bluuebunny/crossref_metadata_2025_split huggingface dataset:
Small for gestational age preterm infants and later adiposity and height: A systematic review and meta‐analysis
Authors: Elmrayed Seham , Pinto Jahaira , Tough Suzanne C. , McDonald Sheila W. , Scime Natalie V. , Wollny Krista , Lee Yoonshin , Kramer Michael S. , Ospina Maria B. , Lorenzetti Diane L. , Madubueze Ada , Leung Alexander A. , Kumar Manoj , Fenton Tanis R. 
Published: August 2023

AbstractBackgroundOverweight and obesity and their consequent morbidities are important worldwide health problems. Some research suggests excess adiposity origins may begin in fetal life, but unknown is whether this applies to infants born preterm.ObjectiveThe objective of the study was to assess the association between small for gestational age (SGA) birth and later adiposity and height among those born preterm.Data sourcesMEDLINE, EMBASE and CINAHL until October 2022.Study selection and data extractionStudies were included if they reported anthropometric (adiposity measures and height) outcomes for participants born preterm with SGA versus non‐SGA. Screening, data extraction and risks of bias assessments were conducted in duplicate by two reviewers.SynthesisWe meta‐analysed across studies using random‐effects models and explored potential heterogeneity sources.ResultsThirty‐nine studies met the inclusion criteria. In later life, preterm SGA infants had a lower body mass index (−0.66 kg/m2, 95% CI −0.79, −0.53; 32 studies, I2 = 16.7, n = 30,346), waist circumference (−1.20 cm, 95% CI −2.17, −0.23; 13 studies, I2 = 19.4, n = 2061), lean mass (−2.62 kg, 95% CI −3.45, 1.80; 7 studies, I2 = 0, n = 205) and height (−3.85 cm, 95% CI −4.73, −2.96; 26 studies, I2 = 52.6, n = 4174) compared with those preterm infants born non‐SGA. There were no differences between preterm SGA and preterm non‐SGA groups in waist/hip ratio, body fat, body fat per cent, truncal fat per cent, fat mass index or lean mass index, although power was limited for some analyses. Studies were rated at high risk of bias due to potential residual confounding and low risk of bias in other domains.ConclusionsCompared to their preterm non‐SGA peers, preterm infants born SGA have lower BMI, waist circumference, lean body mass and height in later life. No differences in adiposity were observed between SGA preterm infants and non‐SGA preterm infants.
Cover Image
Authors: Schrock Morgan S. , Zalenski Abigail A. , Tallman Miranda M. , Kollin Luke , Bratasz Anna , Weeks Griffin , Miller Margaret A. , Sweeney Courtney N. , Pluhar G. Elizabeth , Olin Michael R. , Kisseberth William C. , Bentley R. Timothy , Dickinson Peter J. , York Daniel , Webb Amy , Wang Xu , Moore Sarah , Venere Monica , Summers Matthew K. 
Published: August 2023

The cover image is based on the Original Article Establishment and characterization of two novel patient‐derived lines from canine high‐grade glioma by Morgan S. Schrock et al., https://doi.org/10.1111/vco.12912.
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Critical role for ribonucleoside-diphosphate reductase subunit M2 in ALV-J-induced activation of Wnt/β-catenin signaling via interaction with P27
Authors: Tang Shuang , Leng Mei , Tan Chen , Zhu Lin , Pang Yanling , Zhang Xinheng , Chang Yung-Fu , Lin Wencheng 
Published: August 2023

ABSTRACT
Avian leukemia virus subgroup J (ALV-J) causes various diseases associated with tumor formation and decreased fertility and induced immunosuppressive disease, resulting in significant economic losses in the poultry industry globally. Virus usually exploits the host cellular machinery for their replication. Although there are increasing evidences for the cellular proteins involving viral replication, the interaction between ALV-J and host proteins leading to the pivotal steps of viral life cycle are still unclear. Here, we reported that ribonucleoside-diphosphate reductase subunit M2 (RRM2) plays a critical role during ALV-J infection by interacting with capsid protein P27 and activating Wnt/β-catenin signaling. We found that the expression of RRM2 is effectively increased during ALV-J infection, and that RRM2 facilitates ALV-J replication by interacting with viral capsid protein P27. Furthermore, ALV-J P27 activated Wnt/β-catenin signaling by promoting β-catenin entry into the nucleus, and RRM2 activated Wnt/β-catenin signaling by enhancing its phosphorylation at Ser18 during ALV-J infection. These data suggest that the upregulation of RRM2 expression by ALV-J infection favors viral replication in host cells via activating Wnt/β-catenin signaling.

IMPORTANCE
Our results revealed a novel mechanism by which RRM2 facilitates ALV-J growth. That is, the upregulation of RRM2 expression by ALV-J infection favors viral replication by interacting with capsid protein P27 and activating Wnt/β-catenin pathway in host cells. Furthermore, the phosphorylation of serine at position 18 of RRM2 was verified to be the important factor regulating the activation of Wnt/β-catenin signaling. This study provides insights for further studies of the molecular mechanism of ALV-J infection.
Metabolomic analysis of pig spleen reveals African swine fever virus infection increased acylcarnitine levels to facilitate viral replication
Authors: Yang Xing , Bie Xintian , Liu Huanan , Shi Xijuan , Zhang Dajun , Zhao DengShuai , Hao Yu , Yang Jinke , Yan Wenqian , Chen Guohui , Chen Lingling , Zhu Zixiang , Yang Fan , Ma Xusheng , Liu Xiangtao , Zheng Haixue , Zhang Keshan 
Published: August 2023

ABSTRACT
African swine fever (ASF) is a devastating disease caused by the African swine fever virus (ASFV) that adversely affects the pig industry. The spleen is the main target organ of ASFV; however, the function of metabolites in the spleen during ASFV infection is yet to be investigated. To define the metabolic changes in the spleen after ASFV infection, untargeted and targeted metabolomics analyses of spleens from ASFV-infected pigs were conducted. Untargeted metabolomics analysis revealed 540 metabolites with significant differential levels. Kyoto Encyclopedia of Genes and Genomes pathway analysis showed that these metabolites were mainly enriched in metabolic pathways, including nucleotide metabolism, purine metabolism, arginine biosynthesis, and neuroactive ligand-receptor interaction. Moreover, 134 of 540 metabolites quantified by targeted metabolomics analysis had differential levels and were enriched in metabolic pathways such as the biosynthesis of cofactors, ABC transporters, and biosynthesis of amino acids. Furthermore, coalition analysis of untargeted and targeted metabolomics data revealed that the levels of acylcarnitines, which are intermediates of fatty acid β-oxidation, were significantly increased in ASFV-infected spleens compared with those in the uninfected spleens. Moreover, inhibiting fatty acid β-oxidation significantly reduced ASFV replication, indicating that fatty acid β-oxidation is essential for this process. To our knowledge, this is the first report presenting the metabolite profiles of ASFV-infected pigs. This study revealed a new mechanism of ASFV-mediated regulation of host metabolism. These findings provide new insights into the pathogenic mechanisms of ASFV, which will benefit the development of target drugs for ASFV replication.

IMPORTANCE

African swine fever virus, the only member of the
Asfarviridae
family, relies on hijacking host metabolism to meet the demand for self-replication. However, the change in host metabolism after African swine fever virus (ASFV) infection remains unknown. Here, we analyzed the metabolic changes in the pig spleen after ASFV infection for the first time. ASFV infection increased the levels of acylcarnitines. Inhibition of the production and metabolism of acylcarnitines inhibited ASFV replication. Acylcarnitines are the vital intermediates of fatty acid β-oxidation. This study highlights the critical role of fatty acid β-oxidation in ASFV infection, which may help identify target drugs to control African swine fever disease.
Genomic epidemiology and antibiotic susceptibility profiling of uropathogenic
Escherichia coli
among children in the United States
Authors: Salamzade Rauf , McElheny Christi L. , Manson Abigail L. , Earl Ashlee M. , Shaikh Nader , Doi Yohei 
Published: August 2023

ABSTRACT

Escherichia coli
is the most common cause of urinary tract infections (UTIs) in children, and yet the underlying mechanisms of virulence and antibiotic resistance and the overall population structure of the species is poorly understood within this age group. To investigate whether uropathogenic
E. coli
(UPEC) from children who developed pyelonephritis carried specific genetic markers, we generated whole-genome sequence data for 96 isolates from children with UTIs. This included 57 isolates from children with either radiologically confirmed pyelonephritis or cystitis and 27 isolates belonging to the well-known multidrug-resistant sequence type ST131, selected to investigate their population structure and antibiotic resistance characteristics. We observed a UPEC population structure that is similar to those reported in adults. In comparison with prior investigations, we found that the full
pap
operon was more common among UPEC from pediatric cases of pyelonephritis. Further, in contrast with recent reports that the P-fimbriae adhesin-encoding
papGII
allele is substantially more prevalent in invasive UPEC from adults, we found
papGII
was common to both invasive and non-invasive UPEC from children. Among the set of ST131 isolates from children with UTIs, we found antibiotic resistance was correlated with known genetic markers of resistance, as in adults. Unexpectedly, we observed that
fimH
30, an allele of the fimbrial gene
fimH
often used as a proxy to type ST131 isolates into the most drug-resistant subclade C, was carried by some of the subclade A and subclade B isolates, suggesting that the
fimH
30 allele could confer a selective advantage for UPEC.

IMPORTANCE

Urinary tract infections (UTIs), which are most often caused by
Escherichia coli
, are not well studied in children. Here, we examine genetic characteristics that differentiate UTI-causing bacteria in children that either remain localized to the bladder or are involved in more serious kidney infections. We also examine patterns of antibiotic resistance among strains from children that are part of
E. coli
sequence type 131, a group of bacteria that commonly cause UTIs and are known to have high levels of drug resistance. This work provides new insight into the virulence and antibiotic resistance characteristics of the bacteria that cause UTIs in children.
Evidence-based clinical practice guidelines on postdural puncture headache: a consensus report from a multisociety international working group
Authors: Uppal Vishal , Russell Robin , Sondekoppam Rakesh V , Ansari Jessica , Baber Zafeer , Chen Yian , DelPizzo Kathryn , Dirzu Dan Sebastian , Kalagara Hari , Kissoon Narayan R , Kranz Peter G , Leffert Lisa , Lim Grace , Lobo Clara , Lucas Dominique Nuala , Moka Eleni , Rodriguez Stephen E , Sehmbi Herman , Vallejo Manuel C , Volk Thomas , Narouze Samer 
Published: August 2023

IntroductionPostdural puncture headache (PDPH) can follow unintentional dural puncture during epidural techniques or intentional dural puncture during neuraxial procedures such as a lumbar puncture or spinal anesthesia. Evidence-based guidance on the prevention, diagnosis or management of this condition is, however, currently lacking. This multisociety guidance aims to fill this void and provide practitioners with comprehensive information and patient-centric recommendations to prevent, diagnose and manage patients with PDPH.MethodsBased on input from committee members and stakeholders, the committee cochairs developed 10 review questions deemed important for the prevention, diagnosis and management of PDPH. A literature search for each question was performed in MEDLINE (Ovid) on 2 March 2022. The results from each search were imported into separate Covidence projects for deduplication and screening, followed by data extraction. Additional relevant clinical trials, systematic reviews and research studies published through March 2022 were also considered for the development of guidelines and shared with contributors. Each group submitted a structured narrative review along with recommendations graded according to the US Preventative Services Task Force grading of evidence. The interim draft was shared electronically, with each collaborator requested to vote anonymously on each recommendation using two rounds of a modified Delphi approach.ResultsBased on contemporary evidence and consensus, the multidisciplinary panel generated 50 recommendations to provide guidance regarding risk factors, prevention, diagnosis and management of PDPH, along with their strength and certainty of evidence. After two rounds of voting, we achieved a high level of consensus for all statements and recommendations. Several recommendations had moderate-to-low certainty of evidence.ConclusionsThese clinical practice guidelines for PDPH provide a framework to improve identification, evaluation and delivery of evidence-based care by physicians performing neuraxial procedures to improve the quality of care and align with patients’ interests. Uncertainty remains regarding best practice for the majority of management approaches for PDPH due to the paucity of evidence. Additionally, opportunities for future research are identified.
High pressure effects on ferroelectric tetragonal phase in BaTi1−xFexO3 (x=1%)
Authors: Tran T. A. , Tran T. K. C. , Nguyen L. V. T. , Khan D. T. , Truong-Son L. V. , Thao L. T. P. , Truong V. C. , Thanh-Nghiem N. , Phuc H. T. , Jabarov S. H. , Tien D. P. T. 
Published: August 2023

The pressure-driven phase transformation in polycrystalline BaTi[Formula: see text]FexO3 ([Formula: see text]%), synthesized by a solid-state reaction method, was investigated using synchrotron X-ray diffraction and Raman spectroscopy. All measurements were performed at room temperature within a large pressure range up to 36.5 GPa. The results clearly demonstrate a phase transformation from the ferroelectric tetragonal structure of P4mm symmetry to the paraelectric cubic structure of Pm-3m symmetry in the studied sample at the pressure of about 18 GPa. This phase transformation pressure is much higher than those previously reported for BaTiO3-based systems, indicating the stabilization of the ferroelectric phase by doping 1% Fe into BaTiO3. Feature modes of the tetragonal phase still persist while some new modes appear in the Raman spectra at pressures above 18 GPa. This is probably due to accumulated stress and/or local microscopic disorders in the sample, which are associated with the displacement of the Ti atoms along unit-cell diagonals.
Planetary Relationships to Birth (Imputed Conception) Rates in Humans: A Signature of Cosmic Origin?
Authors: Georgiopoulou E. , Hofmann S. , Maroudas M. , Mastronikolis A. , Matteson E. L. , Tsagri M. , Zioutas K. 
Published: August 2023

This report addresses the time dependence of normal biomedical processes. The conception rate in humans shows relationships that strikingly coincide with planetary periodicities like the orbital period of Jupiter, the 11 years solar cycle and the 237 days Jupiter–Venus synod, and the combined dependence on Jupiter with Mars’ orbital position. The birth rates are used as conception surrogates based on a data set available from the Minnesota Department of Health. The statistical significance of each independent analysis (far) exceeds 5[Formula: see text]. This result cannot be explained with known science. As with other observations in Physics and Medicine (i.e., melanoma), tentatively the only viable explanation we have is the otherwise invisible streaming matter from the dark Universe we live in. The favored dark matter scenario involves streams or clusters as opposed to an isotropic dark sector. The dark Universe scenario has been the driving idea for this type of work. The high sensitivity of living matter to the tiniest external impact might help identify the nature of the dark matter particles, a major problem in all physics since the 1930s. This work is a model for evaluating other biological processes and mutation rates.
Molecular Results and Potential Biomarkers Identified from the Phase 3 MILO/ENGOT-ov11 Study of Binimetinib versus Physician Choice of Chemotherapy in Recurrent Low-Grade Serous Ovarian Cancer
Authors: Grisham Rachel N. , Vergote Ignace , Banerjee Susana , Drill Esther , Kalbacher Elsa , Mirza Mansoor Raza , Romero Ignacio , Vuylsteke Peter , Coleman Robert L. , Hilpert Felix , Oza Amit M. , Westermann Anneke , Oehler Martin K. , Pignata Sandro , Aghajanian Carol , Colombo Nicoletta , Cibula David , Moore Kathleen N. , del Campo Josep M. , Berger Regina , Marth Christian , Sehouli Jalid , O'Malley David M. , Churruca Cristina , Kristensen Gunnar , Clamp Andrew , Farley John , Iyer Gopa , Ray-Coquard Isabelle , Monk Bradley J. 
Published: August 2023

Abstract

Purpose:
We present the results of a post hoc tumor tissue analysis from the phase 3 MILO/ENGOT-ov11 study (NCT01849874).

Patients and Methods:
Mutation/copy-number analysis was performed on tissue obtained pre-randomization. The Kaplan–Meier method was used to estimate progression-free survival (PFS). Unbiased univariate analysis, Cox regression, and binary logistic regression were used to test associations between mutation status and outcomes, including PFS and binary response by local RECIST 1.1.

Results:
MILO/ENGOT-ov11 enrolled 341 patients, ranging in age from 22 to 79, from June, 2013 to April, 2016. Patients were randomized 2:1 to binimetinib or physician's choice of chemotherapy (PCC). The most commonly altered gene was KRAS (33%). In 135 patients treated with binimetinib with response rate (RR) data, other detected MAPK pathway alterations included: NRAS (n = 11, 8.1%), BRAF V600E (n = 8, 5.9%), RAF1 (n = 2, 1.5%), and NF1 (n = 7, 5.2%). In those with and without MAPK pathway alterations, the RRs with binimetinib were 41% and 13%, respectively. PFS was significantly longer in patients with, compared with those without, MAPK pathway alterations treated with binimetinib [HR, 0.5; 95% confidence interval (CI) 0.31–0.79]. There was a nonsignificant trend toward PFS improvement in PCC-treated patients with MAPK pathway alterations compared with those without (HR, 0.82; 95% CI, 0.43–1.59).

Conclusions:
Although this hypothesis-generating analysis is limited by multiple testing, higher RRs and longer PFS were seen in patients with low-grade serous ovarian cancer (LGSOC) treated with binimetinib, and to a lesser extent in those treated with PCC, who harbored MAPK pathway alterations. Somatic tumor testing should be routinely considered in patients with LGSOC and used as a future stratification factor.
SPOP Mutations Target STING1 Signaling in Prostate Cancer and Create Therapeutic Vulnerabilities to PARP Inhibitor–Induced Growth Suppression
Authors: Geng Chuandong , Zhang Man-Chao , Manyam Ganiraju C. , Vykoukal Jody V. , Fahrmann Johannes F. , Peng Shan , Wu Cheng , Park Sanghee , Kondraganti Shakuntala , Wang Daoqi , Robinson Brian D. , Loda Massimo , Barbieri Christopher E. , Yap Timothy A. , Corn Paul G. , Hanash Samir , Broom Bradley M. , Pilié Patrick G. , Thompson Timothy C. 
Published: August 2023

Abstract

Purpose:
Speckle-type POZ protein (SPOP) is important in DNA damage response (DDR) and maintenance of genomic stability. Somatic heterozygous missense mutations in the SPOP substrate-binding cleft are found in up to 15% of prostate cancers. While mutations in SPOP predict for benefit from androgen receptor signaling inhibition (ARSi) therapy, outcomes for patients with SPOP-mutant (SPOPmut) prostate cancer are heterogeneous and targeted treatments for SPOPmut castrate-resistant prostate cancer (CRPC) are lacking.

Experimental Design:
Using in silico genomic and transcriptomic tumor data, proteomics analysis, and genetically modified cell line models, we demonstrate mechanistic links between SPOP mutations, STING signaling alterations, and PARP inhibitor vulnerabilities.

Results:
We demonstrate that SPOP mutations are associated with upregulation of a 29-gene noncanonical (NC) STING (NC-STING) signature in a subset of SPOPmut, treatment-refractory CRPC patients. We show in preclinical CRPC models that SPOP targets and destabilizes STING1 protein, and prostate cancer–associated SPOP mutations result in upregulated NC-STING–NF-κB signaling and macrophage- and tumor microenvironment (TME)–facilitated reprogramming, leading to tumor cell growth. Importantly, we provide in vitro and in vivo mechanism-based evidence that PARP inhibitor (PARPi) treatment results in a shift from immunosuppressive NC-STING–NF-κB signaling to antitumor, canonical cGAS–STING–IFNβ signaling in SPOPmut CRPC and results in enhanced tumor growth inhibition.

Conclusions:
We provide evidence that SPOP is critical in regulating immunosuppressive versus antitumor activity downstream of DNA damage–induced STING1 activation in prostate cancer. PARPi treatment of SPOPmut CRPC alters this NC-STING signaling toward canonical, antitumor cGAS–STING–IFNβ signaling, highlighting a novel biomarker-informed treatment strategy for prostate cancer.
Abstract A003: Kinome-wide siRNA screening identifies DCLK2 as a TBK1 activator and therapeutic target for ccRCC
Authors: Hu Lianxin , Zhang Qing 
Published: August 2023

Abstract
TBK1 has been identified as a potential therapeutic target in multiple cancers. However, it is challenging to target TBK1 in clinical practice due to lack of selectivity for TBK1 inhibitors and its role involved in innate immune signaling. To overcome this difficulty, one approach would be to identify a critical upstream regulator of TBK1 that can be targeted therapeutically, especially in clear cell Renal Cell Carcinoma (ccRCC) displaying hyper-activated TBK1 activity due to VHL loss. In this study, we perform a kinome-wide siRNA screening and identify Doublecortin like kinase 2 (DCLK2) as a novel TBK1 regulator in ccRCC. DCLK2 binds with TBK1 and directly phosphorylates TBK1 on Ser172. Depletion of DCLK2 inhibits anchorage independent colony growth of kidney cancer cells as well as kidney tumorigenesis in orthotopic xenograft models. DCLK2 gene product contains multiple isoforms. Among them, a short isoform called DCLK2203 expresses predominantly in ccRCC. Overexpression of DCLK2203 promotes ccRCC cell growth and tumorigenesis in vivo, which elicits its oncogenic signaling via activating TBK1 phosphorylation. Taken together, our work suggest that DCLK2 is a novel TBK1 activator and potential therapeutic target for ccRCC.
Citation Format: Lianxin Hu, Qing Zhang. Kinome-wide siRNA screening identifies DCLK2 as a TBK1 activator and therapeutic target for ccRCC [abstract]. In: Proceedings of the AACR Special Conference: Advances in Kidney Cancer Research; 2023 Jun 24-27; Austin, Texas. Philadelphia (PA): AACR; Cancer Res 2023;83(16 Suppl):Abstract nr A003.