Miracle-dz/UniFAR-FTUs huggingface dataset:
A new parrot taxon from the Yucatán Peninsula , Mexico-its position within Amazona genus based on morphology and molecular phylogeny ( # 14707 ) 1

Parrots (Psittaciformes) are a diverse group of birds, which need urgent protection. However, many taxa from this order have an unresolved status, which makes their conservation difficult. One of species-rich parrot genus is Amazona, which is widely distributed in the New World. Here we describe a new Amazona form, which is endemic to the Yucatán Peninsula. This parrot is clearly separable from other Amazona species in eleven morphometric characters as well as call and behavior. The clear differences in these features imply that the parrot could represent a new species. However, phylogenetic analyses based on mitochondrial markers show that this parrot groups with strong support within A. albifrons from Central America, which would suggest that it is a subspecies of A. albifrons. Taken together phylogenetic and morphometric analyses, we can conclude that the new parrot represents a recently evolving lineage, whose taxonomic status should be further verified. This lineage diverged from its closest relative about 120,000 years ago and was subjected to accelerated morphological and behavioral changes like some other representatives of the genus Amazona, which makes difficult to establish its taxonomic status and need further studies. Our phylogenies, which are so far the most comprehensive for Amazona taxa enabled us to consider the most feasible scenarios about parrot colonization of the Greater and Lesser Antilles and Central America from South America mainland. The molecular dating of these migrations and diversification rate were correlated with climatic and geological events in the last 5 million years giving an interesting insight into Amazon parrot phylogeography and evolution in general. 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 PeerJ reviewing PDF | (2016:11:14707:1:1:REVIEW 20 Feb 2017) Manuscript to be reviewed
Activation of liver X receptors inhibits experimental fibrosis by interfering with interleukin-6 release from macrophages

Objectives To investigate the role of liver X receptors (LXRs) in experimental skin fibrosis and evaluate their potential as novel antifibrotic targets. Methods We studied the role of LXRs in bleomycin-induced skin fibrosis, in the model of sclerodermatous graft-versus-host disease (sclGvHD) and in tight skin-1 (Tsk-1) mice, reflecting different subtypes of fibrotic disease. We examined both LXR isoforms using LXRα-, LXRβ- and LXR-α/β-double-knockout mice. Finally, we investigated the effects of LXRs on fibroblasts and macrophages to establish the antifibrotic mode of action of LXRs. Results LXR activation by the agonist T0901317 had antifibrotic effects in bleomycin-induced skin fibrosis, in the sclGvHD model and in Tsk-1 mice. The antifibrotic activity of LXRs was particularly prominent in the inflammation-driven bleomycin and sclGvHD models. LXRα-, LXRβ- and LXRα/β-double-knockout mice showed a similar response to bleomycin as wildtype animals. Low levels of the LXR target gene ABCA-1 in the skin of bleomycin-challenged and control mice suggested a low baseline activation of the antifibrotic LXR signalling, which, however, could be specifically activated by T0901317. Fibroblasts were not the direct target cells of LXRs agonists, but LXR activation inhibited fibrosis by interfering with infiltration of macrophages and their release of the pro-fibrotic interleukin-6. Conclusions We identified LXRs as novel targets for antifibrotic therapies, a yet unknown aspect of these nuclear receptors. Our data suggest that LXR activation might be particularly effective in patients with inflammatory disease subtypes. Activation of LXRs interfered with the release of interleukin-6 from macrophages and, thus, inhibited fibroblast activation and collagen release.
The effects of dietary protein restriction and blood-pressure control on the progression of chronic renal disease. Modification of Diet in Renal Disease Study Group.

BACKGROUND Restricting protein intake and controlling hypertension delay the progression of renal disease in animals. We tested these interventions in 840 patients with various chronic renal diseases. METHODS In study 1, 585 patients with glomerular filtration rates of 25 to 55 ml per minute per 1.73 m2 of body-surface area were randomly assigned to a usual-protein diet or a low-protein diet (1.3 or 0.58 g of protein per kilogram of body weight per day) and to a usual- or a low-blood-pressure group (mean arterial pressure, 107 or 92 mm Hg). In study 2, 255 patients with glomerular filtration rates of 13 to 24 ml per minute per 1.73 m2 were randomly assigned to the low-protein diet (0.58 g per kilogram per day) or a very-low-protein diet (0.28 g per kilogram per day) with a keto acid-amino acid supplement, and a usual- or a low-blood-pressure group (same values as those in study 1). An 18-to-45-month follow-up was planned, with monthly evaluations of the patients. RESULTS The mean follow-up was 2.2 years. In study 1, the projected mean decline in the glomerular filtration rate at three years did not differ significantly between the diet groups or between the blood-pressure groups. As compared with the usual-protein group and the usual-blood-pressure group, the low-protein group and the low-blood-pressure group had a more rapid decline in the glomerular filtration rate during the first four months after randomization and a slower decline thereafter. In study 2, the very-low-protein group had a marginally slower decline in the glomerular filtration rate than did the low-protein group (P = 0.07). There was no delay in the time to the occurrence of end-stage renal disease or death. In both studies, patients in the low-blood-pressure group who had more pronounced proteinuria at base line had a significantly slower rate of decline in the glomerular filtration rate. CONCLUSIONS Among patients with moderate renal insufficiency, the slower decline in renal function that started four months after the introduction of a low-protein diet suggests a small benefit of this dietary intervention. Among patients with more severe renal insufficiency, a very-low-protein diet, as compared with a low-protein diet, did not significantly slow the progression of renal disease.
A Study of the Relationship Between Pharmacologic Preconditioning and Adenosine Triphosphate-Sensitive Potassium (KATP) Channels on Cultured Cardiomyocytes Using the Microelectrode Array

The microelectrode array was used to study the pharmacologic preconditioning effect of adenosine triphosphate-sensitive channel activation using potassium channel openers (KCOs) on rat cardiomyocytes over 90 minutes of ischemia. Cell viability and electrophysiological changes between KCOs pretreated and untreated cardiomyocytes were compared. Ischemia caused significant increases in beat frequency, extracellular field potential amplitude, and propagation velocity of spontaneously beating untreated cardiomyocytes. However, these electrophysiological parameters reduced as the duration of ischemia increased. The electrophysiological changes on ischemic cardiomyocytes were abolished by pretreating the cells with KCOs. Pinacidil pretreated cardiomyocytes retained a significantly higher viability than the untreated cardiomyocytes after 90 minutes of ischemia. Because Connexin 43 has a direct correlation with the propagation velocity, the Connexin 43 protein expression was also investigated. Connexin 43 expression levels were lower in KCOs pretreated cardiomyocytes than that of the untreated controls, and this correlated with the propagation velocity results obtained from the microelectrode array. The effect of pinacidil (sarcolemmal adenosine triphosphate-sensitive channel opener) was more prominent than that of diazoxide (mitochondrial K adenosine triphosphate-sensitive channel opener) on ischemic cardiomyocytes as indicated in the present acute ischemia study.
Subjective age estimation using speech sounds: Comparison with facial images

We have defined the perception of one's own age as ldquosubjective agerdquo, and have so far approached using other people's facial images. In this paper, we propose a relative estimation method for subjective age by using people's speech sounds and their chronological age. A relative estimation task is performed, wherein an estimator gives rating values to other people about whether they are older or younger than the estimator. In this task, the difference in the actual age between the estimator and the rating value of the person are measured. We plot the results on a two-dimensional plane with the x-axis as the relative age and the y-axis is the estimation result. Thus, the distribution with the plotted points of upper-right direction is obtained, which is approximated by a logistic function. The zero crossing point in the approximation curve with the x-axis is defined as the shift value in the subjective age. 57 total estimators, including 28 males and 29 females from 25 to 44 years old participated in this experiment. As a result, the subjective age using speech sounds tended to be older than using facial images. The tendency was also more remarkably visible in the male groups than in the female group. However, variance was relatively higher in the male young-middle (35-44) and the female young (25-34) groups than using facial images, which indicated that the subjective age varies according to the profile of estimators, such as age and gender.
Molecular epidemiology of Theileria parva in the field

Summary Molecular tools based on seminested RFLP‐PCR techniques to characterize field parasites in bloodspots dried on filter paper permitted investigation of the extent and the dynamics of diversity of Theileria parva populations in the field. Parallel molecular studies explored the long‐term genome stability of various isolates by probing Southern blots of EcoRI digested total genomic DNA with four different reference nucleic acid probes. Three polymorphic single copy loci encoding for antigen genes were developed for seminested PCR detection in order to apply them for a multilocus approach in population genetic studies. Seven alleles were identified for the polymorphic immunodominant molecule (PIM) locus by using restriction enzymes, and 4 alleles each for the p150 and p104 loci. A simple DNA extraction method gave good results in amplifying these loci from carrier animals using samples of blood dried on filter papers. Results from probing Southern blots of cultures taken at sequential timepoints indicate relative genome stability in T. parva in comparison to other parasitic protozoa such as Plasmodium. Comparatively homogeneous profiles in sympatric isolates from Zambia were identified using all four probes and PCR amplified products which contrasted with the variety found amongst Kenyan stocks. Preliminary characterization of T. parva field samples from the Southern Province of Zambia strongly suggest clonal expansion of one of the components of a non‐Zambian trivalent vaccine used on a limited scale in the Province from 1985 until 1992.
Mislocalization of Fukutin Protein by Disease-causing Missense Mutations Can Be Rescued with Treatments Directed at Folding Amelioration*

Background: The molecular pathogenesis of fukutin-deficient dystroglycanopathy remains unclear, and no effective treatment is available. Results: Some disease-causing missense fukutin mutants showed mislocalization in cultured cells, which can be corrected by treatments directed at folding amelioration. Conclusion: Correction of cellular localization of disease-causing mutants may have a therapeutic benefit. Significance: A possible therapeutic strategy for fukutin-deficient dystroglycanopathy is proposed based on its molecular pathogenesis. Fukuyama-type congenital muscular dystrophy (FCMD), the second most common childhood muscular dystrophy in Japan, is caused by alterations in the fukutin gene. Mutations in fukutin cause abnormal glycosylation of α-dystroglycan, a cell surface laminin receptor; however, the exact function and pathophysiological role of fukutin are unclear. Although the most prevalent mutation in Japan is a founder retrotransposal insertion, point mutations leading to abnormal glycosylation of α-dystroglycan have been reported, both in Japan and elsewhere. To understand better the molecular pathogenesis of fukutin-deficient muscular dystrophies, we constructed 13 disease-causing missense fukutin mutations and examined their pathological impact on cellular localization and α-dystroglycan glycosylation. When expressed in C2C12 myoblast cells, wild-type fukutin localizes to the Golgi apparatus, whereas the missense mutants A170E, H172R, H186R, and Y371C instead accumulated in the endoplasmic reticulum. Protein O-mannose β1,2-N-acetylglucosaminyltransferase 1 (POMGnT1) also mislocalizes when co-expressed with these missense mutants. The results of nocodazole and brefeldin A experiments suggested that these mutant proteins were not transported to the Golgi via the anterograde pathway. Furthermore, we found that low temperature culture or curcumin treatment corrected the subcellular location of these missense mutants. Expression studies using fukutin-null mouse embryonic stem cells showed that the activity responsible for generating the laminin-binding glycan of α-dystroglycan was retained in these mutants. Together, our results suggest that some disease-causing missense mutations cause abnormal folding and localization of fukutin protein, and therefore we propose that folding amelioration directed at correcting the cellular localization may provide a therapeutic benefit to glycosylation-deficient muscular dystrophies.
Dendritic spine actin dynamics in neuronal maturation and synaptic plasticity

The majority of the postsynaptic terminals of excitatory synapses in the central nervous system exist on small bulbous structures on dendrites known as dendritic spines. The actin cytoskeleton is a structural element underlying the proper development and morphology of dendritic spines. Synaptic activity patterns rapidly change actin dynamics, leading to morphological changes in dendritic spines. In this mini‐review, we will discuss recent findings on neuronal maturation and synaptic plasticity‐induced changes in the dendritic spine actin cytoskeleton. We propose that actin dynamics in dendritic spines decrease through actin filament crosslinking during neuronal maturation. In long‐term potentiation, we evaluate the model of fast breakdown of actin filaments through severing and rebuilding through polymerization and later stabilization through crosslinking. We will discuss the role of Ca2+ in long‐term depression, and suggest that actin filaments are dissolved through actin filament severing. © 2016 Wiley Periodicals, Inc.
Analysis of Clostridium difficile infections in patients hospitalized at the nephrological ward in Poland.

BACKGROUND Few studies have evaluated the incidence and risk factors of Clostridium difficile infection (CDI) in the adult Polish population, in particular in solid organ recipients hospitalized at the nephrological ward. AIM The aim of this study was to analyze Clostridium difficile infections (CDI) among patients hospitalized in the Department of Nephrology, Transplantation and Internal Medicine, Medical University of Silesia in Katowice. MATERIAL/METHODS Thirty-seven patients with Clostridium difficile infection diagnosed between October 2011 and November 2013 (26 months), identified among a total of 3728 patients hospitalized in this department during this period, were included in this retrospective, single-center study. The CDI definition was based on the current recommendations of the European Society of Clinical Microbiology and Infectious Diseases. RESULTS The observation period was divided into two 13-month intervals. Increased incidence (of borderline significance) of CDI in the second period compared to the first period was observed (1.33% vs 0.65% respectively; p=0.057). Patients after kidney (n=11), kidney and pancreas (n=2) and liver (n=5) transplantation represented 48% of the analyzed CDI patients, and in half of these patients (50%) CDI symptoms occurred within the first 3 months after transplantation. Clostridium difficile infection leads to irreversible deterioration of graft function in 38% of kidney recipients. Most incidents of CDI (70%) were identified as nosocomial infection. CONCLUSIONS 1. Clostridium difficile infection is particularly common among patients in the early period after solid organ transplantation. 2. Clostridium difficile infection may lead to irreversible deterioration of transplanted kidney function.
Analysis of mRNA expression for steroidogenic enzymes in the remaining adrenal cortices attached to adrenocortical adenomas.

DESIGN AND METHODS We have recently demonstrated that the adrenal cortices attached to aldosterone-producing adenoma (APA) contained microscopic subcapsular micronodules suggestive of active aldosterone production. In this study, we used in situ hybridization to investigate the mRNA expression of steroidogenic enzymes in the adrenal cortices attached to cortisol-producing adenoma (CPA) and clinically silent adenoma (non-functioning adenoma; NFA), in addition to APA. RESULTS Microscopic subcapsular micronodules, which were several hundreds of micrometers in size and spheroid in shape, were observed in the cortices attached to CPA and NFA, as well as APA, at high frequency. Most of the cortical nodules in zona fasciculata to zona reticularis showed a suppressed steroidogenesis in the cortices attached to adenoma, but some expressed intensely all necessary steroidogenic enzyme mRNAs for cortisol synthesis. CONCLUSIONS It is thus necessary to keep in mind, on the occasion of subtotal adrenalectomy, that lesions with the potential to later develop into functional adrenocortical nodules may be present in other parts of the ipsilateral or contralateral adrenal cortices.
Phylogenetic analysis of parthenogenesis‐inducing Wolbachia in the genus Aphytis (Hymenoptera: Aphelinidae)

Parthenogenesis‐inducing intracellular bacteria of the genus Wolbachia are found in a variety of parasitoid wasp genera. The presence of Wolbachia in the uniparental Aphytis species A. fingnanensis Compere, A. diaspidis (Howard), A. chilensis Howard, and A. chrysomphali (Mercet) was tested using primers specific for the ftsZ gene. The symbiont was detected in all of these species. Wolbachia ftsZ genes that were sequenced from the four hosts show a high degree of similarity. Both the PCR with specific primers for group ‘A’ and phylogenetic analysis place these Wolbachia in group ‘A’. The fact that the tested Aphytis species belong to different phylogenetic groups and harbour what seem to be almost identical Wolbachia, lends credence to the horizontal transmission hypothesis.
Invasion of minor veins of tobacco leaves inoculated with tobacco mosaic virus mutants defective in phloem-dependent movement.

To fully understand vascular transport of plant viruses, the viral and host proteins, their structures and functions, and the specific vascular cells in which these factors function must be determined. We report here on the ability of various cDNA-derived coat protein (CP) mutants of tobacco mosaic virus (TMV) to invade vascular cells in minor veins of Nicotiana tabacum L. cv. Xanthi nn. The mutant viruses we studied, TMV CP-O, U1mCP15-17, and SNC015, respectively, encode a CP from a different tobamovirus (i.e., from odontoglossum ringspot virus) resulting in the formation of non-native capsids, a mutant CP that accumulates in aggregates but does not encapsidate the viral RNA, or no CP. TMV CP-O is impaired in phloem-dependent movement, whereas U1mCP15-17 and SNC015 do not accumulate by phloem-dependent movement. In developmentally-defined studies using immunocytochemical analyses we determined that all of these mutants invaded vascular parenchyma cells within minor veins in inoculated leaves. In addition, we determined that the CPs of TMV CP-O and U1mCP15-17 were present in companion (C) cells of minor veins in inoculated leaves, although more rarely than CP of wild-type virus. These results indicate that the movement of TMV into minor veins does not require the CP, and an encapsidation-competent CP is not required for, but may increase the efficiency of, movement into the conducting complex of the phloem (i.e., the C cell/sieve element complex). Also, a host factor(s) functions at or beyond the C cell/sieve element interface with other cells to allow efficient phloem-dependent accumulation of TMV CP-O.
Low‐intensity oral anticoagulation in sickle‐cell disease reverses the prethrombotic state: promises for treatment?

Summary. Increased plasma levels of prothrombin fragment 1 + 2 (Fl + 2) found in patients with sickle‐cell disease reflect enhanced endogenous thrombin generation. We postulate that hypercoagulability contributes to vaso‐ occlusion. The intensity of acenocoumarol treatment required to reduce the Fl + 2 level to 50% of pretreatment level was investigated in seven patients with symptomatic sickle‐cell anaemia during steady‐state disease for a period of 2 months. All patients had increased levels of Fl + 2 compared with an age‐matched control group. Normalization of the Fl + 2 was achieved at a median INR of 1.64 (range 1.18‐2.2). It is concluded that low‐intensity oral anticoagulation normalizes the hypercoagulability in sickle‐cell disease.
Estimating danofloxacin withdrawal time in broiler chickens based on physiologically based pharmacokinetics modeling.

In this study, a physiologically based pharmacokinetics (PBPK) model was firstly developed for danofloxacin in healthy broiler chickens after a single oral administration at 5 mg/kg bw. Then, the model extrapolation from healthy chickens to those infected with Pasteurella multocidaones was performed. The healthy model was validated through a comparison of predicted and previously published concentrations, which indicated that the healthy PBPK model had good predictive ability in plasma, lung, muscle, liver, and kidney, especially at the later sampling time points. Multiple dosing of administration was incorporated into the healthy and infected models. In addition, a Monte Carlo simulation (MCS) included 1000 iterations was further incorporated into both models to predict the withdrawal times of danofloxacin in healthy and infected chickens, which were estimated to be 3 and 2 days, respectively.
Genome-wide association study implicates PARD3B-based AIDS restriction.

BACKGROUND Host genetic variation influences human immunodeficiency virus (HIV) infection and progression to AIDS. Here we used clinically well-characterized subjects from 5 pretreatment HIV/AIDS cohorts for a genome-wide association study to identify gene associations with rate of AIDS progression. METHODS European American HIV seroconverters (n = 755) were interrogated for single-nucleotide polymorphisms (SNPs) (n = 700,022) associated with progression to AIDS 1987 (Cox proportional hazards regression analysis, co-dominant model). RESULTS Association with slower progression was observed for SNPs in the gene PARD3B. One of these, rs11884476, reached genome-wide significance (relative hazard = 0.3; P =3. 370 × 10(-9)) after statistical correction for 700,022 SNPs and contributes 4.52% of the overall variance in AIDS progression in this study. Nine of the top-ranked SNPs define a PARD3B haplotype that also displays significant association with progression to AIDS (hazard ratio, 0.3; P = 3.220 × 10(-8)). One of these SNPs, rs10185378, is a predicted exonic splicing enhancer; significant alteration in the expression profile of PARD3B splicing transcripts was observed in B cell lines with alternate rs10185378 genotypes. This SNP was typed in European cohorts of rapid progressors and was found to be protective for AIDS 1993 definition (odds ratio, 0.43, P = .025). CONCLUSIONS These observations suggest a potential unsuspected pathway of host genetic influence on the dynamics of AIDS progression.