Miracle-dz/UniFAR-FTUs huggingface dataset:
Changes in the epigenome and transcriptome of the poplar shoot apical meristem in response to water availability affect preferentially hormone pathways

The adaptive capacity of long-lived organisms such as trees to the predicted climate changes, including severe and successive drought episodes, will depend on the presence of genetic diversity and phenotypic plasticity. Here, the involvement of epigenetic mechanisms in phenotypic plasticity toward soil water availability was examined in Populus×euramericana. This work aimed at characterizing (i) the transcriptome plasticity, (ii) the genome-wide plasticity of DNA methylation, and (iii) the function of genes affected by a drought-rewatering cycle in the shoot apical meristem. Using microarray chips, differentially expressed genes (DEGs) and differentially methylated regions (DMRs) were identified for each water regime. The rewatering condition was associated with the highest variations of both gene expression and DNA methylation. Changes in methylation were observed particularly in the body of expressed genes and to a lesser extent in transposable elements. Together, DEGs and DMRs were significantly enriched in genes related to phytohormone metabolism or signaling pathways. Altogether, shoot apical meristem responses to changes in water availability involved coordinated variations in DNA methylation, as well as in gene expression, with a specific targeting of genes involved in hormone pathways, a factor that may enable phenotypic plasticity.
Preventive strength training improves working ergonomics during welding

To investigate the effect of a preventive strength training program on cardiovascular, metabolic and muscular strains during welding. Welders are one of the occupation groups which typically have to work in extended forced postures which are known to be an important reason for musculoskeletal disorders. Subjects (exercise group) accomplished a 12-week strength training program, while another group served as controls (control group). Pre and post training examinations included the measurements of the one repetition maximum and an experimental welding test. Local muscle activities were analysed by surface electromyography. Furthermore, heart rate, blood pressure, lactate and rating of perceived exertion were examined. In the exercise group, strength training lead to a significant increase of one repetition maximum in all examined muscles (p<.05). During the experimental welding test muscle activities of trunk and shoulder muscles and arm muscles were significantly reduced in the exercise group after intervention (p<.05). While no changes of neither cardiovascular nor metabolic parameters were found, subjects of the exercise group rated a significantly decreased rate of perceived exertion welding (p<.05). Effects of strength training can be translated in an improved working ergonomics and tolerance against the exposure to high physical demands at work.
The self‐reported use of immunostains and cytogenetic testing in the diagnosis of melanoma by practicing U.S. pathologists of 10 selected states

The diagnosis of melanoma can be challenging, especially in lesions for which the histopathologic criteria bridge two or more taxonomic categories. Newer genomic analytical methods of fluorescence in situ hybridization (FISH) and comparative genomic hybridization (CGH) have been introduced as ancillary techniques to differentiate benign and malignant melanocytic proliferations.
SOCS-1 Binding to Tyrosine 441 of IFN-γ Receptor Subunit 1 Contributes to the Attenuation of IFN-γ Signaling In Vivo1

Suppressor of cytokine signaling (SOCS)-1 is a critical inhibitor of IFN-γ signal transduction in vivo, but the precise biochemical mechanism of action of SOCS-1 is unclear. Studies in vitro have shown that SOCS-1 binds to Jaks and inhibits their catalytic activity, but recent studies indicate SOCS-1 may act in a similar manner to SOCS-3 by firstly interacting with cytokine receptors and then inhibiting Jak activity. Here, we have generated mice, termed Ifngr1441F, in which a putative SOCS-1 binding site, tyrosine 441 (Y441), on the IFN-γ receptor subunit 1 (IFNGR1) is mutated. We confirm that SOCS-1 binds to IFNGR1 in wild-type but not mutant cells. Mutation of Y441 results in impaired negative regulation of IFN-γ signaling. IFN-γ-induced STAT1 activation is prolonged in Ifngr1441F cells, but not to the extent seen in cells completely lacking SOCS-1, suggesting that SOCS-1 maintains activity to modulate IFN-γ signaling via other mechanisms. Despite this, we show that hypersensitivity to IFN-γ results in enhanced innate tumor protection in Ifngr1441F mice in vivo, and unregulated expression of an IFN-γ–dependent chemokine, monokine-induced by IFN-γ. Collectively, these data indicate that Y441 contributes to the regulation of signaling through IFNGR1 via the recruitment of SOCS-1 to the receptor.
Function of a Conserved Checkpoint Recruitment Domain in ATRIP Proteins

ABSTRACT The ATR (ATM and Rad3-related) kinase is essential to maintain genomic integrity. ATR is recruited to DNA lesions in part through its association with ATR-interacting protein (ATRIP), which in turn interacts with the single-stranded DNA binding protein RPA (replication protein A). In this study, a conserved checkpoint protein recruitment domain (CRD) in ATRIP orthologs was identified by biochemical mapping of the RPA binding site in combination with nuclear magnetic resonance, mutagenesis, and computational modeling. Mutations in the CRD of the Saccharomyces cerevisiae ATRIP ortholog Ddc2 disrupt the Ddc2-RPA interaction, prevent proper localization of Ddc2 to DNA breaks, sensitize yeast to DNA-damaging agents, and partially compromise checkpoint signaling. These data demonstrate that the CRD is critical for localization and optimal DNA damage responses. However, the stimulation of ATR kinase activity by binding of topoisomerase binding protein 1 (TopBP1) to ATRIP-ATR can occur independently of the interaction of ATRIP with RPA. Our results support the idea of a multistep model for ATR activation that requires separable localization and activation functions of ATRIP.
Crystal structure of poly[[hexaqua-1κ4 O,2κ2 O-bis(μ3-pyridine-2,4-dicarboxylato-1κO 2:2κ2 N,O 2′;1′κO 4)cobalt(II)strontium(II)] dihydrate]

In the title polymeric complex, {[CoSr(C7H3NO4)2(H2O)6]·2H2O}n, the CoII ion, which is situated on a crystallographic centre of inversion, is six-coordinated by two O atoms and two N atoms from two pyridine-2,4-dicarboxylate (pydc2−) ligands and two terminal water molecules in a slightly distorted octahedral geometry, to form a trans-[Co(pydc)2(H2O)2]2− unit. The SrII ion, situated on a C 2 axis, is coordinated by four O atoms from four pydc2− ligands and four water molecules. The coordination geometry of the SrII atom can be best described as a distorted dodecahedron. Each SrII ion bridges four [Co(pydc)2(H2O)2]2− units by four COO− groups of four pydc2− ligands to form a three-dimensional network structure. Two additional solvent water molecules are observed in the crystal structure and are connected to the three-dimensional coordination polymer by O—H⋯O hydrogen bonds. Further intra- and intermolecular O—H⋯O hydrogen bonds consolidate the overall structure.
The Comparative Molecular Study between Bombycidae and Saturniidae Based on mtDNA RFLP and Cytochrome Oxidase I Gene Sequences: Implication for Molecular Evolution

Abstract Bombycidae, Saturniidae, mtDNA RFLP, Cytochrome Oxidase I Gene The phylogenetic relationships between Bombyx mori and Bombyx mandarina species of Bombycidae, and Antheraea yamamai and Antheraea pernyi species of Saturniidae were investigated based on mtDNA RFLP and cytochrome oxidase I gene. The sizes of the mtDNA of all the species were estimated at approximately 16 kbp ± 500 bp by total length of all the restricted fragments and no variation in size was recognized. Of the fourteen different restriction endonucleases used, BamHl, Hindlll, Pstl, EcoRl and Xbal showed RFLP. Among these, only Hindlll showed RFLP between B. mori and B. mandarina. A comparative analysis of sequences was also conducted with the mitochondrial cytochrome oxidase I genes of each species. The results indicated that B. mori shared a 97% , 85% and 87% sequence identity with B. mandarina, A. yamamai and A. pernyi, respectively. B. mandarina shared a 87% and 88% sequence identity with A. yamamai and A. penyi, respectively. A. yamamai shared 92% sequence identity with A. pernyi. The results of the phylogenetic analysis exhibited monophyly and confidence limits of more than 99% in all trees for both Bombycidae and Saturniidae.
ILAE Commission of European Affairs Subcommission on European Guidelines 1998-2001: The provision of epilepsy care across Europe.

PURPOSE To assess the needs and resources available in the provision of basic epilepsy care across Europe. METHODS A mailed questionnaire was used, the European Epilepsy Services inventory (EESI). The EESI was distributed to all 36 European chapters of the International League Against Epilepsy (ILAE), and answers were obtained from 32, a response rate of 89%. For the purpose of studying trends across Europe, the chapters were divided into a Western, an Eastern, a Central, and a Southern group. RESULTS The survey results showed that there was a wide range in the number of physicians and specialists involved in epilepsy care across Europe, with a trend toward higher numbers of neurologists, pediatricians, and pediatric neurologists in Eastern Europe. Many different specialties were involved in epilepsy care, and many chapters reported differences in the provision of care across their countries, with less possibility for patients to see a specialist in the least provided areas, where most epilepsy patients were cared for by general practitioners and internists. Problems with high costs of the newer antiepileptic drugs were most pronounced in Eastern Europe. Problems with lack of comprehensive care and of epilepsy specialists, with stigma and social problems, and with insufficient professional education and knowledge about epilepsy were reported all across Europe. CONCLUSIONS Knowledge about differences in the pattern of provision of epilepsy care and about the main problems encountered by the European ILAE chapters is of importance in the continuing efforts to improve management of epilepsy all over Europe.
Dietary scores at midlife and healthy ageing in a French prospective cohort

Abstract Although nutrition has been advocated as a major determinant of healthy ageing (HA), studies investigating the link between dietary quality and HA are scarce. We investigated the association between adherence to French food-based and nutrient-based guidelines at midlife, as assessed by three dietary scores, and HA. HA was assessed in 2007–2009, among 2329 participants of the SUpplémentation en Vitamines et Minéraux AntioXydants study aged 45–60 years at baseline (1994–1995) and initially free of diabetes, CVD and cancer. HA was defined as not developing any major chronic disease, good physical and cognitive functioning, no limitations in instrumental activities of daily living, no depressive symptoms, no health-related limitations in social life, good overall self-perceived health and no function-limiting pain. Data from repeated 24-h dietary records provided at baseline permitted the computation of the modified French Programme National Nutrition Santé-Guideline Score (mPNNS-GS), the Probability of Adequate Nutrient Intake Dietary Score (PANDiet) and the Diet Quality Index-International (DQI-I). Associations of these scores with HA were assessed by logistic regression. In 2007–2009, 42 % of men and 36 % of women met our criteria of HA. After adjustment for potential confounders, higher scores of the mPNNS-GS (ORquartile 4 v. quartile 1 1·44; 95 % CI 1·10, 1·87; P trend=0·006) and the PANDiet (1·28; 95 % CI 1·00, 1·64; P trend=0·03) were associated with higher odds of HA. We observed no association between DQI-I and HA. In conclusion, this study suggests a beneficial long-term role of high adherence to both food-based and nutrient-based French dietary guidelines for a HA process.
Understanding the pathogenesis of endometriosis through proteomics: Recent advances and future prospects

Endometriosis is a complex gynecological disease, characterized by the presence and growth of endometrial tissue outside the uterus, resulting in pelvic pain and infertility. It occurs in 10% of women in their reproductive age. The viable endometrial cells enter the peritoneal cavity by retrograde menstruation, implant, and cause lesions ectopically; depending on their ability to survive, attach, grow, and invade. These “normal” endometrial cells turn “endometriotic” apparently because of inherent abnormalities present in them. Information on these molecular abnormalities is now being sought through proteomic approaches. Recent proteome‐based comparisons between the eutopic endometrium from normal women and patients with endometriosis have revealed several proteins (many of which are shown to have a role in several cancers), of which a few have been validated as potential players in the etiology of endometriosis. After an initial in‐flow of information from these proteome studies of eutopic endometrium, focus now needs to be expanded to the changes in the various protein PTMs and their upstream effectors present in these tissues. Early diagnosis of endometriosis through noninvasive means is the need of the hour as well—which would require the use of the presently existing immunoassays, along with the advancing MS‐based proteomics. In this review, we aim to discuss these future thrust areas of human endometriosis proteomics and also present the proteomic advances made so far in understanding the molecular basis of endometriosis.
The expression of nectin-1alpha in normal human skin and various skin tumours.

BACKGROUND A novel cell-cell adhesion system that consists of nectin and afadin has been identified at cadherin-based cell-cell adherens junctions. Nectin is a Ca2+-independent homophilic and heterophilic cell adhesion molecule that belongs to the immunoglobulin superfamily. Nectin has recently been shown to serve as an alpha-herpesvirus entry and cell-cell spread mediator. In spite of the ubiquitous expression of nectin-1alpha, its detailed localization in human skin has not been examined so far. OBJECTIVES To investigate the localization of nectin-1alpha in normal human skin and the alteration of its expression in malignant skin tumours. METHODS Immunohistochemistry was employed to determine the expression of nectin-1alpha and other adhesion molecules. RESULTS We detected nectin-1alpha in normal human epidermis, follicles and eccrine ducts. Nectin-1alpha was colocalized with E-cadherin at cell-cell adherens junctions of the epidermis. The concentration of the nectin-afadin system at cell-cell adherens junctions was reduced in the early stage of malignant transformation of keratinocytes, such as in basal cell carcinomas and squamous cell carcinomas, where the cadherin-catenin system was preserved. Nectin-1alpha at cell-cell adherens junctions was reduced in human epithelial cancer cells located at the advancing border of the tumour. CONCLUSIONS Our results showed that nectin-1alpha is located at cell-cell adherens junctions in human skin and that reduction of nectin-1alpha at cell-cell adherens junctions may be involved in the invasion of squamous cell tumours.
Systemic corticosteroids inhibit bone healing in a rabbit ulnar osteotomy model

Prolonged systemic administration of corticosteroids causes osteoporosis and increased risk of fracture. Despite this well documented side effect of systemic corticosteroids, the effect of these compounds on fracture healing is not well defined. The goal of this study was to test the hypothesis that systemic corticosteroid therapy adversely affects fracture healing in a rabbit ulnar osteotomy model. Non-critical sized (1 mm) defects were created bilaterally in 18 adult female New Zealand White rabbits. Starting 2 months before operative intervention and continuing for 6 weeks during healing of the osteotomies, a subcutaneous dose of either sterile saline or prednisone (0.15 mg/kg) was administered daily. Serial radiographs of the forelimb were taken immediately postoperatively and weekly beginning the second week postoperatively. After killing at 6 weeks, only 3 of 20 limbs from animals treated with prednisone achieved radiographic union while 13 of 16 control limbs achieved union. The radiographic density of bone in the defect as well as callus size were greater in the control limbs than in the limbs from prednisone-treated animals. DEXA confirmed that the bone mineral content was lower in the ulnae of prednisone-treated rabbits both within the defect and in adjacent ulnar bone. Mechanical data indicated that osteotomies from rabbits chronically treated with prednisone were weaker than in controls. In this rabbit ulnar osteotomy model, chronic prednisone treatment clearly inhibited bone healing.
Glutathione transferase zeta: discovery, polymorphic variants, catalysis, inactivation, and properties of Gstz1−/− mice

Glutathione transferase zeta (GSTZ1) is a member of the GST superfamily of proteins that catalyze the reaction of glutathione with endo- and xenobiotics. GSTZ1-1 was discovered by a bioinformatics strategy that searched the human-expressed sequence-tag database with a sequence that matched a putative plant GST. A sequence that was found was expressed and termed GSTZ1-1. In common with other GSTs, GSTZ1-1 showed some peroxidase activity, but lacked activity with most known GST substrates. GSTZ1-1 was also found to be identical with maleylacetoacetate isomerase, which catalyzes the penultimate step in the tyrosine-degradation pathway. Further studies showed that dichloroacetate (DCA) and a range of α-haloalkanoates and α,α-dihaloalkanoates were substrates. A subsequent search of the human-expressed sequence-tag database showed the presence of four polymorphic alleles: 1a, 1b, 1c, and 1d; GSTZ1c was the most common and was designated as the wild-type gene. DCA was shown to be a kcat inactivator of human, rat, and mouse GSTZ1-1; human GSTZ1-1 was more resistant to inactivation than mouse or rat GSTZ1-1. Proteomic analysis showed that hGSTZ1-1 was inactivated when Cys-16 was modified by glutathione and the carbon skeleton of DCA. The polymorphic variants of hGSTZ1-1 differ in their susceptibility to inactivation, with 1a-1a being more resistant to inactivation than the other variants. The targeted deletion of GSTZ1 yielded mice that were not phenotypically distinctive. Phenylalanine proved, however, to be toxic to Gstz1−/− mice, and these mice showed evidence of organ damage and leucopenia.
Localization of FtsI (PBP3) to the Septal Ring Requires Its Membrane Anchor, the Z Ring, FtsA, FtsQ, and FtsL

ABSTRACT Assembly of the division septum in bacteria is mediated by several proteins that localize to the division site. One of these, FtsI (also called penicillin-binding protein 3) of Escherichia coli, consists of a short cytoplasmic domain, a single membrane-spanning segment, and a large periplasmic domain that encodes a transpeptidase activity involved in synthesis of septal peptidoglycan. We have constructed a merodiploid strain with a wild-type copy offtsI at the normal chromosomal locus and a genetic fusion of ftsI to the green fluorescent protein (gfp) at the lambda attachment site. gfp-ftsI was expressed at physiologically appropriate levels under control of a regulatable promoter. Consistent with previous results based on immunofluorescence microscopy GFP-FtsI localized to the division site during the later stages of cell growth and throughout septation. Localization of GFP-FtsI to the cell pole(s) was not observed unless the protein was overproduced about 10-fold. Membrane anchor alterations shown previously to impair division but not membrane insertion or transpeptidase activity were found to interfere with localization of GFP-FtsI to the division site. In contrast, GFP-FtsI localized well in the presence of β-lactam antibiotics that inhibit the transpeptidase activity of FtsI. Septal localization depended upon every other division protein tested (FtsZ, FtsA, FtsQ, and FtsL). We conclude that FtsI is a late recruit to the division site, and that its localization depends on an intact membrane anchor.
Hostility, conflict and cardiovascular responses in married couples: a focus on the dyad

This study examined the relations of one’s own total trait hostility and one’s spouse’s hostility as influences on cardiovascular (CV) responses to couple interactions (including conflict discussions) in 45 married couples aged 24—50. Systolic blood pressure and cardiac index (CI) reactivity to conflict discussion and recovery after conflict was greater in low hostile males if they were interacting with high hostile wives (p < .02). Vascular resistance index (VRI) reactivity to interactions was greater in high hostile husbands with high hostile wives (p < .05). Women showed no adverse CV effects of having a hostile spouse when their own hostility was low. Instead, seeming to anticipate the subsequent couple interactions, wives from duos in which both partners were high in hostility had higher baseline VRI levels and lower baseline CI compared to wives from duos in which both were low in hostility (ps < .05), and they simply maintained these group differences with no greater CV reactivity during the interactions. Findings suggest that CV responses before, during, and after marital discussions, particularly those characterized by conflict, may be influenced not only by one’s own hostility but by the hostility of one’s partner as well.
Classification Network of Gastric Cancer Construction based on Genetic Algorithms and Bayesian Network

One of the most important link in improves diagnostic accuracy and disease cure rate is accurate classification of disease. The current gene chip's development and widely applications making the diagnosis based on tumor gene expression profiling expected to be on a fast and effective clinical diagnostic method. But the sample of gene is small and the expression data is multi-variable. In this article, we uses three data sets on gene expression profiles of gastric cancer for the construction of classification model, First, screened the gene which significantly changed in expression pattern, and use these genes as a set of the feature to reduce the number of variables, and then using genetic algorithms and bayesian network model to build the classifier, the build process uses these three gene expression data to learn classifier. Classification accuracy is calculated by leave-one cross-validation (LOOCV) and it reached 99.8%. Last we use the GO and pathway to analysis the classifier's network structure.