Heavy-Quark Pair Production at Lepton Colliders at NNNLO in QCD.

We compute the total cross section and invariant mass distribution for heavy-quark pair production in e^{+}e^{-} annihilation at the next-to-next-to-next-to-leading order in QCD. The obtained results are expressed as piecewise functions defined by several deeply expanded power series, facilitating a rapid numerical evaluation. Utilizing top-pair production at a collision energy of 500 GeV as a benchmark, we observe a correction of approximately 0.1% for the total cross section and around 10% for the majority of the invariant mass distribution range. These results play a crucial role in significantly reducing theoretical uncertainty: the scale dependence has been diminished to 0.06% for the total cross section and to 5% for the invariant mass distribution. This reduction of uncertainty meets the stringent requirements of future lepton colliders.

Electroweak Corrections to Double Higgs Production at the LHC.

We present the results for the complete next-to-leading order electroweak corrections to pp→HH at the Large Hadron Collider, focusing on the dominant gluon-gluon fusion process. While the corrections at the total cross-section level are approximately -4%, those near the energy of HH production threshold exceed +15%, and corrections at the high-energy region are around -10%, leading to a shape distortion for the differential distributions. Our findings substantially diminish the theoretical uncertainties associated with this pivotal process, providing valuable input for understanding the shape of the Higgs boson potential upon comparison with experimental measurements.

Role of DNA damage response in cyclophosphamide-induced premature ovarian failure in mice.

AIM: To investigate the DNA damage response (DDR) in a cyclophosphamide (CTX)-induced mouse model of premature ovarian failure (POF). METHODS: The POF model was established by injecting mice with CTX. The body, ovarian weights, the estrus cycle, and pathological changes of the ovaries were recorded. The serum levels of 17 ß-estradiol (E2) and follicle-stimulating hormone (FSH) were measured. The expression of Ki67, ß-galactosidase (ß-gal), p21, p53, γH2AX, and pATM in ovarian tissues was detected by immunohistochemistry. The expression of ß-gal, γH2AX, and pATM was analyzed by immunofluorescence staining of primary cultured granulosa cells (GCs). RESULTS: The body and ovarian weights decreased, the estrus cycles were erratic, and the FSH level increased, whereas the E2 level decreased in POF mice compared to controls. The pathological consequences of POF revealed an increase in atretic follicles, corpus luteum, and primordial follicles and a decrease in the number of primary, secondary, and tertiary follicles. Ki67 expression was reduced, ß-gal, p21, p53, γH2AX, and pATM expression were elevated in the ovaries of POF mice. The expression of ß-gal, γH2AX, and pATM increased in GCs with the concentration in a time-dependent manner. CONCLUSION: In total, CTX induced POF in mice, which was mediated by the DDR pathway of ATM-P53-P21.

Circulating LPS from gut microbiota leverages stenosis-induced deep vein thrombosis in mice.

OBJECTIVE AND DESIGN: An accumulating body of evidence has shown that gut microbiota is involved in regulating inflammation; however, it remains undetermined if and how gut microbiota plays an important role in modulating deep venous thrombosis (DVT), which is an inflammation-involved thrombotic event. SUBJECTS: Mice under different treatments were used in this study. METHODS AND TREATMENT: We induced stenosis DVT in mice by partially ligating the inferior vena cava. Mice were treated with antibiotics, prebiotics, probiotics, or inflammatory reagents to modulate inflammatory states, and their effects on the levels of circulating LPS and DVT were examined. RESULTS: Antibiotic-treated mice or germ-free mice exhibited compromised DVT. Treatment of mice with either prebiotics or probiotics effectively suppressed DVT, which was accompanied with the downregulation of circulating LPS. Restoration of circulating LPS in these mice with a low dose of LPS was able to restore DVT. LPS-induced DVT was blocked by a TLR4 antagonist. By performing proteomic analysis, we identified TSP1 as one of the downstream effectors of circulating LPS in DVT. CONCLUSION: These results suggest that gut microbiota may play a nonnegligible role in modulating DVT by leveraging the levels of LPS in circulation, thus shedding light on the development of gut microbiota-based strategies for preventing and treating DVT.

Determining Feynman Integrals with Only Input from Linear Algebra.

We find that all Feynman integrals (FIs), having any number of loops, can be completely determined once linear relations between FIs are provided. Therefore, FI computation is conceptually changed to a linear algebraic problem. Examples up to five loops are given to verify this observation. As a by-product, we obtain a powerful method to calculate perturbative corrections in quantum field theory.

The comparison of biomechanical effects of the conventional and bone-borne palatal expanders on late adolescence with unilateral cleft palate: a 3-dimensional finite element analysis.

BACKGROUND: Patients with unilateral cleft lip and palate were associated with different nasomaxillary complex from the normal population. Although the biomechanical effects of conventional rapid palatal expansion (Hyrax expansion) and bone-borne rapid palatal expansion (micro-implant-assisted expansion) in non-cleft patients have been identified by multiple studies, little is known in patients with unilateral cleft lip and palate. The purpose of this study was to investigate and compare the biomechanical effects of the conventional and bone-borne palatal expanders in a late adolescence with unilateral cleft lip and palate. METHODS: A cone beam CT scan of a late adolescence with unilateral cleft lip and palate was selected to construct the three-dimensional finite element models of teeth and craniofacial structures. The models of conventional and born-borne palatal expanders were established to simulate the clinical maxillary expansion. The geometric nonlinear theory was applied to evaluate the Von Mises stress distribution and displacements in craniofacial structures and teeth. RESULTS: Bone-borne palatal expander achieved more transverse movement than conventional palatal expander in the whole mount of craniofacial regions, and the maximum amount of expansion was occurred anteriorly along the alveolar ridge on cleft-side. The expanding force from born-borne palatal expander resulted in more advancement in nasomaxillary complex than it in conventional palatal expander, especially in the anterior area of the minor segment of maxilla. Stresses from the both expanders distributed in similar patterns, but larger magnitudes and ranges were generated using the bone-borne expander around the maxillary buttresses and pterygoid plates of sphenoid bone. The maximum expanding stresses from born-borne palatal expander were concentrated on palatal slope supporting minscrews, whereas those from conventional palatal expander were concentrated on the anchoring molars. In addition, the buccal tipping effect of teeth generated using the bone-borne expander was less than it using the conventional palatal expander. CONCLUSION: Bone-borne expander generated enhanced skeletal expansion at the levels of alveolar and palate in transversal direction, where the miniscrews contributed increased expanding forces to maxillary buttresses and decreased forces to buccal alveolar. Bone-borne expanders presented a superiority in correcting the asymmetric maxilla without surgical assistant in late adolescence with unilateral cleft lip and palate.

ß3-Endonexin interacts with ninein in vascular endothelial cells to promote angiogenesis.

Anti-angiogenesis serves as an effective tumor therapy approach. In a previous study, we found that ß3-endonexin expressed in vascular endothelial cells was involved in promoting proliferation and angiogenesis partially by facilitating VEGF expression. However, it still remains unclear if ß3-endonexin in vascular endothelial cells also employs other mechanisms in regulating angiogenesis. In this study, we utilized a ß3-endonexin mutant (M2) carrying a defective nuclear localization sequence to disrupt its nuclear localization and evaluated its ability to promote HUVEC proliferation and formation of tube-like vascular structures. In addition, we performed yeast 2-hybrid assay to identify potential functional effectors of ß3-endonexin. We found that both wild type ß3-endonexin and the M2 mutant could localize to centrosomes in HUVECs and both were able to promote HUVEC proliferation and formation of vascular structures. However, the M2 mutant failed to promote VEGF expression in HUVECs. Further, we found that both wild type ß3-endonexin and the M2 mutant were capable of binding to ninein, a centrosomal protein with a proangiogenic effect. Knockdown of ninein in HUVECs impeded centrosome localization of wild type ß3-endonexin and the M2 mutant and inhibited HUVEC proliferation and formation of vascular structures. Taken together, these findings suggest that ß3-endonexin interacts with centrosome ninein and contributes to HUVEC proliferation and formation of vascular structures.

Extraction of Next-to-Next-to-Leading-Order Parton Distribution Functions from Lattice QCD Calculations.

We present for the first time complete next-to-next-to-leading-order coefficient functions to match flavor nonsinglet quark correlation functions in position space, which are calculable in lattice QCD, to parton distribution functions (PDFs). Using PDFs extracted from experimental data and our calculated matching coefficients, we predict valence-quark correlation functions that can be confronted by lattice QCD calculations. The uncertainty of our predictions is greatly reduced with higher order matching coefficients. By performing Fourier transformation, we also obtain matching coefficients for corresponding quasi-PDFs and pseudo-PDFs. Our method of calculations can be readily generalized to evaluate the matching coefficients for sea-quark and gluon correlation functions, making the program to extract partonic structure of hadrons from lattice QCD calculations comparable with and complementary to that from experimental measurements.

Kindlin supports platelet integrin αIIbß3 activation by interacting with paxillin.

Kindlins play an important role in supporting integrin activation by cooperating with talin; however, the mechanistic details remain unclear. Here, we show that kindlins interacted directly with paxillin and that this interaction could support integrin αIIbß3 activation. An exposed loop in the N-terminal F0 subdomain of kindlins was involved in mediating the interaction. Disruption of kindlin binding to paxillin by structure-based mutations significantly impaired the function of kindlins in supporting integrin αIIbß3 activation. Both kindlin and talin were required for paxillin to enhance integrin activation. Interestingly, a direct interaction between paxillin and the talin head domain was also detectable. Mechanistically, paxillin, together with kindlin, was able to promote the binding of the talin head domain to integrin, suggesting that paxillin complexes with kindlin and talin to strengthen integrin activation. Specifically, we observed that crosstalk between kindlin-3 and the paxillin family in mouse platelets was involved in supporting integrin αIIbß3 activation and in vivo platelet thrombus formation. Taken together, our findings uncover a novel mechanism by which kindlin supports integrin αIIbß3 activation, which might be beneficial for developing safer anti-thrombotic therapies.

Multiplicative Renormalizability of Operators defining Quasiparton Distributions.

Extracting parton distribution functions (PDFs) from lattice QCD calculation of quasi-PDFs has been actively pursued in recent years. We extend our proof of the multiplicative renormalizability of the quasiquark operators of Ishikawa et al. [Phys Rev. D 96, 094019 (2017)] to quasigluon operators, and demonstrated that quasigluon operators could be multiplicatively renormalized to all orders in perturbation theory, without mixing with other operators. We find that using a gauge-invariant UV regulator is essential for achieving this proof. With the multiplicative renormalizability of both quasiquark and quasigluon operators, and QCD collinear factorization of hadronic matrix elements of there operators into PDFs, extracting PDFs from lattice QCD calculated hadronic matrix elements of quasiparton operators could have a solid theoretical foundation.