Miracle-dz/UniFAR-FTUs huggingface dataset:
Parasites of crustaceans (Isopoda: Bopyridae) evolved from fish parasites: Molecular and morphological evidence

The phylogenetic origin of isopods that live as parasites of crustaceans (Bopyridae) is examined using ssu rDNA sequences and morphological characters in separate and combined analyses. A study of split-supporting positions proves that information content of the ssu-rDNA alignment is not high, but the signals are sufficient to study relationships of the Bopyridae. The sequences most similar to those of bopyrids are the ones of the Cymothoidae, isopods that are specialized fish parasites. Topologies obtained with different tree reconstructing methods support a sister-group relationship between Bopyridae and Cymothoidae. This finding is in accordance with morphological characters, for which a cladistic analysis was prepared, and a combination of morphological and molecular data gives the same result. As a consequence, we propose to give up the classification of these parasites as a separate suborder "Epicaridea", to name the taxon "Bopyridae", which should have the same rank as the sistertaxon, the family Cymothoidae . The biology of related taxa is discussed to reconstruct an evolutionary scenario. We assume that evolution started with necrophagous and predatory cirolanid-like isopods specialized to feed on fishes, from which step by step temporary and then permanent fish parasites evolved. The latter are represented in the present fauna by the Cymothoidae. A change of hosts must have occurred in cymothoid-like ancestors, who moved from fishes to crustaceans and developed a special life cycle and morphology, giving rise to modern Bopyridae. This host change triggered a new phase of radiation of parasitic isopods.
Effect of Delayed Bleeding after Captive Bolt Stunning on Heart Activity and Blood Removal in Beef Cattle

Twenty Good grade bulls and heifers approximately 18 mo of age from the university crossbred beef herd were stunned and monitored for heart rate by radiotelemetry until ventricular activity ceased. The animals ranged in weight from 335 to 470 kg and were stunned with a captive bolt stunner and allotted to different bleeding treatments. Control animals (three bulls and two heifers) were bled immediately by severing the carotid arteries and jugular veins. The other animals were decapitated by severing the atlas joint and removing the head without previously severing the carotid arteries and jugular veins. Time periods after stunning were 0 rain (two bulls), 3 rain (two bulls and two heifers), 6 rain (two bulls and one heifer), 15 min (three heifers with foreshanks removed immediately after stunning) and 15 rain (three heifers pithed and foreshanks removed immediately after stunning). Respiration ceased in all animals when they were stunned and did not resume. Duration of heart activity after stunning was greater in animals in which bleeding was delayed than in control animals. Weight of blood removed from animals decreased as the time between stunning and bleeding increased. Heart activity ceased 8 to 10 rain after stunning in animals decapitated 15 rain after stunning. Therefore, the majority of blood was removed without ventricular pumping. (
BEETLE POLLINATION OF SHOREA PARVIFOLIA

Pollination ecology of an emergent tree species, Shorea (section Mutica) parvifolia (Dipterocarpaceae), was studied using the canopy observation system in a lowland dipterocarp forest in Sarawak, Malaysia, during a general flowering period in 1996. Although the species has been reported to be pollinated by thrips in Peninsular Malaysia, our observations of flower visitors and pollination experiments indicated that beetles (Chrysomelidae and Curculionidae, Coleoptera) contributed to pollination of S. parvifolia in Sarawak. Beetles accounted for 74% of the flower visitors collected by net-sweeping, and 30% of the beetles carried pollen, while thrips accounted for 16% of the visitors, and 12% of the thrips carried pollen. The apical parts of the petals and pollen served as a reward for the beetles. Thrips stayed inside the flower almost continuously after arrival, and movements among flowers were rare. Fruit set was significantly increased by introduction of beetles to bagged flowers, but not by introduction of thrips. Hand-pollination experiments and comparison of fruit set in untreated, bagged, and open flowers suggested that S. parvifolia was mainly outbreeding.
Antioxidant responses of ‘Selva’ strawberry as affected by salicylic acid under salt stress

BACKGROUND: Salicylic acid (SA) is a phenolic-endogenous plant hormone and its ameliorative effects against abiotic stresses have been well documented. OBJECTIVE: To evaluate the influence of salinity and SA on enzymatic and non-enzymatic antioxidants responses of ‘Selva’ strawberry plants with respect to the time of SA application. METHOD: Well-rooted daughter strawberry plants cv. Selva, were potted in 3 L plastic pots and after their establishment, were sprayed with 0.5 or 1.0 mM salicylic acid solutions one week before, during or one week after being exposed to 40 mM NaCl salinity. Experiments were carried out as bi-factorial in a completely randomized design. RESULTS: The activities of superoxide dismutase and glutathione reductase increased by both salinity and SA treatments. The highest antioxidant enzymes activity was observed in plants treated with SA one week before being exposed to salinity stress. These plants had both higher proline and glycine betaine contents and lower protein degradation. CONCLUSION: Before being exposed to salinity stress, treating strawberry plants with salicylic acid probably by improving their antioxidant systems will prepare them to cope better with the deleterious effects of salt stress.
Induction of cetacean cytochrome P4501A1 by β-naphthoflavone exposure of skin biopsy slices Short title (40 characters max): Inducibility of cetacean cytochrome P4501A1

Marine mammals can accumulate environmental contaminants in their blubber at concentrations harmful to laboratory animals. Induction of the cytochrome P450 1A1 (CYP1A1) enzyme is widely used as a biomarker of exposure and molecular effects in animal species, yet the validity of this biomarker has not been established in marine mammals. In vivo studies are generally precluded in these protected species but skin biopsies (epidermis and dermis) can be collected in a minimally invasive way. We developed an in vitro assay using skin biopsy slices to examine CYP1A1 protein induction in marine mammals in response to chemical exposure. Skin biopsies from sperm whale (Physeter macrocephalus) were exposed for 24 hr to β-naphthoflavone (BNF), a prototypical CYP1A1 inducer and CYP1A1 induction was detected by immunochemical staining in endothelial cells, smooth muscle cells and fibroblasts. Biopsy slices were exposed to a range of BNF concentrations (0.6 -600 μM) and a significant concentrationeffect relationship was observed in both endothelial and smooth muscle cells (p=0.05). This is the first study using skin biopsy slices to examine exposure of cetacean tissue to a CYP1A1 inducer. It demonstrates a causal relationship between chemical exposure and CYP1A1 induction and therefore validates the use of CYP1A1 expression in skin biopsies as a biomarker in cetaceans. Our protocol can be adapted to the investigation of chemicals, mixtures, concentrations, incubation times or biological endpoints of choice. This should prove particularly relevant for these and other protected species that cannot be studied in the laboratory.
A chromosome-wide QTL mapping on chromosome 2 to identify loci affecting live weight and carcass traits in F2 population of Japanese quail

The Japanese quail (Coturnix japonica) is a considerable species which is often used for animal modelling in breeding researches. This study aims to detect quantitative trait loci (QTL) underlying growth and carcass traits in Japanese quail. A three-generation resource population was developed using wild and white Japanese quail strains. The total mapping population consisted of 472 birds. Eight pairs of white and wild birds were mated reciprocally and 34 F1 birds were generated. The F1 birds were intercrossed to produce F2 offspring (422 birds). All of the animals from three generations were genotyped for four microsatellite markers on chromosome 2 in quail. QTL analysis was performed with the Least Squares interval mapping method. The results indicated significant QTL for breast weight, carcass weight, pre-stomach weight, pancreas percentage, head weight, intestine weight, spleen weight, and heart weight. There was also evidence for dominance QTL affecting pre-stomach weight, percentage of pre-stomach weight, and percentage of breast on chromosome 2. The proportion of F2 phenotypic variation explained by significant additive and dominance QTL effects ranged from 1.06 to 3.33% and 0.71 to 4.36%, respectively. There was no evidence for imprinting effect on the studied traits.
Maintaining proton homeostasis is an essential role of glucose metabolism in cell survival

Aerobic glycolysis, termed “the Warburg Effect”, supports cell proliferation, and glucose deprivation directly elicits necrosis or shifts stimuli-induced apoptosis to necrosis. However, how glucose metabolism regulates cell survival or death choice remains largely unclear. Here we use our recently developed method to monitor in real-time cellular apoptosis and necrosis, and uncover a metabolic homeostasis linked to cell death control. We show that glucose metabolism is the major source to maintain both intracellular and extracellular proton homeostasis. Glucose deficiency leads to lack of proton provision, which provokes a compensatory lysosomal proton efflux and resultant increased lysosomal pH. This lysosomal alkalinization can trigger necrosis. Furthermore, artificial proton supplement enables cells to survive glucose deprivation. Taken together, our results reveal a critical role of glucose metabolism in maintaining cellular microenvironment, and provide a better understanding of the essential requirement of aerobic glycolysis for proliferating cells whose active anabolism consumes a great many protons.
cells sensitive and resistant to STI-571 in association with down-regulation of Bcr- Abl, abrogation of STAT5 activity, and Bax conformational change.

Interactions between the histone deacetylase inhibitors (HDACIs) suberanoylanilide hydroxamic acid (SAHA) and sodium butyrate (SB) and the heat shock protein 90 (Hsp90) antagonist 17-AAG have been examined in Bcr-Abl+ human leukemia cells (K562 and LAMA84), including those sensitive and resistant to STI571. Co-administration of 17-AAG with SAHA or SB for 24 h synergistically induced mitochondrial dysfunction (cytochrome c and AIF release), caspase-3 and -8 activation, apoptosis, and growth inhibition. Similar effects were observed in LAMA84 cells and K562 cells resistant to STI-571 as well as in CD34+ leukemic cells obtained from patients with CML including those who had developed a resistance against STI-571. These events were associated with increased association of Bcr/abl, Raf-1, and Akt with Hsp70, whereas the total level of these proteins markedly decreased. A pronounced inactivation of ERK1/2, and activation of JNK were also observed. In addition, 17-AAG/SAHA abrogated DNA binding and transcriptional activities of STAT5 in K562 cells, including those ectopically expressing a constitutively active STAT5A construct. Co-administration of 17-AAG and SAHA also induced downregulation of Mcl-1, Bcl-xL, B-Raf, and p21CIP1, upregulation of Bak, cleavage of 14-3-3 proteins, and a profound conformational change in Bax accompanied by translocation to the membrane fraction. Together, these findings raise the possibility that combining HDACIs with the Hsp90 antagonist 17-AAG may represent a novel strategy against Bcr-Abl+ leukemias, including those resistant to STI571.
TheCytokineInterleukin-6IsSufficientButNotNecessary toMimicthePeripheralConditioningLesionEffecton AxonalGrowth

Lesioningtheperipheralbranchofadorsalrootganglion(DRG)neuronbeforeinjuryofthecentralbranchofthesameneuronenables spontaneous regeneration of these spinal axons. This effect is cAMP and transcription dependent. Here, we show that the cytokine interleukin-6(IL-6)isupregulatedinDRGneuronsaftereitheraconditioninglesionortreatmentwithdibutyryl-cAMP.Inculture,IL-6 allowsneuronstogrowinthepresenceofinhibitorsofregenerationpresentinmyelin.Importantly,intrathecaldeliveryofIL-6toDRG neuronsblocksinhibitionbymyelinbothinvitroandinvivo,effectivelymimickingtheconditioninglesion.BlockingIL-6signalinghas noeffectontheabilityofcAMPtoovercomemyelininhibitors.Consistentwiththis,IL-6-deficientmicerespondtoaconditioninglesion as effectively as wild-type mice. We conclude that IL-6 can mimic both the cAMP effect and the conditioning lesion effect but is not an essentialcomponentofeitherresponse.
Expression of TaTAR2.3-1B, TaYUC9-1 and TaYUC10 correlates with auxin and starch content of developing wheat grains

The role of auxin in developing grains of wheat (Triticum aestivum) is contentious with contradictory reports indicating either positive or negative effects of IAA (indole-3-acetic acid) on grain size. In addition, the contributions to the IAA pool from de novo synthesis via tryptophan, and from hydrolysis of IAA-glucose are unclear. Here we describe the first comprehensive study of tryptophan aminotransferase and indole-3-pyruvate mono-oxygenase expression during wheat grain development from 5 to 20 days after anthesis. A comparison of expression data with measurements of endogenous IAA via combined liquid chromatography-tandem mass spectrometry with heavy isotope labelled internal standards indicates that TaTAR2.3-1B, TaYUC9-A1, TaYUC9-B, TaYUC9-D1, TaYUC10-A and TaYUC10-D are primarily responsible for IAA production in developing grains. Furthermore, we show that IAA synthesis is controlled by genes expressed specifically in developing wheat grains as has already been reported in rice (Oryza sativa) and maize (Zea mays). Our results cast doubt on the proposed role of THOUSAND-GRAIN WEIGHT gene, TaTGW6, in promoting larger grain size via negative effects on grain IAA content. The work on TaTGW6 has overlooked the contribution of the dominant IAA biosynthesis pathway. Although IAA synthesis occurs primarily in the endosperm of wheat grains, we show that the TaYUC9-1 group is also strongly expressed in the embryo. Within the endosperm, TaYUC9-1 expression is highest in aleurone and transfer cells, supporting data from other cereals suggesting that IAA has a key role in differentiation of these tissues.
On the mechanism of sunflower seed deterioration under two different types of accelerated ageing

Action d'une pre-imbibition, de l'equilibrage de l'humidite. Suivi de l'activite de la catalase; etude du comportement des membranes (exsudats, teneur en phospholipides, peroxydation lipidique)
Disinhibitory and neuromodulatory regulation of hippocampal synaptic plasticity

Hippocampal synaptic plasticity, particularly in the Schaffer collateral (SC) to CA1 pyramidal excitatory transmission, is considered as the cellular mechanism underlying learning. The CA1 pyramidal neurons are embedded in an intricate local circuitry that contains a variety of interneurons. The roles these interneurons play in the regulation of the excitatory synaptic plasticity remains largely understudied. Our recent experiments showed that repeated cholinergic activation of α7 nACh receptors expressed in oriens-lacunosum-moleculare (OLMα2) interneurons could induce LTP in SC-CA1 synapses, likely through disinhibition by inhibiting stratum radiatum (s.r.) interneurons that provide feedforward inhibition onto CA1 pyramidal neurons, revealing a potential mechanism for local interneurons to regulate SC-CA1 synaptic plasticity. Here, we pair in vitro studies with biophysically-based modeling to uncover the mechanisms through which cholinergic-activated GABAergic interneurons can disinhibit CA1 pyramidal cells, and how repeated disinhibition modulates hippocampal plasticity at the excitatory synapses. We found that α7 nAChR activation increases OLM activity. OLM neurons, in turn inhibit the fast-spiking interneurons that provide feedforward inhibition onto CA1 pyramidal neurons. This disinhibition, paired with tightly timed SC stimulation, can induce potentiation at the excitatory synapses of CA1 pyramidal neurons. Our work further describes the pairing of disinhibition with SC stimulation as a general mechanism for the induction of hippocampal synaptic plasticity. Disinhibition of the excitatory synapses, paired with SC stimulation, leads to increased NMDAR activation and intracellular calcium concentration sufficient to upregulate AMPAR permeability and potentiate the synapse. Repeated paired disinhibition of the excitatory synapse leads to larger and longer lasting increases of the AMPAR permeability. Our study thus provides a novel mechanism for inhibitory interneurons to directly modify glutamatergic synaptic plasticity. In particular, we show how cholinergic action on OLM interneurons can down-regulate the GABAergic signaling onto CA1 pyramidal cells, and how this shapes local plasticity rules. We identify paired disinhibition with SC stimulation as a general mechanism for the induction of hippocampal synaptic plasticity.
Cornforth and Corey-Suggs reagents as efficient catalysts for sulfonation of aromatic and heteroaromatic compounds using NaHSO3 under solvent free and microwave conditions

Abstract Cornforth and Corey-Suggs reagents Pyridinium Dichromate (PDC) and Pyridinium Chlorochromate (PCC) were explored as efficient catalysts for sulfonation of aromatic and heteroaromatic compounds using NaHSO3 in aqueous acetonitrile medium at room temperature within 1–4 h, while microwave assisted reactions took place within 1–4 min under solvent-free conditions. These observations indicate significant rate accelerations in microwave assisted reactions. which were explained due to the bulk activation of molecules induced by insitu generated high temperatures and pressures when microwaves are transmitted through reaction medium. Graphical Abstract
Learning Code Transformations via Neural Machine Translation

Source code evolves – inevitably – to remain useful, secure, correct, readable, and efficient. Developers perform software evolution and maintenance activities by transforming existing source code via corrective, adaptive, perfective, and preventive changes. These code changes are usually managed and stored by a variety of tools and infrastructures such as version control, issue trackers, and code review systems. Software evolution and maintenance researchers have been mining these code archives in order to distill useful insights regarding the nature of developers’ activities. One of the long-lasting goals of software engineering research is to better support and automate different types of code changes performed by developers. In this thesis we depart from classic manually crafted ruleor heuristic-based approaches, and propose a novel technique to learn code transformations by leveraging the vast amount of publicly available code changes performed by developers. We rely on Deep Learning, and in particular on Neural Machine Translation (NMT), to train models able to learn code change patterns and apply them to novel, unseen, source code. First, we tackle the problem of generating source code mutants for Mutation Testing. In contrast to classic approaches, which rely on handcrafted mutation operators, we propose to automatically learn how to mutate source code by observing real faults. We mine millions of bug fixing commits from GitHub, and then process and abstract this source code. This data is used to train and evaluate an NMT model to translate fixed code into buggy code (i.e., the mutated code). In the second project, we rely on the same dataset of bug-fixes to learn code transformations for the purpose of Automated Program Repair (APR). This represents one of the most challenging research problem in Software Engineering, whose goal is to automatically fix bugs without developers’ intervention. We train a model to translate buggy code into fixed code (i.e., learning patches) and, in conjunction with beam search, generate many different potential patches for a given buggy method. In our empirical investigation we found that such a model is able to fix thousands of unique buggy methods in the wild. Finally, in our third project we push our novel technique to the limits by enlarging the scope to consider not only bug-fixing activities, but any type of meaningful code changes performed by developers. We focus on accepted and merged code changes that have undergone a Pull Request (PR) process. We quantitatively and qualitatively investigate the code transformations learned by the model to build a taxonomy. The taxonomy shows that NMT can replicate a wide variety of meaningful code changes, especially refactorings and bug-fixing activities. In this dissertation we illustrate and evaluate the proposed techniques, which represent a significant departure from earlier approaches in the literature. The promising results corroborate the potential applicability of learning techniques, such as NMT, to a variety of Software Engineering tasks.
The Use of In Vitro Systems for Evaluating Haematotoxicity

ECVAM, JRC Environment Institute, 21020 Ispra (VA), Italy and Consorzio Milano Ricerche, via Ampere, 20129 Milan, Italy; Molecular and Cell Biology, Environment Institute, CIEMAT, Avenida Complutense, 28040 Madrid, Spain; Toxicology Research Laboratories, Lilly Research Laboratories, Greenfield, IN 46140, USA; Department of Hematology, Aarhus University Hospital, Tage-Hansens Gade, 8000 Aarhus, Denmark; 7BIBRA Toxicology International, Woodmansteme Road, Carshalton, Surrey SM5 4DS, UK; 8Hematology and Clinical Chemistry Section, Toxicology and Safety Assessment Department, Pharmacia, via per Pogliano, 20014 Nerviano, Italy; DABAC, University of Tuscia, via S.Camillo DeLellis, 01100 Viterbo, Italy; Center for Drug Evaluation and Research, Food and Drug Administration, 8301 Muirkirk Road, Laurel, MD 20708, USA; Ecole Superieure de Microbiolo! fie, Universite de Bretagne Occidentale, Technopole Brest-b·oise, 29280 Plouzane, France; 2Cell Culture Laboratory, Institute of Medical Microbiology, University of Milan, via Pascal, 20133 Milan, Italy; Advanced Tissue Sciences, 505 Coast Blv. South, La Jolla, CA 92037, USA; Department of Environment, VITOFlemish Institute for Technological Research, Boeretang 200, 2400 Mol, Belgium