bluuebunny/crossref_metadata_2025_split huggingface dataset:
Revised Version of the New Catalogue of Suspected Variable Stars, NSV Release 2
Authors: Kazarovets E. V. , Samus N. N. , Durlevich O. V. 
Published: August 2022

Abstract
We present NSV Release 2, an electronic version of the “New Catalogue of Suspected Variable Stars”. A detailed file-by-file description of the new catalogue version is given. By its structure, we preserve the catalogue as a historical document, but the information it contains has been considerably renewed compared to its first electronic version. Accuracy of coordinates has been drastically improved for the objects in the catalogue; for most of them, we revised photometric and spectroscopic data. Remarks have been renewed. In the cases when there were no finding charts, we recovered variability of 2800 stars of the catalogue, despite large errors of the coordinates earlier published for them. Using photometric data from several sky surveys, we studied and transferred to the General Catalogue of Variable Stars about 5000 NSV stars.
Plasma bupivacaine levels (total and free/unbound) during epidural infusion in liver resection patients: a prospective, observational study
Authors: Burjorjee Jessica , Phelan Rachel , Hopman Wilma M , Ho Anthony M-H , Nanji Sulaiman , Jalink Diederick , Mizubuti Glenio B 
Published: August 2022

IntroductionLiver resection patients may be at an increased risk of local anesthetic (LA) toxicity because the liver is essential for metabolizing LA and producing proteins (mainly α1-acid glycoprotein (AAG)) that bind to it and reduce the free (and pharmacologically active/toxic) levels in circulation. The liver resection itself, manipulation during surgery, and pre-existing liver disease may all interfere with normal hepatic protein synthesis and result in an attenuation of the increased AAG (a positive acute-phase protein) that normally occurs postoperatively. The purpose of this study was to determine whether the AAG response is attenuated postoperatively following liver resection and whether patients approach toxicity thresholds with continuous postoperative epidural infusion of bupivacaine.MethodsProspective, observational study with blood drawn preoperatively, in the postanesthetic care unit, on postoperative day (POD) 2, and prior to discontinuation of epidural analgesia on POD3/POD4. Plasma was analyzed for total and unbound bupivacaine via liquid chromatography–mass spectrometry and AAG via ELISA. Signs/symptoms of local anesthetic systemic toxicity (LAST), pain, and sedation scores were also recorded.ResultsFor the 19 patients completed, total plasma bupivacaine was correlated with total administered, but unbound levels were not associated with the total administered. Unlike non-hepatectomy surgery where unbound LA plasma levels remain stable (or decrease) with continuous postoperative epidural administration, we observed an overall increase. Several patients approached toxicity thresholds and 47% reported at least one symptom of LAST, but no epidurals were discontinued because of LAST. In contrast to the AAG response reported following major non-liver surgery where AAG levels increase twofold, we observed a reduction until POD2 and the magnitude was proportional to resection weight.DiscussionOur results are supported by the literature in suggesting that major liver resection patients may be at an increased vulnerability for LAST. Factors such as the extent of liver disease, resection and intraoperative blood loss should be considered when using continuous postoperative epidural infusion of bupivacaine and vigilance should be used in monitoring, for signs/symptoms of LAST, even for those subtle and non-specific. Future research will be required to verify these findings.Trial registration numberNCT03145805.
Modular Smart Molecules for PSMA-Targeted Chemotherapy
Authors: Olatunji Feyisola P. , Pun Michael , Herman Jacob W. , Romero Oscar , Maniatopoulos Mitchell , Latoche Joseph D. , Parise Robert A. , Guo Jianxia , Beumer Jan H. , Anderson Carolyn J. , Berkman Clifford E. 
Published: August 2022

Abstract
New targeted chemotherapeutics are urgently needed to minimize off-target toxicity and reduce the high-mortality rate associated with metastatic prostate cancer. Herein, we report on the modular synthesis, pharmacokinetics, and efficacy of two small-molecule–drug conjugates (SMDC) targeted to prostate-specific membrane antigen (PSMA) incorporating either: (i) a cathepsin-B–cleavable valine–citrulline (Val–Cit), or (ii) an acid-cleavable phosphoramidate linker. Crucial components used in the design of the conjugates include: (i) CTT1298, a nanomolar affinity ligand that binds irreversibly to PSMA and has proven in past studies to rapidly internalize and shuttle payloads into PSMA-expressing prostate cancer cells, (ii) MMAE, a known potent cytotoxic payload, and (iii) an albumin-binder, proven to improve residence time of drug conjugates. At dose of 0.8 mg/kg (∼250 nmol/kg), the two SMDCs showed significant efficacy in a PSMA(+) PC3-PIP mouse model of human prostate cancer compared with controls, without inducing systemic toxicity. Though localization of the SMDCs was observed in tissues apart from the tumor, release of MMAE was observed predominantly in tumor tissue, at levels that were 2–3 orders of magnitude higher than non-target tissues. Furthermore, SMDC2, which incorporated a novel pH-responsive phosporamidate linker, demonstrated significantly improved efficacy over SMDC1 that has a Val–Cit linker, with a 100% survival over 90 days and 4 out of 8 mice showing complete tumor growth inhibition after 6 weekly doses of 0.8 mg/kg (244 nmol/kg). Our findings demonstrate the potential of irreversible PSMA inhibitors combined with pH-responsive linkers as a way to specifically deliver chemotherapeutic drugs to prostate cancer tumors with minimal toxicity.
“Educar é Higienizar”: as diretrizes do ensino de Higiene nas Escolas Normais paulistas e o papel do professor no livro de Biologia Educacional
Authors: Martins Samira 
Published: August 2022

Este artigo tem como objetivo discorrer sobre as diretrizes de Educação Higiênica e o papel da professora primária na veiculação da mensagem de higiene nas escolas paulistas para a conformação de cidadãos saudáveis e eficientes ao Estado durante a Era Vargas. Para isto, analisamos o livro Biologia Educacional: noções fundamentais (1969) de Antônio de Almeida Junior. Essa obra foi utilizada como livro didático nas Escolas Normais paulistas, a partir de 1938 e sua última edição foi publicada em 1969. As diretrizes sobre higiene contidas no livro visavam instruir a futura professora a seguir seu papel de missionária da mensagem de higiene, para regenerar seus alunos através da educação. A partir da perspectiva foucaultiana, operamos com o conceito de disciplina e biopoder como ferramenta de análise objetivando conhecer a rede de enunciados, da medicina, higiene e da educação escolar. A metodologia adotada para esta discussão volta-se para a pesquisa qualitativa de caráter bibliográfico e análise documental. Um das conclusões que este estudo levantou é que os enunciados veiculados no livro funcionaram como estratégias de disciplinamento de condutas e corpos, objetivando o saneamento dos problemas econômicos do país, tendo a futura professora primária e os alunos como ferramenta e alvos da transformação econômica e social.
ADAR1 Prevents Autoinflammatory Processes in the Heart Mediated by IRF7
Authors: Garcia-Gonzalez Claudia , Dieterich Christoph , Maroli Giovanni , Wiesnet Marion , Wietelmann Astrid , Li Xiang , Yuan Xuejun , Graumann Johannes , Stellos Konstantinos , Kubin Thomas , Schneider Andre , Braun Thomas 
Published: August 2022

Background:
ADAR1 (adenosine deaminase acting on RNA-1)-mediated adenosine to inosine (A-to-I) RNA editing plays an essential role for distinguishing endogenous from exogenous RNAs, preventing autoinflammatory ADAR1 also regulates cellular processes by recoding specific mRNAs, thereby altering protein functions, but may also act in an editing-independent manner. The specific role of ADAR1 in cardiomyocytes and its mode of action in the heart is not fully understood. To determine the role of ADAR1 in the heart, we used different mutant mouse strains, which allows to distinguish immunogenic, editing-dependent, and editing-independent functions of ADAR1.

Methods:

Different
Adar1
-mutant mouse strains were employed for gene deletion or specific inactivation of ADAR1 enzymatic activity in cardiomyocytes, either alone or in combination with
Ifih1
(interferon induced with helicase C domain 1) or
Irf7
(interferon regulatory factor 7) gene inactivation. Mutant mice were investigated by immunofluorescence, Western blot, RNAseq, proteomics, and functional MRI analysis.

Results:

Inactivation of
Adar1
in cardiomyocytes resulted in late-onset autoinflammatory myocarditis progressing into dilated cardiomyopathy and heart failure at 6 months of age.
Adar1
depletion activated interferon signaling genes but not NFκB (nuclear factor kappa B) signaling or apoptosis and reduced cardiac hypertrophy during pressure overload via induction of
Irf7
. Additional inactivation of the cytosolic RNA sensor MDA5 (melanoma differentiation-associated gene 5; encoded by the
Ifih1
gene) in
Adar1
mutant mice prevented activation of interferon signaling gene and delayed heart failure but did not prevent lethality after 8.5 months. In contrast, compound mutants only expressing catalytically inactive ADAR1 in an
Ifih1
-mutant background were completely normal. Inactivation of
Irf7
attenuated the phenotype of
Adar1
-deficient cardiomyocytes to a similar extent as
Ifih1
depletion, identifying IRF7 as the main mediator of autoinflammatory responses caused by the absence of ADAR1 in cardiomyocytes.

Conclusions:
Enzymatically active ADAR1 prevents IRF7-mediated autoinflammatory reactions in the heart triggered by endogenous nonedited RNAs. In addition to RNA editing, ADAR1 also serves editing-independent roles in the heart required for long-term cardiac function and survival.
Inflammatory Role of Milk Fat Globule–Epidermal Growth Factor VIII in Age‐Associated Arterial Remodeling
Authors: Ni Leng , Liu Lijuan , Zhu Wanqu , Telljohann Richard , Zhang Jing , Monticone Robert E. , McGraw Kimberly R. , Liu Changwei , Morrell Christopher H. , Garrido‐Gil Pablo , Labandeira‐Garcia Jose Luis , Lakatta Edward G. , Wang Mingyi 
Published: August 2022

Background

Age‐associated aortic remodeling includes a marked increase in intimal medial thickness (IMT), associated with signs of inflammation. Although aortic wall milk fat globule–epidermal growth factor VIII (MFG‐E8) increases with age, and is associated with aortic inflammation, it is not known whether MFG‐E8 is
required
for the age‐associated increase in aortic IMT. Here, we tested whether MFG‐E8 is
required
for the age‐associated increase in aortic IMT.

Methods and Results

To determine the role of MFG‐E8 in the age‐associated increase of IMT, we compared aortic remodeling in adult (20‐week) and aged (96‐week) MFG‐E8 (−/−) knockout and age matched wild‐type (WT) littermate mice. The average aortic IMT increased with age in the WT from 50±10 to 70±20 μm (
P
<0.0001) but did not significantly increase with age in MFG‐E8 knockout mice. Because angiotensin II signaling is implicated as a driver of age‐associated increase in IMT, we infused 30‐week‐old MFG‐E8 knockout and age‐matched littermate WT mice with angiotensin II or saline via osmotic mini‐pumps to determine whether MFG‐E8 is required for angiotensin II–induced aortic remodeling. (1) In WT mice, angiotensin II infusion substantially increased IMT, elastic lamina degradation, collagen deposition, and the proliferation of vascular smooth muscle cells; in contrast, these effects were significantly reduced in MFG‐E8 KO mice; (2) On a molecular level, angiotensin II treatment significantly increased the activation and expression of matrix metalloproteinase type 2, transforming growth factor beta 1, and its downstream signaling molecule phosphorylated mother against decapentaplegic homolog 2, and collagen type I production in WT mice; however, in the MFG‐E8 knockout mice, these molecular effects were significantly reduced; and (3) in WT mice, angiotensin II increased levels of aortic inflammatory markers phosphorylated nuclear factor‐kappa beta p65, monocyte chemoattractant protein 1, tumor necrosis factor alpha, intercellular adhesion molecule 1, and vascular cell adhesion molecule 1 molecular expression, while in contrast, these inflammatory markers did not change in knockout mice.

Conclusions
Thus, MFG‐E8 is required for both age‐associated proinflammatory aortic remodeling and also for the angiotensin II–dependent induction in younger mice of an aortic inflammatory phenotype observed in advanced age. Targeting MFG‐E8 would be a novel molecular approach to curb adverse arterial remodeling.
microRNA Expression Levels Change in Neonatal Patients During and After Exposure to Cardiopulmonary Bypass
Authors: Hsieh Lance , Tu Lan N. , Paquette Alison , Sheng Quanhu , Zhao Shilin , Bittel Douglas , O’Brien James , Vickers Kasey , Pastuszko Peter , Nigam Vishal 
Published: August 2022

Background
The systemic inflammation that occurs after exposure to cardiopulmonary bypass (CPB), which is especially severe in neonatal patients, is associated with poorer outcomes and is not well understood. In order to gain deeper insight into how exposure to bypass activates inflammatory responses in circulating leukocytes, we studied changes in microRNA (miRNA) expression during and after exposure to bypass. miRNAs are small noncoding RNAs that have important roles in modulating protein levels and function of cells.

Methods and Results

We performed miRNA‐sequencing on leukocytes isolated from neonatal patients with CPB (n=5) at 7 time points during the process of CPB, including before the initiation of bypass, during bypass, and at 3 time points during the first 24 hours after weaning from bypass. We identified significant differentially expressed miRNAs using generalized linear regression models, and miRNAs were defined as statistically significant using a false discovery rate–adjusted
P
<0.05. We identified gene targets of these miRNAs using the TargetScan database and identified significantly enriched biological pathways for these gene targets. We identified 54 miRNAs with differential expression during and after CPB. These miRNAs clustered into 3 groups, including miRNAs that were increased during and after CPB (3 miRNAs), miRNAs that decreased during and after CPB (10 miRNAs), and miRNAs that decreased during CPB but then increased 8 to 24 hours after CPB. A total of 38.9% of the target genes of these miRNAs were significantly differentially expressed in our previous study. miRNAs with altered expression levels are predicted to significantly modulate pathways related to inflammation and signal transduction.

Conclusions
The unbiased profiling of the miRNA changes that occur in the circulating leukocytes of patients with bypass provides deeper insight into the mechanisms that underpin the systemic inflammatory response that occurs in patients after exposure to CPB. These data will help the development of novel treatments and biomarkers for bypass‐associated inflammation.
Renin‐Angiotensin System Inhibitors in Patients With COVID‐19: A Meta‐Analysis of Randomized Controlled Trials Led by the International Society of Hypertension
Authors: Gnanenthiran Sonali R. , Borghi Claudio , Burger Dylan , Caramelli Bruno , Charchar Fadi , Chirinos Julio A. , Cohen Jordana B. , Cremer Antoine , Di Tanna Gian Luca , Duvignaud Alexandre , Freilich Daniel , Gommans D. H. Frank , Gracia‐Ramos Abraham E. , Murray Thomas A. , Pelorosso Facundo , Poulter Neil R. , Puskarich Michael A. , Rizas Konstantinos D. , Rothlin Rodolfo , Schlaich Markus P. , Schreinlecher Michael , Steckelings Ulrike Muscha , Sharma Abhinav , Stergiou George S. , Tignanelli Christopher J. , Tomaszewski Maciej , Unger Thomas , van Kimmenade Roland R. J. , Wainford Richard D. , Williams Bryan , Rodgers Anthony , Schutte Aletta E. ,   the COVID‐METARASI Consortium
Published: August 2022

Background
Published randomized controlled trials are underpowered for binary clinical end points to assess the safety and efficacy of renin‐angiotensin system inhibitors (RASi) in adults with COVID‐19. We therefore performed a meta‐analysis to assess the safety and efficacy of RASi in adults with COVID‐19.

Methods and Results

MEDLINE, EMBASE,
ClinicalTrials.gov
, and the Cochrane Controlled Trial Register were searched for randomized controlled trials that randomly assigned patients with COVID‐19 to RASi continuation/commencement versus no RASi therapy. The primary outcome was all‐cause mortality at ≤30 days. A total of 14 randomized controlled trials met the inclusion criteria and enrolled 1838 participants (aged 59 years, 58% men, mean follow‐up 26 days). Of the trials, 11 contributed data. We found no effect of RASi versus control on all‐cause mortality (7.2% versus 7.5%; relative risk [RR], 0.95; [95% CI, 0.69–1.30]) either overall or in subgroups defined by COVID‐19 severity or trial type. Network meta‐analysis identified no difference between angiotensin‐converting enzyme inhibitors versus angiotensin II receptor blockers. RASi users had a nonsignificant reduction in acute myocardial infarction (2.1% versus 3.6%; RR, 0.59; [95% CI, 0.33–1.06]), but increased risk of acute kidney injury (7.0% versus 3.6%; RR, 1.82; [95% CI, 1.05–3.16]), in trials that initiated and continued RASi. There was no increase in need for dialysis or differences in congestive cardiac failure, cerebrovascular events, venous thromboembolism, hospitalization, intensive care admission, inotropes, or mechanical ventilation.

Conclusions
This meta‐analysis of randomized controlled trials evaluating angiotensin‐converting enzyme inhibitors/angiotensin II receptor blockers versus control in patients with COVID‐19 found no difference in all‐cause mortality, a borderline decrease in myocardial infarction, and an increased risk of acute kidney injury with RASi. Our findings provide strong evidence that RASi can be used safely in patients with COVID‐19.
Inequalities by Income in the Prevalence of Cardiovascular Disease and Its Risk Factors in the Adult Population of Catalonia
Authors: Mullachery Pricila H. , Vela Emili , Cleries Montse , Comin‐Colet Josep , Nasir Khurram , Diez Roux Ana V. , Cainzos‐Achirica Miguel , Mauri Josepa , Bilal Usama 
Published: August 2022

Background
Understanding the magnitude of cardiovascular disease (CVD) inequalities is the first step toward addressing them. The linkage of socioeconomic and clinical data in universal health care settings provides critical information to characterize CVD inequalities.

Methods and Results
We employed a prospective cohort design using electronic health records data from all residents of Catalonia aged 18+ between January and December of 2019 (N=6 332 228). We calculated age‐adjusted sex‐specific prevalence of 5 CVD risk factors (diabetes, hypertension, hyperlipidemia, obesity, and smoking), and 4 CVDs (coronary heart disease, cerebrovascular disease, atrial fibrillation, and heart failure). We categorized income into high, moderate, low, and very low according to individual income (tied to prescription copayments) and receipt of welfare support. We found large inequalities in CVD and CVD risk factors among men and women. CVD risk factors with the largest inequalities were diabetes, smoking, and obesity, with prevalence rates 2‐ or 3‐fold higher for those with very low (versus high) income. CVDs with the largest inequalities were cerebrovascular disease and heart failure, with prevalence rates 2 to 4 times higher for men and women with very low (versus high) income. Inequalities varied by age, peaking at midlife (30–50 years) for most diseases, while decreasing gradually with age for smoking.

Conclusions
We found wide and heterogeneous inequalities by income in 5 CVD risk factors and 4 CVD. Our findings in a region with a high‐quality public health care system and universal coverage stress that strong equity‐promoting policies are necessary to reduce disparities in CVD.
Reconsidering ‘Art’ and ‘Life’
Authors: Routledge Laura 
Published: August 2022

Abstract
The categories of ‘art’ and ‘life’ play a central role in the critical reception of Allan Kaprow’s Happenings, which have predominantly been read as a generalized, “blithely affirmative” and even “faintly embarrassing” attempt to fuse the two. This paper attempts to rethink the definition and relation of these two categories in Kaprow’s work. Rather than an uncritical attempt to fuse art and life, I suggest, Kaprow’s Happenings developed an increasingly complex, branching and networked structure, capable of staging a plurality of different modes of interaction between work and world. This paper explores both the modes and the contexts of these interactions in three of Kaprow’s Happenings of the 1960s.
Early childhood developmental vulnerability associated with parental mental disorder comorbidity
Authors: Watkeys Oliver J , O’Hare Kirstie , Dean Kimberlie , Laurens Kristin R , Harris Felicity , Carr Vaughan J , Green Melissa J 
Published: August 2022

Objectives: Parental mental health has a profound influence on the mental health and well-being of their offspring. With comorbid mental disorders generally the rule rather than the exception, increased knowledge of the impact of parental mental disorder comorbidity on early child development may facilitate improved targeting and delivery of early intervention for vulnerable offspring. Methods: Participants were 66,154 children and their parents in the New South Wales Child Development Study – a prospective, longitudinal, record-linkage study of a population cohort of children born in NSW between 2002 and 2004. Early childhood developmental vulnerability was assessed at age ~5 years using the Australian Early Development Census, and information on parental mental disorders was obtained from administrative health records. Binomial and multinomial logistic regression were used to assess the relationship between parental mental disorders and early childhood developmental vulnerability on emotional and behavioural domains, as well as membership of latent developmental risk classes reflecting particular classes of vulnerability. Results: Multiple diagnoses of mental disorders in mothers and fathers were associated with an increased likelihood of early childhood emotional and behavioural developmental vulnerability in offspring, relative to parents without mental disorder. The likelihood of offspring vulnerability increased with the number of parental comorbidities, particularly maternal comorbidities. Conclusion: Early childhood developmental vulnerability was strongly associated with parental mental ill-health, with the strength of associations increasing in line with a greater number of mental disorder diagnoses among mothers and fathers. New and expectant parents diagnosed with multiple mental disorders should be prioritised for intervention, including attention to the developmental well-being of their offspring.