bluuebunny/crossref_metadata_2025_split huggingface dataset:
Somitic origin of the medial border of the mammalian scapula and its homology to the avian scapula blade
Authors: Valasek Petr , Theis Susanne , Krejci Eliska , Grim Milos , Maina Flavio , Shwartz Yulia , Otto Anthony , Huang Ruijin , Patel Ketan 
Published: January 2010

AbstractThe scapula is the main skeletal element of the pectoral girdle allowing muscular fixation of the forelimb to the axial skeleton. The vertebrate limb skeleton has traditionally been considered to develop from the lateral plate mesoderm, whereas the musculature originates from the axial somites. However, in birds, the scapular blade has been shown to develop from the somites. We investigated whether a somitic contribution was also present in the mammalian scapula. Using genetic lineage‐tracing techniques, we show that the medial border of the mammalian scapula develops from somitic cells. The medial scapula border serves as the attachment site of girdle muscles (serratus anterior, rhomboidei and levator scapulae). We show that the development of these muscles is independent of the mechanism that controls the formation of all other limb muscles. We suggest that these muscles be specifically referred to as medial girdle muscles. Our results establish the avian scapular blade and medial border of the mammalian scapula as homologous structures as they share the same developmental origin.
Investigation of childhood central nervous system vasculitis: magnetic resonance angiography versus catheter cerebral angiography
Authors: ELEFTHERIOU DESPINA , COX TIM , SAUNDERS DAWN , KLEIN NIGEL J , BROGAN PAUL A , GANESAN VIJEYA 
Published: January 2010

Aim  We compared the clinical utility of magnetic resonance angiography (MRA) to catheter cerebral angiography (CA) in the investigation of children with suspected central nervous system (CNS) vasculitis.Method  Single‐centre retrospective review of children with a suspected diagnosis of CNS vasculitis studied with both MRA and CA. MRA and CA‐detected abnormalities (location, multiplicity, and morphology) were compared; sensitivity and specificity were calculated on a per lesion and per patient basis for MRA, with CA as the reference standard.Results  Findings in fourteen patients (median age at presentation of 5y 10mo [range 1y 5mo–14y 5mo]; eight males, six females) relating to sixteen paired studies of MRA and CA were reviewed. CA‐detected lesions were commonly bilateral (13/16 studies, p<0.05), and likely to be proximally distributed (15/16 studies, p<0.05).The sensitivity and specificity of MRA for CA lesion detection was 63% (95% confidence interval [CI] 48–78) and 89% (95% CI 81–93), respectively with moderate agreement between the two modalities (κ=0.51, 95% CI 0.37–0.66). The majority of the false negative observations involved the posterior circulation (9/14). The overall sensitivity for MRA diagnosis of vasculitis per patient was 94% (95% CI 67–99).Interpretation  MRA failed to identify all lesions detected on CA, particularly those in the posterior circulation. MRA is a reasonable initial modality in the investigation of suspected CNS vasculitis but in cases of abnormal parenchymal MRI and normal MRA, CA should be considered.
Mechanical properties of the plantarflexor musculotendinous unit during passive dorsiflexion in children with cerebral palsy compared with typically developing children
Authors: ALHUSAINI ADEL AA , CROSBIE JACK , SHEPHERD ROBERTA B , DEAN CATHERINE M , SCHEINBERG ADAM 
Published: January 2010

Aim  To examine the passive length–tension relations in the myotendinous components of the plantarflexor muscles of children with and without cerebral palsy (CP) under conditions excluding reflex muscle contraction.Method  A cross‐sectional, non‐interventional study was conducted in a hospital outpatient clinic. Passive torque–angle characteristics of the ankle were quantified from full plantarflexion to full available dorsiflexion in 26 independently ambulant children with CP (11 females, 15 males; mean age: 6y 11mo, range 4y 7mo–9y 7mo) and 26 age‐matched typically developing children (18 females, 8 males; mean age 7y 2mo, range 4y 1mo–10y 4mo). In the children with CP, the affected (hemiplegia; n=21) or more affected (diplegia; n=5) leg was tested; in typically developing children, the leg tested was randomly selected. Gross Motor Function Classification System levels were I (n=15) and II (n=11). Care was taken to eliminate active or reflex muscle contribution to the movement, confirmed by the absence of electromyographic activity.Results  There were small but significant differences between the two groups for maximum ankle dorsiflexion (p=0.003), but large and significant differences in the torques required to produce the same displacement (p<0.001). Further, the hysteresis of the average loading cycle in the children with CP was over three times that of the typically developing children (p<0.001).Interpretation  We believe that the plantarflexor muscles of children with CP are stiffer and intrinsically more resistant to stretch, even though they retain near normal excursion. This increased stiffness is a non‐neurally‐mediated feature demonstrated by these children. The extent to which it influences function and predisposes the children to development of soft tissue contracture is unknown.
Characterization of spasticity in cerebral palsy: dependence of catch angle on velocity
Authors: WU YI‐NING , REN YUPENG , GOLDSMITH ASHLEE , GAEBLER DEBORAH , LIU SHU Q , ZHANG LI‐QUN 
Published: January 2010

Aim  To evaluate spasticity under controlled velocities and torques in children with cerebral palsy (CP) using a manual spasticity evaluator.Method  The study involved 10 children with spastic CP (six males, four females; mean age 10y 1mo, SD 2y 9mo, range 7–16y; one with quadriplegia, six with right hemiplegia, three with left hemiplegia; Gross Motor Function Classification System levels I [n=2], II [n=3], III [n=2], IV [n=2], and V [n=1]; Manual Ability Classification System levels II [n=5], III [n=4], and V [n=1]) and 10 typically developing participants (four males, six females; mean age 10y 3mo, SD 2y 7mo, range 7–15y). Spasticity and catch angle were evaluated using joint position, resistance torque, and torque rate at velocities of 90°, 180°, and 270° per second, controlled using real‐time audio‐visual feedback. Biomechanically, elbow range of motion (ROM), stiffness, and energy loss were determined during slow movement (30°/s) and under controlled terminal torque.Results  Compared with typically developing children, children with CP showed higher reflex‐mediated torque (p<0.001) and the torque increased more rapidly with increasing velocity (p<0.001). Catch angle was dependent on velocity and occurred later with increasing velocity (p=0.005). Children with CP showed smaller ROM (p<0.05), greater stiffness (p<0.001), and more energy loss (p=0.003).Interpretation  Spasticity with velocity dependence may also be position‐dependent. The delayed catch angle at higher velocities indicates that the greater resistance felt by the examiner at higher velocities was also due to position change, because the joint was moved further to a stiffer position at higher velocities.
Noradrenaline activation of neurotrophic pathways protects against neuronal amyloid toxicity
Authors: Counts Scott E. , Mufson Elliott J. 
Published: January 2010

J. Neurochem. (2010) 113, 649–660.AbstractDegeneration of locus coeruleus (LC) noradrenergic forebrain projection neurons is an early feature of Alzheimer’s disease. The physiological consequences of this phenomenon are unclear, but observations correlating LC neuron loss with increased Alzheimer’s disease pathology in LC projection sites suggest that noradrenaline (NA) is neuroprotective. To investigate this hypothesis, we determined that NA protected both hNT human neuronal cultures and rat primary hippocampal neurons from amyloid‐β (Aβ1–42 and Aβ25–35) toxicity. The noradrenergic co‐transmitter galanin was also effective at preventing Aβ‐induced cell death. NA inhibited Aβ25–35‐mediated increases in intracellular reactive oxygen species, mitochondrial membrane depolarization, and caspase activation in hNT neurons. NA exerted its neuroprotective effects in these cells by stimulating canonical β1 and β2 adrenergic receptor signaling pathways involving the activation of cAMP response element binding protein and the induction of endogenous nerve growth factor (NGF) and brain‐derived neurotrophic factor (BDNF). Treatment with functional blocking antibodies for either NGF or BDNF blocked NA’s protective actions against Aβ1–42 and Aβ25–35 toxicity in primary hippocampal and hNT neurons, respectively. Taken together, these data suggest that the neuroprotective effects of noradrenergic LC afferents result from stimulating neurotrophic NGF and BDNF autocrine or paracrine loops via β adrenoceptor activation of the cAMP response element binding protein pathway.
TRP channels of intracellular membranes
Authors: Dong Xian‐Ping , Wang Xiang , Xu Haoxing 
Published: January 2010

J. Neurochem. (2010) 113, 313–328.AbstractIon channels are classically understood to regulate the flux of ions across the plasma membrane in response to a variety of environmental and intracellular cues. Ion channels serve a number of functions in intracellular membranes as well. These channels may be temporarily localized to intracellular membranes as a function of their biosynthetic or secretory pathways, i.e., en route to their destination location. Intracellular membrane ion channels may also be located in the endocytic pathways, either being recycled back to the plasma membrane or targeted to the lysosome for degradation. Several channels do participate in intracellular signal transduction; the most well known example is the inositol 1,4,5‐trisphosphate receptor (IP3R) in the endoplasmic reticulum. Some organellar intracellular membrane channels are required for the ionic homeostasis of their residing organelles. Several newly‐discovered intracellular membrane Ca2+ channels actually play active roles in membrane trafficking. Transient receptor potential (TRP) proteins are a superfamily (28 members in mammal) of Ca2+‐permeable channels with diverse tissue distribution, subcellular localization, and physiological functions. Almost all mammalian TRP channels studied thus far, like their ancestor yeast TRP channel (TRPY1) that localizes to the vacuole compartment, are also (in addition to their plasma membrane localization) found to be localized to intracellular membranes. Accumulated evidence suggests that intracellularly‐localized TRP channels actively participate in regulating membrane traffic, signal transduction, and vesicular ion homeostasis. This review aims to provide a summary of these recent works. The discussion will also be extended to the basic membrane and electrical properties of the TRP‐residing compartments.
Disclosure “Bunching”
Authors: DYE RONALD A. 
Published: January 2010

ABSTRACTThis paper studies managers' preferences among information acquisition and disclosure policies when their firms are required to engage in “real‐time” or “continuous” financial reporting. The paper predicts that for many, but not all, processes describing the distribution of their firms' cash flows, when subject to such reporting requirements, managers will engage in disclosure “bunching,” that is, they will bunch the discretionary component of the information they acquire and disclose into a single point in time rather than spread the acquisition and disclosure of that information over time. We show that managers' preferred bunching period depends on managers' strategy for trading in their firms' shares, managers' risk aversion, the risk premium the capital market attaches to firms' shares, and the size of managers' initial ownership stakes in their firms. We also study and characterize how the equilibrium prices of firms' shares vary over time and also how managers' optimal trading strategies vary with their most preferred “bunching” strategies. Several extensions confirm the robustness of the optimality of disclosure “bunching.”
The Relation Between Voluntary Disclosure and Financial Reporting: Evidence from Synthetic Leases
Authors: ZECHMAN SARAH L. C. 
Published: January 2010

ABSTRACTI investigate how the use and voluntary disclosure of synthetic leases is affected by incentives to defer cash outflows and manage the financial statements by keeping debt off the balance sheet. I find that managers of cash‐constrained firms with incentives to defer cash payments are more likely to finance asset purchases with synthetic leases. The mandated reporting for synthetic leases allows managers to avoid disclosing the financial consequences of these transactions. Managers of firms with incentives to use off‐balance‐sheet financing do not provide transparent disclosure about their synthetic leases. However, managers of cash‐constrained firms, which are less likely to use synthetic leases for financial reporting reasons, do voluntarily disclose the existence and financial consequences of these contracts. Alternative tests around FIN 46 adoption corroborate these findings.
Stimulation of angiotensin AT2receptors by the non‐peptide agonist, Compound 21, evokes vasodepressor effects in conscious spontaneously hypertensive rats
Authors: Bosnyak S , Welungoda IK , Hallberg A , Alterman M , Widdop RE , Jones ES 
Published: January 2010

Background and purpose: Angiotensin type 2 receptor (AT2receptor) stimulation evokes vasodilator effectsin vitroandin vivothat oppose the vasoconstrictor effects of angiotensin type 1 receptors (AT1receptors). Recently, a novel non‐peptide AT2receptor agonist, Compound 21, was described, which exhibited high AT2receptor selectivity.Experimental approach: Functional cardiovascular effects of the drug candidate Compound 21 were assessed, using mouse isolated aorta and rat mesenteric arteriesin vitroand in conscious spontaneously hypertensive rats (SHR).Key results: Compound 21 evoked dose‐dependent vasorelaxations in aortic and mesenteric vessels, abolished by the AT2receptor antagonist, PD123319.In vivo, Compound 21 administered alone, at doses ranging from 50 to 1000 ng·kg−1·min−1over 4 h did not decrease blood pressure in conscious normotensive Wistar‐Kyoto rats or SHR. However, when given in combination with the AT1receptor antagonist, candesartan, Compound 21 (300 ng·kg−1·min−1) lowered blood pressure in SHR only. Further analysis in separate groups of conscious SHR revealed that, at a sixfold lower dose, Compound 21 (50 ng·kg−1·min−1) still evoked a significant depressor response in adult SHR (∼30 mmHg) when combined with different doses of candesartan (0.01 or 0.1 mg·kg−1). Moreover, the Compound 21‐evoked depressor effect was abolished when co‐infused (50 µg·kg−1·min−1for 2 h) with the AT2receptor antagonist PD123319.Conclusion and implications: Collectively, our results indicate that acute administration of Compound 21 evoked blood pressure reductions via AT2receptor stimulation. Thus Compound 21 can be considered an excellent drug candidate for further study of AT2receptor function in cardiovascular disease.
Oxaliplatin responses in colorectal cancer cells are modulated by CHK2 kinase inhibitors
Authors: Pires IM , Ward TH , Dive C 
Published: January 2010

Background and purpose:  Checkpoint kinase 2 (CHK2) is activated by DNA damage and can contribute to p53 stabilization, modulating growth arrest and/or apoptosis. We investigated the contribution of CHK2 to oxaliplatin‐mediated toxicity in a colorectal cancer model.Experimental approach:  We evaluated the ability of CHK2 small molecule inhibitors to potentiate oxaliplatin‐induced toxicity. The role of CHK2 in oxaliplatin‐induced apoptosis was investigated in HCT116 cells that were wild‐type (WT) or KO for CHK2. Small molecule inhibitors of CHK2 were used in combination studies with oxaliplatin in this cell model.Key results:  In oxaliplatin‐treated CHK2 KO cells, accelerated apoptosis was accompanied by attenuated p53 stabilization and p21WAF‐1 up‐regulation correlating with increased Bax expression, cytochrome c release and elevated caspase activity. The higher levels of apoptosis in CHK2 KO cells were restored to control (WT) levels when CHK2 was re‐introduced. This ‘uncoupling’ of p53 stabilization and Bax up‐regulation in CHK2 KO cells suggested oxaliplatin‐induced apoptosis was due to a p53‐independent response. Combination studies revealed that CHK2 inhibitor II or debromohymenialdisine antagonized the responses to oxaliplatin. This inhibitory effect correlated with decreases in apoptosis, p53 stabilization and DNA inter‐strand cross‐link formation, and was dependent on the presence (but not activity) of CHK2.Conclusions and implications:  Combinations of CHK2 inhibitors with oxaliplatin should further sensitize cells to oxaliplatin treatment. However, these inhibitors produced an antagonistic effect on the response to oxaliplatin, which was reversed on the re‐introduction of CHK2. These observations may have implications for the use of oxaliplatin in colorectal cancer therapy in combination with therapies targeting CHK2.
Cilostazol is anti‐inflammatory in BV2 microglial cells by inactivating nuclear factor‐kappaB and inhibiting mitogen‐activated protein kinases
Authors: Jung Won‐Kyo , Lee Da‐Young , Park Cheol , Choi Yung Hyun , Choi Inhak , Park Sae‐Gwang , Seo Su‐Kil , Lee Soo‐Woong , Yea Sung Su , Ahn Soon‐Cheol , Lee Chang‐Min , Park Won Sun , Ko Jae‐Hong , Choi Il‐Whan 
Published: January 2010

Background and purpose:  Cilostazol is a specific inhibitor of 3′‐5′‐cyclic adenosine monophosphate (cAMP) phosphodiesterase, which is widely used to treat ischemic symptoms of peripheral vascular disease. Although cilostazol has been shown to exhibit vasodilator properties as well as antiplatelet and anti‐inflammatory effects, its cellular mechanism in microglia is unknown. In the present study, we assessed the anti‐inflammatory effect of cilostazol on the production of pro‐inflammatory mediators in lipopolysaccharide (LPS)‐stimulated murine BV2 microglia.Experimental approach:  We examined the effects of cilostazol on LPS‐induced nuclear factor‐kappaB (NF‐κB) activation and phosphorylation of mitogen‐activated protein kinases (MAPKs).Key results:  Cilostazol suppressed production of nitric oxide (NO), prostaglandin E2 (PGE2) and the proinflammatory cytokines, interleukin‐1 (IL‐1), tumour necrosis factor‐α, and monocyte chemoattractant protein‐1 (MCP‐1), in a concentration‐dependent manner. Inhibitory effects of cilostazol were not affected by treatment with an adenylate cyclase inhibitor, SQ 22536, indicating that these actions of cilostazol were cAMP‐independent. Cilostazol significantly inhibited the DNA binding and transcriptional activity of NF‐κB. Moreover, cilostazol blocked signalling upstream of NF‐κB activation by inhibiting extracellular signal‐regulated kinases 1 and 2 (ERK1/2) and c‐Jun N‐terminal kinase (JNK), but without affecting the activity of p38 MAPK.Conclusion and implications:  Our results demonstrate that suppression of the NF‐κB, ERK, JNK signalling pathways may inhibit LPS‐induced NO and PGE2 production. Therefore, cilostazol may have therapeutic potential for neurodegenerative diseases by inhibiting pro‐inflammatory mediators and cytokine production in activated microglia.
Upper Cervical Facet Joint and Spinal Rami Blocks for the Treatment of Cervicogenic Headache
Authors: Zhou Linqiu , Hud‐Shakoor Zarinah , Hennessey Christopher , Ashkenazi Avi 
Published: January 2010

(Headache 2010;50:657‐663)Objective.— To evaluate the efficacy of upper cervical facet joint injections and spinal rami blocks in the treatment of cervicogenic headache.Background.— Cervicogenic headache has been recognized as a common and often disabling disorder. The treatment of this headache type remains challenging.Methods.— We conducted a retrospective chart review of 31 patients with refractory cervicogenic headache who underwent fluoroscopically guided C1/2, C2/3 facet joint injections and C2, C3 spinal rami blocks using a mixture of 0.25% bupivacaine and 3 mg betamehtasone. The outcome measures were the change in headache severity, assessed using an 11‐point numerical pain scale, after treatment, and the duration of head pain relief.Results.— Twenty‐eight (90.3%) patients experienced >50% headache relief after treatment, with an average duration of 21.7 (1‐90) days. Mean (±SD) head pain intensity decreased from 7.5 ± 1.3 before treatment to 2.7 ± 1.9 immediately after it (P < .0001). The procedures were well tolerated.Conclusions.— C1/2, C2/3 facet joint injections and C2, C3 spinal rami blocks were effective and well tolerated for the treatment of cervicogenic headache in this study. The procedures provided significant and prolonged pain relief in the majority of patients. Larger controlled studies are needed to further evaluate the efficacy of this treatment modality in cervicogenic headache.
Prenatal Alcohol Exposure Alters Biobehavioral Reactivity to Pain in Newborns
Authors: Oberlander Tim F. , Jacobson Sandra W. , Weinberg Joanne , Grunau Ruth E. , Molteno Christopher D. , Jacobson Joseph L. 
Published: January 2010

Objectives:  To examine biobehavioral responses to an acute pain event in a Cape Town, South Africa, cohort consisting of 28 Cape Colored (mixed ancestry) newborns (n = 14) heavily exposed to alcohol during pregnancy (exposed), and born to abstainers (n = 14) or light (≤0.5 oz absolute alcohol/d) drinkers (controls).Methods:  Mothers were recruited during the third trimester of pregnancy. Newborn data were collected on postpartum day 3 in the maternity obstetrical unit where the infant had been delivered. Heavy prenatal alcohol exposure was defined as maternal consumption of at least 14 drinks/wk or at least 1 incident of binge drinking/mo. Acute stress‐related biobehavioral markers [salivary cortisol, heart rate (HR), respiratory sinus arrhythmia (RSA), spectral measures of heart rate variability (HRV), and videotaped facial actions] were collected thrice during a heel lance blood collection (baseline, lance, and recovery). After a feeding and nap, newborns were administered an abbreviated Brazelton Neonatal Behavioral Assessment Scale.Results:  There were no between‐group differences in maternal age, marital status, parity, gravidity, depression, anxiety, pregnancy smoking, maternal education, or infant gestational age at birth (all ps > 0.15). In both groups, HR increased with the heel lance and decreased during the postlance period. The alcohol‐exposed group had lower mean HR than controls throughout, and showed no change in RSA over time. Cortisol levels showed no change over time in controls but decreased over time in exposed infants. Although facial action analyses revealed no group differences in response to the heel lance, behavioral responses assessed on the Brazelton Neonatal Scale showed less arousal in the exposed group.Conclusions:  Both cardiac autonomic and hypothalamic–pituitary–adrenal stress reactivity measures suggest a blunted response to an acute noxious event in alcohol‐exposed newborns. This is supported by results on the Brazelton Neonatal Scale indicating reduced behavioral arousal in the exposed group. To our knowledge, these data provide the first biobehavioral examination of early pain reactivity in alcohol‐exposed newborns and have important implications for understanding neuro‐/biobehavioral effects of prenatal alcohol exposure in the newborn period.