bluuebunny/crossref_metadata_2025_split huggingface dataset:
Role of stem cells during diabetic liver injury
Authors: Wan Ying , Garner Jessica , Wu Nan , Phillip Levine , Han Yuyan , McDaniel Kelly , Annable Tami , Zhou Tianhao , Francis Heather , Glaser Shannon , Huang Qiaobing , Alpini Gianfranco , Meng Fanyin 
Published: December 2015

AbstractDiabetes mellitus is one of the most severe endocrine metabolic disorders in the world that has serious medical consequences with substantial impacts on the quality of life. Type 2 diabetes is one of the main causes of diabetic liver diseases with the most common being non‐alcoholic fatty liver disease. Several factors that may explain the mechanisms related to pathological and functional changes of diabetic liver injury include: insulin resistance, oxidative stress and endoplasmic reticulum stress. The realization that these factors are important in hepatocyte damage and lack of donor livers has led to studies concentrating on the role of stem cells (SCs) in the prevention and treatment of liver injury. Possible avenues that the application of SCs may improve liver injury include but are not limited to: the ability to differentiate into pancreatic β‐cells (insulin producing cells), the contribution for hepatocyte regeneration, regulation of lipogenesis, glucogenesis and anti‐inflammatory actions. Once further studies are performed to explore the underlying protective mechanisms of SCs and the advantages and disadvantages of its application, there will be a greater understand of the mechanism and therapeutic potential. In this review, we summarize the findings regarding the role of SCs in diabetic liver diseases.
Measurement of hematological and serum biochemical normal values of captive housed Chlorocebus aethiops sabaeus monkeys and correlation with the age
Authors: Castro Jorge , Puente Pedro , Martínez Rafael , Hernández Alexander , Martínez Leticia , Pichardo Dagmara , Aldana Lizet , Valdés Iris , Cosme Karelia 
Published: December 2015

AbstractBackgroundSome factors such as sex, age, and captivity conditions have a direct influence on the normal hematological and serum biochemical parameters of African green monkeys. On the other hand, reliability in reported values is in many cases limited by studied animal number (<200) and there is not report on the correlation of these parameters with the age in each sex animal group. Thus, this study sought determining normal hematological (11) and serum biochemical parameters (9) of 400 captive housed African green monkeys and also correlate them with the age of the animals.MethodsA total of 200 females and 200 males were grouped by the sex and age groups (1–2, 3–4, 5–6, and 7–8 years old) for measuring normal values of hematological and serum biochemical parameters and to study the correlation of these parameters with the age of the animals.ResultsAs key outcome, the main hematological and serum biochemical reference values of African green monkeys were determined. Significant differences (P < 0.05) were found among 95% of studied parameters between males and females. About 75% and 95% of the parameters were influenced by the age in the female and male groups, respectively. About 35% of hematological and serum biochemical parameters correlated positively (R2 > 0.5) with the age in the female monkeys. On the contrary in the male monkeys, only 45% of parameters correlated positively with the age (R2 > 0.5).ConclusionsThus, authors believe that results of this study are important for assisting researchers in the assessment of health status of captive housed African green monkeys for preclinical studies.
Role of d‐amino acid oxidase in the production of kynurenine pathway metabolites from d‐tryptophan in mice
Authors: Notarangelo Francesca M. , Wang Xiao‐Dan , Horning Kyle J. , Schwarcz Robert 
Published: December 2015

AbstractThe kynurenine pathway (KP), the major catabolic route of the essential amino acid l‐tryptophan (l‐TRP), contains several neuroactive compounds, including kynurenic acid, 3‐hydroxykynurenine (3‐HK), and quinolinic acid (QUIN). The role of the d‐enantiomer (d‐TRP) in KP metabolism has received little attention so far. d‐TRP can be converted to l‐TRP by d‐amino acid oxidase, and the same enzyme can produce d‐kynurenine, a known bioprecursor of KYNA. To analyze these complex metabolic events systematically in vivo, we injected mice with d‐TRP (300 mg/kg, i.p.) and examined KP metabolism in the absence or presence of the d‐amino acid oxidase inhibitor 3‐methylpyrazole‐5‐carboxylic acid (MPC; 100 mg/kg, i.p.,). After 90 min, newly formed l‐TRP was recovered in plasma, liver, forebrain, and cerebellum, and MPC prevented its neosynthesis in all tissues. In the same animals, de novo production of d‐kynurenine from d‐TRP was also observed, but was much higher in the periphery than in the brain. d‐TRP administration raised KYNA, 3‐HK, and QUIN levels in all tissues examined, and KYNA production from d‐TRP was significantly reduced after pre‐treatment with MPC. These results indicate that catabolic routes other than those classically ascribed to l‐TRP and l‐kynurenine can account for the synthesis of KYNA, 3‐HK and QUINin vivo.
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The essential amino acid l‐tryptophan is catabolized via the kynurenine pathway (KP). We explored the role of the d‐enantiomer in KP metabolism in mice in vivo. We report that d‐tryptophan is metabolized in both brain and periphery and converted to KP metabolites, including d‐kynurenine and l‐kynurenine, kynurenic acid, 3‐hydroxykynurenine, and quinolinic acid. Pharmacological experiments confirm the involvement of d‐amino acid oxidase in these processes. Our results indicate that this enzyme participates in the synthesis of KP metabolites from d‐tryptophan.
In vivo and in vitro effects of multiple sclerosis immunomodulatory therapeutics on glutamatergic excitotoxicity
Authors: Luchtman Dirk , Gollan René , Ellwardt Erik , Birkenstock Jérôme , Robohm Kerstin , Siffrin Volker , Zipp Frauke 
Published: December 2015

AbstractIn multiple sclerosis (MS), a candidate downstream mechanism for neuronal injury is glutamate (Glu)‐induced excitotoxicity, leading to toxic increases in intraneuronal Ca2+. Here, we used in vivo two‐photon imaging in the brain of TN‐XXL transgenic Ca2+ reporter mice to test whether promising oral MS therapeutics, namely fingolimod, dimethyl fumarate, and their respective metabolites fingolimod‐phosphate and monomethyl fumarate, can protect neurons against acute glutamatergic excitotoxic damage. We also assessed whether these drugs can protect against excitotoxicity in vitro using primary cortical neurons, and whether they can directly inhibit Glu release from pathogenic T‐helper 17 lymphocytes. In vivo, direct and acute (1 h) administration of 100 mM Glu to the brainstem resulted in a rapid and significant up‐regulation in neuronal Ca2+ signaling as well as morphological excitotoxic changes that were attenuated by the NMDA‐receptor antagonist MK801. Direct CNS administration of MS drugs prior to Glu significantly delayed or reduced, but did not prevent the neuronal Ca2+ increase or morphological changes. In vitro, prolonged (24 h) treatment of primary neurons with the fumarates significantly protected against neurotoxicity induced by Glu as well as NMDA, similar to MK801. Furthermore, monomethyl fumerate significantly reduced Glu release from pathogenic T‐helper 17 lymphocytes. Overall, these data suggest that MS drugs may mediate neuroprotection via excitotoxicity modulating effects.imageEvidence suggests MS pathogenesis may involve neuronal excitotoxicity, induced by local release of glutamate. However, current MS drugs, including dimethyl fumerate (DMF) and fingolimod (FTY720) are largely anti‐inflammatory and not yet fully tested for their neuroprotective potential. Here, we show that the drugs, in particular DMF metabolite monomethyl fumerate (MMF), protect neurons by excitotoxicity modulating effects. Th17, T‐helper 17.
Glyceraldehyde 3‐phosphate dehydrogenase augments the intercellular transmission and toxicity of polyglutamine aggregates in a cell model of Huntington disease
Authors: Mikhaylova Elena R. , Lazarev Vladimir F. , Nikotina Alina D. , Margulis Boris A. , Guzhova Irina V. 
Published: December 2015

AbstractThe common feature of Huntington disease is the accumulation of oligomers or aggregates of mutant huntingtin protein (mHTT), which causes the death of a subset of striatal neuronal populations. The cytotoxic species can leave neurons and migrate to other groups of cells penetrating and damaging them in a prion‐like manner. We hypothesized that the glycolytic enzyme glyceraldehyde 3‐phosphate dehydrogenase (GAPDH), previously shown to elevate the aggregation of mHTT, is associated with an increased efficiency of intercellular propagation of mHTT. GAPDH, on its own or together with polyglutamine species, was shown to be released into the extracellular milieu mainly from dying cells as assessed by a novel enzyme immunoassay, western blotting, and ultrafiltration. The conditioned medium of cells with growing GAPDH‐polyQ aggregates was toxic to naïve cells, whereas depletion of the aggregates from the medium lowered this cytotoxicity. The GAPDH component of the aggregates was found to increase their toxicity by two‐fold in comparison with polyQ alone. Furthermore, GAPDH‐polyQ complexes were shown to penetrate acceptor cells and to increase the capacity of polyQ to prionize its intracellular homolog containing a repeat of 25 glutamine residues. Finally, inhibitors of intracellular transport showed that polyQ‐GAPDH complexes, as well as GAPDH itself, penetrated cells using clathrin‐mediated endocytosis. This suggested a pivotal role of the enzyme in the intercellular transmission of Huntington disease pathogenicity. In conclusion, GAPDH occurring in complexes with polyglutamine strengthens the prion‐like activity and toxicity of the migrating aggregates.imageAggregating polygluatmine tracts were shown to release from the cells over‐expressing mutant huntingtin in a complex with glyceraldehyde 3‐phosphate dehydrogenase (GAPDH). The enzyme enhances the intracellular transport of aggregates to healthy cells, prionization of normal cellular proteins and finally cell death, thus demonstrating the pivotal role of GAPDH in the horizontal transmission of neurodegeneration.
Xerostomia Among Older Adults With Low Income: Nuisance or Warning?
Authors: Lee Young‐Shin , Kim Hee‐Gerl , Moreno Kim 
Published: December 2015

AbstractPurposeThe purpose of this study was to identify the prevalence of xerostomia and related factors among low‐income older adults in South Korea.Study DesignA cross‐sectional, population‐based study.MethodsUsing data from the Home Healthcare Service Project, a population‐based interview survey with home healthcare service, a total of 9,840 adults 65 years of age and older were assessed for the presence of xerostomia in association with aspects of health lifestyles, chronic disease, oral conditions, and oral function.ResultsOverall, 40% of participants reported experiencing xerostomia. Multivariate regression analysis indicated xerostomia was more likely to be reported by women having symptoms of gingival bleeding/pain, having difficulty swallowing liquid or chewing solid food, and having multiple chronic diseases. Interestingly, older adults who live alone and drink alcohol (two or more times per week) reported fewer problems with xerostomia.ConclusionsIncreased focus on the detrimental health consequences of xerostomia would make treatment a higher priority. Improved assessment of at‐risk populations, particularly among the elderly, could lead to earlier preventative interventions, lessening the negative impact on quality of life.Clinical RelevanceHealth professionals along with the general public need increased knowledge about the detrimental effects of xerostomia on overall health. There is a need for earlier assessment and treatment to facilitate optimal health promotion and disease prevention.
Oral Cobalamin Supplementation in Dogs with Chronic Enteropathies and Hypocobalaminemia
Authors: Toresson L. , Steiner J.M. , Suchodolski J.S. , Spillmann T. 
Published: December 2015

BackgroundCobalamin deficiency is commonly associated with chronic enteropathies (CE) in dogs and current treatment protocols recommend parenteral supplementation. In humans, several studies have reported equal efficacy of oral and parenteral cobalamin administration of cobalamin.ObjectivesTo retrospectively evaluate whether oral cobalamin supplementation can restore normocobalaminemia in dogs with CE and hypocobalaminemia.AnimalsFifty‐one client‐owned dogs with various signs of CE and hypocobalaminemia.Material and MethodsRetrospective study based on a computerized database search for dogs treated at Evidensia Specialist Animal Hospital, Helsingborg, Sweden during January 2012–March 2014. Inclusion criteria were dogs with signs of CE, an initial serum cobalamin ≤270 ng/L (reference interval: 234–811 ng/L) and oral treatment with cobalamin tablets. Serum cobalamin for follow‐up was analyzed 20–202 days after continuous oral cobalamin supplementation started.ResultsAll dogs became normocobalaminemic with oral cobalamin supplementation. The mean increase in serum cobalamin concentration after treatment was 794 ± 462 ng/L. Serum cobalamin concentrations were significantly higher after supplementation (mean 1017 ± 460 ng/L; P < .0001) than at baseline (mean 223 ± 33 ng/L).Conclusion and Clinical ImportanceOur results suggest that oral cobalamin supplementation is effective in normalizing serum cobalamin concentrations in dogs with CE. Prospective studies comparing cellular cobalamin status in dogs being treated with parenteral versus oral cobalamin supplementation are warranted before oral supplementation can be recommended for routine supplementation.
cmv1 is a gate for Cucumber mosaic virus transport from bundle sheath cells to phloem in melon
Authors: Guiu‐Aragonés Cèlia , Sánchez‐Pina María Amelia , Díaz‐Pendón Juan Antonio , Peña Eduardo J. , Heinlein Manfred , Martín‐Hernández Ana Montserrat 
Published: December 2015

SummaryCucumber mosaic virus (CMV) has the broadest host range among plant viruses, causing enormous losses in agriculture. In melon, strains of subgroup II are unable to establish a systemic infection in the near‐isogenic line SC12‐1‐99, which carries the recessive resistance gene cmv1 from the accession PI 161375, cultivar ‘Songwhan Charmi’. Strains of subgroup I overcome cmv1 resistance in a manner dependent on the movement protein. We characterized the resistance conferred by cmv1 and established that CMV‐LS (subgroup II) can move from cell to cell up to the veins in the inoculated leaf, but cannot enter the phloem. Immunogold labelling at transmission electron microscopy level showed that CMV‐LS remains restricted to the bundle sheath (BS) cells in the resistant line, and does not invade vascular parenchyma or intermediary cells, whereas, in the susceptible line ‘Piel de Sapo’ (PS), the virus invades all vein cell types. These observations indicate that the resistant allele of cmv1 restricts systemic infection in a virus strain‐ and cell type‐specific manner by acting as an important gatekeeper for virus progression from BS cells to phloem cells. Graft inoculation experiments showed that CMV‐LS cannot move from the infected PS stock into the resistant cmv1 scion, thus suggesting an additional role for cmv1 related to CMV transport within or exit from the phloem. The characterization of this new form of recessive resistance, based on a restriction of virus systemic movement, opens up the possibility to design alternative approaches for breeding strategies in melon.
Diagnosis and management of aspergillosis in the Netherlands: a national survey
Authors: Lestrade Pieter P. A. , Meis Jacques F. , Arends Jan P. , van der Beek Martha T. , de Brauwer Els , van Dijk Karin , de Greeff Sabine C. , Haas Pieter‐Jan , Hodiamont Caspar J. , Kuijper Ed J. , Leenstra Tjalling , Muller Anouk E. , Oude Lashof Astrid M. L. , Rijnders Bart J. , Roelofsen Eveline , Rozemeijer Wouter , Tersmette Mathijs , Terveer Elizabeth M. , Verduin Cees M. , Wolfhagen Maurice J. H. M. , Melchers Willem J. G. , Verweij Paul E. 
Published: December 2015

SummaryA survey of diagnosis and treatment of invasive aspergillosis was conducted in eight University Medical Centers (UMCs) and eight non‐academic teaching hospitals in the Netherlands. Against a background of emerging azole resistance in Aspergillus fumigatus routine resistance screening of clinical isolates was performed primarily in the UMCs. Azole resistance rates at the hospital level varied between 5% and 10%, although rates up to 30% were reported in high‐risk wards. Voriconazole remained first choice for invasive aspergillosis in 13 out of 16 hospitals. In documented azole resistance 14 out of 16 centres treated patients with liposomal amphotericin B.
Comparison of biotyping methods as alternative identification tools to molecular typing of pathogenic Cryptococcus species in sub‐Saharan Africa
Authors: Nyazika Tinashe K. , Robertson Valerie J. , Nherera Brenda , Mapondera Prichard T. , Meis Jacques F. , Hagen Ferry 
Published: December 2015

SummaryCryptococcal meningitis is the leading fungal infection and AIDS defining opportunistic illness in patients with late stage HIV infection, particularly in South‐East Asia and sub‐Saharan Africa. Given the high mortality, clinical differences and the extensive ecological niche of Cryptococcus neoformans and Cryptococcus gattii species complexes, there is need for laboratories in sub‐Sahara African countries to adopt new and alternative reliable diagnostic algorithms that rapidly identify and distinguish these species. We biotyped 74 and then amplified fragment length polymorphism (AFLP) genotyped 66 Cryptococcus isolates from a cohort of patients with HIV‐associated cryptococcal meningitis. C. gattii sensu lato was isolated at a prevalence of 16.7% (n = 11/66) and C. neoformans sensu stricto was responsible for 83.3% (n = 55/66) of the infections. l‐Canavanine glycine bromothymol blue, yeast‐carbon‐base‐d‐proline‐d‐tryptophan and creatinine dextrose bromothymol blue thymine were able to distinguish pathogenic C. gattii sensu lato from C. neoformans sensu stricto species when compared with AFLP genotyping. This study demonstrates high C. gattii sensu lato prevalence in Zimbabwe. In addition, biotyping methods can be used as alternative diagnostic tools to molecular typing in resource‐limited areas for differentiating pathogenic Cryptococcus species.
Introgression of antioxidant activity into cassava (Manihot esculenta C.): an effective technique for extending fresh storage roots shelf life
Authors: Nduwumuremyi Athanase , Melis Rob , Shanahan Paul , Asiimwe Theodore 
Published: December 2015

AbstractPhysiological postharvest deterioration (PPD) of cassava is the main constraint affecting its nutritional and economical values. PPD is induced by wounds when detaching storage roots from mother plant during harvesting. It is accelerated by the reactive oxygen species (ROS) such as oxygen ion (O2) and peroxide (O2)−2. The carotenoid content and its antioxidant property can help in extending shelf life of cassava storage roots. The primary mode of action of carotenoids as antioxidant is to quench singlet oxygen. Cassava breeding was reported to successfully introgress and improve carotenoid content into cassava. The two types of phytoene synthase (PSY) enzymes (PSY1 and PSY2) are key regulators of carotenoids accumulation in cassava. Carotenoids formation and accumulation in cassava storage roots are induced by a single nucleotide polymorphism in PSY2 which causes a non‐conservative amino acid exchange. This single nucleotide polymorphism in PSY gene is co‐segregated with β‐carotene in cassava storage roots, a phenomenon that could help to unravel the mechanism of introgression of carotenoids into cassava. This article investigates breeding feasibility for improving quality of cassava landraces in developing countries.
Functional characterization of the chaperon‐like protein Cdc48 in cryptogein‐induced immune response in tobacco
Authors: Rosnoblet Claire , Bègue Hervé , Blanchard Cécile , Pichereaux Carole , Besson‐Bard Angélique , Aimé Sébastien , Wendehenne David 
Published: December 2015

AbstractCdc48, a molecular chaperone conserved in different kingdoms, is a member of the AAA+ family contributing to numerous processes in mammals including proteins quality control and degradation, vesicular trafficking, autophagy and immunity. The functions of Cdc48 plant orthologues are less understood. We previously reported that Cdc48 is regulated by S‐nitrosylation in tobacco cells undergoing an immune response triggered by cryptogein, an elicitin produced by the oomycete Phytophthora cryptogea. Here, we inv estigated the function of NtCdc48 in cryptogein signalling and induced hypersensitive‐like cell death. NtCdc48 was found to accumulate in elicited cells at both the protein and transcript levels. Interestingly, only a small proportion of the overall NtCdc48 population appeared to be S‐nitrosylated. Using gel filtration in native conditions, we confirmed that NtCdc48 was present in its hexameric active form. An immunoprecipitation‐based strategy following my mass spectrometry analysis led to the identification of about a hundred NtCdc48 partners and underlined its contribution in cellular processes including targeting of ubiquitylated proteins for proteasome‐dependent degradation, subcellular trafficking and redox regulation. Finally, the analysis of cryptogein‐induced events in NtCdc48‐overexpressing cells highlighted a correlation between NtCdc48 expression and hypersensitive cell death. Altogether, this study identified NtCdc48 as a component of cryptogein signalling and plant immunity.
Compensatory mechanisms mitigate the effect of warming and drought on wood formation
Authors: Balducci Lorena , Cuny Henri E. , Rathgeber Cyrille B. K. , Deslauriers Annie , Giovannelli Alessio , Rossi Sergio 
Published: December 2015

AbstractBecause of global warming, high‐latitude ecosystems are expected to experience increases in temperature and drought events. Wood formation will have to adjust to these new climatic constraints to maintain tree mechanical stability and long‐distance water transport. The aim of this study is to understand the dynamic processes involved in wood formation under warming and drought. Xylogenesis, gas exchange, water relations and wood anatomy of black spruce [Picea mariana (Mill.) B.S.P.] saplings were monitored during a greenhouse experiment where temperature was increased during daytime or night‐time (+6 °C) combined with a drought period. The kinetics of tracheid development expressed as rate and duration of the xylogenesis sub‐processes were quantified using generalized additive models. Drought and warming had a strong influence on cell production, but little effect on wood anatomy. The increase in cell production rate under warmer temperatures, and especially during the night‐time warming at the end of the growing season, resulted in wider tree‐rings. However, the strong compensation between rates and durations of cell differentiation processes mitigates warming and drought effects on tree‐ring structure. Our results allowed quantification of how wood formation kinetics is regulated when water and heat stress increase, allowing trees to adapt to future environmental conditions.