bluuebunny/crossref_metadata_2025_split huggingface dataset:
Long continued applications of N fertilizer to cereals on sandy loam: grain and straw response to residual N
Authors: Thomsen I.K. , Djurhuus J. , Christensen B.T. 
Published: February 2009

Abstract. The residual value of mineral N fertilizer applied in the spring was investigated in a field experiment where four cereals (winter wheat, winter barley, spring barley and spring oats) had been grown at reduced (0.7N), normal (1N) or high (1.3N) N fertilizer rates for 20 to 28 years. The effect of previous N fertilizer dressing was tested in two succeeding years by replacing the original N rate with five test N rates ranging from 0 to 240 kg N ha−1 for winter cereals and 0 to 200 kg N ha−1 for spring cereals. In the first test year, winter wheat grown on plots previously supplied with the high rate of mineral fertilizer (202 kg N ha−1 yr−1) yielded more grain and straw and had a higher total N uptake than wheat on plots previously supplied with the normal (174 kg N ha−1 yr−1) or reduced (124 kg N ha−1 yr−1) rate. The grain yield response and N uptake was not significantly affected by the N supply in the test year. The winter wheat grown in the second test year was unaffected by the previous N supply. Grain and straw yield response and total N uptake for spring barley, winter barley and oats, were almost identical irrespective of the previous N rate.After 20 to 28 years there were no significant differences in soil C and N (0 to 20 cm) between soil receiving three rates of N fertilizer. Soil from differently fertilized oat plots showed no significant differences in N mineralizing capacity. Nitrate leaching losses from the soils at the three N rates were estimated and the N balances for the 20 to 28 years experimental period calculated. The data indicated a reduction in overall loss of 189 to 466 kg N ha−1 at the normal and high N rates compared with the reduced N rate. We conclude that the N supplying capacity and soil organic matter content of this fertile sandy loam soil under continuous cereal cropping with straw removal was not significantly affected by differences in N fertilizer residues.
Initial Evidence on the Role of Accounting Earnings in the Bond Market
Authors: EASTON PETER D. , MONAHAN STEVEN J. , VASVARI FLORIN P. 
Published: February 2009

ABSTRACTWe document that: (1) the incidence of bond trade increases during the days surrounding earnings announcements, (2) there is a bond‐price reaction to the announcement of earnings, and (3) there is a positive association between annual bond returns and both annual changes in earnings and annual analysts' forecast errors. All of these effects are larger when earnings convey bad news or when the underlying bond is more risky. Taken together, our results suggest that the nonlinear payoff structure of bond securities affects the role of accounting earnings in the bond market.
Depreciation Rules and the Relation between Marginal and Historical Cost
Authors: RAJAN MADHAV V. , REICHELSTEIN STEFAN 
Published: February 2009

ABSTRACTThe reported cost of a product frequently contains historical cost components that reflect past investments in productive capacity. We examine a setting wherein a firm makes a sequence of overlapping capacity investments. Earlier research has identified particular accrual accounting (depreciation) rules with the property that, on a per unit basis, the historical cost of a product captures precisely its marginal cost. Relative to this benchmark, we investigate and characterize the direction and magnitude of the bias in reported historical cost that results from alternative depreciation rules, including in particular straight‐line depreciation in conjunction with partial direct expensing. In addition, we demonstrate that for a reasonable range of parameter specifications the resulting bias is rather small. Finally, we apply our framework to two specific settings. First, in a regulatory context, we establish the extent to which the accounting profit margin is indicative of a firm's pricing power in the product market. Second, we model an internal control scenario in which a manager's performance is evaluated using residual income, and identify the distortions in investment levels that result from the use of alternative depreciation rules.
Montelukast inhibits neutrophil pro‐inflammatory activity by a cyclic AMP‐dependent mechanism
Authors: Anderson Ronald , Theron Annette J , Gravett Cornelia M , Steel Helen C , Tintinger Gregory R , Feldman Charles 
Published: February 2009

Background and purpose: The objective of this study was to characterize the effects of the cysteinyl leukotriene receptor antagonist, montelukast (0.1–2 µmol·L−1), on Ca2+‐dependent pro‐inflammatory activities, cytosolic Ca2+fluxes and intracellular cAMP in isolated human neutrophils activated with the chemoattractants, N‐formyl‐L‐methionyl‐L‐leucyl‐L‐phenylalanine (1 µmol·L−1) and platelet‐activating factor (200 nmol·L−1).Experimental approach: Generation of reactive oxygen species was measured by lucigenin‐ and luminol‐enhanced chemiluminescence, elastase release by a colourimetric assay, leukotriene B4and cAMP by competitive binding ELISA procedures, and Ca2+fluxes by fura‐2/AM‐based spectrofluorimetric and radiometric (45Ca2+) procedures.Key results: Pre‐incubation of neutrophils with montelukast resulted in dose‐related inhibition of the generation of reactive oxygen species and leukotriene B4by chemoattractant‐activated neutrophils, as well as release of elastase, all of which were maximal at 2 µmol·L−1(mean percentages of the control values of 30 ± 1, 12 ± 3 and 21 ± 3 respectively;P < 0.05). From a mechanistic perspective, treatment of chemoattractant‐activated neutrophils with montelukast resulted in significant reductions in both post‐peak cytosolic Ca2+concentrations and store‐operated Ca2+influx. These montelukast‐mediated alterations in Ca2+handling by the cells were associated with a significant elevation in basal cAMP levels, which resulted from inhibition of cyclic nucleotide phosphodiesterases.Conclusions and implications: Montelukast, primarily a cysteinyl leukotriene (CysLT1) receptor antagonist, exhibited previously undocumented, secondary, neutrophil‐directed anti‐inflammatory properties, which appeared to be cAMP‐dependent.
Inotropy and L‐type Ca2+current, activated by β1‐ and β2‐adrenoceptors, are differently controlled by phosphodiesterases 3 and 4 in rat heart
Authors: Christ Torsten , Galindo‐Tovar Alejandro , Thoms Marcus , Ravens Ursula , Kaumann Alberto J. 
Published: February 2009

Background and purpose: β1‐ and β2‐adrenoceptors coexist in rat heart but β2‐adrenoceptor‐mediated inotropic effects are hardly detectable, possibly due to phosphodiesterase (PDE) activity. We investigated the influence of the PDE3 inhibitor cilostamide (300 nmol·L−1) and the PDE4 inhibitor rolipram (1 µmol·L−1) on the effects of (−)‐catecholamines.Experimental approach: Cardiostimulation evoked by (−)‐noradrenaline (ICI118551 present) and (−)‐adrenaline (CGP20712A present) through β1‐ and β2‐adrenoceptors, respectively, was compared on sinoatrial beating rate, left atrial and ventricular contractile force in isolated tissues from Wistar rats. L‐type Ca2+‐current (ICa‐L) was assessed with whole‐cell patch clamp.Key results: Rolipram caused sinoatrial tachycardia. Cilostamide and rolipram did not enhance chronotropic potencies of (−)‐noradrenaline and (−)‐adrenaline. Rolipram but not cilostamide potentiated atrial and ventricular inotropic effects of (−)‐noradrenaline. Cilostamide potentiated the ventricular effects of (−)‐adrenaline but not of (−)‐noradrenaline. Concurrent cilostamide + rolipram uncovered left atrial effects of (−)‐adrenaline. Both rolipram and cilostamide augmented the (−)‐noradrenaline (1 µmol·L−1) evoked increase in ICa‐L. (−)‐Adrenaline (10 µmol·L−1) increased ICa‐Lonly in the presence of cilostamide but not rolipram.Conclusions and implications: PDE4 blunts the β1‐adrenoceptor‐mediated inotropic effects. PDE4 reduces basal sinoatrial rate in a compartment distinct from compartments controlled by β1‐ and β2‐adrenoceptors. PDE3 and PDE4 jointly prevent left atrial β2‐adrenoceptor‐mediated inotropy. Both PDE3 and PDE4 reduce ICa‐Lresponses through β1‐adrenoceptors but the PDE3 component is unrelated to inotropy. PDE3 blunts both ventricular inotropic and ICa‐Lresponses through β2‐adrenoceptors.
Anti‐nociceptive properties of the xanthine oxidase inhibitor allopurinol in mice: role of A1adenosine receptors
Authors: Schmidt AP , Böhmer AE , Antunes C , Schallenberger C , Porciúncula LO , Elisabetsky E , Lara DR , Souza DO 
Published: February 2009

Background and purpose: Allopurinol is a potent inhibitor of the enzyme xanthine oxidase, used primarily in the treatment of hyperuricemia and gout. It is well known that purines exert multiple effects on pain transmission. We hypothesized that the inhibition of xanthine oxidase by allopurinol, thereby reducing purine degradation, could be a valid strategy to enhance purinergic activity. The aim of this study was to investigate the anti‐nociceptive profile of allopurinol on chemical and thermal pain models in mice.Experimental approach: Mice received an intraperitoneal (i.p.) injection of vehicle (Tween 10%) or allopurinol (10–400 mg kg−1). Anti‐nociceptive effects were measured with intraplantar capsaicin, intraplantar glutamate, tail‐flick or hot‐plate tests.Key results: Allopurinol presented dose‐dependent anti‐nociceptive effects in all models. The opioid antagonist naloxone did not affect these anti‐nociceptive effects. The non‐selective adenosine‐receptor antagonist caffeine and the selective A1adenosine‐receptor antagonist, DPCPX, but not the selective A2Aadenosine‐receptor antagonist, SCH58261, completely prevented allopurinol‐induced anti‐nociception. No obvious motor deficits were produced by allopurinol, at doses up to 200 mg kg−1. Allopurinol also caused an increase in cerebrospinal fluid levels of purines, including the nucleosides adenosine and guanosine, and decreased cerebrospinal fluid concentration of uric acid.Conclusions and implications: Allopurinol‐induced anti‐nociception may be related to adenosine accumulation. Allopurinol is an old and extensively used compound and seems to be well tolerated with no obvious central nervous system toxic effects at high doses. This drug may be useful to treat pain syndromes in humans.
Galantamine improves apomorphine‐induced deficits in prepulse inhibition via muscarinic ACh receptors in mice
Authors: Yano K , Koda K , Ago Y , Kobayashi H , Kawasaki T , Takuma K , Matsuda T 
Published: February 2009

Background and purpose: Galantamine, a weak acetylcholine esterase (AChE) inhibitor and allosteric potentiator of nicotinic ACh receptors (nAChRs), improves apomorphine‐induced deficits in prepulse inhibition (PPI), sensory information‐processing deficits, via a nAChR‐independent mechanism. The present study examined the role of muscarinic ACh receptors (mAChRs) in the effect of galantamine, and studied the mechanism of galantamine‐induced increases in prefrontal ACh levels in mice.Experimental approach: Apomorphine (1 mg kg−1) was administered to male ddY mice (9–10 weeks old) to create a PPI deficit model. Extracellular ACh concentrations in the prefrontal cortex were measured byin vivomicrodialysis.Key results: Galantamine‐ and donepezil‐mediated improvements in apomorphine‐induced PPI deficits were blocked by the preferential M1mAChR antagonist telenzepine. The mAChR agonist oxotremorine also improved apomorphine‐induced PPI deficits. Galantamine, like donepezil, increased extracellular ACh concentrations in the prefrontal cortex. Galantamine‐induced increases in prefrontal ACh levels were partially blocked by the dopamine D1receptor antagonist SCH23390, but not by antagonists of mAChRs (telenzepine) and nAChRs (mecamylamine). Galantamine increased dopamine, but not 5‐HT, release in the prefrontal cortex.Conclusions and implications: Galantamine improves apomorphine‐induced PPI deficits by stimulating mAChRs through increasing brain ACh levels via a dopamine D1receptor‐dependent mechanism and AChE inhibition.
Magnetic resonance spectroscopy reveals an epileptic network in juvenile myoclonic epilepsy
Authors: Lin Katia , Carrete Jr Henrique , Lin Jaime , Peruchi Mirella Maccarini , De Araújo Filho Gerardo Maria , Guaranha Mirian Salvadori Bittar , Guilhoto Laura Maria Figueiredo Ferreira , Sakamoto Américo Ceiki , Yacubian Elza Márcia Targas 
Published: February 2009

SummaryPurpose:  To investigate the cerebral metabolic differences between patients with juvenile myoclonic epilepsy (JME) and normal controls and to evaluate to what extent these metabolic alterations reflect involvement of an epileptic network.Methods:  Sixty patients with JME were submitted to multi‐voxel proton spectroscopy (1H‐MRS) at 1.5 T over medial prefrontal cortex (MPC), primary motor cortex (PMC), thalamus, striatum, posterior cingulate gyrus (PCG), and insular, parietal, and occipital cortices. We determined ratios for integral values of N‐acetyl‐aspartate (NAA) and glutamate‐glutamine (GLX) over creatine‐phosphocreatine (Cr). The control group (CTL) consisted of 30 age‐ and sex‐matched healthy volunteers.Results:  The NAA/Cr ratio, a measure of neuronal injury, was reduced in PMC, MPC, and thalamus among patients. In addition, they had an altered GLX/Cr ratio, which is involved in excitatory activity, on PMC, MPC, and PCG, where it was reduced, whereas it was increased on insula and striatum. Multiple regression analysis revealed the strongest correlation between thalamus and MPC, but the thalamus was also correlated with insula, occipital cortex, and striatum among patients. Lower NAA/Cr was observed with advancing age and duration of epilepsy, regardless of frequency of seizures and antiepileptic drug therapy in thalamus and frontal cortex.Discussion:  The identification of a specific network of neurochemical dysfunction in patients with JME, with diverse involvement of particular structures within the thalamocortical circuitry, suggests that cortical hyperexcitability in JME is not necessarily diffuse, supporting the knowledge that the focal/generalized distinction of epileptogenesis should be reconsidered. Furthermore, evidence is provided toward progressive neuronal dysfunction in JME.
Ketogenic diet in the treatment of refractory continuous spikes and waves during slow sleep
Authors: Nikanorova Marina , Miranda Maria J. , Atkins Mary , Sahlholdt Lene 
Published: February 2009

SummaryPurpose: To evaluate the effect of the ketogenic diet on electroclinical characteristics and cognitive function in children with continuous spikes and waves during slow sleep (CSWS).Methods: Five children (four boys, one girl) aged between 8 and 13 years with CSWS refractory to conventional antiepileptic drugs (AEDs), including levetiracetam, and steroids were included. The prospective electroclinical assessment was performed prior to the ketogenic diet and once every 6 months post initiation during the 2‐year period. All children underwent neuropsychological testing prior to the ketogenic diet and four of the children again 12 months after the diet’s introduction. In case 4 the testing has been performed after 7 months and the diet was withdrawn after 9 months because of the lack of efficacy and the parent’s wishes. In two patients the cognitive functions were also evaluated after 24 months since the diet’s initiation. During the period on the ketogenic diet the concomitant AED treatment was unchanged.Results: Electrographic evaluation after 24 months on the ketogenic diet showed CSWS resolution in one patient, mild decrease of the spike–wave index in one, and lack of response in three patients. The ketogenic diet did not influence the neuropsychological outcome, and intelligence quotient (IQ) scores remained low at the end of the follow‐up period. However, in two patients an improvement in attention and behavior was demonstrated.Discussion: This is the first study evaluating the efficacy of the ketogenic diet in children with CSWS. Five presented cases were refractory to AEDs and steroids. Only one case responded with complete CSWS disappearance; in one the effect of the ketogenic diet was partial and intermittent, whereas in three patients no response has been observed. These results show that the ketogenic diet did not appear to influence the neuropsychological outcome; however, the absence of a control group makes it impossible to conclude with certainty.
Arthroscopic Documentation of Elbow Cartilage Pathology in Dogs with Clinical Lameness without Changes on Standard Radiographic Projections
Authors: PUNKE JOHN P. , HULSE DON A. , KERWIN SHARON C. , PEYCKE LAURA E. , BUDSBERG STEVEN C. 
Published: February 2009

Objective—To document cartilage damage associated with elbow lameness in dogs without radiographic signs.Study Design—Case series.Animals—Dogs (n=16).Methods—Medical records (November 2004–January 2006) of dogs with undiagnosed forelimb lameness localized to the elbow but without radiographic signs that had lesions identified by either computed tomography (CT) or nuclear scintigraphy and confirmed by arthroscopy were included. Signalment, duration of clinical signs before admission, surgical diagnosis, and treatment were recorded.Results—Sixteen dogs (10 left, 6 right elbows) were identified. Median age was 30.1 months and median duration of clinical signs before admission was 15.6 months. CT or scintigraphy were strongly suggestive of elbow pathology before confirmation by arthroscopy. Medial coronoid pathology was identified in every abnormal elbow and osteochondrosis dissecans in 2 elbows.Conclusions—Elbow pathology not associated with radiographic changes can be identified by CT and scintigraphy. Coronoid pathology is the most likely diagnosis.Clinical Relevance—Absence of radiographic signs in elbows with clinical signs of lameness should be evaluated with advanced imaging techniques (CT, scintigraphy) and arthroscopy to identify the cause of lameness.
Effect of Limb Position on Elbow Congruity with CT Evaluation
Authors: HOUSE MARK R. , MARINO DOMINIC J. , LESSER MARTIN L. 
Published: February 2009

Objective—To determine if computed tomographic (CT) measurement of radio‐ulnar congruence (RUC) is affected by limb position.Study Design—Prospective study.Animals—Labrador Retrievers (n=10).Methods—Each dog had both elbows imaged in neutral, supination, and pronation positions using helical CT acquisition, at 1 mm increments, in a transverse plane. RUC was calculated using a previously reported method and a new technique using 3‐D image processing and measurements determined by a coordinate system.Results—The limits of agreement showed that comparing any pair of elbow positions yielded large discrepancies in measurements with the previously reported technique. Better agreement between pairs of elbow positions with reduced discrepancy was achieved using the 3‐D technique. Variation in antebrachium positioning did yield a difference in congruence.Conclusions—Limb position (supination, pronation) affects elbow congruity measurements using CT analysis. Use of 3‐D image processing may allow for improved elbow congruity measurements compared with other 2‐D measurement techniques.Clinical Relevance—Limb position must be controlled when performing CT evaluation of elbows for incongruity. 3‐D imaging appears to be less affected by limb position than conventional 2‐D analysis when assessing radioulnar incongruence.
Un‐United Medial Epicondyle of the Humerus: Radiographic Prevalence and Association with Elbow Osteoarthritis in a Cohort of Labrador Retrievers
Authors: PASTER ERIN R. , BIERY DARRYL N. , LAWLER DENNIS F. , EVANS RICHARD H. , KEALY RICHARD D. , GREGOR THOMAS P. , McKELVIE PAMELA J. , SMITH GAIL K. 
Published: February 2009

Objective—To longitudinally characterize the radiographic appearance of un‐united medial epicondyle (UME) of the humerus, evaluate UME association with osteoarthritis (OA) and consider its relevance to the elbow dysplasia complex.Study Design—Longitudinal cohort study.Animals—Labrador retrievers (n=48) from 7 litters.Methods—Forty‐eight same‐sex littermates were paired for this lifetime feeding study. One of each pair was control‐fed; the pair mate was fed 25% less than the control each day. Elbows of 46 surviving dogs were radiographed at ages 6 and 8 years, and/or at end‐of‐life (EOL). Elbow histopathology was done EOL, although UME lesions were not evaluated histologically.Results—Seven dogs (15%) had UME, representing 5 litters; 4 were control‐fed, 3 diet‐restricted. Six (86%) dogs had unilateral lesions; 1 was bilateral. UME was evident on craniocaudal (CrCd) radiographic projections by 8 years in all dogs. UME was detected in only 1 elbow by mediolateral radiographic projection. Elbow OA frequency in UME affected dogs was not significantly different from the remaining study population. Histopathologic lesions were bilateral in dogs with unilateral UME.Conclusions—UME may be more common than previously thought. Most cases were unilateral and diet restriction had no effect on frequency. The CrCd view was critical for diagnosis. Elbow OA was not directly associated with UME.Clinical Relevance—Infrequent diagnosis of UME could result from infrequent radiography and use of only the flexed lateral radiographic projection required by the Orthopedic Foundation for Animals for elbow screening. Like hip evaluations, screening for UME should be continued for life, until genetics are better understood. Lack of association between UME and elbow OA suggests that UME is not likely a component of elbow dysplasia.
Treatment of Incomplete Ossification of the Humeral Condyle with Autogenous Bone Grafting Techniques
Authors: FITZPATRICK NOEL , SMITH THOMAS J. , O'RIORDAN JERRY , YEADON RUSSELL 
Published: February 2009

Objective—To report clinical experience with autogenous bone grafting, with and without metallic implants, for treatment of lameness attributed to incomplete ossification of the humeral condyle (IOHC).Study Design—Case series.Animals—Dogs (n=8; 9 elbows) with IOHC.Methods—A transcondylar humeral bone core was removed and the resultant socket grafted using autogenous bone harvested as either free cancellous bone or a corticocancellous dowel using an osteochondral autograph transfer system. In 8 elbows, additional support for the humeral condyle was provided with metallic implants. Postoperative outcome was assessed by clinical, radiographic, computed tomographic (CT) and owner questionnaire examinations in the short and medium term.Results—Eight dogs (9 elbows) were treated surgically for IOHC. Graft types were free cancellous graft (n=2) or corticocancellous dowel (7). Condylar augmentation was performed using epicondylar cross pins (1); transcondylar Acutrak™(AT) screw and epicondylar cortical screw (1); and a single transcondylar AT screw (7). Lameness resolved in 1–12 weeks. Bone bridging was documented in 7 of 8 elbows assessed by CT examination. Owner questionnaires (6 dogs) assessing daily functions were available for 7 of 9 elbows (follow‐up, 6–45 months). Relevant follow‐up function scores were significantly improved compared with preoperative values. One dog was intermittently lame and was administered nonsteroidal antiinflammatory medication.Conclusion—Use of autogenous bone grafting techniques leads to resolution of lameness attributed to IOHC. Augmentation of grafts with implants like the AT screw is recommended.Clinical Relevance—Autogenous bone grafting techniques represent a viable alternative or adjunct to existing techniques for clinical management of IOHC in the dog.