bluuebunny/crossref_metadata_2025_split huggingface dataset:
Review of interaction of bullets and fragments with skin-bone-muscle parenchyma
Authors: Pandey Punit , Joshi Yugal , Ganpule Shailesh 
Published: February 2025

Abstract
Penetrating projectile injuries from bullets and fragments remain a leading cause of casualties in modern warfare. Understanding the mechanical interaction of these projectiles with biological tissues is crucial for designing and optimizing both modern ammunition and protective systems. Towards this end, we review the mechanics of the interaction of the projectiles with various biological tissues. The review focuses on the relationship between projectile characteristics (velocity, shape, design), specific tissue, and the resulting injury. The aim is to understand the relationship between these factors and the energy or energy density required to inflict specific tissue-specific injuries. The review highlights the distinct failure mechanisms for each tissue for bullets and fragments. Skin failure is manifested by a combination of crushing, shearing, and elastic hole enlargement. Bone fracture predominantly shows conical cavity formation and associated radial and concentric cracks. Muscle and brain failures involve shearing and temporary cavity formation. Eye, due to its delicate nature, is highly susceptible to penetration by small projectiles with minimal compression. The data suggests significant variations in the energy density needed for perforation depending on the tissue type and projectile characteristics. For example, skin perforation requires a lower energy density (0.1-0.2 J/mm2) compared to bone (0.05-3.2 J/mm2). Further, the traditional 80 J energy criteria of a projectile for defining the lethality threshold might be overly conservative, especially for smaller projectiles. This review also highlights the importance of considering energy density as casualty criteria.
A comparison of Bayesian and frequentist confidence intervals in the presence of a late Universe degeneracy
Authors: Ó. Colgáin Eoin , Pourojaghi Saeed , Sheikh-Jabbari M. M. , Sherwin Darragh 
Published: February 2025

Abstract
Hubble tension is a problem in one-dimensional (1D) posteriors, since local

$$H_0$$

H
0

determinations are only sensitive to a single parameter. Projected 1D posteriors for

$$\Lambda $$

Λ

CDM cosmological parameters become more non-Gaussian with increasing effective redshift when the model is fitted to redshift-binned data in the late Universe. We explain mathematically why this non-Gaussianity arises and show, using observational Hubble data (OHD), that Markov chain Monte Carlo (MCMC) marginalisation leads to 1D posteriors that fail to track the

$$\chi ^2$$

χ
2

minimum at

$$68\%$$

68
%

confidence level in high redshift bins. To gain a second perspective, we resort to profile likelihoods as a complementary technique. Doing so, we observe that

$$z \gtrsim 1$$

z
≳
1

cosmic chronometer (CC) data currently prefer a non-evolving (constant) Hubble parameter over a Planck-

$$\Lambda $$

Λ

CDM cosmology at

$$\sim 2 \sigma $$

∼
2
σ

. Within the Hubble tension debate, it is imperative that subsamples of data sets with differing redshifts yield similar

$$H_0$$

H
0

values. In addition, we confirm that MCMC degeneracies observed in 2D posteriors are not due to curves of constant

$$\chi ^2$$

χ
2

. Finally, on the assumption that the Planck-

$$\Lambda $$

Λ

CDM cosmological model is correct, using profile likelihoods we confirm a

$$>2 \sigma $$

>
2
σ

discrepancy with Planck-

$$\Lambda $$

Λ

CDM in a combination of CC and baryon acoustic oscillations (BAO) data beyond

$$z \sim 1.5$$

z
∼
1.5

. This confirms a discrepancy reported earlier with fresh methodology.
Beyond the inert doublet: imprints of Scotogenic Yukawa interactions at FCC-ee
Authors: Marzo Carlo , Melis Aurora 
Published: February 2025

Abstract
It is tempting to interpret the minuscule scale of neutrino masses as a symptom of its radiative origin. In light of the notable leap in precision expected at the Future Circular Collider, we explore areas of the parameter space that can simultaneously support the detectable Higgs-strahlung signal with parallel ones from forthcoming measurements in low-energy observables. We pinpoint the role that the extra fermions have in shaping a signal distinct from the pure Inert Doublet one. The details of the full one-loop computation and on-shell renormalization are presented. Both normal and inverted hierarchies for the radiatively generated neutrino masses and angles are investigated.
Theoretical study of the open-flavored tetraquark $$T_{c\bar{s}}(2900)$$ in the process $$\Lambda _b\rightarrow K^0D^0\Lambda $$
Authors: Lyu Wen-Tao , Lyu Yun-He , Duan Man-Yu , Wang Guan-Ying , Chen Dian-Yong , Wang En 
Published: February 2025

Abstract
Recently, the LHCb Collaboration has measured the processes

$$B^+\rightarrow D^-D_s^+\pi ^+$$

B
+

→

D
-

D
s
+

π
+

and

$$B^+\rightarrow \bar{D}^0D_s^+\pi ^+$$

B
+

→

D

¯

0

D
s
+

π
+

, where the

$$D_s^+\pi ^-$$

D
s
+

π
-

and

$$D_s^+\pi ^+$$

D
s
+

π
+

invariant mass distributions show the significant signals of two new open-flavored tetraquark states

$$T_{c\bar{s}}(2900)^0$$

T

c

s

¯

(
2900
)

0

and

$$T_{c\bar{s}}(2900)^{++}$$

T

c

s

¯

(
2900
)

+
+

, as the two of the isospin triplet. In this work, we have investigated the process

$$\Lambda _b\rightarrow K^0D^0\Lambda $$

Λ
b

→

K
0

D
0

Λ

by taking into account the tetraquark state

$$T_{c\bar{s}}(2900)^0$$

T

c

s

¯

(
2900
)

0

and the intermediate nucleon resonance

$$N^*(1535)$$

N
∗

(
1535
)

, which could be dynamically generated by the interactions of the

$$D^*K^*/D^*_s\rho $$

D
∗

K
∗

/

D
s
∗

ρ

and the pseudoscalar meson-octet baryon, respectively. Our results show that a clear peak of the open-flavored tetraquark

$$T_{c\bar{s}}(2900)$$

T

c

s

¯

(
2900
)

may appear in the

$$K^0D^0$$

K
0

D
0

invariant mass distribution of the process

$$\Lambda _b\rightarrow K^0D^0\Lambda $$

Λ
b

→

K
0

D
0

Λ

, which could be tested by future experiments.
Exhibiting stable model of dark energy compact star with Tolman-VI solution under complexity free system
Authors: Nazar Hammad , Majeed Abdul , Abbas Ghulam , Ashraf Asifa , Channuie Phongpichit 
Published: February 2025

Abstract
Several recent developments have highlighted the significance of the vanishing complexity factor formalism in understanding the structure and evolution of stellar relativistic compact objects. This formalism, introduced through a novel definition proposed by Herrera (Phys. Rev. D 97:044010, 2018), offers valuable insights into the dynamics of such systems. In this manuscript, we explored a class of realistic solutions to the static and spherically symmetric field equations characterized by two fluid distributions: ordinary stellar matter and dark energy, within the framework of this formalism. Utilizing the well-known Tolman-VI solution as the seed ansatz for the metric coefficient

$$g_{rr},$$

g

rr

,

we employed the complexity-free format to derive an analytic solution for the other metric coefficient,

$$g_{tt}.$$

g

tt

.

Subsequently, we obtained the solutions of gravitational field equations for our proposed spacetime model by incorporating the linear dark energy equation of state. These results were applied to the astrophysical compact star candidate LMC X-4, with

$$M =1.04 M_\odot $$

M
=
1.04

M
⊙

and

$$R =8.4~\text {km}.$$

R
=
8.4

km
.

The potential viability and credibility of the proposed dark star solutions were thoroughly analyzed by examining key constraints, including the regularity of metric functions, physical adequacy through matter variables, state parameter behavior, energy conditions, stability tests (such as pressure anisotropy and hydrostatic equilibrium), the speed of sound, and the mass–radius relation for this compact star candidate. Notably, the estimated values of the dark energy coupling factor, presented in Table 1, highlight the exotic nature of the fluid distribution and effectively quantify the contribution of dark energy to the structure and evolution of an ultra-relativistic dark compact star. These findings strongly support our model solutions and demonstrate improvements over previously reported results in Rej et al. (Chin J Phys 87:608, 2024).
Abstract A007: Regulation of DNA methylation and gene expression in T-cell acute lymphoblastic leukemia by IKAROS tumor suppressor
Authors: Ding Yali , He Bing , Bogush Daniel , Schramm Joseph W , Desai Dhimant , Dovat Sinisa 
Published: February 2025

Abstract
The IKZF1 gene encodes IKAROS - a DNA-binding zinc finger protein that functions as a tumor suppressor in T-cell acute lymphoblastic leukemia (T-ALL). Deletion of IKZF1 results in the development of high-risk leukemia. The mechanisms through which IKAROS regulates gene expression and cellular proliferation in T-ALL are largely unknown. We studied IKAROS role in regulation of DNA methylation and epigenomic regulation of gene expression in Ikzf1-null mouse T-ALL cells and following Ikzf1 re-introduction into Ikzf1-null mouse T-ALL cells. We used reduced representation bisulfite sequencing (RRBS), with ChIP-seq of IKAROS, histone deacetylase 1 (HDAC1), EZH2, and ATAC-seq along with CUT&Tag of histone modification markers, coupled with RNA-seq to study dynamic effect of IKAROS in IKZF1-null T-ALL and at several time points following Ikzf1 re-introduction. Deletion of Ikzf1 results in severe depletion of facultative heterochromatin, associated with DNA methylation at promoters of several tumor suppressor genes. Re-introduction of Ikzf1 within 24 hours results in global re-distribution of DNA methylation. IKAROS DNA binding was directly associated with de novo DNA methylation at promoters of genes that positively regulate several oncogenic pathways. DNA binding of IKAROS also resulted in the loss of DNA methylation, HDAC1 recruitment to promoters, EZH2 re-distribution, and de novo formation of H3K27me3 facultative heterochromatin. This was associated with cessation of cellular proliferation and induction of T-cell differentiation. Dynamic analysis of DNA methylation for 3 days following Ikzf1 re-introduction, revealed that the large fraction of DNA with altered methylation status due to IKAROS binding, preserved the altered DNA methylation pattern for at least two additional days, despite lack of IKAROS DNA binding in subsequent days following Ikzf1 re-introduction. In conclusion, our results demonstrated that IKAROS’ tumor suppressor function in T-ALL, occurs via regulation of DNA methylation and recruitment of HDAC1 and EZH2 to the promoters of its target genes. Results provide novel insight into the role of DNA methylation in regulation of gene expression in T-ALL with IKZF1-deletion and epigenomic regulation of tumor suppression in T-ALL.
Citation Format: Yali Ding, Bing He, Daniel Bogush, Joseph W Schramm, Dhimant Desai, Sinisa Dovat. Regulation of DNA methylation and gene expression in T-cell acute lymphoblastic leukemia by IKAROS tumor suppressor [abstract]. In: Proceedings of the AACR Special Conference in Cancer Research: DNA Methylation, Clonal Hematopoiesis, and Cancer; 2025 Feb 1-4; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2025;85(3 Suppl):Abstract nr A007.
Abstract A010: Dnmt3a2 ensures proper enhancer DNA methylation during embryonic development
Authors: Liu Minmin , Urrutia Guillermo A , Shereda Rachel , Liang Gangning , Jones Peter A 
Published: February 2025

Abstract
Proper enhancer function and switching is essential for the development of vertebrates and is known to be controlled by DNA cytosine methylation. We used isoform-specific knockouts of the two known DNA methyltransferase variants, Dnmt3a1 and Dnmt3a2 to probe their roles in enhancer methylation in embryogenesis and in postnatal development. Mouse embryos lacking Dnmt3a1 showed minimal loss of genomic methylation confirming that this isoform is not required for embryonic development. However, they were smaller than their littermates and died about 4 weeks after birth with considerable demethylation in the brain as has been previously reported. On the other hand, embryos lacking Dnmt3a2 showed widespread genomic hypomethylation which was particularly prevalent in enhancers and imprinted genes. Interestingly these methylation deficits were largely repaired after birth, presumably by the remaining Dnmt3a1 isoform. The mice were viable; however, they showed an increased prevalence of sporadic phenotypes including anophthalmia, hydronephrosis, hydrocephalus and male infertility which have previously been observed in laboratory mice. Hypomethylation of several imprinted genes was also observed in sperm which might potentially explain the infertility phenotype. There is therefore an interplay between the 2 isoforms which is developmentally regulated and a key role for Dnmt3a2 might be the stabilization of enhancer states which lessening the chance of sporadic phenotypes arising after birth.
Citation Format: Minmin Liu, Guillermo A Urrutia, Rachel Shereda, Gangning Liang, Peter A Jones. Dnmt3a2 ensures proper enhancer DNA methylation during embryonic development [abstract]. In: Proceedings of the AACR Special Conference in Cancer Research: DNA Methylation, Clonal Hematopoiesis, and Cancer; 2025 Feb 1-4; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2025;85(3 Suppl):Abstract nr A010.
Abstract A016: DNA methylation variability in aging and Clonal Hematopoiesis
Authors: Pompetti Anthony J , Chung Woonbok , Jelinek Jaroslav , Egodage Tanya , Issa Jean-Pierre 
Published: February 2025

Abstract
DNA methylation (DNAm) reflects regions of the genome that are transcriptionally repressed or active depending on the methylation level. Multitudes of DNAm “clocks” have been created to predict biological age and health outcomes. Deviations in biological age from chronological age reflect an alteration in the normal biological aging process. Clonal hematopoiesis of indeterminate potential (CHIP) arises in hematopoietic stem cells that have accumulated somatic mutations in key driver genes which provide a selective advantage for clonal expansion. Subjects with CHIP mutations are more prone to negative clinical outcomes such as coronary heart disease. While DNAm and CHIP have been studied for the past decade, the associations between the two are only now starting to become apparent. In this study we propose an improved measurement of aging based on the Jenson-Shannon distance (JSD) and associate this measurement with CHIP and adverse clinical outcomes. Bisulfite amplicon sequencing of 20 CpG-rich targets that change in methylation with age was performed on an initial cohort of 155 individuals from the National Institute of Neurological Disorders and Stroke (NINDS). JSD was used to construct a DNA methylation chaos clock (DMC) on these targets. DMC provided better predictions of chronological age than DNAm alone (r=0.9; p&lt;0.0001). We validated our findings in 286 individuals from Cooper University Hospital for Management of Trauma where the accuracy of the DMC was confirmed in correlations of predicted vs actual age (r=0.86; p&lt;0.0001). We next examined the association between DMC age acceleration and clinical outcomes. It was found that in individuals over the age of 50, DMC acceleration was associated with smoking and disease incidence (e.g. congestive heart failure and chronic obstructive pulmonary disease) independent of chronological age. The incidence of CHIP mutations in three key driver genes (DNMT3A, TET2, and ASXL1) was assayed in a subset of 345 individuals from both cohorts. Individuals with CHIP mutations in key driver genes had greater deviations in their predicted age than individuals without CHIP mutations (p&lt;0.001). This study demonstrates that the DMC assay is a candidate for improvements in our measurements of biological age and it reflects important changes in an individual’s biological aging process.
Citation Format: Anthony J Pompetti, Woonbok Chung, Jaroslav Jelinek, Tanya Egodage, Jean-Pierre Issa. DNA methylation variability in aging and Clonal Hematopoiesis [abstract]. In: Proceedings of the AACR Special Conference in Cancer Research: DNA Methylation, Clonal Hematopoiesis, and Cancer; 2025 Feb 1-4; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2025;85(3 Suppl):Abstract nr A016.
Abstract A020: Clonal hematopoiesis is associated with acute kidney injury in the context of breast, endometrial, and ovarian cancers
Authors: Ruthen Neil , Kim Minsoo , Tan Hui Zhuan , Khandwala Yash , Hakimi A. Ari , Won Alice , Reznik Ed , Jaimes Edgar A 
Published: February 2025

Abstract
Clonal hematopoiesis of indeterminate potential (CHIP) has been linked to a higher risk for acute kidney injury (AKI) (Vlasschaert et al. 2024). The high rate of AKI in the context of cancer is often attributed to the administration of nephrotoxic therapies or comorbidities. However, the effect of the interplay between tumor-associated physiologies, treatment, and CHIP on AKI incidence has yet to be characterized. Here, we model the prognostic value of CHIP in predicting AKI across twenty cancer types. Leveraging a single institutional database, we identified 25,189 patients with longitudinal serum creatinine (sCr) measurements, targeted sequencing of paired tumor and blood samples (MSKCC-IMPACT), and well-documented treatment histories. We called AKI events directly from longitudinal measurements by evaluating increases in sCr compared to the average sCr over the prior 90-day window using diagnostic criteria from the Kidney Disease Improving Global Outcomes (KDIGO) consortium. CHIP mutations were called using a previously reported two-tiered filtering schema (Bolton et al. 2020). In our cohort, we found that 26.5% of patients experienced at least one AKI event and 38.0% of patients presented with at least one CHIP mutation. We then performed competing risks analyses over cox proportional hazards models to test for the association of CHIP and time to AKI from the first creatinine measurement, adjusting for age, gender, histories of diabetes, smoking, and prior receipt of cisplatin. CHIP was significantly associated with decreased time to AKI in the context of breast, endometrial, and ovarian cancers (Benjamini-Hochberg-corrected p &lt; 0.05). Subsequent univariate Kaplan-Meier analyses revealed TP53, PPM1D, SRFS2 mutations were associated with 7.50, 9.05, and 9.73-year decreases in median time to AKI (p &lt; 0.01). Our study reveals specific CHIP mutations as prognostic markers for AKI for patients with breast, endometrial, and ovarian cancers. These findings may guide future clinical decision-making regarding treatment for patients with CHIP mutations.
Citation Format: Neil Ruthen, Minsoo Kim, Hui Zhuan Tan, Yash Khandwala, A. Ari Hakimi, Alice Won, Ed Reznik, Edgar A Jaimes. Clonal hematopoiesis is associated with acute kidney injury in the context of breast, endometrial, and ovarian cancers [abstract]. In: Proceedings of the AACR Special Conference in Cancer Research: DNA Methylation, Clonal Hematopoiesis, and Cancer; 2025 Feb 1-4; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2025;85(3 Suppl):Abstract nr A020.
Abstract B002: DNA methylation protects cancer cells against senescence
Authors: Chen Xiaoying , Yamaguchi Kosuke , Rodgers Brianna , Goehrig Delphine , Vindrieux David , Lahaye Xavier , Nolot Matthieu , Ferry Laure , Martin Nadine , Dubus Pierre , Miura Fumihito , Ito Takashi , Manel Nicolas , Kanemaki Masato , Bernard David , Defossez Pierre-Antoine 
Published: February 2025

Abstract
Inhibitors of DNA methylation such as 5-aza-deoxycytidine are widely used in experimental and clinical settings. However, their mechanism of action is such that DNA damage inevitably cooccurs with loss of DNA methylation, making it challenging to discern their respective effects. Here we deconvolute the effects of decreased DNA methylation and DNA damage on cancer cells, by using degron alleles of key DNA methylation regulators (DNMT1 and UHRF1). We report that cancer cells with decreased DNA methylation — but no DNA damage— enter cellular senescence, with G1 arrest, senescence-associated secretory phenotype (SASP) expression, and senescence-associated beta-galactosidase (SA-β-gal) positivity. This senescence is independent of p53 and Rb, but involves p21, which is cytoplasmic and inhibits apoptosis. The suppression of cyclic GMP-AMP synthase (cGAS) alleviates SASP response and lysosomal activity, and this process is independent of stimulator of interferon genes (STING). Xenograft experiments show that tumor cells can be made senescent in vivo by decreasing DNA methylation. These findings reveal the intrinsic effects of loss of DNA methylation in cancer cells and have practical implications for future therapeutic approaches.
Citation Format: Xiaoying Chen, Kosuke Yamaguchi, Brianna Rodgers, Delphine Goehrig, David Vindrieux, Xavier Lahaye, Matthieu Nolot, Laure Ferry, Nadine Martin, Pierre Dubus, Fumihito Miura, Takashi Ito, Nicolas Manel, Masato Kanemaki, David Bernard, Pierre-Antoine Defossez. DNA methylation protects cancer cells against senescence [abstract]. In: Proceedings of the AACR Special Conference in Cancer Research: DNA Methylation, Clonal Hematopoiesis, and Cancer; 2025 Feb 1-4; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2025;85(3 Suppl):Abstract nr B002.
Abstract B003: BRAFV600E is essential for maintenance of the CpG island methylator phenotype and DNA methylation of PRC2 target genes in colon cancer
Authors: El Bouazzaoui Layla , Bugter Jeroen M , Küçükköse Emre , Verheem André , Post Jasmin B , Fenderico Nicola , Borel Rinkes Inne H.M , Snippert Hugo J.G , Maurice Madelon M , Kranenburg Onno 
Published: February 2025

Abstract
In colon cancer, the BRAFV600E mutation is strongly associated with the CpG island methylator phenotype (CIMP). Here, we characterized the contribution of BRAFV600E to maintenance of aberrant DNA methylation. A reverse CRISPR gene editing approach was applied to revert the V600E mutation in BRAF back to wildtype (E600V) in organoids derived from a late-stage tumour. DNA methylation analyses identified 5187 differentially methylated CpGs within CpG islands, predominantly hypermethylated (82%) in BRAFV600E organoids, including genes associated with CIMP, as well as Polycomb Repressor Complex 2 (PRC2) target genes. RNA sequencing showed that expression of those genes was concordantly repressed. Furthermore, BRAFV600Einduced high expression of PRC2 core components (EZH2, SUZ12, EED), caused PRC2-induced H3K27 trimethylation in promoter regions, and maintained a PRC2-associated embryonic phenotype. This phenotype was lost following mutation correction or pharmacological inhibition of DNA methylation. These findings show that BRAFV600E maintains aberrant DNA and histone methylation patterns in advanced colon cancer, likely preserving the transformed phenotype by silencing of PRC2 target genes. Epigenetic therapies may have value in the treatment of BRAFV600E-mutant colon cancer.
Citation Format: Layla El Bouazzaoui, Jeroen M Bugter, Emre Küçükköse, André Verheem, Jasmin B Post, Nicola Fenderico, Inne H.M Borel Rinkes, Hugo J.G Snippert, Madelon M Maurice, Onno Kranenburg. BRAFV600E is essential for maintenance of the CpG island methylator phenotype and DNA methylation of PRC2 target genes in colon cancer [abstract]. In: Proceedings of the AACR Special Conference in Cancer Research: DNA Methylation, Clonal Hematopoiesis, and Cancer; 2025 Feb 1-4; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2025;85(3 Suppl):Abstract nr B003.