bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cell autonomous and cell‐type specific circadian rhythms in Arabidopsis
Authors: Yakir Esther , Hassidim Miriam , Melamed‐Book Naomi , Hilman Dror , Kron Ido , Green Rachel M. 
Published: July 2011

SummaryThe circadian system of plants regulates a wide range of rhythmic physiological and cellular output processes with a period of about 24 h. The rhythms are generated by an oscillator mechanism that, in Arabidopsis, consists of interlocking feedback loops of several components including CIRCADIAN CLOCK ASSOCIATED 1 (CCA1), LATE ELONGATED HYPOCOTYL (LHY), TIMING OF CAB EXPRESSION 1 (TOC1) and CCA1 HIKING EXPEDITION (CHE). Over recent years, researchers have gained a detailed picture of the clock mechanism at the resolution of the whole plant and several tissue types, but little information is known about the specificities of the clock mechanism at the level of individual cells. In this paper we have addressed the question of cell‐type‐specific differences in circadian systems. Using transgenic Arabidopsis plants with fluorescence‐tagged CCA1 to measure rhythmicity in individual leaf cells in intact living plants, we showed that stomatal guard cells have a different period from surrounding epidermal and mesophyll leaf cells. By comparing transcript levels in guard cells with whole plants, we identified differences in the expression of some oscillator genes that may underlie cell‐specific differences in clock properties. In addition, we demonstrated that the oscillators of individual cells in the leaf are robust, but become partially desynchronized in constant conditions. Taken together our results suggest that, at the level of individual cells, there are differences in the canonical oscillator mechanism that has been described for plants.
Losartan and amlodipine on myocardial structure and function: a prospective, randomized, clinical trial
Authors: Fogari R. , Mugellini A. , Destro M. , Corradi L. , Lazzari P. , Zoppi A. , Preti P. , Derosa G. 
Published: July 2011

Diabet. Med. (2011) 29, 24–31 (2012)AbstractAims  To compare the effects of losartan and amlodipine on myocardial structure and function in hypertensive patients with Type 2 diabetes and left ventricular hypertrophy.Methods  After a 4‐week placebo period, patients were randomized to losartan 50 mg (n = 90) or amlodipine 5 mg (n = 91) for 12 months, with a doubling of the dose in patients who did not respond after 4 weeks. Blood pressure was measured in the clinic every month, while conventional echocardiography and acoustic densitometry (integrated backscatter analysis) were performed at the end of the placebo period and after 12 months of treatment.Results  Both drugs reduced systolic/diastolic blood pressure to a comparable extent. Losartan significantly reduced left ventricular mass index (−19%, P < 0.001), interventricular septal thickness (−16.6%, P < 0.01) and left ventricular posterior wall thickness in diastole (−13.7%, P < 0.01). Amlodipine also decreased such measurements (−10%, P < 0.01 for left ventricular mass index, −9.3%, P < 0.05 for interventricular septal thickness in diastole and −10.1%, P < 0.05 for posterior wall thickness in diastole), but to a lesser extent than losartan. Both drugs significantly increased the ratio of peak filling velocity at early diastole to that at atrial contraction (E/A ratio) and decreased isovolumetric relaxation time: +13.7% and −8.5% with losartan,(both P < 0.01), and +7.9% and −4.9%, with amlopidine (both P < 0.05). Losartan, but not amlodipine, significantly reduced the relative integrated backscatter compared to baseline of the intraventricular septum (−10%, P < 0.01), and of the left ventricular posterior wall (−12%, P < 0.01), while increasing the cyclic variation of integrated backscatter of both the intraventricular septum (+35%, P < 0.001) and the left ventricular posterior wall (+32%, P < 0.001).Conclusions  Losartan provided a greater attenuation of left ventricular hypertrophy than amlodipine, seemingly as a result of a greater reduction of myocardial fibrosis.
Efficacy and safety of linagliptin in persons with Type 2 diabetes inadequately controlled by a combination of metformin and sulphonylurea: a 24‐week randomized study1
Authors: Owens D. R. , Swallow R. , Dugi K. A. , Woerle H. J. 
Published: July 2011

Diabet. Med. 28, 1352–1361 (2011)AbstractAims  To examine the efficacy and safety of the dipeptidyl peptidase‐4 inhibitor linagliptin in persons with Type 2 diabetes mellitus inadequately controlled [HbA1c 53–86 mmol/mol (7.0–10.0%)] by metformin and sulphonylurea combination treatment.Methods  A multi‐centre, 24‐week, randomized, double‐blind, parallel‐group study in 1058 patients comparing linagliptin (5 mg once daily) and placebo when added to metformin plus sulphonylurea. The primary endpoint was the change in HbA1c after 24 weeks.Results  At week 24, the linagliptin placebo‐corrected HbA1c adjusted mean change from baseline was −7 mmol/mol (−0.62%) [95% CI −8 to −6 mmol/mol (−0.73 to −0.50%); P < 0.0001]. More participants with baseline HbA1c≥ 53 mmol/mol (≥ 7.0%) achieved an HbA1c < 53 mmol/mol (< 7.0%) with linagliptin compared with placebo (29.2% vs. 8.1%, P < 0.0001). Fasting plasma glucose was reduced with linagliptin relative to placebo (−0.7 mmol/l, 95% CI −1.0 to −0.4; P < 0.0001). Improvements in homeostasis model assessment of β‐cell function were seen with linagliptin (P < 0.001). The proportion of patients who reported a severe adverse event was low in both groups (linagliptin 2.4%; placebo 1.5%). Symptomatic hypoglycaemia occurred in 16.7 and 10.3% of the linagliptin and placebo groups, respectively. Hypoglycaemia was generally mild or moderate; severe hypoglycaemia was reported in 2.7 and 4.8% of the participants experiencing hypoglycaemic episodes in the linagliptin and placebo groups, respectively. No significant weight changes were noted.Conclusions  In patients with Type 2 diabetes, adding linagliptin to metformin given in combination with a sulphonylurea significantly improved glycaemic control and this was well tolerated. Linagliptin could provide a valuable treatment option for individuals with inadequate glycaemic control despite ongoing combination therapy with metformin and a sulphonylurea.
Are arterial and venous samples clinically equivalent for the estimation of pH, serum bicarbonate and potassium concentration in critically ill patients?
Authors: Herrington W. G. , Nye H. J. , Hammersley M. S. , Watkinson P. J. 
Published: July 2011

Diabet. Med. 29, 32–35 (2012)AbstractAims  To assess the comparability of venous and arterial samples for pH, bicarbonate and potassium measurements in critically ill patients.Methods  Simultaneous arterial and venous samples from 206 critically ill patients were analysed in duplicate. Coefficients of variation and 95% limits of agreement were calculated for arterial and venous samples. Bland‐Altman plots were constructed to assess agreement between sampling sites.Results  The median (range) of arterial pH, bicarbonate concentrations, potassium concentrations and glucose concentrations were 7.40 (7.01–7.56), 25 (9–41) mmol/l, 4.2 (3.1–6.8) mmol/l and 7.4 (3.0–13.5) mmol/l, respectively. Coefficients of variation for arterial and venous pH were both 0.1%, with bias (95% limits of agreement) of –0.01 (–0.03 to 0.01) for arterial and −0.01 (−0.02 to 0.01) for venous samples. The bias (95% limits of agreement) between arterial and venous samples was 0.03 (−0.02 to 0.08). Coefficients of variation for arterial and venous bicarbonate results were 0.8 and 0.7%, respectively, with bias (95% limits of agreement) of 0 (−0.5 to 0.5) mmol/l for both sample types. The bias (95% limits of agreement) between venous and arterial samples was 0 (−1.3 to 1.3) mmol/l. Coefficients of variation for arterial and venous potassium samples were 0.8 and 1.1%, respectively, with bias (95% limits of agreement) of 0 (−0.1 to 0.1) for both sample types. The bias (95% limits of agreement) between venous and arterial samples was 0.1 (−0.4 to 0.6) mmol/l.Conclusions  A venous blood sample, analysed on a blood gas machine, is sufficiently reliable to assess pH, bicarbonate and potassium concentrations in critically ill patients, suggesting that venous sampling alone is appropriate in the management of diabetic ketoacidosis.
Functional characterization of vesicular excitatory amino acid transport by human sialin
Authors: Miyaji Takaaki , Omote Hiroshi , Moriyama Yoshinori 
Published: July 2011

J. Neurochem.(2011)119, 1–5.AbstractSialin, the protein coded by SLC17A5, is responsible for membrane potential (Δψ)‐driven aspartate and glutamate transport into synaptic vesicles in addition to H+/sialic acid co‐transport in lysosomes. Rodent sialin mutants harboring the mutations associated with Salla disease in humans did not transport aspartate and glutamate whereas H+/sialic acid co‐transport activity was about one‐third of the wild‐type protein. In this study, we investigate the effects of various mutations on the transport activities of human sialin. Proteoliposomes containing purified heterologously expressed human sialin exhibited both Δψ‐driven aspartate and glutamate transport activity and H+/sialic acid co‐transport activity. Aspartate and glutamate transport was not detected in the R39C and K136E mutant forms of SLC17A5 protein associated with Salla disease, whereas H+/sialic acid co‐transport activity corresponded to 30–50% of the recombinant wild‐type protein. In contrast, SLC17A5 protein harboring the mutations associated with infantile sialic acid storage disease, H183R and Δ268SSLRN272 still showed normal levels of Δψ‐driven aspartate and glutamate transport even though H+/sialic acid co‐transport activity was absent. Human sialin carrying the G328E mutation that causes both phenotypes, and P334R and G378V mutations that cause infantile sialic acid storage disease showed no transport activity. These results support the idea that people suffering from Salla disease have been defective in aspartergic and glutamatergic neurotransmissions.
A monoclonal antibody against synthetic Aβ dimer assemblies neutralizes brain‐derived synaptic plasticity‐disrupting Aβ
Authors: O’Nuallain Brian , Klyubin Igor , Mc Donald Jessica M. , Foster James S. , Welzel Alfred , Barry Andrew , Dykoski Richard K. , Cleary James P. , Gebbink Martijn F.B.G. , Rowan Michael J. , Walsh Dominic M. 
Published: July 2011

J. Neurochem. (2011) 119, 189–201.AbstractDiverse lines of evidence indicate that pre‐fibrillar, diffusible assemblies of the amyloid β‐protein (Aβ) play an important role in Alzheimer’s disease pathogenesis. Although the precise molecular identity of these soluble toxins remains unsettled, recent experiments suggest that sodium dodecyl sulfate (SDS)‐stable Aβ dimers may be the basic building blocks of Alzheimer’s disease‐associated synaptotoxic assemblies and as such present an attractive target for therapeutic intervention. In the absence of sufficient amounts of highly pure cerebral Aβ dimers, we have used synthetic disulfide cross‐linked dimers (free of Aβ monomer or fibrils) to generate conformation‐specific monoclonal antibodies. These dimers aggregate to form kinetically trapped protofibrils, but do not readily form fibrils. We identified two antibodies, 3C6 and 4B5, which preferentially bind assemblies formed from covalent Aβ dimers, but do not bind to Aβ monomer, amyloid precursor protein, or aggregates formed by other amyloidogenic proteins. Monoclonal antibody 3C6, but not an IgM isotype‐matched control antibody, ameliorated the plasticity‐disrupting effects of Aβ extracted from the aqueous phase of Alzheimer’s disease brain, thus suggesting that 3C6 targets pathogenically relevant Aβ assemblies. These data prove the usefulness of covalent dimers and their assemblies as immunogens and recommend further investigation of the therapeutic and diagnostic utility of monoclonal antibodies raised to such assemblies.
The action of Semaphorin7A on thalamocortical axon branching
Authors: Fukunishi Akiko , Maruyama Takuro , Zhao Hong , Tiwari Manisha , Kang Sujin , Kumanogoh Atsushi , Yamamoto Nobuhiko 
Published: July 2011

J. Neurochem. (2011) 118, 1008–1015.AbstractDeveloping axons form extensive branches to make synaptic contacts with their target cells. Despite the important role of axon branching in neural circuit formation, its underlying molecular mechanism is still largely unknown. In this study, we investigated the involvement of Semaphorin7A (Sema7A) in thalamocortical (TC) axon branching. In situ hybridization demonstrated that sema7a was expressed specifically in layer 4, the TC recipient layer, when TC axons form extensive arbors. A similar protein expression pattern was observed by immunohistochemistry with an anti‐Sema7A antibody. The effect of Sema7A on axon branching was investigated in dissociated cell cultures from embryonic rat thalamus. TC axon branching increased dramatically on Sema7A‐coated dishes. We further studied the activity of Sema7A in vivo using loss‐ and gain‐of‐function analyses. The number of vesicular glutamate transporter 2‐positive puncta was markedly reduced in the Sema7A‐deficient cortex. In contrast, their number increased significantly when Sema7A was over‐expressed in layer 4 cells by in utero electroporation. Taken together, these findings suggest that Sema7A acts as a positive regulator for TC axon branching and/or pre‐synaptic puncta formation.
Δ9‐THC increases endogenous AHA1 expression in rat cerebellum and may modulate CB1 receptor function during chronic use
Authors: Filipeanu Catalin M. , Guidry Jesse J. , Leonard Stuart T. , Winsauer Peter J. 
Published: July 2011

J. Neurochem. (2011) 118, 1101–1112.AbstractTo characterize the long‐term effects of adolescent marijuana abuse, we performed a proteomic analysis of cerebellar extracts from adult female rats with and without ovariectomy that were treated with Δ9‐THC for 40 days during adolescence. Six proteins were found to significantly differ among the four treatment groups, with Δ9‐THC and ovariectomy (OVX) decreasing the mitochondrial proteins, pyruvate carboxylase and NADH dehydrogenase, whereas the levels of putative cytosolic molecular chaperones NM23B, translationally controlled tumor protein, DJ‐1 and activator of heat‐shock 90kDa protein ATPase homolog 1 (AHA1) were increased. We further analyzed the effects of AHA1, a HSP90 co‐chaperone, on CB1R and CB2R trafficking and signaling in transfected HEK293T and Neuro‐2A cells. In HEK293T cells, AHA1 over‐expression enhanced plasma membrane levels of CB1R and increased CB1R‐mediated effects on cAMP levels and on MAPK phosphorylation. AHA1 over‐expression also enhanced cell surface levels of endogenous CB1R and the effects of Δ9‐THC on the cAMP levels in Neuro‐2A cells. In contrast, over‐expression of AHA1 did not affect the subcellular localization and signaling of CB2R. Our data indicate that chronic Δ9‐THC administration in adolescence altered the endogenous levels of specialized proteins in the cerebellum, such as AHA1, and that this protein can change CB1R cell surface levels and signaling.
Trace metal leaching in a spodosol irrigated with tomato packinghouse wastewater
Authors: Chahal M. K. , Toor G. S. 
Published: July 2011

AbstractTomato packinghouse wastewater is often applied to land in Florida, but the sandy soils, low levels of organic matter, shallow groundwater and abundant rainfall present favourable conditions for leaching of wastewater‐borne trace metals. We investigated the leaching of copper (Cu), iron (Fe), manganese (Mn) and zinc (Zn) from a sandy siliceous, hyperthermic Oxyaquic Alorthods packed in two distinct soil horizons (Ap and A/E) in 12 polyvinyl chloride soil columns (30 cm internal diameter × 50 cm length). Thirty leaching events were conducted by daily applying tomato packinghouse wastewater at low (0.84 cm/day), medium (1.68 cm/day) and high (2.51 cm/day) rates for 30‐days period. Control treatment received de‐ionized water at the same application rate as the medium treatment (1.68 cm/day). Application of wastewater at three rates did not affect the mean concentrations of Cu in leachate (0.19–0.2 mg/L) because of retention of Cu in the soil profile. However, leachate Zn concentrations were twice as much (0.3–0.32 mg/L) following wastewater application than for the control (0.13 mg/L) treatment. Leaching losses of Cu and Zn were smaller with the medium wastewater treatment (similar to control treatment) than for the high wastewater treatment. Concentrations of Cu and Zn at the 50 cm soil depth were much less than the drinking water standards, suggesting a minimum risk of groundwater contamination under fields to which wastewater was applied. Our results imply that tomato packinghouse wastewater can be safely land‐applied at 1.68 cm/day to Florida’s Spodosols under vegetable production without concerns of significant trace metal leaching.
A Novel Movement Disorder in Related Male Labrador Retrievers Characterized by Extreme Generalized Muscular Stiffness
Authors: Vanhaesebrouck A.E. , Shelton G.D. , Garosi L. , Harcourt‐Brown T.R. , Couturier J. , Behr S. , Harvey R.J. , Jeffery N.D. , Matiasek K. , Blakemore W.F. , Granger N. 
Published: July 2011

Objectives: To describe the clinical phenotype of a new motor disorder in Labrador Retrievers.
Animals and Methods: Case series study. Seven young male Labrador Retrievers presented for evaluation of stiff gait.
Results: All affected dogs had generalized muscular stiffness, persistent at rest and resulting in restricted joint movements. They showed a forward flexed posture, festinating gait, and bradykinesia. Signs developed between 2 and 16 months of age and tended to stabilize in adulthood. Needle electromyogram in the conscious state showed continuous motor unit activity in resting epaxial and proximal limb muscles. This activity was abolished by general anesthesia. Muscle and nerve histopathology was normal. In 2 dogs necropsied, astrocytosis was evident throughout the spinal cord gray matter, reticular formation and caudate nuclei. Decreased neuronal counts were selectively found in the spinal cord Rexed's lamina VII, but not in VIII and IX. Pedigree analysis showed that the affected dogs were from 5 related litters.
Conclusions and Clinical Importance: This new hypertonicity syndrome in Labrador Retrievers is unique because of the selective distribution of the histological lesions, the lack of progression in adulthood, and its exclusive occurrence in male dogs. Pedigree analysis suggests an X‐linked hereditary disease, although other modes of inheritance cannot be ruled out with certainty. We hypothesize that altered output from basal nuclei and reticular formation together with motor neuron disinhibition caused by a decreased number of spinal cord interneurons leads to the muscular stiffness.
Distribution of Flunixin Meglumine and Firocoxib into Aqueous Humor of Horses
Authors: Hilton H.G. , Magdesian K.G. , Groth A.D. , Knych H. , Stanley S.D. , Hollingsworth S.R. 
Published: July 2011

Background: Nonsteroidal anti‐inflammatory drugs (NSAIDs) are commonly used systemically for the treatment of inflammatory ocular disease in horses. However, little information exists regarding the ocular penetration of this class of drugs in the horse.
Objective: To determine the distribution of orally administered flunixin meglumine and firocoxib into the aqueous humor of horses.
Animals: Fifteen healthy adult horses with no evidence of ophthalmic disease.
Methods: Horses were randomly assigned to a control group and 2 treatment groups of equal sizes (n = 5). Horses assigned to the treatment groups received an NSAID (flunixin meglumine, 1.1 mg/kg PO q24h or firocoxib, 0.1 mg/kg PO q24h for 7 days). Horses in the control group received no medications. Concentrations of flunixin meglumine and firocoxib in serum and aqueous humor and prostaglandin (PG) E2 in aqueous humor were determined on days 1, 3, and 5 and aqueous : serum ratios were calculated.
Results: Firocoxib penetrated the aqueous humor to a significantly greater extent than did flunixin meglumine at days 3 and 5. Aqueous : serum ratios were 3.59 ± 3.32 and 11.99 ± 4.62% for flunixin meglumine and firocoxib, respectively. Ocular PGE2 concentrations showed no differences at any time point among study groups.
Conclusions and Clinical Importance: Both flunixin meglumine and firocoxib penetrated into the aqueous humor of horses. This study suggests that orally administered firocoxib penetrates the aqueous humor better than orally administered flunixin meglumine at label dosages in the absence of ocular inflammation. Firocoxib should be considered for the treatment of inflammatory ophthalmic lesions in horses at risk for the development of adverse effects associated with nonselective NSAID administration.
Descente fidèlement plate pour les n-champs d’Artin
Authors: Toën Bertrand 
Published: July 2011

AbstractWe prove two flat descent results in the setting of Artin n-stacks. First of all, a stack for the etale topology which is an Artin n-stack (in the sense of Simpson and Toën–Vezzosi) is also a stack for the flat (fppf) topology. Moreover, an n-stack, for the fppf topology, which admits a flat (fppf) n-atlas is an Artin n-stack (i.e. possesses a smooth n-atlas). We deduce from these two results a comparison between etale and fppf cohomologies (with coefficients in non-smooth group schemes and also non-abelian). This work is written in the setting of the derived stacks of Toën and Vezzosi, and all of these results are therefore also valid for derived Artin n-stacks.
From the Phan–Thien–Tanner/Oldroyd-B Non-Newtonian Model to the Double Shear Thining Rabinowisch Thin Film Model
Authors: Bayada Guy , Chupin Laurent , Martin Sébastien 
Published: July 2011

Abstract
In this paper, an asymptotic expansion is used to derive a description of Phan–Tien– Tanner (PTT)/Oldroyd-B flows in the thin film situation without the classical “upper convective maxwell”(UCM) assumption. We begin with a short presentation of the Phan–Thien–Tanner/Oldroyd-B models, which introduce viscoelastic effects in a solute–solvent mixture. The three-dimensional flow is described using five parameters, namely the Deborah number (De) (or the relaxation parameter λ), the viscosity ratio r, the bulk fluid viscosity η, the material slip parameter a related to the “convected derivative” and an elongation number κ. Then we focus on the thin film assumption and the related asymptotic analysis that allows us to derive a reduced model. A perturbation procedure for “not too small” values of κ allows us to obtain further results such as an asymptotic “effective viscosity/ shear rate” law, which appears to be a perturbation of the double Rabinowisch model, whose parameters are completely defined by those of the original three-dimensional model. And last a numerical procedure is proposed based on a penalized Uzawa method, to compute the corresponding solution. This algorithm can also be used for any generalized double Newtonian shear thinning Carreau law.