bluuebunny/crossref_metadata_2025_split huggingface dataset:
Mitochondrial DNA copy number and function decrease with age in the short‐lived fish Nothobranchius furzeri
Authors: Hartmann Nils , Reichwald Kathrin , Wittig Ilka , Dröse Stefan , Schmeisser Sebastian , Lück Claudia , Hahn Christin , Graf Michael , Gausmann Ulrike , Terzibasi Eva , Cellerino Alessandro , Ristow Michael , Brandt Ulrich , Platzer Matthias , Englert Christoph 
Published: May 2011

SummaryAmong vertebrates that can be kept in captivity, the annual fish Nothobranchius furzeri possesses the shortest known lifespan. It also shows typical signs of aging and is therefore an ideal model to assess the role of different physiological and environmental parameters on aging and lifespan determination. Here, we used Nothobranchius furzeri to study whether aging is associated with mitochondrial DNA (mtDNA) alterations and changes in mitochondrial function. We sequenced the complete mitochondrial genome of N. furzeri and found an extended control region. Large‐scale mtDNA deletions have been frequently described to accumulate in other organisms with age, but there was no evidence for the presence of detectable age‐related mtDNA deletions in N. furzeri. However, mtDNA copy number significantly decreased with age in skeletal muscle, brain, liver, skin and dorsal fin. Consistent with this finding, expression of Pgc‐1α that encodes a transcriptional coactivator of mitochondrial biogenesis and expression of Tfam and mtSsbp both encoding mtDNA binding factors was downregulated with age. The investigation of possible changes in mitochondrial function revealed that the content of respiratory chain complexes III and IV was reduced in skeletal muscle with age. In addition, ADP‐stimulated and succinate‐dependent respiration was decreased in mitochondria of old fish. These findings suggest that despite the short lifespan, aging in N. furzeri is associated with a decline in mtDNA copy number, the downregulation of mtDNA‐associated genes and an impairment of mitochondrial function.
Insulin‐activated Akt rescues Aβ oxidative stress‐induced cell death by orchestrating molecular trafficking
Authors: Picone Pasquale , Giacomazza Daniela , Vetri Valeria , Carrotta Rita , Militello Valeria , Biagio Pier L. San , Di Carlo Marta 
Published: May 2011

SummaryIncreasing evidence indicates that Alzheimer’s disease, one of the most diffused aging pathologies, and diabetes may be related. Here, we demonstrate that insulin signalling protects LAN5 cells by amyloid‐β42 (Aβ)‐induced toxicity. Aβ affects both activation of insulin receptors and the levels of phospho‐Akt, a critical signalling molecule in this pathway. In contrast, oxidative stress induced by Aβ can be antagonized by active Akt that, in turn, inhibits Foxo3a, a pro‐apoptotic transcription factor activated by reactive oxygen species generation. Insulin cascade protects against mitochondrial damage caused by Aβ treatment, restoring the mitochondrial membrane potential. Moreover, we show that the recovery of the organelle integrity recruits active Akt translocation to the mitochondrion. Here, it plays a role both by maintaining unimpaired the permeability transition pore through increase in HK‐II levels and by blocking apoptosis through phosphorylation of Bad, coming from cytoplasm after Aβ stimulus. Together, these results indicate that the Akt survival signal antagonizes the Aβ cell death process by balancing the presence and modifications of common molecules in specific cellular environments.
Implementation quality of whole‐school mental health promotion and students’ academic performance
Authors: Dix Katherine L. , Slee Phillip T. , Lawson Michael J. , Keeves John P. 
Published: May 2011

Background:  This paper argues for giving explicit attention to the quality of implementation of school‐wide mental health promotions and examines the impact of implementation quality on academic performance in a major Australian mental health initiative.Method:  Hierarchical linear modelling was used to investigate change in standardised academic performance across the 2‐year implementation of a mental health initiative in 96 Australian primary (or elementary) schools that was focused on improving student social‐emotional competencies.Results:  After controlling for differences in socioeconomic background, a significant positive relationship existed between quality of implementation and academic performance. The difference between students in high‐ and low‐implementing schools was equivalent to a difference in academic performance of up to 6 months of schooling.
Opioids and the immune system: what is their mechanism of action?
Authors: Eisenstein Toby K 
Published: May 2011

There is a significant amount of literature showing that morphine and other opioids modulate immune responses. The findings support many mechanisms by which this may occur. In vitro experiments provide evidence for direct actions of opioids on immune cells using a variety of functional end points. When these drugs are given in vivo, a plethora of immune parameters are also altered. The paper in this issue of the journal by Zhang et al. provides new information on morphine alteration of immune cell subsets in the spleen and thymus of mice and the potential role of glucocorticoids in these observed phenomena. This Commentary reviews the in vitro activities of morphine on leucocytes, as well as other documented mechanisms by which morphine can alter immune function in vivo.LINKED ARTICLE This article is a commentary on Zhang et al., pp. 1829–1844 of this issue. To view this paper visit http://dx.doi.org/10.1111/j.1476‐5381.2011.01475.x
Antiparkinsonian potential of targeting group III metabotropic glutamate receptor subtypes in the rodent substantia nigra pars reticulata
Authors: Broadstock M , Austin PJ , Betts MJ , Duty S 
Published: May 2011

BACKGROUND AND PURPOSEIncreased firing of the glutamatergic pathway between the subthalamic nucleus and substantia nigra pars reticulata (SNpr) contributes to the abnormal firing of motor circuits and subsequent motor deficits seen in Parkinson's disease. Broad spectrum agonist‐induced activation of presynaptic group III metabotropic glutamate (mGlu) receptors within the SNpr reduced glutamate release and reversed akinesia in the reserpine‐treated rat model of Parkinson's disease. Here, we have sought to identify which subtypes of group III mGlu receptor in the SNpr were responsible for these beneficial effects.EXPERIMENTAL APPROACHThe ability of the mGlu4 positive allosteric modulator, N‐phenyl‐7‐(hydroxyminocyclopropa[b]chromen‐1a‐carboxamide) (PHCCC), the mGlu7 allosteric agonist, N,N′‐dibenzhydrylethane‐1,2‐diamine dihydrochloride (AMN082) and the mGlu8‐selective agonist (S)‐3,4‐dicarboxyphenylglycine [(S)‐3,4‐DCPG] to inhibit KCl‐evoked [3H]‐D‐aspartate release was examined in vitro in rat nigral prisms. Reversal of akinesia in reserpine‐treated rats was also assessed following intranigral injection of these agents.KEY RESULTSPHCCC and AMN082 inhibited [3H]‐D‐aspartate release by 42% and 53%, respectively when given alongside a sub‐threshold concentration of the broad spectrum group III agonist, L‐2‐amino‐4‐phosphonobutyrate (L‐AP4; 1 µM). In contrast (S)‐3,4‐DCPG failed to inhibit [3H]‐D‐aspartate release. All three agents also reversed reserpine‐induced akinesia although only the effects of PHCCC and AMN082 were inhibited by pre‐treatment with the group III antagonist (RS)‐α‐cyclopropyl‐4‐phosphonophenylglycine (CPPG).CONCLUSIONS AND IMPLICATIONSThese findings reveal that targeting SNpr mGlu4 or mGlu7 receptors, but not mGlu8 receptors, provided relief from akinesia in the reserpine‐treated rat model of Parkinson's disease, most likely reflecting inhibition of excess glutamate release in this region.
Experimental High‐Volume Hemofiltration With Predilutional Tris‐Hydroxymethylaminomethane for Correction of Low Tidal Volume Ventilation‐Induced Acidosis
Authors: Russ Martin , Deja Maria , Ott Sascha , Bedarf Janis , Keckel Tobias , Hiebl Bernhard , Wagner Johanna J. , Unger Juliane K. 
Published: May 2011

AbstractThe most common method of controlling acidemia during lung‐protective ventilation is CO2 removal with an extracorporeal lung assist (ECLA) system. Another possibility to prevent acidemia is based on intravenous (i.v.) application of tris‐hydroxymethyl‐aminomethane (3 mol/L, THAM) buffer, which can bind hydrogen protons and which can be removed from the body via renal replacement therapy (RRT). We investigated whether RRT combined with predilutional (prefilter) THAM‐application provides an alternative to ECLA for a rescue situation. For this, anesthetized pigs, 40 kg of body weight, six animals per group, underwent 5 h of acidemia (pH 7.19–7.24) induced by acid infusion and permissive hypercapnia (low tidal volume ventilation, PaCO2 80–90 mm Hg). Isovolemic, high‐volume hemofiltration (HVHF) was operated with predilutional THAM‐infusion for treatment. To evaluate adverse effects of this approach, we set up further groups: HVHF with postdilutional (post‐filter) THAM‐application; i.v.‐THAM without HVHF; normal pH homeostasis with HVHF. Acid‐base parameters, hemodynamics, renal function, and lung morphology were investigated. HVHF with predilutional THAM‐infusion of 8 mmol/kg/h allowed fast pH normalization, significant reduction in PaCO2 to 56 mm Hg and tolerable hemodynamics. HVHF alone or lower dose i.v. THAM (2 mmol/kg/h) failed to produce a comparable result. A postdilutional THAM infusion reduced hemodynamic tolerability and increased lung edema formation. HVHF in pigs with normal acid‐base status resulted in a decreased base excess and urine acidification. In conclusion, predilutional THAM‐application and HVHF corrected the acid‐base disorder and improved pulmonary hemodynamics. Further studies are necessary to optimize the protocol including the dosage.
Ictal head turning in frontal and temporal lobe epilepsy
Authors: Rémi Jan , Wagner Philipp , O’Dwyer Rebecca , Silva Cunha João P. , Vollmar Christian , Krotofil Isabella , Noachtar Soheyl 
Published: May 2011

SummaryPurpose: To quantitatively evaluate the difference of ictal head turning movements between patients with temporal lobe epilepsy (TLE) and frontal lobe epilepsy (FLE).Methods: We investigated 38 seizures of 31 patients with unilateral TLE and 22 seizures of 14 patients with unilateral FLE where head turning occurred in the seizure evolution. The head movements were defined as ipsilateral or contralateral in reference to the lateralization of the patient’s focal epilepsy syndrome. Head movements were quantified by either referencing the head position with manually placed markers or by automatic detection of infrared marked reference points. The time of onset, duration, and angular speed of the head movements were computed, and interindividual and intraindividual analyses were performed.Key Findings: All of the TLE seizures had both contralateral and ipsilateral head turning, whereas all FLE had contralateral head turning; only 6 of 22 seizures were associated with ipsilateral head turning. Ipsilateral head turning always preceded contralateral head turning in both TLE and FLE. The head turning occurred significantly sooner after clinical seizure onset in FLE than in TLE patients (ipsilateral 0.5 vs. 16.0 s, contralateral: 4.5 vs. 21.3 s; p < 0.001). Furthermore, the duration of head turning was shorter in FLE for contralateral head turning (4.1 s) than in TLE (contralateral 6.0 s, p < 0.01); the ipsilateral head turning in the two groups did not differ (3.0 vs. 2.9 s) in duration. The angular speed of head turning did not differ for ipsilateral and for contralateral head turning in FLE and TLE.Significance: Quantitative analysis of head turning demonstrates significant differences between patients with FLE and TLE. These differences likely represent differences in spread of epileptic activity. This information may be useful in the seizure evaluation of patients considered for resective epilepsy surgery.
Aphasic status epilepticus: Electroclinical correlation
Authors: Ericson Eric J. , Gerard Elizabeth E. , Macken Michael P. , Schuele Stephan U. 
Published: May 2011

SummaryPurpose:  Aphasic status epilepticus (ASE) in otherwise awake patients is a rare phenomenon. We present a series of nine consecutive patients with ASE to characterize clinical, electrophysiologic, and imaging findings.Methods:  Nine patients in ASE were identified between July 2006 and December 2009 at our institution. Each was evaluated by the neurology service and monitored with video‐electroencephalography (EEG) for at least 24 h. Thorough, repeated language testing was correlated with EEG findings.Key Findings:  All nine patients were right‐handed with subacute or chronic left hemispheric lesions on magnetic resonance imaging (MRI). All patients had mixed aphasia, three presenting with persistent aphasia from onset and six with episodic speech impairment, which became persistent in five of the six. The initial 30‐min EEG demonstrated electrographic seizure in only five patients (56%), despite the presence of aphasia during the recording. Left hemispheric periodic lateralized epileptiform discharges (PLEDS) were seen in two patients, and left hemispheric slowing in two patients. Continuous video‐EEG monitoring confirmed electrographic seizure activity in all nine patients. Peak electrographic seizure frequency varied from continuous to once every 2 h and was not associated with fluctuations in the speech deficit. EEG seizures resolved abruptly in three patients and gradually over up to 4 days in six patients. Clinical improvement was delayed in eight of the nine patients, and four patients retained some aphasia at discharge, 2–4 days after EEG seizure resolution.Significance:  Standard EEG is sensitive for detection of abnormalities in the dominant hemisphere in patients with ASE. However, continuous EEG is necessary to confirm the diagnosis and monitor treatment, since clinical symptoms do not correlate with electrographic seizure activity and do not provide sufficient information to guide treatment decisions.
Understanding the differences in prevalence of epilepsy in tropical regions
Authors: Yemadje Luce‐Perrine , Houinato Dismand , Quet Fabrice , Druet‐Cabanac Michel , Preux Pierre‐Marie 
Published: May 2011

SummaryEpilepsy is a frequent chronic neurologic disorder that affects nearly 70 million people worldwide. The majority of people with epilepsy live in developing countries, where epilepsy remains a major public health problem. Wide prevalence differences exist among various populations across sub‐Saharan Africa, Latin America, and Asia. In particular, prevalence is lower in Southeast Asia than in sub‐Saharan Africa and Latin America. Methodologic problems alone do not seem to explain these differences shown in recent review papers. The distribution of numerous risk or etiologic factors such as infectious diseases with neurologic sequel, head injuries, or genetic factors could explain these differences. Stigmatization of people with epilepsy could lead to underestimating the prevalence of epilepsy, even in well‐conducted studies. It is important to standardize the process of epidemiologic monitoring of epilepsy in order to improve the reliability in data comparison. Understanding the reasons for these differences is a crucial issue for eventually raising new hypotheses or prevention strategies.
Noninvasive Risk Stratification Techniques in Pediatric Patients with Ventricular Preexcitation
Authors: CZOSEK RICHARD J. , ANDERSON JEFFREY B. , MARINO BRADLEY S. , MELLION KATELYN , KNILANS TIMOTHY K. 
Published: May 2011

Background: Individuals with ventricular preexcitation (VP) are known to have an increased risk of sudden death. This risk has been associated with conduction properties of the accessory pathway.Methods: Patients with VP underwent risk stratification through the use of exercise and transesophageal testing. All patients were initially screened with exercise testing and those with preexcitation throughout exercise went on to have transesophageal testing. Patients who demonstrated high‐risk pathway characteristics by transesophageal testing or developed clinical indications for an electrophysiology (EP) study underwent ablation. This stepwise risk stratification technique was evaluated for the ability to avoid the need for intracardiac EP study. Patients stratified as low risk were contacted for follow‐up.Results: One hundred and twenty‐nine exercise studies were performed in 127 patients. Thirty‐five of 129 exercise studies demonstrated accessory pathway block during exercise. Twenty‐seven of 35 underwent no additional testing. Sixty‐six patients underwent transesophageal testing. Forty‐nine of 66 patients demonstrated low‐risk pathway characteristics and 40 of 49 underwent no further testing. In total, 68 of 129 (53%) patients avoided the need for intracardiac EP study and ablation. A noncardiac indication for the initial diagnostic electrocardiogram was associated with lower likelihood of intracardiac EP study. None of the patients stratified as low risk had additional invasive procedures or life‐threatening arrhythmias upon follow‐up.Conclusions: Successful risk stratification of pediatric patients with VP is possible through the use of exercise and transesophageal testing. In this patient population, half of the patients were able to avoid an intracardiac EP study. (PACE 2011; 34:555–562)
Cardiac Resynchronization Therapy and Obstructive Sleep‐Related Breathing Disorder in Patients with Congestive Heart Failure
Authors: SHALABY ALAA , ATWOOD CHARLES W. , SELZER FAITH , SUFFOLETTO MATTHEW , GORCSAN III JOHN , STROLLO PATRICK 
Published: May 2011

Objectives:
To assess the impact of cardiac resynchronization therapy (CRT) with or without atrial overdrive pacing, on sleep‐related breathing disorder (SRBD).
Introduction:
CRT may have a positive influence on SRBD in patients who qualify for the therapy. Data are inconclusive in patients with obstructive SRBD.
Methods:
Consenting patients eligible for CRT underwent a baseline polysomnography (PSG) 2 weeks after implantation during which pacing was withheld. Patients with an apnea hypopnea index (AHI) ≥15 but <50 were enrolled and randomized to atrial overdrive pacing (DDD) versus atrial synchronous pacing (VDD) with biventricular pacing in both arms. Patients underwent two further PSGs 12 weeks apart.
Results:
Nineteen men with New York Heart Association class III congestive heart failure participated in the study (age 67.2 ± 7.5, Caucasian 78.9%, ischemic 73.7%). The score on Epworth Sleepiness Score was 7.3 ± 4.0, Pittsburgh Sleep Quality Index 7.4 ± 3.1, and Minnesota Living with Heart Failure Questionnaire 36.9 ± 21.9. There were no differences between the groups. At baseline, patients exhibited poor sleep efficiency (65.3 ± 16.6%) with nadir oxygen saturation of 83.5 ± 5.3% and moderate to severe SRBD (AHI 21.5 ± 15.3) that was mainly obstructive (central apnea index 3.3 ± 6.7/hour). On both follow‐up assessments, there was no improvement in indices of SRBD (sleep efficiency [68.3 ± 17.9%], nadir oxygen saturation of 82.8 ± 4.6%, and AHI 24.9 ± 21.9).
Conclusion:
In a cohort of elderly male CHF patients receiving CRT, CRT had no impact on obstructive SRBD burden with or without atrial overdrive pacing. (PACE 2011; 34:593–603)
Angiogenesis in Mesenteric Microvascular Networks from Spontaneously Hypertensive Versus Normotensive Rats
Authors: YANG MING , ARAGON MARIO , MURFEE WALTER L. 
Published: May 2011

Please cite this paper as: Yang, Aragon and Murfee (2011). Angiogenesis in Mesenteric Microvascular Networks from Spontaneously Hypertensive Versus Normotensive Rats. Microcirculation 18(7), 574–582.AbstractObjective:  Elevated blood pressure during hypertension has been associated with microvascular rarefaction, defined as a loss of microvessels. However, whether rarefaction is a result of impaired angiogenesis remains unclear. The objective of this study was to compare angiogenesis across the time course of mesenteric microvascular network remodeling in adult spontaneously hypertensive versus normotensive rats.Methods:  Angiogenic responses in 15‐ to 16‐week‐old SHR and Wistar rats at 0, 3, 5, 10 or 25 days post 20‐minute exteriorization of the mesentery were quantified.Results:  Consistent with the phenomenon of rarefaction, vascularized area in unstimulated SHR was decreased compared to Wistar. By 25 days, SHR vascular area had increased to the Wistar level and vascular length density and capillary sprouting were comparable. At 3 and 5 days, SHR and Wistar tissues displayed an increase in the capillary sprouting and vascular density relative to their unstimulated controls. At 10 days, capillary sprouting in the SHR remained elevated. The percent change in vascular density was elevated in the SHR compared to the Wistar group at 3 and 5 days and by 25 days the rate of change was more negative.Conclusions:  Our results suggest that SHR networks undergo an increased rate of growth followed by an increased rate of pruning.
Low gestational weight gain and the risk of preterm birth and low birthweight: a systematic review and meta‐analyses
Authors: HAN ZHEN , LUTSIV OLHA , MULLA SOHAIL , ROSEN ALLISON , BEYENE JOSEPH , MCDONALD SARAH D. ,   on behalf of the Knowledge Synthesis Group
Published: May 2011

AbstractBackground. Low gestational weight gain is common, with potential adverse perinatal outcomes. Objective. To determine the relation between low gestational weight gain and preterm birth and low birthweight in singletons in developing and developed countries. Data sources. Medline, EMBASE and reference lists were searched, identifying 6 283 titles and abstracts. Methods of study selection. Following the MOOSE consensus statement, two assessors independently reviewed titles, abstracts, full articles, extracted data and assessed quality. Results. Fifty‐five studies, 37 cohort and 18 case‐control, were included, involving 3 467 638 women. In the cohort studies (crude data, generally supported where available by adjusted data and case‐control studies), women with low total gestational weight gain had increases in preterm birth <37 weeks [RR 1.64 (95%CI 1.62–1.65)], 32–36 weeks [RR 1.39 (95%CI 1.38–1.40)] and ≤32 weeks [RR 3.80 (95%CI 3.72–3.88)]. Low total gestational weight gain was associated with increased risks of low birthweight <2 500 g [RR 1.85 (95%CI 1.72–2.00)], in developing and developed countries [RR 1.84 (95%CI 1.71–1.99) and RR 3.02 (95%CI 1.37–6.63), respectively], 1 500–2 500 g [RR 2.02 (95%CI 1.88–2.17)] and <1 500 g (RR 2.00 (95%CI 1.67–2.40)]. Women with low weekly gestational weight gain were at increased risk of preterm birth [RR 1.56 (95%CI 1.26–1.94)], 32–36 weeks [RR 2.43 (95%CI 2.37–2.50)] and ≤32 weeks [RR 2.31 (95%CI 2.20–2.42)] but not low birthweight [RR 1.64 (95%CI 0.89–3.02)]. Conclusions. In this systematic review, we determined that singletons born to women with low total gestational weight gain have higher risks of preterm birth and low birthweight, with the lower the gain, the higher the risks.