Miracle-dz/UniFAR-FTUs huggingface dataset:
NEW CULTIVAR

The metabolomic content determines many of the important features of a fruit, such as its taste, flavor, color, nutritional value, and abiotic or biotic resistance. Peach ( Prunus persica (L.) Batsch) is one of the best genetically characterized species used as a model for Rosaceae, the drupes of which are a source of minerals, vitamins, fiber, and antioxidant compounds for healthy diets around the world. During the last few years, a great advance in the analysis of the metabolic diversity and reconfiguration in different peach varieties in response to developmental and environmental factors has occurred. These studies have shown that the great phenotypic diversity among different peach varieties is correlated with differential metabolomic content. Besides, the fruit metabolome of each peach variety is not static; on the contrary, it is drastically configured in response to both developmental and environmental signals, and moreover, it was found that these metabolic reconfigurations are also variety-dependent. In the present review, the main sources of metabolic diversity and conditions that induce modifications in the peach fruit metabolome are summarized. It is postulated that comparison of the metabolic reconfigurations that take place among the fruits from different varieties may help us better understand peach fruit metabolism and their key drivers, which in turn may aid in the future design of high-quality peach fruits.
Regularity of the conditional expectations with respect to signal to noise ratio

Let $(W,H,\mu)$ be the classical Wiener space, assume that $U_\la=I_W+u_\la$ is an adapted perturbation of identity where the perturbation $u_\la$ is an $H$-valued map, defined up to $\mu$-equivalence classes, such that its Lebesgue density $s\to \dot{u}_\la(s)$ is almost surely adapted to the canonical filtration of the Wiener space and depending measurably on a real parameter $\la$. Assuming some regularity for $u_\la$, its Sobolev derivative and integrability of the divergence of the resolvent operator of its Sobolev derivative, we prove the almost sure and $L^p$-regularity w.r. to $\la$ of the estimation $E[\dot{u}_\la(s)|\calU_\la(s)]$ and more generally of the conditional expectations of the type $E[F\mid\calU_\la(s)]$ for nice Wiener functionals, where $(\calU_\la(s),s\in [0,1])$ is the the filtration which is generated by $U_\la$. These results are applied to prove the invertibility of the adapted perturbations of identity, hence to prove the strong existence and uniqueness of functional SDE's; convexity of the entropy and the quadratic estimation error and finally to the information theory.
Transcriptome Profile of Thyroid Glands in Bile Duct Ligation Mouse Model

Thyroid hormone (TH) contributes to multiple cellular mechanisms in the liver, muscle cells, adipose tissue, and brain, etc. In particular, the liver is an important organ in TH metabolism for the conversion of thyronine (T4) into triiodothyronine (T3) by the deiodinase enzyme. TH levels were significantly decreased and thyroid-stimulating hormone (TSH) levels were significantly increased in patients with liver failure compared with normal subjects. Among liver failure diseases, hepatic encephalopathy (HE) deserves more attention because liver damage and neuropathologies occur simultaneously. Although there is numerous evidence of TH dysregulation in the HE model, specific mechanisms and genetic features of the thyroid glands in the HE model are not fully understood. Here, we investigated the significantly different genes in the thyroid glands of a bile duct ligation (BDL) mouse model as the HE model, compared to the thyroid glands of the control mouse using RNA sequencing. We also confirmed the alteration in mRNA levels of thyroid gland function-related genes in the BDL mouse model. Furthermore, we evaluated the increased level of free T4 and TSH in the BDL mouse blood. Thus, we emphasize the potential roles of TH in liver metabolism and suggest that thyroid dysfunction-related genes in the HE model should be highlighted for finding the appropriate solution for an impaired thyroid system in HE.
Molecular phylogeny of Cosmetocleithrum Kritsky, Thatcher & Boeger, 1986 (Monogenoidea: Dactylogyridae), gill parasites of Neotropical catfishes (Siluriformes)

Abstract Cosmetocleithrum Kritsky, Thatcher & Boeger, 1986 (Dactylogyridae) represents one of the most species-rich groups (22 species currently recognized as valid) of all dactylogyrid parasites infecting Neotropical catfishes. Species of Cosmetocleithrum exhibit a remarkable affinity towards catfishes of the Doradidae and the Auchenipteridae. However, phylogenetic relationships between members of this genus have not been yet analysed. This study analysed newly obtained partial sequences of the 28S ribosomal RNA gene of seven species of Cosmetocleithrum, including its type species C. gussevi Kritsky, Thatcher & Boeger, 1986, along with several other dactylogyrids infecting siluriform, gymnotiform, perciform and characiform fishes. Cosmetocleithrum appeared as an evolutionary recent group, composed of two well-defined lineages: lineage 1 includes parasites of doradids – namely, C. bulbocirrus, C. confusum, C. parvum and C. bifurcum – whereas lineage 2 is composed of species from doradids – that is, C. rarum, C. gussevi, C. gigas, C. trachydorasi and C. falsunilatum – together with parasites of auchenipterids – namely, C. laciniatum and C. baculum. The search for synapomorphies to characterize taxonomic groups within Cosmetocleithrum appears challenging, since the morphology of their haptoral elements is quite conservative, and that of the copulatory complex is highly variable between species. The results of the present study support the recent synonymization of Paracosmetocleithrum Acosta, Scholz, Blasco-Costa, Alves & Silva, 2018 with Cosmetocleithrum. Whereas the 28S ribosomal DNA data resolved Cosmetocleithrum as monophyletic, the statistical support for the lineage was low, rendering its phylogenetic position between other Neotropical dactylogyrids yet undefined.
Measles virus-imposed remodeling of the autophagy machinery determines the outcome of bacterial coinfection

ABSTRACT Although it is admitted that secondary infection can complicate viral diseases, the consequences of viral infection on cell susceptibility to other infections remain underexplored at the cellular level. We though to examine whether the sustained macroautophagy/autophagy associated with measles virus (MeV) infection could help cells oppose invasion by Salmonella Typhimurium, a bacterium sensitive to autophagic restriction. We report here the unexpected finding that Salmonella markedly replicated in MeV-infected cultures due to selective growth within multinucleated cells. Hyper-replicating Salmonella localized outside of LAMP1-positive compartments to an extent that equaled that of the predominantly cytosolic sifA mutant Salmonella. Bacteria were subjected to effective ubiquitination but failed to be targeted by LC3 despite an ongoing productive autophagy. Such a phenotype could not be further aggravated upon silencing of the selective autophagy regulator TBK1 or core autophagy factors ATG5 or ATG7. MeV infection also conditioned primary human epithelial cells for augmented Salmonella replication. The analysis of selective autophagy receptors able to target Salmonella revealed that a lowered expression level of SQSTM1/p62 and TAX1BP1/T6BP autophagy receptors prevented effective anti-Salmonella autophagy in MeV-induced syncytia. Conversely, as SQSTM1/p62 is promoting the cytosolic growth of Shigella flexneri, MeV infection led to reduced Shigella replication. The results indicate that the rarefaction of dedicated autophagy receptors associated with MeV infection differentially affects the outcome of bacterial coinfection depending on the nature of the functional relationship between bacteria and such receptors. Thus, virus-imposed reconfiguration of the autophagy machinery can be instrumental in determining the fate of bacterial coinfection.Abbreviations: ACTB/β-ACTIN: actin beta; ATG: autophagy related; BAFA1: bafilomycin A1; CFU: colony-forming units; CALCOCO2/NDP52: calcium binding and coiled-coil domain 2; FIP: fusion inhibitory peptide; GFP: green fluorescent protein; LAMP1: lysosomal associated membrane protein 1; LIR: MAP1LC3/LC3-interacting region; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MeV: measles virus; MOI: multiplicity of infection; OPTN: optineurin; PHH: primary human hepatocyte; SCV: Salmonella-containing vacuoles; SQSTM1/p62: sequestosome 1; S. flexneri: Shigella flexneri; S. Typhimurium: Salmonella enterica serovar Typhimurium; TAX1BP1/T6BP: Tax1 binding protein 1; TBK1: TANK binding kinase 1
The Damaging Effects of Long UVA (UVA1) Rays: A Major Challenge to Preserve Skin Health and Integrity

Within solar ultraviolet (UV) light, the longest UVA1 wavelengths, with significant and relatively constant levels all year round and large penetration properties, produce effects in all cutaneous layers. Their effects, mediated by numerous endogenous chromophores, primarily involve the generation of reactive oxygen species (ROS). The resulting oxidative stress is the major mode of action of UVA1, responsible for lipid peroxidation, protein carbonylation, DNA lesions and subsequent intracellular signaling cascades. These molecular changes lead to mutations, apoptosis, dermis remodeling, inflammatory reactions and abnormal immune responses. The altered biological functions contribute to clinical consequences such as hyperpigmentation, inflammation, photoimmunosuppression, sun allergies, photoaging and photocancers. Such harmful impacts have also been reported after the use of UVA1 phototherapy or tanning beds. Furthermore, other external aggressors, such as pollutants and visible light (Vis), were shown to induce independent, cumulative and synergistic effects with UVA1 rays. In this review, we synthetize the biological and clinical effects of UVA1 and the complementary effects of UVA1 with pollutants or Vis. The identified deleterious biological impact of UVA1 contributing to clinical consequences, combined with the predominance of UVA1 rays in solar UV radiation, constitute a solid rational for the need for a broad photoprotection, including UVA1 up to 400 nm.
Use of health care utilization as a metric of intervention success may perpetuate racial disparities: An outcome evaluation of a homeless transitional care program

Abstract Objective This study explored race‐based differences in disease burden, health care utilization, and mortality for Black and White persons experiencing homelessness (PEH) who were referred to a transitional care program, and health care utilization and program outcomes for program participants. Design This was a quantitative program evaluation. Sample Black and White PEH referred to a transitional care program (n = 450). We also analyzed data from the subgroup of program participants (N = 122). Of the 450 referrals, 122 participants enrolled in the program. Measures We included chronic disease burden, mental illness, substance use, health care utilization, and mortality rates for all PEH referred. For program participants, we added 6‐month pre/post health care utilization and program outcomes. All results were dichotomized by race. Results Black PEH who were referred to the program had higher rates of hypertension, diabetes, renal failure, and HIV and similar post‐referral mortality rates compared to White PEH. Black and White PEH exhibited similar program outcomes; however, Black PEH revisited the emergency department (ED) less frequently than White PEH at 30 and 90 days after participating in the program. Conclusions Health care utilization may be a misleading indicator of medical complexity and morbidity among Black PEH. Interventions that rely on health care utilization as an outcome measure may unintentionally contribute to racial disparities.
Enhanced antitumor activity induced by a DNA vaccine encoding E7 antigen fused to an ERAD-targeting sequence

Abstract The endoplasmic reticulum (ER) is a key organelle in cell homeostasis and cell health through antigen presentation to immune cells. Thus, the ER has become a therapeutic target to induce cellular immune responses. We previously reported the antitumor effect of a DNA vaccine that expresses the E7 antigen fused to the cyclooxygenase-2 (COX-2) protein. This inflammation-related enzyme contains a degradation cassette associated with the endoplasmic reticulum-associated degradation (ERAD) pathway. To avoid the use of full-length COX-2 and any risk of adverse effects due to the activity of its catalytic site, we designed new versions of the fusion protein. These new constructs encode the E7 antigen fused to the signal peptide and the ERAD sequence of COX-2 with or without the membrane-binding domain (MBD) as well as deletion of the catalytic site. We evaluated the antigen-specific antitumor effect of these DNA constructs in murine prophylactic and therapeutic cancer models. These assays showed that the ERAD cassette is the minimum sequence in the COX-2 protein that induces an antitumor effect when fused to the E7 antigen with the advantage of eliminating any potential adverse effects from the use of full-length COX-2.
Role of ferroptosis-related genes in periodontitis based on integrated bioinformatics analysis

Background Cell survival or death is one of the key scientific issues of inflammatory response. To regulate cell death during the occurrence and development of periodontitis, various forms of programmed cell death, such as pyroptosis, ferroptosis, necroptosis, and apoptosis, have been proposed. It has been found that ferroptosis characterized by iron-dependent lipid peroxidation is involved in cancer, degenerative brain diseases and inflammatory diseases. Furthermore, NCOA4 is considered one of ferroptosis-related genes (FRGs) contributing to butyrate-induced cell death in the periodontitis. This research aims to analyze the expression of FRGs in periodontitis tissues and to explore the relationship between ferroptosis and periodontitis. Method Genes associated with periodontitis were retrieved from two Gene Expression Omnibus datasets. Then, we normalized microarray data and removed the batch effect using the R software. We used R to convert the mRNA expression data and collected the expression of FRGs. Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG), transcription factor (TF) and protein-protein interaction (PPI) network analyses were used. In addition, we constructed a receiver operating characteristic curve and obtained relative mRNA expression verified by quantitative reverse-transcription polymerase chain reaction (PCR). Results Eight and 10 FRGs related to periodontitis were upregulated and downregulated, respectively. GO analysis showed that FRGs were enriched in the regulation of glutathione biosynthetic, glutamate homeostasis, and endoplasmic reticulum-nucleus signaling pathway. The top TFs included CEBPB, JUND, ATF2. Based on the PPI network analysis, FRGs were mainly linked to the negative regulation of IRE1-mediated unfolded protein response, regulation of type IIa hypersensitivity, and regulation of apoptotic cell clearance. The expression levels of NCOA4, SLC1A5 and HSPB1 using PCR were significantly different between normal gingival samples and periodontitis samples. Furthermore, the diagnostic value of FRGs for periodontitis were “Good”. Conclusions We found significant associations between FRGs and periodontitis. The present study not only provides a new possible pathomechanism for the occurrence of periodontitis but also offers a new direction for the diagnosis and treatment of periodontitis.
Men's experiences of receiving a prostate cancer diagnosis after opportunistic screening—A qualitative descriptive secondary analysis

Prostate cancer is one of the most common types of cancer in men and could occur without symptoms. Screening has been debated but remains controversial and, in most countries, organized population‐based screening does not exist. The aim of this study was to describe men's experiences of receiving a prostate cancer diagnosis after opportunistic screening.
Three different short-interval intracortical inhibition methods in early diagnosis of amyotrophic lateral sclerosis

Abstract Objectives: To compare the utility of conventional amplitude measurements of short-interval intracortical inhibition (A-SICI) with two threshold-tracking (T-SICI) methods, as aids to early diagnosis of amyotrophic lateral sclerosis (ALS). The new parallel threshold-tracking method (T-SICIp) was compared with the previously used serial tracking method (T-SICIs). Methods: 112 consecutive patients referred with the suspicion of ALS and 40 healthy controls were prospectively included. Based on clinical follow-up, patients were divided into 67 patients with motor neuron disease (MND) comprising progressive muscular atrophy (PMA) as well as ALS, and 45 patient controls. SICI was recorded from first dorsal interosseus muscle using the three different protocols. Results: MND patients had significantly reduced T-SICIp, T-SICIs and A-SICI, compared with healthy controls and patient controls, while healthy and patient controls were similar. Paradoxically, T-SICIp was least affected in MND patients with the most upper motor neuron (UMN) signs (Spearman ρ = 0.537, P < 0.0001) whereas there was no correlation for T-SICIs or A-SICI. T-SICIp also provided the best discrimination between patient controls and MND as determined by the receiver operating characteristic (ROC) curves. For patients with no UMN signs, area under ROC curve for 2-3ms inter-stimulus intervals was 0.931 for T-SICIp, 0.771 for T-SICIs and 0.786 for A-SICI. Conclusions: SICI is a sensitive measure for detection of cortical involvement in ALS patients. T-SICIp has higher sensitivity and specificity than T-SICIs and A-SICI, particularly in patients without any upper motor neuron signs.
Efficacy of n-3 fatty acid supplementation on rheumatoid arthritis’ disease activity indicators: a systematic review and meta-analysis of randomized placebo-controlled trials

Abstract Theoretical evidence and previous studies suggest that oralnutrient supplementation (ONS) with n-3 fatty acids for rheumatoid arthritis (RA) has the potential to lower disease activity indicators and non-steroidal anti-inflammatory drug (NSAID) uptake. A systematic search was conducted on five databases/registries from inception until May 23, 2021 with the aim to identify randomized placebo-controlled trials comparing n-3 supplements to placebo on disease-specific outcomes. A total of 23 studies matched the criteria (PROSPERO: CRD42019137041). Pooled analyses revealed that n-3 ONS provided a small effect in reducing pain [standardized mean difference (SMD): −0.16, 95% confidence intervals (CI): −0.40 to 0.09], and tender (SMD: −0.20, 95% CI: −0.46 to 0.05) and swollen joint count (SMD: −0.10, 95% CI: −0.28 to 0.07). In sensitivity analyses, there was a small effect in the reduction of NSAIDs intake (SMD: −0.22, 95% CI: −0.90 to 0.46), and c-reactive protein was reduced only by 0.21 mg/dL (95% CI: −0.75 to 0.33). Similar findings were observed regarding other objective/subjective outcomes. The certainty of the evidence was mostly of “very low/low” quality. Overall, n-3 ONS in RA might have a limited clinical benefit. Previous findings suggesting a reduction in NSAID intake may have been biased from the inadequate blinding of interventions.
Domain Decomposition Methods for Discontinuous Galerkin Approximations of Elliptic Problems

The application of the techniques of domain decomposition to construct effective preconditioners for systems generated by standard methods such as finite difference or finite element methods has been well-researched in the past few decades. However, results concerning the application of these techniques to systems created by the discontinuous Galerkin method (DG) are much more rare. This dissertation represents the effort to extend the study of two-level nonoverlapping and overlapping additive Schwarz methods for DG discretizations of secondand fourth-order elliptic partial differential equations. In particular, the general Schwarz framework is used to find theoretical bounds for the condition numbers of the preconditioned systems corresponding to both the nonoverlapping and overlapping additive Schwarz methods. In addition, the impact on the performance of the preconditioners caused by varying the penalty parameters inherent to DG methods is investigated. Another topic of investigation is the choice of course subspace made for the two-level Schwarz methods. The results of in-depth computational experiments performed to validate and study various aspects of the theory are presented. In addition, the design and implementation of the methods are discussed.
Early Life Short-Term Exposure to Polychlorinated Biphenyl 126 in Mice Leads to Metabolic Dysfunction and Microbiota Changes in Adulthood

Early life exposure to environmental pollutants may have long-term consequences and harmful impacts on health later in life. Here, we investigated the short- and long-term impact of early life 3,3′,4,4′,5-pentacholorobiphenyl (PCB 126) exposure (24 μg/kg body weight for five days) in mice on the host and gut microbiota using 16S rRNA gene sequencing, metagenomics, and 1H NMR- and mass spectrometry-based metabolomics. Induction of Cyp1a1, an aryl hydrocarbon receptor (AHR)-responsive gene, was observed at 6 days and 13 weeks after PCB 126 exposure consistent with the long half-life of PCB 126. Early life, Short-Term PCB 126 exposure resulted in metabolic abnormalities in adulthood including changes in liver amino acid and nucleotide metabolism as well as bile acid metabolism and increased hepatic lipogenesis. Interestingly, early life PCB 126 exposure had a greater impact on bacteria in adulthood at the community structure, metabolic, and functional levels. This study provides evidence for an association between early life environmental pollutant exposure and increased risk of metabolic disorders later in life and suggests the microbiome is a key target of environmental chemical exposure.