bluuebunny/crossref_metadata_2025_split huggingface dataset:
Expression of TaCYP78A3, a gene encoding cytochrome P450 CYP78A3 protein in wheat (Triticum aestivum L.), affects seed size
Authors: Ma Meng , Wang Qian , Li Zhanjie , Cheng Huihui , Li Zhaojie , Liu Xiangli , Song Weining , Appels Rudi , Zhao Huixian 
Published: June 2015

SummarySeveral studies have described quantitative trait loci (QTL) for seed size in wheat, but the relevant genes and molecular mechanisms remain largely unknown. Here we report the functional characterization of the wheat TaCYP78A3 gene and its effect on seed size. TaCYP78A3 encoded wheat cytochrome P450 CYP78A3, and was specifically expressed in wheat reproductive organs. TaCYP78A3 activity was positively correlated with the final seed size. Its silencing caused a reduction of cell number in the seed coat, resulting in an 11% decrease in wheat seed size, whereas TaCYP78A3 over‐expression induced production of more cells in the seed coat, leading to an 11–48% increase in Arabidopsis seed size. In addition, the cell number in the final seed coat was determined by the TaCYP78A3 expression level, which affected the extent of integument cell proliferation in the developing ovule and seed. Unfortunately, TaCYP78A3 over‐expression in Arabidopsis caused a reduced seed set due to an ovule developmental defect. Moreover, TaCYP78A3 over‐expression affected embryo development by promoting embryo integument cell proliferation during seed development, which also ultimately affected the final seed size in Arabidopsis. In summary, our results indicated that TaCYP78A3 plays critical roles in influencing seed size by affecting the extent of integument cell proliferation. The present study provides direct evidence that TaCYP78A3 affects seed size in wheat, and contributes to an understanding of the cellular basis of the gene influencing seed development.
An unusual xylan in Arabidopsis primary cell walls is synthesised by GUX3, IRX9L, IRX10L and IRX14
Authors: Mortimer Jenny C. , Faria‐Blanc Nuno , Yu Xiaolan , Tryfona Theodora , Sorieul Mathias , Ng Yao Z. , Zhang Zhinong , Stott Katherine , Anders Nadine , Dupree Paul 
Published: June 2015

SummaryXylan is a crucial component of many plant primary and secondary cell walls. However, the structure and function of xylan in the dicotyledon primary cell wall is not well understood. Here, we characterized a xylan that is specific to tissues enriched in Arabidopsis primary cell walls. Unlike previously described xylans, this xylan carries a pentose linked 1–2 to the α‐1,2‐d‐glucuronic acid (GlcA) side chains on the β‐1,4‐Xyl backbone. The frequent and precisely regular spacing of GlcA substitutions every six xylosyl residues along the backbone is also unlike that previously observed in secondary cell wall xylan. Molecular genetics, in vitro assays, and expression data suggest that IRX9L, IRX10L and IRX14 are required for xylan backbone synthesis in primary cell wall synthesising tissues. IRX9 and IRX10 are not involved in the primary cell wall xylan synthesis but are functionally exchangeable with IRX9L and IRX10L. GUX3 is the only glucuronyltransferase required for the addition of the GlcA decorations on the xylan. The differences in xylan structure in primary versus secondary cell walls might reflect the different roles in cross‐linking and interaction with other cell wall components.
Interaction of MYC2 and GBF1 results in functional antagonism in blue light‐mediated Arabidopsis seedling development
Authors: Maurya Jay P. , Sethi Vishmita , Gangappa Sreeramaiah N. , Gupta Nisha , Chattopadhyay Sudip 
Published: June 2015

SummaryRegulations of Arabidopsis seedling growth by two proteins, which belong to different classes of transcription factors, are poorly understood. MYC2 and GBF1 belong to bHLH and bZIP classes of transcription factors, respectively, and function in cryptochrome‐mediated blue light signaling. Here, we have investigated the molecular and functional interrelation of MYC2 and GBF1 in blue light‐mediated photomorphogenesis. Our study reveals that MYC2 and GBF1 colocalize and physically interact in the nucleus. This interaction requires the N‐terminal domain of each protein. The atmyc2 gbf1 double mutant analyses and transgenic studies have revealed that MYC2 and GBF1 act antagonistically and inhibit the activity of each other to regulate hypocotyl growth and several other biological processes. This study further reveals that MYC2 and GBF1 bind to HYH promoter and inhibit each other through non‐DNA binding bHLH–bZIP heterodimers. These results, taken together, provide insights into the mechanistic view on the concerted regulatory role of MYC2 and GBF1 in Arabidopsis seedling development.
Secondary siRNAs from Medicago NB‐LRRs modulated via miRNA–target interactions and their abundances
Authors: Fei Qili , Li Pingchuan , Teng Chong , Meyers Blake C. 
Published: June 2015

SummarySmall RNAs are a class of non‐coding RNAs that are of great importance in gene expression regulatory networks. Different families of small RNAs are generated via distinct biogenesis pathways. One such family specific to plants is that of phased, secondary siRNAs (phasiRNAs); these require RDR6, DCL4, and (typically) a microRNA (miRNA) trigger for their biogenesis. Protein‐encoding genes are an important source of phasi‐RNAs. The model legume Medicago truncatula generates phasiRNAs from many PHAS loci, and we aimed to investigate their biogenesis and mechanism by which miRNAs trigger these molecules. We modulated miRNA abundances in transgenic tissues showing that the abundance of phasiRNAs correlates with the levels of both miRNA triggers and the target, precursor transcripts. We identified sets of phasiRNAs or PHAS loci that predominantly and substantially increase in response to miRNA overexpression. In the process of validating targets from miRNA overexpression tissues, we found that in the miRNA‐mRNA target pairing, the 3′ terminal nucleotide (the 22nd position), but not the 10th position, is important for phasiRNA production. Mutating the single 3′ terminal nucleotide dramatically diminishes phasiRNA production. Ectopic expression of Medicago NB‐LRR‐targeting miRNAs in Arabidopsis showed that only a few NB‐LRRs are capable of phasiRNA production; our data indicate that this might be due to target inaccessibility determined by sequences flanking target sites. Our results suggest that target accessibility is an important component in miRNA–target interactions that could be utilized in target prediction, and the evolution of mRNA sequences flanking miRNA–target sites may be impacted.
Cryopreservation alters the membrane and cytoskeletal protein profile of platelet microparticles
Authors: Raynel Sarah , Padula Matthew P. , Marks Denese C. , Johnson Lacey 
Published: June 2015

BACKGROUNDCryopreservation of platelets (PLTs) in dimethyl sulfoxide (DMSO) and storage at −80°C extends the PLT shelf life to at least 2 years, allowing greater accessibility in military and rural environments. While cryopreserved PLTs have been extensively characterized, the microparticles formed as a result of cryopreservation are yet to be fully described.STUDY DESIGN AND METHODSApheresis PLTs were cryopreserved at −80°C with 5% DMSO and sampled before freezing and after thawing. Microparticle number, size, surface receptor phenotype, and function were assessed by microscopy, flow cytometry, dynamic light scattering, and thrombin‐generating capacity. Proteomic changes were examined using two‐dimensional gel electrophoresis and Western blotting.RESULTSPLT cryopreservation resulted in a 15‐fold increase in the number of microparticles compared to fresh PLTs. The surface receptor phenotype of these microparticles differed to microparticles from fresh PLTs, with more microparticles expressing glycoprotein (GP)IV, GPIIb, and the GPIb‐V‐IX complex. Cryopreservation drastically altered the abundance of many cytoskeletal proteins in the PLT microparticles, including actin, filamin, gelsolin, and tropomyosin. Despite these changes, PLT microparticles were functional and contributed to phosphatidylserine‐ and tissue factor– induced thrombin generation.CONCLUSIONThis study demonstrates that PLT microparticles formed by cryopreservation are phenotypically distinct from those present before freezing. These differences may be associated with the procoagulant properties of cryopreserved PLTs.
Bilateral removal of the mandibular and medial retropharyngeal lymph nodes through a single ventral midline incision for staging of head and neck cancers in dogs: a description of surgical technique
Authors: Green K. , Boston S. E. 
Published: June 2015

AbstractCurrently, there is no standard protocol for removal of regional lymph nodes for the staging of head and neck cancers in dogs. Palpation and fine needle aspiration of mandibular lymph nodes are most commonly performed for staging of head and neck cancers. Although cytology is commonly performed for staging of head and neck, cancers histopathology is required for definitive lymph node staging. When regional lymph node biopsy is performed, mandibular lymph nodes are most commonly sampled due to their accessibility. The medial retropharyngeal lymph nodes may be the most relevant draining lymph node of the head and neck, but they are not routinely sampled due to their anatomic location medial to the salivary glands. The technique described here will allow for a standardized surgical approach for the efficient removal of both mandibular and medial retropharyngeal lymph nodes for staging of head and neck tumours via a single ventral midline approach.
The activity and inhibition of poly(ADP‐ribose) polymerase‐1 in equine peripheral blood mononuclear cells in vitro
Authors: Douglas Hope F. , Southwood Louise L. , Meyer‐Ficca Mirella L. , Hart Samantha K. , Meyer Ralph G. 
Published: June 2015

AbstractObjectivesTo evaluate the poly (ADP‐ribose) polymerase‐1 (PARP1) enzyme and its inhibition in horses and explore its potential as a novel therapeutic target for equine intestinal ischemia‐reperfusion injury by (1) identifying poly (ADP‐ribose) (PAR) as an indication of PARP1 activation in equine cells using available immunoblot analytical techniques, (2) inducing PARP1 activation in an in vitro oxidative DNA damage model, (3) and demonstrating the inhibition of PARP1 in equine cells using commercially available PARP1 inhibitors.DesignExperimental study.AnimalsBlood samples were collected from systemically healthy ponies (n= 3) and horses (n= 3).Interventions(1) Equine peripheral blood mononuclear cells were exposed to 3 different concentrations of hydrogen peroxide (H2O2) and were lysed at specific time points. PARP1 activity was then assessed by using immunoblot analyses to determine PAR levels. (2) Equine peripheral blood mononuclear cells were preincubated with defined concentrations of PARP1 inhibitors prior to H2O2‐mediated PARP1 stimulation. PAR levels reflecting PARP1 activity were determined using immunoblot analyses.Measurements and Main ResultsCommercially available anti‐PAR antibodies were used successfully to identify equine PAR. There was a significant increase in PAR accumulation following treatment with H2O2. All of the tested PARP inhibitors significantly reduced PAR accumulation to or below basal levels following treatment with H2O2.ConclusionsThis proof of principle study demonstrated that PAR, an indicator of PARP1 activity, can be identified in the equine species using immunoblot techniques, that equine PARP1 can be activated by H2O2‐induced DNA damage, and that this activation can be inhibited by PARP1 enzyme inhibitors. The data suggest that the PARP1 pathway plays a role in the equine cellular response to oxidative DNA damage and supports its potential as a novel therapeutic target. Further research documenting an increase in PAR levels in vivo and the efficacy of PARP1 inhibitors in an equine intestinal ischemia‐reperfusion model is needed.
Protozoal infections of the cornea and conjunctiva in dogs associated with chronic ocular surface disease and topical immunosuppression
Authors: Beckwith‐Cohen Billie , Gasper David J. , Bentley Ellison , Gittelman Howard , Ellis Angela E. , Snowden Karen F. , Shock Barbara C. , Yabsley Michael J. , Dubielzig Richard R. 
Published: June 2015

AbstractObjectiveTo describe five cases of protozoal keratitis or conjunctivitis in dogs with chronic preexisting ocular surface disease treated with long‐term immunosuppression.Animals studiedFive dogs that developed corneal or conjunctival mass lesions.ProceduresThe database of the Comparative Ocular Pathology Laboratory of Wisconsin was searched for canine cases diagnosed with corneal or conjunctival protozoal infection. Five cases were identified, and tissues were examined using routine and special histochemical stains: immunohistochemical labels forNeospora caninum,Toxoplasma gondii, andLeishmaniaspp., and tissue sample PCR forLeishmaniaspp., Trypanosoma cruzi,tissue coccidia (i.e.,T. gondii/Sarcocystis/Neospora),piroplasms, trichomonads, andAcanthamoeba. Electron microscopy was performed for two cases, and serology forN. caninumandT. gondiiwas available for three cases.ResultsPreexisting ocular diseases included keratoconjunctivitis sicca and pigmentary keratitis (n = 4) and pyogranulomatous meibomian adenitis (n = 1). All dogs were treated with tacrolimus or cyclosporine for at least 1.2 years. Dogs were presented with fleshy corneal or conjunctival masses that were clinically suspected to be neoplastic (n = 4) or immune mediated (n = 1). Histologic examination revealed granulomatous inflammation with intralesional protozoal organisms. Amoeba (n = 2),T. gondii(n = 2), orLeishmania mexicana(n = 1) were identified using molecular techniques. Serological tests were negative.ConclusionsProtozoal keratitis and conjunctivitis without systemic involvement appears rare and may be associated with chronic preexisting ocular surface disease treated with long‐term immunosuppression. Based upon clinical appearance, lesions could be confused with neoplasia. This is the first report of amoebic keratoconjunctivitis in dogs and ofL. mexicanain dogs in the United States.
Postexercise orthostatic intolerance: influence of exercise intensity
Authors: Mündel Toby , Perry Blake G. , Ainslie Philip N. , Thomas Kate N. , Sikken Elisabeth L. G. , Cotter James D. , Lucas Samuel J. E. 
Published: June 2015

New Findings

What is the central question of this study?
Following exercise, hypotension is often reported and syncope is more likely. It is unresolved whether the postexercise hypotension associated with different exercise intensities contributes to the rate at which syncope develops.

What is the main finding and its importance?
The physiological events that induce presyncope are the same both before and after exercise; however, more intense exercise accelerated the development of hypocapnia, hypotension and, ultimately, syncope. These data indicate that higher intensity exercise induces a postexercise hypotension that reduces cardiovascular reserve, an earlier development of hypocapnia and, ultimately, cerebral hypoperfusion.

After exercise, a reduction in mean arterial pressure is often experienced and is referred to as postexercise hypotension. Whilst syncope is more likely following exercise, it is unknown whether orthostatic tolerance is impacted by any exercise intensity‐mediated effect on postexercise hypotension. We examined the effect of exercise intensity on time to presyncope, induced via combined head‐up tilt and lower body negative pressure following 1 h of cycling at 30 and 70% of heart rate range. Healthy participants (n = 8; mean ± SD, 28 ± 5 years old) completed orthostatic testing to presyncope before and after exercise. Beat‐to‐beat middle cerebral artery blood flow velocity (MCAv), mean arterial pressure and cerebral oxygenation (measured by near‐infrared spectroscopy) were recorded continuously throughout orthostatic testing. During exercise, heart rates were 95 ± 6 and 147 ± 5 beats min−1 for 30 and 70% heart rate range, respectively, with average power outputs of 103 ± 22 and 221 ± 45 W, respectively. Time to presyncope occurred 32% sooner after the 70% heart rate range trial (952 ± 484 versus 1418 ± 435 s; P = 0.004). Both before and after exercise, presyncope occurred at the same reduction in MCAv (grouped mean, −30 ± 11 cm s−1), mean arterial pressure (−18 ± 13 mmHg), total oxygenation index (−6 ± 2%) and partial pressure of end‐tidal CO2 (−16 ± 8 mmHg; all P > 0.1). At presyncope following exercise, the MCAv response was related more to the change in partial pressure of end‐tidal CO2 from the baseline preceding orthostatic testing (r2 = 0.50, P = 0.01) than to the hypotension (r2 = 0.12, P = 0.17). Presyncope both before and after exercise occurred as a result of the same physiological perturbations, albeit greatly accelerated following more intense exercise.
Glucocorticoids as regulatory signals during intrauterine development
Authors: Fowden Abigail L. , Forhead Alison J. 
Published: June 2015

New Findings

What is the topic of this review?
This review discusses the role of the glucocorticoids as regulatory signals during intrauterine development. It examines the functional significance of these hormones as maturational, environmental and programming signals in determining offspring phenotype.

What advances does it highlight?
It focuses on the extensive nature of the regulatory actions of these hormones. It highlights the emerging data that these actions are mediated, in part, by the placenta, other endocrine systems and epigenetic modifications of the genome.

Glucocorticoids are important regulatory signals during intrauterine development. They act as maturational, environmental and programming signals that modify the developing phenotype to optimize offspring viability and fitness. They affect development of a wide range of fetal tissues by inducing changes in cellular expression of structural, transport and signalling proteins, which have widespread functional consequences at the whole organ and systems levels. Glucocorticoids, therefore, activate many of the physiological systems that have little function in utero but are vital at birth to replace the respiratory, nutritive and excretory functions previously carried out by the placenta. However, by switching tissues from accretion to differentiation, early glucocorticoid overexposure in response to adverse conditions can programme fetal development with longer term physiological consequences for the adult offspring, which can extend to the next generation. The developmental effects of the glucocorticoids can be direct on fetal tissues with glucocorticoid receptors or mediated by changes in placental function or other endocrine systems. At the molecular level, glucocorticoids can act directly on gene transcription via their receptors or indirectly by epigenetic modifications of the genome. In this review, we examine the role and functional significance of glucocorticoids as regulatory signals during intrauterine development and discuss the mechanisms by which they act in utero to alter the developing epigenome and ensuing phenotype.
Cytokine Profiles from Antigen-Stimulated Whole-Blood Samples among Patients with Pulmonary or Nonmeningeal Disseminated Coccidioidomycosis
Authors: Ampel Neil M. , Nesbit Lance A. , Nguyen Chinh T. , Chavez Suzette , Knox Kenneth S. , Johnson Suzanne M. , Pappagianis Demosthenes 
Published: June 2015

ABSTRACT

The outcome of coccidioidomycosis depends on a robust specific cellular immune response. A T-helper type 1 (Th1) cellular immune response has been previously associated with resolution of clinical illness. However, the precise elements of this response and whether cytokines not involved with the Th1 response play a role in coccidioidomycosis are not known. Whole-blood samples were obtained from subjects with active coccidioidomycosis and controls and incubated for 18 h with T27K, a coccidioidal antigen preparation. The supernatant was then assayed for gamma interferon (IFN-γ), interleukin-2 (IL-2), tumor necrosis factor alpha (TNF-α), IL-4, IL-6, IL-10, and IL-17A. A total of 43 subjects, 16 with acute pneumonia, 9 with pulmonary sequelae of nodules and cavities, and 18 with nonmeningeal disseminated coccidioidomycosis, were studied. Compared to concentrations in healthy immune and nonimmune donors, the median concentration of IL-17A was significantly higher in those with active coccidioidomycosis (for both,
P
< 0.01). In addition, IL-6 concentrations were higher while IL-2 and IFN-γ concentrations were significantly lower in those with nonmeningeal disseminated disease diagnosed within 12 months than in those with acute pneumonia (for all,
P
< 0.05). The cytokine profile among patients with active coccidioidomycosis is distinct in that IL-17A is persistently present. In addition, those with nonmeningeal disseminated disease have an increased inflammatory cytokine response and diminished Th1 responses that modulate over time.
Performance of a Noninvasive Test for Detecting Mycobacterium bovis Shedding in European Badger (Meles meles) Populations
Authors: King Hayley C. , Murphy Andrew , James Phillip , Travis Emma , Porter David , Sawyer Jason , Cork Jennifer , Delahay Richard J. , Gaze William , Courtenay Orin , Wellington Elizabeth M. 
Published: June 2015

ABSTRACT

The incidence of
Mycobacterium bovis
, the causative agent of bovine tuberculosis, in cattle herds in the United Kingdom is increasing, resulting in substantial economic losses. The European badger (
Meles meles
) is implicated as a wildlife reservoir and is the subject of control measures aimed at reducing the incidence of infection in cattle populations. Understanding the epidemiology of
M. bovis
in badger populations is essential for directing control interventions and understanding disease spread; however, accurate diagnosis in live animals is challenging and currently uses invasive methods. Here we present a noninvasive diagnostic procedure and sampling regimen using field sampling of latrines and detection of
M. bovis
with quantitative PCR tests, the results of which strongly correlate with the results of immunoassays in the field at the social group level. This method allows
M. bovis
infections in badger populations to be monitored without trapping and provides additional information on the quantities of bacterial DNA shed. Therefore, our approach may provide valuable insights into the epidemiology of bovine tuberculosis in badger populations and inform disease control interventions.