this study was to evaluate the accuracy of automatic cephalometric landmark localization and measurements using cephalometric analysis via artificial intelligence (AI) compared with computer-assisted manual analysis. Methods: Reconstructed lateral cephalograms (RLCs) from cone-beam computed tomography (CBCT) in 85 patients were selected. Computer-assisted manual analysis (Dolphin Imaging 11.9) and AI automatic analysis (Planmeca Romexis 6.2) were used to locate 19 landmarks and obtain 23 measurements. Mean radial error (MRE) and successful detection rate (SDR) values were calculated to assess the accuracy of automatic landmark digitization. Paired t tests and Bland‒Altman plots were used to compare the differences and consistencies in cephalometric measurements between manual and automatic analysis programs. Results: The MRE for 19 cephalometric landmarks was 2.07 ± 1.35 mm with the automatic program. The average SDR within 1 mm, 2 mm, 2.5 mm, 3 and 4 mm were 18.82%, 58.58%, 71.70%, 82.04% and 91.39%, respectively. Soft tissue landmarks (1.54 ± 0.85 mm) had the most consistency, while dental landmarks (2.37 ± 1.55 mm) had the most variation. In total, 15 out of 23 measurements were within the clinically acceptable level of accuracy, 2 mm or 2°. The rates of consistency within the 95% limits of agreement were all above 90% for all measurement parameters. Conclusion: Automatic analysis software collects cephalometric measurements almost effectively enough to be acceptable in clinical work. Nevertheless, automatic cephalometry is not capable of completely replacing manual tracing. Additional manual supervision and adjustment for automatic programs can increase accuracy and efficiency.

Orthodontic tooth movement (OTM) is induced by biomechanical stimuli and facilitated by periodontal tissue remodeling, where multiple immune cells participate in this progression. It has been demonstrated that macrophage is essential for mechanical force‐induced tissue remodeling. In this study, we first found that mechanical force significantly induced macrophage proliferation in human periodontal samples and murine OTM models. Yet, how macrophages perceive mechanical stimuli and thereby modulate their biological behaviors remain elusive. To illustrate the mechanisms of mechanical force‐induced macrophage proliferation, we subsequently identified Piezo1, a novel mechanosensory ion channel, to modulate macrophage response subjected to mechanical stimuli. Mechanical force upregulates Piezo1 expression in periodontal tissues and cultured bone‐marrow‐derived macrophages (BMDMs). Remarkably, suppressing Piezo1 with GsMTx4 retarded OTM through reduced macrophage proliferation. Moreover, knockdown of Piezo1 effectively inhibited mechanical force‐induced BMDMs proliferation. RNA sequencing was further performed to dissect the underlying mechanisms of Piezo1‐mediated mechanotransduction utilizing mechanical stretch system. We revealed that Piezo1‐activated AKT/GSK3β signaling was closely associated with macrophage proliferation upon mechanical stimuli. Importantly, Cyclin D1 (Ccnd1) was authenticated as a critical downstream factor of Piezo1 that facilitated proliferation by enhancing Rb phosphorylation. We generated genetically modified mice in which Ccnd1 could be deleted in macrophages in an inducible manner. Conditional ablation of Ccnd1 inhibited periodontal macrophage proliferation and therefore delayed OTM. Overall, our findings highlight that proliferation driven by mechanical force is a key process by which macrophages infiltrate in periodontal tissue during OTM, where Piezo1‐AKT‐Ccnd1 axis plays a pivotal role.