bluuebunny/crossref_metadata_2025_split huggingface dataset:
Central European parasitic flatworms of the family Renicolidae Dollfus, 1939 (Trematoda: Plagiorchiida): molecular and comparative morphological analysis rejects the synonymization ofRenicola pinguiscomplex suggested by Odening
Authors: HENEBERG PETR , SITKO JILJÍ , BIZOS JIŘÍ , HORNE ELIZABETH C. 
Published: June 2016

SUMMARYThe Renicolidae are digenean parasites of piscivorous and molluscivorous birds. Although they exhibit few morphological autapomorphies and are highly variable, the numerous suggested re-classifications within the family have never been supported by any molecular analyses. We address the possible synonymization of species within theRenicola pinguiscomplex suggested previously by Odening. We provide and analyse sequences of two nuclear (ITS2, 28S rDNA) and two mitochondrial (CO1, ND1) DNA loci of central European species of the Renicolidae, namelyRenicola lari, Renicola pinguisandRenicola sternaesp. n., and we also provide first sequences ofRenicola sloanei. The combined molecular and comparative morphological analysis confirms the previously questioned validity of the threeRenicolaspp. of highly similar morphology, which display strict niche separation in terms of host specificity and selectivity. We identify two previously unreported clades within the genusRenicola; however, only one of them is supported by the analysis of adult worms. We also provide comparative measurements of the three examined closely related central European renicolids, and describe the newly proposed tern-specialized speciesRenicola sternaesp. n., which was previously repeatedly misidentified asRenicola paraquinta. Based on the extensive dataset collected in 1962–2015, we update the host spectrum of Renicolidae parasitizing central European birds (Renicola bretensis, R. lari, Renicola mediovitellata, R. pinguis, Renicola secundaandR. sternaesp. n.) and discuss their host-specific prevalence and intensity of infections.
Debates on Constitutionalism and the Legacies of the Cultural Revolution
Authors: Changchang Wu 
Published: June 2016

AbstractThis article focuses on the debate surrounding constitutionalism that has been driven by a constitutionalist alliance of media reporters, intellectuals and lawyers since 2010, and follows its historical trajectory. It argues that this debate forms a discourse with a structuring absence, the roots of which can be traced back to the taboos surrounding the Cultural Revolution, the 1975 Constitution, and everything associated with them. The absence manifests itself in the silence on workers' right to strike, a right which was deleted from the 1982 Constitution in an attempt to correct the ultra-leftist anarchy of the Cultural Revolution. Previous and in contrast to that, there was a Maoist constitutional movement in the Cultural Revolution, represented by the 1975 Constitution, that aimed to protect the constituent power of the workers by legalizing their right to strike. Today, we are witnessing the rise of migrant workers as they struggle for trade union reform and collective bargaining with little support from the party-state or local trade unions. In this context, a third constitutional transformation should be considered that is not a return to the 1975 Constitution but which instead adds some elements which protect labour's right to strike to the 1982 Constitution.
High and novel genetic diversity ofFrancisella tularensisin Germany and indication of environmental persistence
Authors: SCHULZE C. , HEUNER K. , MYRTENNÄS K. , KARLSSON E. , JACOB D. , KUTZER P. , GROßE K. , FORSMAN M. , GRUNOW R. 
Published: June 2016

SUMMARYIn Germany tularemia is a re-emerging zoonotic disease. Therefore, we investigated wild animals and environmental water samples for the presence and phylogenetic diversity ofFrancisella tularensisin the poorly studied Berlin/Brandenburg region. The phylogenomic analysis of three isolates from wild animals revealed three new subclades within the phylogenetic tree ofF. tularensis[B.71 from a raccoon dog (Nyctereutes procyonoides); B.74 from a red fox (Vulpes vulpes), and B.75 from a Eurasian beaver (Castor fiber albicus)]. The results from histological, PCR, and genomic investigations on the dead beaver showed that the animal suffered from a systemic infection. Indications were found that the bacteria were released from the beaver carcass into the surrounding environment. We demonstrated unexpectedly high and novel phylogenetic diversity ofF. tularensisin Germany and the fact that the bacteria persist in the environment for at least one climatic season. These findings support a broader host species diversity than previously known regarding Germany. Our data further support the assumption derived from previous serological studies of an underestimated frequency of occurrence of the pathogen in the environment and in wild animals.F. tularensiswas isolated from animal species not previously reported as natural hosts in Germany.
Twenty years of Hendra virus: laboratory submission trends and risk factors for infection in horses
Authors: SMITH C. S. , McLAUGHLIN A. , FIELD H. E. , EDSON D. , MAYER D. , OSSEDRYVER S. , BARRETT J. , WALTISBUHL D. 
Published: June 2016

SUMMARYHendra virus (HeV) was first described in 1994 in an outbreak of acute and highly lethal disease in horses and humans in Australia. Equine cases continue to be diagnosed periodically, yet the predisposing factors for infection remain unclear. We undertook an analysis of equine submissions tested for HeV by the Queensland government veterinary reference laboratory over a 20-year period to identify and investigate any patterns. We found a marked increase in testing from July 2008, primarily reflecting a broadening of the HeV clinical case definition. Peaks in submissions for testing, and visitations to the Government HeV website, were associated with reported equine incidents. Significantly differing between-year HeV detection rates in north and south Queensland suggest a fundamental difference in risk exposure between the two regions. The statistical association between HeV detection and stockhorse type may suggest that husbandry is a more important risk determinant than breedper se. The detection of HeV in horses with neither neurological nor respiratory signs poses a risk management challenge for attending veterinarians and laboratory staff, reinforcing animal health authority recommendations that appropriate risk management strategies be employed for all sick horses, and by anyone handling sick horses or associated biological samples.
Effect of Gas Pores on Mechanical Properties of High-Pressure Die-Casting AM50 Magnesium Alloy
Authors: Jiang Wei , Cao Zhanyi , Liu Liping , Jiang Bo 
Published: June 2016

AbstractHigh-pressure die-casting (HPDC) AM50 tensile specimens were used to investigate characteristics of gas pores and its effect on mechanical properties of HPDC AM50 magnesium alloy. Combining microstructure morphology gained from optical microscopy, scanning electron microscopy (SEM), and three-dimensional (3D) reconstruction with the experimental data from uniaxial tensile testing, we pursued the relationship between gas pores and the mechanical properties of HPDC AM50 Mg alloy. Results indicate that comparing with 3D reconstruction models, 2D images like optical metallography images and SEM images have one-sidedness. Furthermore, the size and maximum areal fraction of gas pores have negative effects on the mechanical properties of HPDC AM50 Mg alloy. With increase of the maximum size of gas pores in the specimen, the ultimate tensile strength (UTS) and elongation decrease. In addition, with the maximum areal fraction becoming larger, both the UTS and elongation decrease linearly.
ADJOINT FUNCTORS BETWEEN CATEGORIES OF HILBERT -MODULES
Authors: Clare Pierre , Crisp Tyrone , Higson Nigel 
Published: June 2016

Let$E$be a (right) Hilbert module over a$C^{\ast }$-algebra$A$. If$E$is equipped with a left action of a second$C^{\ast }$-algebra$B$, then tensor product with$E$gives rise to a functor from the category of Hilbert$B$-modules to the category of Hilbert$A$-modules. The purpose of this paper is to study adjunctions between functors of this sort. We shall introduce a new kind of adjunction relation, called a local adjunction, that is weaker than the standard concept from category theory. We shall give several examples, the most important of which is the functor of parabolic induction in the tempered representation theory of real reductive groups. Each local adjunction gives rise to an ordinary adjunction of functors between categories of Hilbert space representations. In this way we shall show that the parabolic induction functor has a simultaneous left and right adjoint, namely the parabolic restriction functor constructed in Clareet al.[Parabolic induction and restriction via$C^{\ast }$-algebras and Hilbert$C^{\ast }$-modules,Compos. Math.FirstView(2016), 1–33, 2].
Electoral rule choice in transitional economies
Authors: CLEMENT JESSICA 
Published: June 2016

AbstractThe Arab Spring and subsequent global unrest sparked a debate about whether a fourth wave of democracy emerged in the global political arena starting in 2010. A key issue arises from these emerging democracies, or ‘countries in transition’, about what types of government institutions will be adopted by the new democracies. The previous literature on advanced democracies shows the economic structure of a nation impacted its choice of electoral rule system. This paper looks at what determines electoral rule choice in transitional nations. Using a panel database with 65 transitional countries with data for 18 years (1995 to 2012), this paper tests the argument that more coordinated market economies (CMEs) tend to adopt more proportional representative electoral rule systems during a political transition. Findings show that countries characterized as CMEs due to widespread primary education, which supports co-specific assets, and prominent industrial sectors have more proportional electoral rule systems.
Transferrin receptor facilitates TGF-β and BMP signaling activation to control craniofacial morphogenesis
Authors: Lei R , Zhang K , Liu K , Shao X , Ding Z , Wang F , Hong Y , Zhu M , Li H , Li H 
Published: June 2016

AbstractThe Pierre Robin Sequence (PRS), consisting of cleft palate, glossoptosis and micrognathia, is a common human birth defect. However, how this abnormality occurs remains largely unknown. Here we report that neural crest cell (NCC)-specific knockout of transferrin receptor (Tfrc), a well known transferrin transporter protein, caused micrognathia, cleft palate, severe respiratory distress and inability to suckle in mice, which highly resemble human PRS. Histological and anatomical analysis revealed that the cleft palate is due to the failure of palatal shelves elevation that resulted from a retarded extension of Meckel’s cartilage. Interestingly, Tfrc deletion dramatically suppressed both transforming growth factor-β (TGF-β) and bone morphogenetic protein (BMP) signaling in cranial NCCs-derived mandibular tissues, suggesting that Tfrc may act as a facilitator of these two signaling pathways during craniofacial morphogenesis. Together, our study uncovers an unknown function of Tfrc in craniofacial development and provides novel insight into the etiology of PRS.
ZnCl2 sustains the adriamycin-induced cell death inhibited by high glucose
Authors: Garufi A , Trisciuoglio D , Cirone M , D'Orazi G 
Published: June 2016

AbstractHyperglycemia, the condition of high blood glucose, is typical of diabetes and obesity and represents a significant clinical problem. The relationship between hyperglycemia and cancer risk has been established by several studies. Moreover, hyperglycemia has been shown to reduce cancer cell response to therapies, conferring resistance to drug-induced cell death. Therefore, counteracting the negative effects of hyperglycemia may positively improve the cancer cell death induced by chemotherapies. Recent studies showed that zinc supplementation may have beneficial effects on glycemic control. Here we aimed at evaluating whether ZnCl2 could counteract the high-glucose (HG) effects and consequently restore the drug-induced cancer cell death. At the molecular level we found that the HG-induced expression of genes known to be involved in chemoresistance (such as HIF-1α, GLUT1, and HK2 glycolytic genes, as well as NF-κB activity) was reduced by ZnCl2 treatment. In agreement, the adryamicin (ADR)-induced apoptotic cancer cell death was significantly impaired by HG and efficiently re-established by ZnCl2 cotreatment. Mechanistically, the ADR-induced c-Jun N-terminal kinase/stress-activated protein kinase (JNK/SAPK) phosphorylation, inhibited by HG, was efficiently restored by ZnCl2. The JNK involvement in apoptotic cell death was assessed by the use of JNK dominant-negative expression vector that indeed impaired the ZnCl2 ability to restore drug-induced cell death in HG condition. Altogether, these findings indicate that ZnCl2 supplementation efficiently restored the drug-induced cancer cell death, inhibited by HG, by both sustaining JNK activation and counteracting the glycolytic pathway.
Tubular epithelial cells in renal clear cell carcinoma express high RIPK1/3 and show increased susceptibility to TNF receptor 1-induced necroptosis
Authors: Al-Lamki R S , Lu W , Manalo P , Wang J , Warren A Y , Tolkovsky A M , Pober J S , Bradley J R 
Published: June 2016

AbstractWe previously reported that renal clear cell carcinoma cells (RCC) express both tumor necrosis factor receptor (TNFR)-1 and -2, but that, in organ culture, a TNF mutein that only engages TNFR1, but not TNFR2, causes extensive cell death. Some RCC died by apoptosis based on detection of cleaved caspase 3 in a minority TUNEL-positive cells but the mechanism of death in the remaining cells was unexplained. Here, we underpin the mechanism of TNFR1-induced cell death in the majority of TUNEL-positive RCC cells, and show that they die by necroptosis. Malignant cells in high-grade tumors displayed threefold to four fold higher expression of both receptor-interacting protein kinase (RIPK)1 and RIPK3 compared with non-tumor kidney tubular epithelium and low-grade tumors, but expression of both enzymes was induced in lower grade tumors in organ culture in response to TNFR1 stimulation. Furthermore, TNFR1 activation induced significant MLKLSer358 and Drp1Ser616 phosphorylation, physical interactions in RCC between RIPK1-RIPK3 and RIPK3-phospho-MLKLSer358, and coincidence of phospho-MLKLser358 and phospho-Drp1Ser616 at mitochondria in TUNEL-positive RCC. A caspase inhibitor only partially reduced the extent of cell death following TNFR1 engagement in RCC cells, whereas three inhibitors, each targeting a different step in the necroptotic pathway, were much more protective. Combined inhibition of caspases and necroptosis provided additive protection, implying that different subsets of cells respond differently to TNF-α, the majority dying by necroptosis. We conclude that most high-grade RCC cells express increased amounts of RIPK1 and RIPK3 and are poised to undergo necroptosis in response to TNFR1 signaling.
Does murine spermatogenesis require WNT signalling? A lesson from Gpr177 conditional knockout mouse models
Authors: Chen Su-Ren , Tang J-X , Cheng J-M , Hao X-X , Wang Y-Q , Wang X-X , Liu Y-X 
Published: June 2016

AbstractWingless-related MMTV integration site (WNT) proteins and several other components of the WNT signalling pathway are expressed in the murine testes. However, mice mutant for WNT signalling effector β-catenin using different Cre drivers have phenotypes that are inconsistent with each other. The complexity and overlapping expression of WNT signalling cascades have prevented researchers from dissecting their function in spermatogenesis. Depletion of the Gpr177 gene (the mouse orthologue of Drosophila Wntless), which is required for the secretion of various WNTs, makes it possible to genetically dissect the overall effect of WNTs in testis development. In this study, the Gpr177 gene was conditionally depleted in germ cells (Gpr177flox/flox, Mvh-Cre; Gpr177flox/flox, Stra8-Cre) and Sertoli cells (Gpr177flox/flox, Amh-Cre). No obvious defects in fertility and spermatogenesis were observed in these three Gpr177 conditional knockout (cKO) mice at 8 weeks. However, late-onset testicular atrophy and fertility decline in two germ cell-specific Gpr177 deletion mice were noted at 8 months. In contrast, we did not observe any abnormalities of spermatogenesis and fertility, even in 8-month-old Gpr177flox/flox, Amh-Cre mice. Elevation of reactive oxygen species (ROS) was detected in Gpr177 cKO germ cells and Sertoli cells and exhibited an age-dependent manner. However, significant increase in the activity of Caspase 3 was only observed in germ cells from 8-month-old germ cell-specific Gpr177 knockout mice. In conclusion, GPR177 in Sertoli cells had no apparent influence on spermatogenesis, whereas loss of GPR177 in germ cells disrupted spermatogenesis in an age-dependent manner via elevating ROS levels and triggering germ cell apoptosis.
Acetate functions as an epigenetic metabolite to promote lipid synthesis under hypoxia
Authors: Gao Xue , Lin Shu-Hai , Ren Feng , Li Jin-Tao , Chen Jia-Jia , Yao Chuan-Bo , Yang Hong-Bin , Jiang Shu-Xia , Yan Guo-Quan , Wang Di , Wang Yi , Liu Ying , Cai Zongwei , Xu Ying-Ying , Chen Jing , Yu Wenqiang , Yang Peng-Yuan , Lei Qun-Ying 
Published: June 2016

AbstractBesides the conventional carbon sources, acetyl-CoA has recently been shown to be generated from acetate in various types of cancers, where it promotes lipid synthesis and tumour growth. The underlying mechanism, however, remains largely unknown. We find that acetate induces a hyperacetylated state of histone H3 in hypoxic cells. Acetate predominately activates lipogenic genes ACACA and FASN expression by increasing H3K9, H3K27 and H3K56 acetylation levels at their promoter regions, thus enhancing de novo lipid synthesis, which combines with its function as the metabolic precursor for fatty acid synthesis. Acetyl-CoA synthetases (ACSS1, ACSS2) are involved in this acetate-mediated epigenetic regulation. More importantly, human hepatocellular carcinoma with high ACSS1/2 expression exhibit increased histone H3 acetylation and FASN expression. Taken together, this study demonstrates that acetate, in addition to its ability to induce fatty acid synthesis as an immediate metabolic precursor, also functions as an epigenetic metabolite to promote cancer cell survival under hypoxic stress.
LATS-YAP/TAZ controls lineage specification by regulating TGFβ signaling and Hnf4α expression during liver development
Authors: Lee Da-Hye , Park Jae Oh , Kim Tae-Shin , Kim Sang-Kyum , Kim Tack-hoon , Kim Min-chul , Park Gun Soo , Kim Jeong-Hwan , Kuninaka Shinji , Olson Eric N. , Saya Hideyuki , Kim Seon-Young , Lee Ho , Lim Dae-Sik 
Published: June 2016

AbstractThe Hippo pathway regulates the self-renewal and differentiation of various adult stem cells, but its role in cell fate determination and differentiation during liver development remains unclear. Here we report that the Hippo pathway controls liver cell lineage specification and proliferation separately from Notch signalling, using mice and primary hepatoblasts with liver-specific knockout of Lats1 and Lats2 kinase, the direct upstream regulators of YAP and TAZ. During and after liver development, the activation of YAP/TAZ induced by loss of Lats1/2 forces hepatoblasts or hepatocytes to commit to the biliary epithelial cell (BEC) lineage. It increases BEC and fibroblast proliferation by up-regulating TGFβ signalling, but suppresses hepatoblast to hepatocyte differentiation by repressing Hnf4α expression. Notably, oncogenic YAP/TAZ activation in hepatocytes induces massive p53-dependent cell senescence/death. Together, our results reveal that YAP/TAZ activity levels govern liver cell differentiation and proliferation in a context-dependent manner.
Prosaposin is a regulator of progranulin levels and oligomerization
Authors: Nicholson Alexandra M. , Finch NiCole A. , Almeida Marcio , Perkerson Ralph B. , van Blitterswijk Marka , Wojtas Aleksandra , Cenik Basar , Rotondo Sergio , Inskeep Venette , Almasy Laura , Dyer Thomas , Peralta Juan , Jun Goo , Wood Andrew R. , Frayling Timothy M. , Fuchsberger Christian , Fowler Sharon , Teslovich Tanya M. , Manning Alisa K. , Kumar Satish , Curran Joanne , Lehman Donna , Abecasis Goncalo , Duggirala Ravindranath , Pottier Cyril , Zahir Haaris A. , Crook Julia E. , Karydas Anna , Mitic Laura , Sun Ying , Dickson Dennis W. , Bu Guojun , Herz Joachim , Yu Gang , Miller Bruce L. , Ferguson Shawn , Petersen Ronald C. , Graff-Radford Neill , Blangero John , Rademakers Rosa 
Published: June 2016

AbstractProgranulin (GRN) loss-of-function mutations leading to progranulin protein (PGRN) haploinsufficiency are prevalent genetic causes of frontotemporal dementia. Reports also indicated PGRN-mediated neuroprotection in models of Alzheimer’s and Parkinson’s disease; thus, increasing PGRN levels is a promising therapeutic for multiple disorders. To uncover novel PGRN regulators, we linked whole-genome sequence data from 920 individuals with plasma PGRN levels and identified the prosaposin (PSAP) locus as a new locus significantly associated with plasma PGRN levels. Here we show that both PSAP reduction and overexpression lead to significantly elevated extracellular PGRN levels. Intriguingly, PSAP knockdown increases PGRN monomers, whereas PSAP overexpression increases PGRN oligomers, partly through a protein–protein interaction. PSAP-induced changes in PGRN levels and oligomerization replicate in human-derived fibroblasts obtained from a GRN mutation carrier, further supporting PSAP as a potential PGRN-related therapeutic target. Future studies should focus on addressing the relevance and cellular mechanism by which PGRN oligomeric species provide neuroprotection.
Deficient methylation and formylation of mt-tRNAMet wobble cytosine in a patient carrying mutations in NSUN3
Authors: Van Haute Lindsey , Dietmann Sabine , Kremer Laura , Hussain Shobbir , Pearce Sarah F. , Powell Christopher A. , Rorbach Joanna , Lantaff Rebecca , Blanco Sandra , Sauer Sascha , Kotzaeridou Urania , Hoffmann Georg F. , Memari Yasin , Kolb-Kokocinski Anja , Durbin Richard , Mayr Johannes A. , Frye Michaela , Prokisch Holger , Minczuk Michal 
Published: June 2016

AbstractEpitranscriptome modifications are required for structure and function of RNA and defects in these pathways have been associated with human disease. Here we identify the RNA target for the previously uncharacterized 5-methylcytosine (m5C) methyltransferase NSun3 and link m5C RNA modifications with energy metabolism. Using whole-exome sequencing, we identified loss-of-function mutations in NSUN3 in a patient presenting with combined mitochondrial respiratory chain complex deficiency. Patient-derived fibroblasts exhibit severe defects in mitochondrial translation that can be rescued by exogenous expression of NSun3. We show that NSun3 is required for deposition of m5C at the anticodon loop in the mitochondrially encoded transfer RNA methionine (mt-tRNAMet). Further, we demonstrate that m5C deficiency in mt-tRNAMet results in the lack of 5-formylcytosine (f5C) at the same tRNA position. Our findings demonstrate that NSUN3 is necessary for efficient mitochondrial translation and reveal that f5C in human mitochondrial RNA is generated by oxidative processing of m5C.