bluuebunny/crossref_metadata_2025_split huggingface dataset:
Reinstatement and recircumscription ofJupunbaandPunjuba(Fabaceae) based on phylogenetic evidence
Authors: Soares Marcos Vinicius Batista , Guerra Ethiéne , Morim Marli Pires , Iganci João Ricardo Vieira 
Published: January 2021

AbstractAmong the mimosoid legumes (Fabaceae, Caesalpinioideae, mimosoid clade), many genera have complex nomenclatural histories, including Abarema that stands out due to numerous nomenclatural changes. Abarema is a Neotropical genus that currently comprises c. 50 species, with centres of diversity in the Amazon and Atlantic rain forests. Recent phylogenetic studies of Abarema have demonstrated the non-monophyly of the genus, which was shown to be polyphyletic with species traditionally recognized under the genus placed in three main clades that are intermingled with other genera of the former tribe Ingeae. The type species of Abarema groups with Inga, Macrosamanea, Enterolobiump.p., Zygia and Blanchetiodendron, whereas the other two clades correspond to the former genera Jupunba and Punjuba. The aim of this study is to build a phylogenetic tree of Abarema s.l. supporting the reinstatement of Jupunba and Punjuba, based on morphological and phylogenetic evidence, and to carry out a nomenclatural overhaul of the species and implement necessary typifications. For Punjuba we reinstate three species and add three new combinations. Jupunba comprises 37 species, of which eight are reinstated; in addition, the resurrection of one species with a new synonym is proposed and 29 new combinations are made. In total, 63 taxa are revised, including accepted names, synonyms and excluded names. A taxonomic key is presented for the identification of Punjuba, Jupunba and related genera. We present 40 new combinations, one new taxonomic status and 18 corrections of nomenclature category for lectotypes and two neotypes. One lectotype is designated, one species is reinstated with a new synonym and a second step neotypification is made. We located 97 unreported types during the revision, which are cited here for the first time.
Molecular mechanism mediating enteric bacterial translocation after severe burn: the role of cystic fibrosis transmembrane conductance regulator
Authors: Liu Xinzhu , Chen Yu , You Bo , Peng Yuan , Chen Yajie , Yang Zichen , Zhang Yixin , Chen Jing 
Published: January 2021

Abstract

Background
Gut ischemia and hypoxia post severe burn leads to breakdown of intestinal epithelial barrier and enteric bacterial translocation (EBT), resulting in serious complications, such as systemic inflammatory response syndrome, sepsis and multiple organ failure. Cystic fibrosis transmembrane conductance regulator (CFTR) is known to be downregulated by hypoxia and modulate junctional complexes, which are crucial structures maintaining the intestinal barrier. This study aimed to investigate whether CFTR plays a role in both regulating the intestinal barrier and mediating EBT post severe burn, as well as the signaling pathways involved in these processes.

Methods
An in vitro Caco-2 cell model subjected to hypoxic injury and an in vivo mouse model with a 30% total body surface area full-thickness dermal burn were established. DF 508 mice (mice with F508del CFTR gene mutation) were used as an in vivo model to further demonstrate the role of CFTR in maintaining normal intestinal barrier function. QRT-PCR, western blot, ELISA, TER assay and immunofluorescence staining were used to detect the expression and localization of CFTR and tight junction proteins, as well as the function of tight junctions.

Results
Our data indicated that, in Caco-2 cells, the hypoxia condition significantly reduced CFTR expression; activated extracellular signal-regulated kinase and nuclear factor-κB signaling; elevated secretion of inflammatory factors (tumor necrosis factor-α, interleukin-1β and interleukin-8); downregulated zonula occludens-1, occludin and E-cadherin expression; decreased transepithelial electrical resistance values; and led to a cellular mislocation of ZO-1. More importantly, knockdown of CFTR caused similar alterations. The upregulation of inflammatory factors and downregulation of tight junction proteins (ZO-1 and occludin) induced by knockdown of CFTR could be reversed by specific extracellular signal-regulated kinase or nuclear factor-κB inhibition. In support of the in vitro data, exuberant secretion of pro-inflammatory mediators and EBT was observed in the intestine of severely burnt mice in vivo. EBT occurred in DF508 mice (mice with the F508del CFTR gene mutation), accompanied by augmented tumor necrosis factor-α, interleukin-1β and interleukin-8 levels in the ileum compared to wildtype mice. In addition, vitamin D3 was shown to protect the intestinal epithelial barrier from hypoxic injury.

Conclusions
Collectively, the present study illustrated that CFTR and downstream signaling were critical in modulating the intestinal epithelial junction and EBT post severe burn.
Sulcal Morphology in Cingulate Cortex is Associated with Voluntary Oro-Facial Motor Control and Gestural Communication in Chimpanzees (Pan troglodytes)
Authors: Hopkins William D , Procyk Emmanuel , Petrides Michael , Schapiro Steven J , Mareno Mary Catherine , Amiez Celine 
Published: January 2021

AbstractIndividual differences in sulcal variation within the anterior and mid-cingulate cortex of the human brain, particularly the presence or absence of a paracingulate sulcus (PCGS), are associated with various motor and cognitive processes. Recently, it has been reported that chimpanzees possess a PCGS, previously thought to be a unique feature of the human brain. Here, we examined whether individual variation in the presence or absence of a PCGS as well as the variability in the intralimbic sulcus (ILS) are associated with oro-facial motor control, handedness for manual gestures, and sex in a sample of MRI scans obtained in 225 chimpanzees. Additionally, we quantified the depth of the cingulate sulcus (CGS) along the anterior–posterior axis and tested for association with oro-facial motor control, handedness, and sex. Chimpanzees with better oro-facial motor control were more likely to have a PCGS, particularly in the left hemisphere compared to those with poorer control. Male chimpanzees with better oro-facial motor control showed increased leftward asymmetries in the depth of the anterior CGS, whereas female chimpanzees showed the opposite pattern. Significantly, more chimpanzees had an ILS in the left compared to the right hemisphere, but variability in this fold was not associated with sex, handedness, or oro-facial motor control. Finally, significant population-level leftward asymmetries were found in the anterior portion of the CGS, whereas significant rightward biases were evident in the posterior regions. The collective results suggest that the emergence of a PCGS and enhanced gyrification within the anterior and mid-cingulate gyrus may have directly or indirectly evolved in response to selection for increasing oro-facial motor control in primates.
Development of a Treatment-decision Algorithm for Human Immunodeficiency Virus–uninfected Children Evaluated for Pulmonary Tuberculosis
Authors: Gunasekera Kenneth S , Walters Elisabetta , van der Zalm Marieke M , Palmer Megan , Warren Joshua L , Hesseling Anneke C , Cohen Ted , Seddon James A 
Published: January 2021

Abstract

Background
Limitations in the sensitivity and accessibility of diagnostic tools for childhood tuberculosis contribute to the substantial gap between estimated cases and cases notified to national tuberculosis programs. Thus, tools to make accurate and rapid clinical diagnoses are necessary to initiate antituberculosis treatment in more children.

Methods
We analyzed data from a prospective cohort of children &lt;13 years old being routinely evaluated for pulmonary tuberculosis in Cape Town, South Africa, from March 2012 to November 2017. We developed a regression model to describe the contributions of baseline clinical evaluation to the diagnosis of tuberculosis using standardized, retrospective case definitions. We included baseline chest radiographic and Xpert MTB/RIF assay results to the model to develop an algorithm with ≥90% sensitivity in predicting tuberculosis.

Results
Data from 478 children being evaluated for pulmonary tuberculosis were analyzed (median age, 16.2 months; interquartile range, 9.8–30.9 months); 242 (50.6%) were retrospectively classified with tuberculosis, bacteriologically confirmed in 104 (43.0%). The area under the receiver operating characteristic curve for the final model was 0.87. Clinical evidence identified 71.4% of all tuberculosis cases in this cohort, and inclusion of baseline chest radiographic results increased the proportion to 89.3%. The algorithm was 90.1% sensitive and 52.1% specific, and maintained a sensitivity of &gt;90% among children &lt;2 years old or with low weight for age.

Conclusions
Clinical evidence alone was sufficient to make most clinical antituberculosis treatment decisions. The use of evidence-based algorithms may improve decentralized, rapid treatment initiation, reducing the global burden of childhood mortality.
Chitinase 3 like 1 is a regulator of smooth muscle cell physiology and atherosclerotic lesion stability
Authors: Tsantilas Pavlos , Lao Shen , Wu Zhiyuan , Eberhard Anne , Winski Greg , Vaerst Monika , Nanda Vivek , Wang Ying , Kojima Yoko , Ye Jianqin , Flores Alyssa , Jarr Kai-Uwe , Pelisek Jaroslav , Eckstein Hans-Henning , Matic Ljubica , Hedin Ulf , Tsao Philip S , Paloschi Valentina , Maegdefessel Lars , Leeper Nicholas J 
Published: January 2021

Abstract

Aims
Atherosclerotic cerebrovascular disease underlies the majority of ischaemic strokes and is a major cause of death and disability. While plaque burden is a predictor of adverse outcomes, plaque vulnerability is increasingly recognized as a driver of lesion rupture and risk for clinical events. Defining the molecular regulators of carotid instability could inform the development of new biomarkers and/or translational targets for at-risk individuals.

Methods and results
Using two independent human endarterectomy biobanks, we found that the understudied glycoprotein, chitinase 3 like 1 (CHI3L1), is up-regulated in patients with carotid disease compared to healthy controls. Further, CHI3L1 levels were found to stratify individuals based on symptomatology and histopathological evidence of an unstable fibrous cap. Gain- and loss-of-function studies in cultured human carotid artery smooth muscle cells (SMCs) showed that CHI3L1 prevents a number of maladaptive changes in that cell type, including phenotype switching towards a synthetic and hyperproliferative state. Using two murine models of carotid remodelling and lesion vulnerability, we found that knockdown of Chil1 resulted in larger neointimal lesions comprised by de-differentiated SMCs that failed to invest within and stabilize the fibrous cap. Exploratory mechanistic studies identified alterations in potential downstream regulatory genes, including large tumour suppressor kinase 2 (LATS2), which mediates macrophage marker and inflammatory cytokine expression on SMCs, and may explain how CHI3L1 modulates cellular plasticity.

Conclusion
CHI3L1 is up-regulated in humans with carotid artery disease and appears to be a strong mediator of plaque vulnerability. Mechanistic studies suggest this change may be a context-dependent adaptive response meant to maintain vascular SMCs in a differentiated state and to prevent rupture of the fibrous cap. Part of this effect may be mediated through downstream suppression of LATS2. Future studies should determine how these changes occur at the molecular level, and whether this gene can be targeted as a novel translational therapy for subjects at risk of stroke.
Coronary stent CD31-mimetic coating favours endothelialization and reduces local inflammation and neointimal development in vivo
Authors: Diaz-Rodriguez Sergio , Rasser Charlotte , Mesnier Jules , Chevallier Pascale , Gallet Romain , Choqueux Christine , Even Guillaume , Sayah Neila , Chaubet Frédéric , Nicoletti Antonino , Ghaleh Bijan , Feldman Laurent J , Mantovani Diego , Caligiuri Giuseppina 
Published: January 2021

Abstract

Aims
The rapid endothelialization of bare metal stents (BMS) is counterbalanced by inflammation-induced neointimal growth. Drug-eluting stents (DES) prevent leukocyte activation but impair endothelialization, delaying effective device integration into arterial walls. Previously, we have shown that engaging the vascular CD31 co-receptor is crucial for endothelial and leukocyte homeostasis and arterial healing. Furthermore, we have shown that a soluble synthetic peptide (known as P8RI) acts like a CD31 agonist. The aim of this study was to evaluate the effect of CD31-mimetic metal stent coating on the in vitro adherence of endothelial cells (ECs) and blood elements and the in vivo strut coverage and neointimal growth.

Methods and results
We produced Cobalt Chromium discs and stents coated with a CD31-mimetic peptide through two procedures, plasma amination or dip-coating, both yielding comparable results. We found that CD31-mimetic discs significantly reduced the extent of primary human coronary artery EC and blood platelet/leukocyte activation in vitro. In vivo, CD31-mimetic stent properties were compared with those of DES and BMS by coronarography and microscopy at 7 and 28 days post-implantation in pig coronary arteries (n = 9 stents/group/timepoint). Seven days post-implantation, only CD31-mimetic struts were fully endothelialized with no activated platelets/leukocytes. At day 28, neointima development over CD31-mimetic stents was significantly reduced compared to BMS, appearing as a normal arterial media with the absence of thrombosis contrary to DES.

Conclusion
CD31-mimetic coating favours vascular homeostasis and arterial wall healing, preventing in-stent stenosis and thrombosis. Hence, such coatings seem to improve the metal stent biocompatibility.
All-cause mortality and location of death in patients with established cardiovascular disease before, during, and after the COVID-19 lockdown: a Danish Nationwide Cohort Study
Authors: Butt Jawad H , Fosbøl Emil L , Gerds Thomas A , Andersson Charlotte , Kragholm Kristian , Biering-Sørensen Tor , Andersen Julie , Phelps Mathew , Andersen Mikkel Porsborg , Gislason Gunnar , Torp-Pedersen Christian , Køber Lars , Schou Morten 
Published: January 2021

Abstract

Background
On 13 March 2020, the Danish authorities imposed extensive nationwide lockdown measures to prevent the spread of the coronavirus disease 2019 (COVID-19) and reallocated limited healthcare resources. We investigated mortality rates, overall and according to location, in patients with established cardiovascular disease before, during, and after these lockdown measures.

Methods and results
Using Danish nationwide registries, we identified a dynamic cohort comprising all Danish citizens with cardiovascular disease (i.e. a history of ischaemic heart disease, ischaemic stroke, heart failure, atrial fibrillation, or peripheral artery disease) alive on 2 January 2019 and 2020. The cohort was followed from 2 January 2019/2020 until death or 16/15 October 2019/2020. The cohort comprised 340 392 and 347 136 patients with cardiovascular disease in 2019 and 2020, respectively. The overall, in-hospital, and out-of-hospital mortality rate in 2020 before lockdown was significantly lower compared with the same period in 2019 [adjusted incidence rate ratio (IRR) 0.91, 95% confidence interval (CI) CI 0.87–0.95; IRR 0.95, 95% CI 0.89–1.02; and IRR 0.87, 95% CI 0.83–0.93, respectively]. The overall mortality rate during and after lockdown was not significantly different compared with the same period in 2019 (IRR 0.99, 95% CI 0.97–1.02). However, the in-hospital mortality rate was lower and out-of-hospital mortality rate higher during and after lockdown compared with the same period in 2019 (in-hospital, IRR 0.92, 95% CI 0.88–0.96; out-of-hospital, IRR 1.04, 95% CI1.01–1.08). These trends were consistent irrespective of sex and age.

Conclusions
Among patients with established cardiovascular disease, the in-hospital mortality rate was lower and out-of-hospital mortality rate higher during lockdown compared with the same period in the preceding year, irrespective of age and sex.
Genotype-environment interactions and the maintenance of polygenic variation.
Authors: Gillespie J H , Turelli M 
Published: January 2021

Abstract
Genotype-environment interactions may be a potent force maintaining genetic variation in quantitative traits in natural populations. This is shown by a simple model of additive polygenic inheritance in which the additive contributions of alleles vary with the environment. Under simplifying symmetry assumptions, the model implies that the variance of the phenotypes produced across environments by a multilocus genotype decreases as the number of heterozygous loci increases. In the region of an optimal phenotype, the mapping from the quantitative trait into fitness is concave, and the mean fitness of a genotype will increase with the number of heterozygous loci. This leads to balancing selection, polymorphism, and potentially high levels of additive genetic variance, even though all allelic effects remain additive within each specific environment. An important implication of the model is that the variation maintained by genotype-environment interactions is difficult to study with the restricted range of environments represented in typical experiments. In particular, if fluctuations in allelic effects are pervasive, as suggested by the extensive literature on genotype-environment interactions, efforts to estimate genetic parameters in a single environment may be of limited value.
Repair of single- and multiple-substitution mismatches during recombination in Streptococcus pneumoniae.
Authors: Gasc A M , Sicard A M , Claverys J P 
Published: January 2021

Abstract
The use as genetic markers, during transformation of Streptococcus pneumoniae, of 19 sequences differing from wild type, located throughout the amiA locus, enabled us to examine the fate of 24 single- and 11 multiple-mismatches during recombination. Tentative mismatch ranking as a function of decreasing repair efficiency by the Hex mismatch repair system is G/T = A/C = G/G (maximum repair: 90-95%) greater than C/T (mostly 75 to 90% repair) greater than A/A (from 50 to 90% repair) greater than T/T (50-65% repair) greater than A/G (from 0 to 20% repair) greater than C/C. No indication of correction of the latter has been obtained. Over the limited number of samples examined, we observed no influence of the base composition of the surrounding sequence on correction efficiency for both transition mismatches and for G/G and C/C. Variations in the surrounding sequence affect repair of A/G and C/T, and, even more strongly, of A/A and T/T. No simple correlation to the G:C content of the surrounding sequence is apparent from our results, in contrast to the conclusion drawn for the Mut mismatch repair system of Escherichia coli. Examination of the fate of multiple mismatches suggests that C/C may sometimes impede recognition of otherwise corrected mismatches.
Hybrid dysgenesis in Drosophila simulans lines transformed with autonomous P elements.
Authors: Daniels S B , Chovnick A , Kidwell M G 
Published: January 2021

Abstract
The molecular and phenotypic analysis of several previously described P element-transformed lines of Drosophila simulans was extended in order to determine whether they had the potential to produce a syndrome of P-M hybrid dysgenesis analogous to the one in Drosophila melanogaster. The transformed line with the highest number of P elements at the beginning of the analysis, DsP pi-5C, developed strong P activity potential and P element regulation, properties characteristic of D. melanogaster P strains. The subsequent analysis of sublines derived from 34 single pair matings of DsP pi-5C revealed that they were heterogeneous with respect to both their P element complements and P activity potentials, but similar with respect to their regulatory capabilities. The subline with the highest P activity, DsP pi-5C-27, was subsequently used as a reference P strain in the genetic analysis of the D. simulans transformants. In these experiments, the reciprocal cross effect was observed with respect to both gonadal sterility and male recombination. As in D. melanogaster, the induction of gonadal sterility in D. simulans was shown to be temperature-dependent. Molecular analysis of DsP pi-5C-27 revealed that it has approximately 30 P elements per genome, at least some of which are defective. The number of potentially complete P elements in its genome is similar to the number in the D. melanogaster P strain, Harwich-77. Overall our analysis indicates that P-transformed lines of D. simulans are capable of expressing the major features of P-M hybrid dysgenesis previously demonstrated in D. melanogaster and that P elements appear to behave in a similar way in the two sibling species.
Phage genetic sites involved in lambda growth inhibition by the Escherichia coli rap mutant.
Authors: Guzmán P , Guarneros G 
Published: January 2021

Abstract
The rap mutation of Escherichia coli prevents the growth of bacteriophage lambda. We have isolated phage mutants that compensate for the host deficiency. The mutations, named bar, were genetically located to three different loci of the lambda genome: barI in the attP site, barII in the cIII ea10 region, and barIII within or very near the imm434 region. The level of lambda leftward transcription correlates with rap exclusion. Phage lambda mutants partially defective in the pL promoter or in pL-transcript antitermination showed a Bar- phenotype. Conversely, mutants constitutive for transcription from the pI or pL promoters were excluded more stringently by rap bacteria. We conclude that rap exclusion depends on the magnitude of transcription through the wild type bar loci in the phage genome.
The maintenance of genetic variability in two-locus models of stabilizing selection.
Authors: Nagylaki T 
Published: January 2021

Abstract
The maintenance of genetic variability at two diallelic loci under stabilizing selection is investigated. Generations are discrete and nonoverlapping; mating is random; mutation and random genetic drift are absent; selection operates only through viability differences. The determination of the genotypic values is purely additive. The fitness function has its optimum at the value of the double heterozygote and decreases monotonically and symmetrically from its optimum, but is otherwise arbitrary. The resulting fitness scheme is identical to the symmetric viability model. Linkage disequilibrium is neglected, but the results are otherwise exact. Explicit formulas are found for all the equilibria, and explicit conditions are derived fro their existence and stability. A complete classification of the six possible global convergence patterns is presented. In addition to the symmetric equilibrium (with gene frequency 1/2 at both loci), a pair of unsymmetric equilibria may exist; the latter are usually, but not always, unstable. If the ratio of the effect of the major locus to that of the minor one exceeds a critical value, both loci will be stably polymorphic. If selection is weak at the minor locus, the more rapidly the fitness function decreases near the optimum, the lower is this critical value; for rapidly decreasing fitness functions, the critical value is close to one. If the fitness function is smooth at the optimum, then a stable polymorphism exists at both loci only if selection is strong at the major locus.