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At least 757 records · Page 42

Flavor fragmentation function factorization

A definition of partonic jet flavor that is both theoretically well-defined and experimentally robust would have profound implications for measurements and predictions especially for heavy flavor applications. Recently, a definition of jet flavor was introduced as the net flavor flowing along the direction of the Winner-Take-All axis of a jet which is soft safe to all orders, but not collinear safe. Here, we exploit the lack of collinear safety and propose a factorization theorem of perturbative flavor fragmentation functions that resum collinear divergences and describe the evolution of flavor from the short distance of jet production to the long distance at which hadronization occurs. Collinear flavor evolution is governed by a small modification of the DGLAP equations. We present a detailed all-orders analysis and identify exact relations that must hold amongst the various anomalous dimensions by probability conservation and the existence of fixed points of the renormalization group flow. We explicitly validate the factorization theorem at one-loop order, and demonstrate its consistency at two loops in particular flavor channels. Starting at two-loops, constraints on phase space imposed by flavor measurements potentially allow for non-trivial soft contributions, but we demonstrate that they are scaleless and so explicitly vanish, ensuring that soft particles are summed inclusively and all divergences are exclusively collinear in nature. This factorization theorem opens the door to precision calculations with identified flavor in the infrared.

72 PHYSICS OF ELEMENTARY PARTICLES AND FIELDS↗

Factorization connecting continuum & lattice TMDs

Transverse-momentum-dependent parton distribution functions (TMDs) can be studied from first principles by a perturbative matching onto lattice-calculable quantities: so-called lattice TMDs, which are a class of equal-time correlators that includes quasi-TMDs and TMDs in the Lorentz-invariant approach. We introduce a general correlator that includes as special cases these two Lattice TMDs and continuum TMDs, like the Collins scheme. Then, to facilitate the derivation of a factorization relation between lattice and continuum TMDs, we construct a new scheme, the Large Rapidity (LR) scheme, intermediate between the Collins and quasi-TMDs. The LR and Collins schemes differ only by an order of limits, and can be matched onto one another by a multiplicative kernel. We show that this same matching also holds between quasi and Collins TMDs, which enables us to prove a factorization relation between these quantities to all orders in α s . Our results imply that there is no mixing between various quark flavors or gluons when matching Collins and quasi TMDs, making the lattice calculation of individual flavors and gluon TMDs easier than anticipated. We cross-check these results explicitly at one loop and discuss implications for other physical-to-lattice scheme factorizations.

72 PHYSICS OF ELEMENTARY PARTICLES AND FIELDS↗

Perturbative calculations of gravitational form factors at large momentum transfer

We perform a perturbative QCD analysis of the gravitational form factors (GFFs) of nucleon at large momentum transfer. We derive the explicit factorization formula of the GFFs in terms of twist-3 and twist-4 light-cone distribution amplitudes of nucleon. Power behaviors for these GFFs are obtained from the leading order calculations. Numeric results of the quark and gluon contributions to various GFFs are presented with model assumptions for the distribution amplitudes in the literature. We also present the perturbative calculations of the scalar form factor $\langle P$' $|F^2|P \rangle$ for pion and proton at large momentum transfer.

72 PHYSICS OF ELEMENTARY PARTICLES AND FIELDS↗

Effective field theory factorization for diffraction

We derive a factorization formula for coherent and incoherent ep diffraction using the soft collinear effective theory, utilizing multiple power expansion parameters to handle different kinematic regions. This goes beyond the known hard-collinear diffractive factorization to address the small-x Regge dynamics and Pomeron exchange from first principles. The effective field theory analysis also uncovers and factorizes an important irreducible incoherent background generated by color-nonsinglet exchange, dubbed “quasi-diffraction”, for which we calculate the associated Sudakov suppression. For unpolarized scattering we show that there are four diffractive structure functions at leading power, and point out the importance of studying ${F}_{3,4}^D$ through asymmetries, in addition to ${F}_{2,L}^D$. For the quasi-diffractive background, we make model independent predictions for ratios of the corresponding structure functions in a perturbative kinematic region. Our analysis also makes predictions for six leading-power spin-dependent structure functions. Finally, we provide connections to diffractive parton distributions, and assess the Ingelman-Schlein model. Our work lays a path for further QCD-based studies of diffraction.

72 PHYSICS OF ELEMENTARY PARTICLES AND FIELDS↗

Transverse Λ polarization in e + e – processes within a TMD factorization approach and the polarizing fragmentation function

We perform a re-analysis of Belle data for the transverse Λ and Λ¯ polarization in e + e – annihilation processes within a transverse momentum dependent (TMD) factorization approach. We consider two data sets, one referring to the associated production of Λ’s with a light unpolarized hadron in an almost back-to-back configuration, and one for the inclusive Λ production, with the reconstruction of the thrust axis. We adopt the Collins-Soper-Sterman framework and employ the recent formulation on the factorization of single-inclusive hadron production. This extends a previous phenomenological study carried out in a more simplified TMD approach, leading to a new extraction of the polarizing fragmentation function (FF). While confirming several features of the previous analysis, here we include the proper QCD scale dependence of this TMD FF and carefully exploit the role of its nonperturbative component. Here, the compatibility, within a unique TMD factorization scheme, of double and single-inclusive hadron production is discussed in detail. Moreover, we consider another data set for inclusive Λ production, at much larger energies, from the OPAL Collaboration, in order to test the consistency of the entire approach. Finally, we elaborate on some fundamental issues like the role of SU(2) isospin symmetry and the heavy quark contributions.

72 PHYSICS OF ELEMENTARY PARTICLES AND FIELDS↗

Enhancing Interpretability in Generative Modeling: Statistically Disentangled Latent Spaces Guided by Generative Factors in Scientific Datasets

This study addresses the challenge of statistically extracting generative factors from complex, high-dimensional datasets in unsupervised or semi-supervised settings. We investigate encoder-decoder-based generative models for nonlinear dimensionality reduction, focusing on disentangling low-dimensional latent variables corresponding to independent physical factors. Introducing Aux-VAE, a novel architecture within the classical Variational Autoencoder framework, we achieve disentanglement with minimal modifications to the standard VAE loss function by leveraging prior statistical knowledge through auxiliary variables. These variables guide the shaping of the latent space by aligning latent factors with learned auxiliary variables. We validate the efficacy of Aux-VAE through comparative assessments on multiple datasets, including astronomical simulations.

97 MATHEMATICS AND COMPUTING↗

Identification and overexpression of endogenous transcription factors to enhance lipid accumulation in the biotechnologically relevant species Chlamydomonas pacifica

Sustainable low-carbon energy solutions are critical to mitigating global carbon emissions. Algae-based platforms offer potential by converting carbon dioxide into valuable products while aiding carbon sequestration. However, scaling algae cultivation faces challenges like contamination in outdoor systems. Previously, our lab evolved Chlamydomonas pacifica, an extremophile green alga, which tolerates high temperature, pH, salinity, and light, making it ideal for large-scale bioproduct production, including biodiesel. Here, we enhanced lipid accumulation in evolved C. pacifica by identifying and overexpressing key endogenous transcription factors through genome-wide in-silico analysis and in-vivo testing. These factors include Lipid Remodeling Regulator 1 (CpaLRL1), Nitrogen Response Regulator 1 (CpaNRR1), Compromised Hydrolysis of Triacylglycerols 7 (CpaCHT7), and Phosphorus Starvation Response 1 (CpaPSR1). Under nitrogen deprivation, CpaLRL1, CpaNRR1, and CpaCHT7 overexpression enhanced lipid accumulation compared to wild-type. However, CpaPSR1 increased lipid accumulation compared to wild-type in normal media and did not increase further under nitrogen deprivation, highlighting the difference in function based on media conditions. Notably, lipid analysis of CpaPSR1 under normal media conditions revealed a 2.4-fold increase in triglycerides (TAGs) compared to the wild-type, highlighting its potential for biodiesel production. This approach provides a framework for transcription factor-focused metabolic engineering in algae, advancing bioenergy and biomaterial production.

Biofuels↗

Extension of the discrete generalized multigroup method using SPH factors

The discrete generalized multigroup (DGM) method provides a way to treat the energy dependence of neutron transport similarly to the standard multigroup approximation. However, DGM uses an orthogonal basis to retain the energy dependence in higher-order terms. Using correction factors similar to traditional Superhomogénéisation (SPH) factors, the DGM method may be extended to produce cross sections that are homogenized over both space and energy. Additionally, since some fine-group energy dependence is retained, the resulting homogenized cross sections are more problem-independent than cross sections homogenized by SPH factors alone. In particular, a 44-group set of cross sections is collapsed to approximately a 1% error in the pincell fission densities for a test problem using three DOF per coarse energy group.

22 GENERAL STUDIES OF NUCLEAR REACTORS↗

Autoantibodies in dilated cardiomyopathy induce vascular endothelial growth factor expression in cardiomyocytes

Background: Autoantibodies have been identified as major predisposing factors for dilated cardiomyopathy (DCM). Patients with DCM show elevated serum levels of vascular endothelial growth factor (VEGF) whose source is unknown. Besides its well-investigated effects on angiogenesis, evidence is present that VEGF signaling is additionally involved in fibroblast proliferation and cardiomyocyte hypertrophy, hence in cardiac remodeling. Whether autoimmune effects in DCM impact cardiac VEGF signaling needs to be elucidated. Methods: Five DCM patients were treated by the immunoadsorption (IA) therapy on five consecutive days. The eluents from the IA columns were collected and prepared for cell culture. Cardiomyocytes from neonatal rats (NRCM) were incubated with increasing DCM-immunoglobulin-G (IgG) concentrations for 48 h. Polyclonal IgG (Venimmun N), which was used to restore IgG plasma levels in DCM patients after the IA therapy was additionally used for control cell culture purposes. Results: Elevated serum levels of VEGF decreased significantly after IA (Serum VEGF (ng/ml); DCM pre-IA: 45 ± 9.1 vs. DCM post–IA: 29 ± 6.7; P < 0.05). In cell culture, pretreatment of NRCM by DCM-IgG induced VEGF expression in a time and dose dependent manner. Biologically active VEGF that was secreted by NRCM significantly increased BNP mRNA levels in control cardiomyocytes and induced cell-proliferation of cultured cardiac fibroblast (Fibroblast proliferation; NRCM medium/HC-IgG: 1 ± 0.0 vs. NRCM medium/DCM-IgG 100 ng/ml: 5.6 ± 0.9; P < 0.05). Conclusion: The present study extends the knowledge about the possible link between autoimmune signaling in DCM and VEGF induction. Whether this observation plays a considerable role in cardiac remodeling during DCM development needs to be further elucidated. - Highlights: • Mechanisms of remodeling in dilated cardiomyopathy (DCM) are not fully understood. • Autoantibodies have been identified as major predisposing factors for DCM. • DCM patients show high serum levels of VEGF. • Recent data indicate that VEGF is involved in cardiac remodeling processes. • Whether autoimmune processes in DCM are involved in VEGF signaling are unclear.

60 APPLIED LIFE SCIENCES↗

The forkhead-like transcription factor (Fhl1p) maintains yeast replicative lifespan by regulating ribonucleotide reductase 1 (RNR1) gene transcription

In eukaryotes, numerous genetic factors contribute to the lifespan including metabolic enzymes, signal transducers, and transcription factors. As previously reported, the forkhead-like transcription factor (FHL1) gene was required for yeast replicative lifespan and cell proliferation. To determine how Fhl1p regulates the lifespan, we performed a DNA microarray analysis of a heterozygous diploid strain deleted for FHL1. We discovered numerous Fhl1p-target genes, which were then screened for lifespan-regulating activity. We identified the ribonucleotide reductase (RNR) 1 gene (RNR1) as a regulator of replicative lifespan. RNR1 encodes a large subunit of the RNR complex, which consists of two large (Rnr1p/Rnr3p) and two small (Rnr2p/Rnr4p) subunits. Heterozygous deletion of FHL1 reduced transcription of RNR1 and RNR3, but not RNR2 and RNR4. Chromatin immunoprecipitation showed that Fhl1p binds to the promoter regions of RNR1 and RNR3. Cells harboring an RNR1 deletion or an rnr1-C428A mutation, which abolishes RNR catalytic activity, exhibited a short lifespan. In contrast, cells with a deletion of the other RNR genes had a normal lifespan. Overexpression of RNR1, but not RNR3, restored the lifespan of the heterozygous FHL1 mutant to the wild-type (WT) level. The Δfhl1/FHL1 mutant conferred a decrease in dNTP levels and an increase in hydroxyurea (HU) sensitivity. These findings reveal that Fhl1p regulates RNR1 gene transcription to maintain dNTP levels, thus modulating longevity by protection against replication stress. - Highlights: • Fhl1p regulates replicative lifespan and transcription of RNR large subunit genes. • Rnr1p uniquely acts as a lifespan regulator independent of the RNR complex. • dNTP levels modulate longevity by protection against replication stress.

60 APPLIED LIFE SCIENCES↗

miR-141-3p functions as a tumor suppressor modulating activating transcription factor 5 in glioma

Glioma is the most common malignant primary brain tumor which arises from the central nervous system. Our studies reported that an anti-apoptotic factor, activating transcription factor 5 (ATF5), is highly expressed in malignant glioma specimens and cell lines. Downregulation by dominant-negetive ATF5 could repress glioma cell proliferation and accelerate apoptosis. Here, we further investigate the upstream factor which regulates ATF5 expression. Bioinformatic analysis showed that ATF5 was a potential target of miR-141-3p. Luciferase reporter assay verified that miR-141-3p specifically targeted the ATF5 3′-UTR in glioma cells. Functional studied suggested that miR-141-3p overexpression inhibited proliferation and promoted apoptosis of glioma cells (U87MG and U251). Xenograft experiments proved the inhibition of miR-141-3p on glioma growth in vivo. Moreover, exogenous ATF5 without 3′-UTR restored the cell proliferation inhibition triggered by miR-141-3p. Taken together, we put forward that miR-141-3p is a new upstream target towards ATF5. It can serve as a crucial tumor suppressor in regulating the ATF5-regulated growth of malignant glioma. - Highlights: • ATF5 was highly expressed in gliomas and was essential for cell proliferation and apoptosis. • MiR-141-3p specifically targeted the ATF5 3′-UTR in glioma cells. • MiR-141-3p was significantly downregulated in glioma tissues and cell lines. • MiR-141-3p inhibited glioma growth through repressing ATF5 expression in vitro and in vivo. • Exogenous expression of ATF5 rescued cells from proliferation inhibition triggered by miR-141-3p.

60 APPLIED LIFE SCIENCES↗

An AT-hook protein DEPRESSED PALEA1 physically interacts with the TCP Family transcription factor RETARDED PALEA1 in rice

Highlights: • The AT-hook protein DP1 physically interacts with the TCP family transcription factor REP1 in rice. • In maize, the AT-hook protein BAD1 physically interacts with the TCP family transcription factor BAF1. • The interaction between AT-hook proteins and TCP proteins may be conserved in rice and maize. The cereal crops (such as rice and maize) which belong to the grass family, are the most important grain crops for human beings, and the development of their flower and inflorescence architecture has attracted extensive attention. Although multiple genes involved in the regulation of floral and inflorescence organogenesis have been identified, the underlying molecular mechanisms are largely unknown. Previously, we identified rice depressed palea1 (dp1) mutants with defects in main structure of palea and its enhancer RETARDED PALEA1 (REP1). DP1 is an AT-hook protein while REP1 is a TCP transcription factor, both of which are important regulators of palea development. However, the relationship of these two proteins has not been elucidated yet. Here, we demonstrated that DP1 interacts physically with REP1 both in yeast and in rice protoplasts. Considering the close phylogenetic relationship between maize and rice, we further hypothesize that their orthologs in maize, BARREN STALK FASTIGIATE (BAF1) and BRANCH ANGLE DEFECTIVE 1 (BAD1), may interact physically. Subsequently, we verified their physical interaction, indicating that the interaction between AT-hook proteins and TCP proteins is conserved in rice and maize. Our findings may reveal a novel molecular mechanism of floral and inflorescence development in grasses.

60 APPLIED LIFE SCIENCES↗

Kruppel-like factor 4 (KLF-4) plays a crucial role in simvastatin (SVT)-induced differentiation of rabbit articular chondrocytes

Highlights: • SVT was shown to exhibit a protective effect on chondrocytes. • KLF-4 regulates the SVT-mediated differentiation of chondrocytes. • KLF-4 plays critical role in SVT-mediated chondrocyte differentiation. Simvastatin is a cholesterol-lowing reagent that is derived synthetically from the fermentation of Aspergillus terreus. Recently, SVT has been shown to possess a protective effect of chondrocytes. Kruppel-like factor 4 (KLF-4) is a zinc finger transcription factor that plays crucial roles during the development and maintenance of multiple organs. However, the roles of KLF-4 in chondrocytes have not been well unknown. Here, we investigated whether KLF-4 regulates SVT-caused differentiated phenotype of chondrocytes. A KLF-4 cDNA or KLF-4 siRNA was transfected into SVT-treated chondrocytes. Western blot analysis, RT-PCR and immunofluorescence staining analyzed expression of type II collagen and SOX-9, marker proteins of differentiation. The results showed overexpression of KLF-4 accelerates SVT-induced type II collagen expression, as determined by western blot analysis and causes sulfated-proteoglycan synthesis, as detected by Alcian blue staining. RT-PCR revealed that ectopic expression of KLF-4 induces SVT-caused SOX-9, a transcription factor of type II collagen, expression. Transfection of KLF-4 siRNA reversed SVT-caused type II collagen and SOX-9 expression and inhibited SVT-induced sulfated proteoglycan production. This study indicates that KLF-4 plays critical role in SVT-caused chondrocytes differentiation.

60 APPLIED LIFE SCIENCES↗

Fibroblast growth factor 19 protects the heart from oxidative stress-induced diabetic cardiomyopathy via activation of AMPK/Nrf2/HO-1 pathway

Highlights: • FGF19 Improves Cardiac Dysfunction and Fibrosis in Diabetic Cardiomyopathy. • FGF19 Prevent Cardiac Oxidative Stress in the Diabetic Heart. • FGF 19 induces expression Nrf2/HO-1 signaling axis through activation of AMPK. Diabetes affects cardiac structure and function, where it leads to diabetic cardiomyopathy. Reactive oxygen species (ROS) produced by oxidative stress play an important role in the development of diabetic cardiomyopathy. Fibroblast growth factor (FGF) 19, an enterokine, is synthesized and released into the ileum. In the present study, we revealed that FGF19 induced an antioxidant response through stimulating the expression of nuclear erythroid factor 2 (NE-F2)-related factor 2 (Nrf2) and as well as reducing ROS production through the AMPK signaling pathway. Additionally, AMPK inhibition by the AMPK-specific inhibitor compound C decreased Nrf2 and heme oxygenase-1 (HO-1) protein expression. Taken together, these results suggested that FGF19, through the anti-oxidative defense system, attenuated the development of diabetic cardiomyopathy and restored cardiac function.

60 APPLIED LIFE SCIENCES↗

The cytoskeletal protein Zyxin interacts with the zinc-finger transcription factor Zic1 and plays the role of a scaffold for Gli1 and Zic1 interactions during early development of Xenopus laevis

Highlights: • Zyxin can interact with the transcription factor Zic1. • Zyxin, Zic1 and Gli1 can form a triple complex in the nucleus. • Triple complex Gli1 + Zic + Zyxin enhances the activity of Gli1 + Zic complex. We have shown recently that the cytoskeletal protein Zyxin participates in the fine tuning of the neural plate pattering in Xenopus laevis embryos by modulating activity of one of the effectors of Hedgehog (Shh) signaling cascade, the transcription factor Gli1. In the present work, we show that Zyxin can also interact with the potential modulator of the Shh pathway, the transcription factor Zic1. The interaction of proteins occurs primarily by mean of the zinc-finger domain of Zic1 and 2nd LIM domain of Zyxin. Moreover, we have also revealed the ability of the Zyxin, Zic1 and Gli1 to form a ternary complex. The activity of this complex resembles that of the previously described by other authors protein complex formed by Gli1 and Zic1, amplifying effect of the latter. The data obtained provide evidence for the scaffolding role of Zyxin for Gli1 and Zic1 interactions and confirm its role in the regulation of Shh signaling cascade.

60 APPLIED LIFE SCIENCES↗

p-Coumaric acid stimulates longitudinal bone growth through increasing the serum production and expression levels of insulin-like growth factor 1 in rats

The aim of the present study was to examine the effects of p-coumaric acid on the longitudinal growth of the long bone in adolescent male rats. Teatment with p-coumaric acid significantly increased the tibial length and the height of each growth plate zone and the ratio of 5-bromo-2′-deoxyuridine-positive cells relative to total proliferative cells. Expression of insulin-like growth factor 1 and its receptor in the proliferative and hypertrophic zones, and serum levels of growth hormone and insulin-like growth factor 1 were significantly increased as well in the p-coumaric acid-treated group. Via increasing both the serum level of insulin-like growth factor 1 and its expression, p-coumaric acid could promote cell proliferation in growth plate zones. These results suggest that p-coumaric acid has the potential to increase height and may be a feasible alternative to growth hormone therapy.

60 APPLIED LIFE SCIENCES↗

Transforming growth factor alpha promotes tumorigenesis and regulates epithelial-mesenchymal transition modulation in colon cancer

Highlights: • TGFα facilitates short-term and long-term proliferations of colon cancer cells. • TGFα was suggested as a migration-and-invasion promoting factor of colon cancer. • TGFα modulates epithelial-mesenchymal transition markers and NFκB signaling pathway in colon cancer cells. Colon cancer is one of the most common cancers in the developed countries. The association between transforming growth factor TGFα and human cancer incidence has been suggested, yet, the regulatory roles of TGFα and the molecular mechanisms remain unknown, especially in colon cancer. We aim to investigate the functional regulations of TGFα in colon cancer progression. Two colon cancer cell lines were applied, and plasmid overexpression and siRNA-mediated depletion techniques were used to verify the role of TGFα in colon cancer. Cell proliferation was analyzed by MTS assay and colony formation assay, and western blot assay was used to examine protein expression. Migration, invasion, and reporter assays were also carried out to study the regulations of TGFα in colon cancer. Our results evidenced that expression of TGFα facilitates short-term and long-term proliferations of colon cancer cells. Moreover, TGFα was suggested as a migration-and-invasion promoting factor of colon cancer. Finally, our data indicated that TGFα modulates epithelial-mesenchymal transition (EMT) markers and NFκB signaling pathway in colon cancer cells. We provide the first time evidence of the promoting role TGFα plays in colon cancer tumorigenesis with proposed regulatory mechanisms involving EMT alteration and NFκB signaling pathway.

60 APPLIED LIFE SCIENCES↗

Insulin-like growth factor binding Protein-3 suppresses osteoblast differentiation via bone morphogenetic protein-2

Highlights: • The maintenance of bone mass after induction of bone formation is difficult. • Insulin-like growth factor (IGF)-1 regulates bone mass including osteogenesis. • IGF-binding proteins (IGFBPs) are important for IGF-1 stability. • Bone morphogenetic protein-2 (BMP-2) induces osteoblast differentiation. • IGFBP-3 counteracts the effect of BMP-2 and suppresses bone formation. Bone augmentation therapy is used in dental implantation. While techniques to induce bone formation are generally successful, the maintenance of bone mass is more difficult. Therefore, it is important to understand the mechanisms that regulate this process. Insulin-like growth factor-1 (IGF-1) is one of the most abundant growth factors that regulate bone mass, promote osteoblast differentiation, and accelerate bone formation. The activity of IGF-1 is regulated by IGF-binding proteins (IGFBPs). IGFBP-3 forms a ternary complex with IGF-1, extending its half-life in the circulating system. Therefore, IGFBP-3 acts as a stabilizer and transporter of IGF-1. Recent studies reported new IGF-1-independent functions of IGFBP-3 related with bone metabolism. In this study, we investigated the function of IGFBP-3 in osteoblast differentiation. Our results showed that IGFBP-3 decreases the expression of osteoblast differentiation markers, whose expression is enhanced by bone morphogenetic protein-2 (BMP-2). IGFBP-3 also reduced BMP-2 effect on ALP activity and mineral nodule formation. In addition, IGFBP-3 suppresses the activity of the Smad Binding Element (SBE) reporter, induced by BMP-2 signaling. These results suggest that IGFBP-3 inhibits osteoblast differentiation through the BMP-2 signal pathway, and that IGFBP-3 might play a role in bone mass maintenance in an IGF-1-dependent and -independent manner.

60 APPLIED LIFE SCIENCES↗