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Slowing
Kinds of Slowing Terms modified by Slowing Selected AbstractsContralateral EEG Slowing and Amobarbital Distribution in Wada Test: An Intracarotid SPECT StudyEPILEPSIA, Issue 2 2000Seung Bong Hong Summary: Purpose: To relate the occurrence of contralateral electroencephalogram slowing (CES) to amobarbital distribution, we performed electroencephalogram (EEG) monitoring and intracarotid single photon emission computed tomography (SPECT) during an intracarotid amobarbital procedure (IAP). Methods: IAP was performed on 22 patients with temporal lobe epilepsy. CES was defined as the occurrence of significant EEG slowing on the contralateral hemisphere (>50% of the ipsilateral hemisphere slowing) after amobarbital injection. To map the distribution of the amobarbital, we injected a mixture of amobarbital and 99m technetium-ethylcysteinate dimer (99m Tc-ECD) into the internal carotid artery and performed a brain SPECT 2 h later. In the SPECT images, regions of interest were determined by ipsilateral and contralateral anterior cerebral artery territories (iACA, cACA), ipsilateral and contralateral middle cerebral artery territories (iMCA, cMCA), and ipsilateral and contralateral posterior cerebral artery territories (iPCA, cPCA), as well as ipsilateral and contralateral anterior and posterior mesial temporal regions (iAMT, cAMT, iPMT, cPMT). The perfusion of amobarbital was interpreted visually in each region. Results: Amobarbital was distributed in the iMCA in all the patients; in the iACA in 20 (90.9%) patients; in the iAMT in 14 (63.5%); and in the iPCA and iPMT in only two (9.1%). CES was observed in 13 (59.1%) patients. Cross-perfusion of amobarbital in limited areas of the cACA were observed in only four of 13 patients. Wada retention memory scores (WRMS) showed no significant difference between the CES- (n = 9) and CES+ (n = 13) groups. Conclusions: Amobarbital rarely perfused the iPCA territory and the iPMT region and was rarely delivered to the contralat-eral hemisphere. The occurrence of CES was not related to the cross-perfusion of amobarbital. CES appears to be produced by a transient functional disconnection from the ipsilateral hemisphere. [source] Mechanisms Associated with the Negative Inotropic Effect of Deuterium Oxide in Single Rat Ventricular MyocytesEXPERIMENTAL PHYSIOLOGY, Issue 2 2000K. Hongo Deuterium oxide (D2O) is known to cause a negative inotropic effect in muscle although the mechanisms associated with this response in cardiac muscle are not well understood. We studied the effects of D2O in single rat ventricular myocytes in order to characterise the mechanisms associated with its negative inotropic effect and to assess its possible use as an acute modulator of microtubules. D2O rapidly reduced the magnitude of contraction in rat ventricular myocytes, and there was some recovery of contraction in the presence of D2O. Colchicine, an agent known to depolymerise microtubules, did not modify the effect of D2O. D2O decreased the L-type Ca2+ current (ICa), measured under whole cell and perforated patch clamp conditions. Slowing of the time to peak and a delay in inactivation of ICa were observed. Intracellular calcium ([Ca2+]i) and sodium ([Na+]i) were measured using the fluorescent indicators fura-2 and SBFI, respectively. The fall in contraction upon exposure to D2O was not associated with a fall in the [Ca2+]i transient; this response is indicative of a reduction in myofilament Ca2+ sensitivity. Both the [Ca2+]i transient and [Na+]i increased during the partial recovery of contraction in the presence of D2O. We conclude that a decrease in the myofilament sensitivity for Ca2+ and a reduction in Ca2+ influx via ICa are principally responsible for the negative inotropic effect of D2O in cardiac muscle. We found no evidence to explain the negative inotropic effect of D2O in terms of microtubule proliferation. In addition we suggest that acute application of D2O is not a useful procedure for the investigation of the role of microtubules in excitation-contraction coupling in cardiac muscle. [source] Neuroprotective therapy in Parkinson's disease and motor complications: A search for a pathogenesis-targeted, disease-modifying strategyMOVEMENT DISORDERS, Issue S11 2005C. Warren Olanow MD, FRCPC Abstract The introduction of levodopa in the late 1960s represented a landmark in the therapy of Parkinson's disease (PD). However, motor complications of chronic levodopa therapy have emerged as a major limitation of this otherwise effective therapy. Advancing medical and surgical treatment of these complications has been the main objective of clinical trials during the past few decades. In addition, basic research has focused on better understanding of the mechanisms of motor complications and how to prevent them. Slowing or delaying the progression of the disease delays the need for levodopa therapy; therefore, neuroprotective strategies may play an important role in preventing the onset and reducing the severity of levodopa-related adverse effects. In this introductory review, we present the rationale for current and experimental therapies designed to favorably modify the progression of PD. If implemented early in the course of the disease, such treatments, if found effective, may not only alter the natural progression of the disease but may also delay or minimize motor and nonmotor complications associated with levodopa. © 2005 Movement Disorder Society [source] Rotigaptide (ZP123) Improves Atrial Conduction Slowing in Chronic Volume Overload-Induced Dilated AtriaBASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 1 2006Ketil Haugan Rotigaptide (ZP123) is a selective gap junction modifier that increases cardiac gap junctional intercellular communication. We hypothesised that rotigaptide treatment would increase atrial conduction velocity and reduce the inducibility to atrial tachyarrhythmias in a model of chronic volume overload induced chronic atrial dilatation characterized by atrial conduction velocity slowing. Chronic volume overload was created in Japanese white rabbits by arterio-venous shunt formation. Atrial conduction velocity and atrial tachyarrhythmias inducibility were examined in Langendorff-perfused chronic volume overload hearts (n=12) using high-resolution optical mapping before and after treatment with rotigaptide. Moreover, expression levels of atrial gap junction proteins (connexin40 and connexin43) were examined in chronic volume overload hearts (n=6) and compared to sham-operated controls (n=6). Rotigaptide treatment significantly increased atrial conduction velocity in chronic volume overload hearts, however, rotigaptide did not decrease susceptibility to the induction of atrial tachyarrhythmias. Protein expressions of Cx40 and Cx43 were decreased by 32% and 72% (P<0.01), respectively, in chromic volume overload atria compared to control. To conclude, rotigaptide increased atrial conduction velocity in a rabbit model of chromic volume overload induced atrial conduction velocity slowing. The demonstrated effect of rotigaptide on atrial conduction velocity did not prevent atrial tachyarrhythmias inducibility. Whether rotigaptide may possess antiarrhythmic efficacy in other models of atrial fibrillation remains to be determined. [source] Slowing Down in Chemical Tristability SystemsCHINESE JOURNAL OF CHEMISTRY, Issue 8 2001Ye-Hong Zhan Abstract In this paper two kinds of slowing down in the chemical tristability systems are studied. One is the critical slowing down at the edges of tristable region, and the other is the slowing down far from the critical point, which has much to do with the unstable steady-points. The results possess some universal properties. [source] Modulation of rabbit sinoatrial node activation sequence by acetylcholine and isoproterenol investigated with optical mapping techniqueACTA PHYSIOLOGICA, Issue 4 2009D. V. Abramochkin Abstract Aims:, Changes in the rabbit sinoatrial node (SAN) activation sequence with the cholinergic and adrenergic factors were studied. The correlation between the sinus rhythm rate and the leading pacemaker site shift was determined. The hypothesis concerning the cholinergic suppression of nodal cell excitability as one of the mechanisms associated with pacemaker shift was tested. Methods:, A high-resolution optical mapping technique was used to register beat-to-beat changes in the SAN activation pattern under the influence of the cholinergic and adrenergic factors. Results:, Acetylcholine (10 ,m) and strong intramural parasympathetic nerve stimulation caused a pacemaker shift as well as rhythmic slowing and the formation of an inexcitable region in the central part of SAN. In this region the generation of action potentials was suppressed. The slowing of the sinus rhythm (which exceeded 12.8 ± 3.1% of the rhythm control rate) always accompanied the pacemaker shift. Isoproterenol (10, 100 nm, 1 ,m) and sympathetic postganglionic nerve stimulation also evoked a pacemaker shift but without formation of an inexcitable zone. The acceleration of the sinus rhythm, which exceeded 10.5 ± 1.3% of the control rate of the rhythm, always accompanied the shift. Conclusions:, Both cholinergic and adrenergic factors cause pacemaker shifts in the rabbit SAN. While modest changes in the sinus rhythm do not coincide with the pacemaker shift, greater changes always accompany the shift and may be caused by it, according to one hypothesis. The formation of an inexcitable zone at the place where the leading pacemaker is situated is one of the mechanisms associated with pacemaker shift. [source] Partial reversal of conduction slowing during repetitive stimulation of single sympathetic efferents in human skinACTA PHYSIOLOGICA, Issue 3 2004M. Campero Abstract Aims:, To describe and identify the function of a class of human C fibre with an unusual response to repetitive electrical stimulation. Other C fibres slow progressively at 2 Hz (type 1), reach a latency plateau (type 2) or hardly slow at all (type 3). Methods:, C fibres innervating hairy skin were recorded by microneurography in the superficial peroneal nerves of 19 healthy volunteers. Baseline electrical stimulation of the skin was at 0.25 Hz, and activity-dependent slowing recorded during stimulation at 2 Hz for 3 min and after a 3-min pause in stimulation. Results:, In 41 units, there was a partial recovery of latency during repetitive stimulation. These were classified as ,type-4' units, and identified as sympathetic efferents, since they exhibited spontaneously activity, which was enhanced by manoeuvres that increase sympathetic outflow (15 of 16 cases) and/or suppressed by a proximal anaesthetic block (eight of eight cases). The peak slowing during 2 Hz trains averaged 6.47 ± 2.06% (mean ± SD, n = 41), but after 3 min the slowing had reduced to 4.90 ± 2.20%, which was less than in all type 1 (nociceptor) fibres but similar to that in type 2 (cold) fibres. Compared with cold fibres, type-4 sympathetic fibres slowed more after the first 10 impulses at 2 Hz (2.57 ± 0.45%) and also after a pause in stimulation (1.66 ± 0.51%). Conclusions:, The distinctive activity-dependent slowing profiles of these type-4 sympathetic C units may help identification in vitro, and suggest that hyperpolarization-activated channels have a particularly prominent role in the axonal membrane. [source] Is bipolar II depression phenotypically distinctive?ACTA PSYCHIATRICA SCANDINAVICA, Issue 6 2009G. B. Parker Objective:, We examine the depressive symptom profile of bipolar II disorder patients compared with a comparator (composite) group of those with unipolar depression, with stratification by melancholic and non-melancholic subtypes. Method:, Out-patients (n = 394) attending a specialist depression clinic comprised the sample. Data on severity and prototypic status of depressive symptoms were analysed. Results:, Age-matched analyses revealed minimal differentiation between bipolar II and composite unipolar groups. Stratified analyses suggested that ,bipolar II depression' more closely approximated melancholic depression in terms of psychomotor and cognitive slowing. Severity-based analyses and prototypic symptom patterns yielded differing results, suggesting that definition of bipolar II depression is influenced by rating strategies, and age. Conclusion:, We found limited differentiation of bipolar II depression from unipolar, melancholic and non-melancholic depression. Differences suggested previously may reflect age, gender and severity differences, highlighting the need for appropriately matched groups in defining bipolar II depression. [source] Fixing the Hole in the Bucket: Household Poverty Dynamics in the Peruvian AndesDEVELOPMENT AND CHANGE, Issue 5 2006Anirudh Krishna ABSTRACT Achieving the Millennium Development Goal of halving poverty will require simultaneous action on two separate fronts: helping poor people escape from poverty, and stemming the flow of people into poverty. This article examines forty Peruvian communities, and finds that descents into poverty have occurred alongside escapes in every one of them. Escape and descent are asymmetric in terms of reasons: while one set of reasons is responsible for escapes from poverty, another and different set of reasons is associated with descent. Making progress in poverty reduction will require measures to accelerate escapes whilst at the same time slowing down descents. The article looks at the different policies which will be required to serve these two separate purposes. [source] Neural agrin increases postsynaptic ACh receptor packing by elevating rapsyn protein at the mouse neuromuscular synapseDEVELOPMENTAL NEUROBIOLOGY, Issue 9 2008Jennifer Brockhausen Abstract Fluorescence resonance energy transfer (FRET) experiments at neuromuscular junctions in the mouse tibialis anterior muscle show that postsynaptic acetylcholine receptors (AChRs) become more tightly packed during the first month of postnatal development. Here, we report that the packing of AChRs into postsynaptic aggregates was reduced in 4-week postnatal mice that had reduced amounts of the AChR-associated protein, rapsyn, in the postsynaptic membrane (rapsyn+/, mice). We hypothesize that nerve-derived agrin increases postsynaptic expression and targeting of rapsyn, which then drives the developmental increase in AChR packing. Neural agrin treatment elevated the expression of rapsyn in C2 myotubes by a mechanism that involved slowing of rapsyn protein degradation. Similarly, exposure of synapses in postnatal muscle to exogenous agrin increased rapsyn protein levels and elevated the intensity of anti-rapsyn immunofluorescence, relative to AChR, in the postsynaptic membrane. This increase in the rapsyn-to-AChR immunofluorescence ratio was associated with tighter postsynaptic AChR packing and slowed AChR turnover. Acute blockade of synaptic AChRs with ,-bungarotoxin lowered the rapsyn-to-AChR immunofluorescence ratio, suggesting that AChR signaling also helps regulate the assembly of extra rapsyn in the postsynaptic membrane. The results suggest that at the postnatal neuromuscular synapse agrin signaling elevates the expression and targeting of rapsyn to the postsynaptic membrane, thereby packing more AChRs into stable, functionally-important AChR aggregates. © 2008 Wiley Periodicals, Inc. Develop Neurobiol, 2008 [source] Androgen modulates the kinetics of the delayed rectifying K+ current in the electric organ of a weakly electric fishDEVELOPMENTAL NEUROBIOLOGY, Issue 12 2007M. Lynne McAnelly Abstract Weakly electric fish such as Sternopygus macrurus utilize a unique signal production system, the electric organ (EO), to navigate within their environment and to communicate with conspecifics. The electric organ discharge (EOD) generated by the Sternopygus electric organ is quasi-sinusoidal and sexually dimorphic; sexually mature males produce long duration EOD pulses at low frequencies, whereas mature females produce short duration EOD pulses at high frequencies. EOD frequency is set by a medullary pacemaker nucleus, while EOD pulse duration is determined by the kinetics of Na+ and K+ currents in the electric organ. The inactivation of the Na+ current and the activation of the delayed rectifying K+ current of the electric organ covary with EOD frequency such that the kinetics of both currents are faster in fish with high (female) EOD frequency than those with low (male) EOD frequencies. Dihydrotestosterone (DHT) implants masculinize the EOD centrally by decreasing frequency at the pacemaker nucleus (PMN). DHT also acts at the electric organ, broadening the EO pulse, which is at least partly due to a slowing of the inactivation kinetics of the Na+ current. Here, we show that chronic DHT treatment also slows the activation and deactivation kinetics of the electric organ's delayed rectifying K+ current. Thus, androgens coregulate the time-varying kinetics of two distinct ion currents in the EO to shape a sexually dimorphic communication signal. © 2007 Wiley Periodicals, Inc. Develop Neurobiol, 2007 [source] Maturation of action monitoring from adolescence to adulthood: an ERP studyDEVELOPMENTAL SCIENCE, Issue 6 2005Alexandra M. Hogan This study investigated the development of the frontal lobe action-monitoring system from late childhood and adolescence to early adulthood using ERP markers of error processing. Error negativity (ERN) and correct response negativity (CRN) potentials were recorded while adolescents and adults (aged 12,22 years, n = 23) performed two forced-choice visual reaction time tasks of differing complexity. Significant age differences were seen for behavioural and ERP responses to complex (infrequent, incompatible) trials: adolescents elicited an error negativity of reduced magnitude compared with adults. Furthermore, in contrast to adults, adolescents showed a non-significant differentiation between response-locked ERP components elicited by correct (CRN) and error responses (ERN). Behaviourally, adolescents corrected fewer errors in incompatible trials, and with increasing age there was greater post-error slowing. In conclusion, the neural systems underlying action-monitoring continue to mature throughout the second decade of life, and are associated with increased efficiency for fast error detection and correction during complex tasks. [source] Exenatide effects on glucose metabolism and metabolic disorders common to overweight and obese patients with type 2 diabetesDRUG DEVELOPMENT RESEARCH, Issue 8 2006David M. Webb Abstract The risks of cardiovascular disease (CVD) and type 2 diabetes increase as body mass index increases in overweight (25,30,kg/m2) and obese (>30,kg/m2) individuals. However, these risks can be reduced with even modest weight loss. In patients with established type 2 diabetes, control of both glycemia and body weight are important to minimize the risk of future diabetic complications. Exenatide is a 39-amino-acid peptide incretin mimetic currently approved in the United States for the treatment of type 2 diabetes as an adjunct to sulfonylurea and/or metformin. Phase-3 clinical studies showed exenatide therapy for 30 weeks significantly reduced glycosylated hemoglobin (HbA1c), and fasting and postprandial plasma glucose, while significantly reducing body weight. Open-label extensions from these pivotal trials demonstrated patients treated with exenatide for 2 years had sustained reductions in glycemic control at 30 weeks and a progressive reduction in body weight. Patients treated with exenatide also had improvement in blood pressure, inflammatory markers, and lipid profiles. The glucoregulatory and weight-reducing effects of exenatide are the result of multiple modes of action that mimic several of the glucoregulatory actions of the naturally occurring peptide, glucagon-like peptide-1 (GLP-1). These include restoration of first phase insulin response, enhancement of glucose-dependent insulin secretion, suppression of inappropriate glucagon secretion, slowing of gastric emptying, and affects on satiety leading to reduced food intake. Further research is required to fully understand the role for exenatide to potentially alleviate metabolic disorders associated with type 2 diabetes, including CVD and obesity. Drug Dev. Res. 67:666,676, 2006. © 2006 Wiley-Liss, Inc. [source] Febrile infection,related epilepsy syndrome (FIRES): A nonencephalitic encephalopathy in childhoodEPILEPSIA, Issue 7 2010Andreas Van Baalen Summary Encephalitis is generally presumed, even when seizures follow banal febrile infection, and pathogen detection in cerebrospinal fluid fails. This retrospective multicenter case series reports on 22 previously healthy children aged 3,15 years (median 6.5 years) with prolonged or recurrent seizures occurring 2,14 days (median 5 days) after fever onset (19 children with respiratory or nonspecific infections). Cerebrospinal fluid studies revealed 2,42 cells/,l (median 5 cells/,l) and no pathogens. Electroencephalography showed diffuse slowing or multifocal discharges. Neuroimaging demonstrated normal findings in 10 children. Brain biopsies were performed in seven children showing gliosis but no inflammation. Anesthetic barbiturates were used in 14 children with refractory status epilepticus, and immunotherapy in 9. Two children died, eight remained in a state of impaired consciousness, eight developed therapy-refractory epilepsies, two had behavioral disturbances, and two recovered. The lack of evidence for encephalitis suggests another infection-related pathogenesis of this disastrous epileptic encephalopathy. Therefore, we propose the term "febrile infection,related epilepsy syndrome" (FIRES). [source] Cognitive Deficits during Status Epilepticus and Time Course of Recovery: A Case ReportEPILEPSIA, Issue 10 2007Wim Van Paesschen Summary:, We describe a young woman with progressive cognitive and neurological deficits during a parietal lobe status epilepticus (SE). Ictal FDG-PET showed left parietal lobe hypermetabolism and frontal lobe hypometabolism with concomitant EEG slowing. Cognitive and neurological deficits fully reversed more than 1 year after seizure remission, and were associated with normalization of FDG-PET and EEG. Our findings suggest that ictal hypometabolism and EEG delta activity at a distance from the epileptic focus were seizure-related phenomena, possibly representing inhibition in seizure propagation pathways, which could be responsible for the epileptic encephalopathy. [source] Clinical and Electrographic Features of Epileptic Spasms Persisting Beyond the Second Year of LifeEPILEPSIA, Issue 6 2002Márcio A. Sotero De Menezes Summary: ,Purpose: Few reports detailing the electroclinical features of epileptic spasms persisting beyond infancy have been published. We sought to characterize this unique population further. Methods: We retrospectively reviewed the clinical and video-EEG data on 26 patients (4,17 years; mean, 93 months) with a confirmed diagnosis of epileptic spasms and who were evaluated at our tertiary referral center between 1993 and 2000. Results: In half of our cases, epileptic spasms were associated with disorders of neuronal migration, severe perinatal asphyxia, and genetic anomalies. Interictal EEGs showed generalized slowing in the majority of patients, and a slow-wave transient followed by an attenuation of the background amplitude was the most common ictal EEG pattern associated with an epileptic spasm (19 cases). Other seizure types (number of cases in parentheses) included tonic seizures with or without a preceding spasm (13), partial seizures (11), myoclonic seizures (11), generalized tonic,clonic seizures (six), atypical absence seizures (two), and atonic seizures (one). Cases with a more organized EEG background (especially with frequencies ,7 Hz) were more likely to have better cognition. Continued disorganization of the EEG background and persistence of hypsarrhythmia were associated with poor developmental outcome. Conclusions: Patients with epileptic spasms persisting beyond age 2 years constitute a truly refractory population, one that should be better recognized by clinicians. Interestingly, although many therapies resulted in a >50% reduction in seizures, neither neurocognitive function nor quality of life was substantially improved with intervention. The interictal EEG background is the most helpful in predicting neurologic outcome. [source] Contralateral EEG Slowing and Amobarbital Distribution in Wada Test: An Intracarotid SPECT StudyEPILEPSIA, Issue 2 2000Seung Bong Hong Summary: Purpose: To relate the occurrence of contralateral electroencephalogram slowing (CES) to amobarbital distribution, we performed electroencephalogram (EEG) monitoring and intracarotid single photon emission computed tomography (SPECT) during an intracarotid amobarbital procedure (IAP). Methods: IAP was performed on 22 patients with temporal lobe epilepsy. CES was defined as the occurrence of significant EEG slowing on the contralateral hemisphere (>50% of the ipsilateral hemisphere slowing) after amobarbital injection. To map the distribution of the amobarbital, we injected a mixture of amobarbital and 99m technetium-ethylcysteinate dimer (99m Tc-ECD) into the internal carotid artery and performed a brain SPECT 2 h later. In the SPECT images, regions of interest were determined by ipsilateral and contralateral anterior cerebral artery territories (iACA, cACA), ipsilateral and contralateral middle cerebral artery territories (iMCA, cMCA), and ipsilateral and contralateral posterior cerebral artery territories (iPCA, cPCA), as well as ipsilateral and contralateral anterior and posterior mesial temporal regions (iAMT, cAMT, iPMT, cPMT). The perfusion of amobarbital was interpreted visually in each region. Results: Amobarbital was distributed in the iMCA in all the patients; in the iACA in 20 (90.9%) patients; in the iAMT in 14 (63.5%); and in the iPCA and iPMT in only two (9.1%). CES was observed in 13 (59.1%) patients. Cross-perfusion of amobarbital in limited areas of the cACA were observed in only four of 13 patients. Wada retention memory scores (WRMS) showed no significant difference between the CES- (n = 9) and CES+ (n = 13) groups. Conclusions: Amobarbital rarely perfused the iPCA territory and the iPMT region and was rarely delivered to the contralat-eral hemisphere. The occurrence of CES was not related to the cross-perfusion of amobarbital. CES appears to be produced by a transient functional disconnection from the ipsilateral hemisphere. [source] Functional electrical stimulation in neurological disordersEUROPEAN JOURNAL OF NEUROLOGY, Issue 5 2008O. K. Sujith Functional electrical stimulation (FES) refers to electrical stimulation of muscles in order to improve the impaired motor function. This is achieved by activating skeletal muscles with constant frequency trains of stimulations. This method has been found useful in various neurological disorders like hemiplegia, foot drop and paraplegia including spinal cord injuries. The first half of this review focuses on the broad clinical applications of functional electrical stimulation, its mechanism of action and the complications of this mode of therapy. Advanced Parkinson's disease (PD) is characterized by marked slowing of gait and frequent freezing episodes. Medical and surgical treatments are often ineffective in managing freezing episodes. The second half of this review discusses briefly the gait abnormalities in PD and the available treatment options. The possible role of FES in improving gait in parkinsonism and the importance of future research in this direction are highlighted. [source] Neuropathic pain in spinal cord injury: significance of clinical and electrophysiological measuresEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 1 2009Susanne Wydenkeller Abstract A large percentage of spinal cord-injured subjects suffer from neuropathic pain below the level of the lesion (bNP). The neural mechanisms underlying this condition are not clear. The aim of this study was to elucidate the general effects of spinal deafferentiation and of bNP on electroencephalographic (EEG) activity. In addition, the relationship between the presence of bNP and impaired function of the spinothalamic tract was studied. Measurements were performed in complete and incomplete spinal cord-injured subjects with and without bNP as well as in a healthy control group. Spinothalamic tract function, assessed by contact heat evoked potentials, did not differ between subjects with and without bNP; nevertheless, it was impaired in 94% of subjects suffering from bNP. In the EEG recordings, the degree of deafferentiation was reflected in a slowing of EEG peak frequency in the 6,12-Hz band. Taking into account this unspecific effect, spinal cord-injured subjects with bNP showed significantly slower EEG activity than subjects without bNP. A discrimination analysis in the subjects with spinothalamic tract dysfunction correctly classified 84% of subjects as belonging to either the group with bNP or the group without bNP, according to their EEG peak frequency. These findings could be helpful for both the development of an objective diagnosis of bNP and for testing the effectiveness of new therapeutic agents. [source] Remote myocardium gene expression after 30 and 120 min of ischaemia in the ratEXPERIMENTAL PHYSIOLOGY, Issue 2 2006Miguel S. Guerra The aim of the present study was to investigate how early the onset of ischaemia-induced changes in gene expression is in remote myocardium, and whether these changes would be different for left and right ventricles. Wistar rats (n= 27) were randomly assigned to left coronary artery (LCA) ligation for 30 or 120 min and sham groups. Evans Blue infusion revealed antero-apical left ventricle (LV) and left intraventricular (IV) septal ischaemia (35.5 ± 0.6% of LV mass). LCA ligation induced transient LV systolic dysfunction and sustained biventricular slowing of relaxation. Regarding mRNA levels, type B natriuretic peptide (BNP) was upregulated in the LV at 30 (+370 ± 191%) and 120 min (+221 ± 112%), whilst in the right ventricle (RV) this was only significant at 120 min (+128 ± 39%). Hipoxia-inducible factor 1, and interleukin 6 overexpression positively correlated with BNP. Inducible NO synthase upregulation was present in both ventricles at 120 min (LV, +327 ± 195%; RV, +311 ± 122%), but only in the RV at 30 min (+256 ± 88%). Insulin-like growth factor 1 increased in both ventricles at 30 (RV, +59 ± 18%; LV, +567 ± 192%) and 120 min (RV, +69 ± 33%; LV, +120 ± 24%). Prepro-endothelin-1 was upregulated in the RV at 120 min (+77 ± 25%). Ca2+ -handling proteins were selectively changed in the LV at 120 min (sarcoplasmic reticulum Ca2+ ATPase, 53 ± 7%; phospholamban, +31 ± 4%; Na+,Ca2+ exchanger, 31 ± 6%), while Na+,H+ exchanger was altered only in the RV (,79 ± 5%, 30 min; +155 ± 70%, 120 min). Tumour necrosis factor-, and angiotensin converting enzyme were not significantly altered. A very rapid modulation of remote myocardium gene expression takes place during myocardial ischaemia, involving not only the LV but also the RV. These changes are different in the two ventricles and in the same direction as those observed in heart failure. [source] The regulation of the endosomal compartment by p53 the tumor suppressor geneFEBS JOURNAL, Issue 8 2009Xin Yu The endosomal compartment of the cell is involved in a number of functions including: (a) internalizing membrane proteins to multivesicular bodies and lysosomes; (b) producing vesicles that are secreted from the cell (exosomes); and (c) generating autophagic vesicles that, especially in times of nutrient deprivation, supply cytoplasmic components to the lysosome for degradation and recycling of nutrients. The p53 protein responds to various stress signals by initiating a transcriptional program that restores cellular homeostasis and prevents the accumulation of errors in a cell. As part of this process, p53 regulates the transcription of a set of genes encoding proteins that populate the endosomal compartment and impact upon each of these endosomal functions. Here, we demonstrate that p53 regulates transcription of the genes TSAP6 and CHMP4C, which enhance exosome production, and CAV1 and CHMP4C, which produce a more rapid endosomal clearance of the epidermal growth factor receptor from the plasma membrane. Each of these p53-regulated endosomal functions results in the slowing of cell growth and division, the utilization of catabolic resources and cell-to-cell communication by exosomes after a stress signal is detected by the p53 protein. These processes avoid errors during stress and restore homeostasis once the stress is resolved. [source] Pilot RCT of Aged Garlic Extract finds slowing of atherosclerotic progression as measured by electron beam tomographyFOCUS ON ALTERNATIVE AND COMPLEMENTARY THERAPIES AN EVIDENCE-BASED APPROACH, Issue 2 2005Article first published online: 14 JUN 2010 [source] New perspectives on Holocene landscape development in the southern English chalklands: The upper Allen valley, Cranborne Chase, DorsetGEOARCHAEOLOGY: AN INTERNATIONAL JOURNAL, Issue 2 2005C. French A combination of on- and off-site paleoenvironmental and archaeological investigations of the upper Allen valley of Dorset, conducted from 1998,2002, has begun to indicate a different model of prehistoric landscape development to those previously put forward for this part of the southern English chalk downlands. Woodland growth in the earlier Holocene appears to have been slower and patchier than the presumed model of full climax deciduous woodland rapidly attained in a warming environment. With open areas still strongly present in the Mesolithic, the area witnessed its first exploitation, thus slowing and altering soil development. Consequently, many areas perhaps never developed thick, well-structured, brown forest earths, but more probably thin brown earths. By the later Neolithic period, these soils had become thin rendzinas, largely as a consequence of human exploitation and the predominance of pastoral land use. The early presence of thinner and less well-developed soils over large areas of downland removes the necessity for envisaging extensive soil erosion and the accumulation of thick colluvial and alluvial deposits in the dry valleys and valley floor as often postulated. If there were major changes in the vegetation and soil complexes in this area of chalk downland, these had already occurred by the Neolithic rather than the Bronze Age as often suggested, and the area has remained relatively stable ever since. This has major implications for models of prehistoric land use in the southern chalkland region, such as a much greater degree of stability in prehistoric and historic times, variability within sub-regions, and differences between different parts of the chalk downlands than had previously been envisaged. © 2005 Wiley Periodicals, Inc. [source] Recurrent Wernicke's Aphasia: Migraine and Not Stroke!HEADACHE, Issue 5 2009Nishant Kumar Mishra MBBS We report the clinical findings of a 40-year-old woman with recurrent migraine presenting with Wernicke's aphasia in accordance with the results of a standardized battery for language assessment (Boston Aphasia Diagnostic Examination). The patient had no evidence of parenchymal or vascular lesions on MRI and showed delta and theta slowing over the left posterior temporal leads on the EEG. Although the acute onset of a fluent aphasia suggested stroke as a likely etiology, the recurrence of aphasia as the initial symptom of migraine was related to cortical spreading depression and not to stroke. [source] Gastric Stasis Occurs in Spontaneous, Visually Induced, and Interictal MigraineHEADACHE, Issue 10 2007Sheena Aurora MD Objective., To evaluate and compare gastric motility and emptying during spontaneous migraine to previous observations from induced migraine. Blackground., We have previously demonstrated a delay in gastric emptying both during the interictal period and during an induced migraine. A limitation noted in these studies was whether there are differences gastrointestinally during a visually induced migraine compared to spontaneous migraines. To address this, 9 additional studies have been performed to ascertain if there is a similar delay during spontaneous migraine Methods., Gastric scintigraphy using a standard meal was performed in 3 subjects during 3 periods: spontaneous migraine, induced migraine, and interictal period. Results., On average, the time to half emptying was delayed during spontaneous migraine (124 minutes), during induced migraine (182 minutes), and during the interictal period migraine (243 minutes) compared to normative values established at our center (112 minutes). On average, similar gastric slowing was seen in all 3 groups when the percentage of nuclear material remaining in the stomach at 2 hours was measured. Conclusions., This study provides additional evidence of gastric stasis in migraineurs interictally during induced and spontaneous migraine. [source] Hashimoto's Encephalopathy Mimicking Migraine With AuraHEADACHE, Issue 1 2007Adolfo Jimenez Huete MD We describe a patient with Hashimoto's encephalopathy presenting as long-standing episodes of aphasia associated with migraine-like headache. Repeated thyroid hormone levels were within normal values, but high titers of antithyroid antibodies in serum, and diffuse EEG slowing and CSF abnormalities during one episode led to the diagnosis. [source] Clinical application of measurement of hippocampal atrophy in degenerative dementiasHIPPOCAMPUS, Issue 6 2009Josephine Barnes Abstract Hippocampal atrophy is a characteristic and early feature of Alzheimer's disease. Volumetry of the hippocampus using T1-weighted magnetic resonance imaging (MRI) has been used not only to assess hippocampal involvement in different neurodegenerative diseases as a potential diagnostic biomarker, but also to understand the natural history of diseases, and to track changes in volume over time. Assessing change in structure circumvents issues surrounding interindividual variability and allows assessment of disease progression. Disease-modifying effects of putative therapies are important to assess in clinical trials and are difficult using clinical scales. As a result, there is increasing use of serial MRI in trials to detect potential slowing of atrophy rates as an outcome measure. Automated and yet reliable methods of quantifying such change in the hippocampus would therefore be very valuable. Algorithms capable of measuring such changes automatically have been developed and may be applicable to predict decline to a diagnosis of dementia in the future. This article details the progress in using MRI to understand hippocampal changes in the degenerative dementias and also describes attempts to automate hippocampal segmentation in these diseases. © 2009 Wiley-Liss, Inc. [source] Effect of pneumatic power tool use on nerve conduction velocity across the wristHUMAN FACTORS AND ERGONOMICS IN MANUFACTURING & SERVICE INDUSTRIES, Issue 4 2005John Rosecrance The purpose of this study was to determine if the use of pneumatic power tools altered electrophysiologic properties of the median and ulnar nerves at the wrist during the work shift. Sensory nerve conduction velocities were measured in hands of workers before work and then at 2-hour intervals during the workday. Ten workers exposed to pneumatic power tool use and 10 workers not exposed to intensive hand activity were evaluated. The conduction velocities slowed significantly across the wrist in the median and ulnar nerves among workers using pneumatic tools but not among control workers. This investigation demonstrated that short-term exposure to highly intensive hand tasks causes significant slowing in nerve conduction velocity across the wrist. © 2005 Wiley Periodicals, Inc. Hum Factors Man 15: 339,352, 2005. [source] Interactions between alcohol and caffeine in relation to psychomotor speed and accuracyHUMAN PSYCHOPHARMACOLOGY: CLINICAL AND EXPERIMENTAL, Issue 3 2002Michelle Mackay Abstract Unlike other CNS depressants, alcohol intoxication can be associated with increased error rates, coupled with unaffected (or speeded) response rates during psychomotor and cognitive processing. The present study examined whether concurrent consumption of caffeine may differentially affect these aspects of alcohol and performance. A randomised, double-blind, placebo-controlled design was utilised in which 64 healthy young volunteers received either 0.66,g/kg alcohol, caffeine (110,120,mg), both or neither. Performance was assessed using a four choice reaction time task (FCRT) with elements of repetitive (predictable) and random stimuli sequences and the digit symbol substitution task (DSST). Individuals on alcohol made significantly more errors during both fixed and random FCRT sequences, and there was evidence of weak antagonism of these effects by caffeine on the latter measure. On the DSST test of psychomotor speed, alcohol was associated with a significant slowing, the caffeine group were significantly faster and there was clear antagonism of the effects of alcohol by caffeine. These findings confirm that alcohol consumption is associated a greater number of errors and provide some evidence for task-specific antagonism of alcohol's cognitive effects by caffeine. Copyright © 2002 John Wiley & Sons, Ltd. [source] Is food availability limiting African Penguins Spheniscus demersus at Boulders?IBIS, Issue 1 2006A comparison of foraging effort at mainland, island colonies The African Penguin Spheniscus demersus (Vulnerable) formed three new colonies during the 1980s, two on the South African mainland (Stony Point and Boulders) and one on Robben Island. One of the mainland colonies, at Boulders, Simon's Town, is in a suburban area, resulting in conflict with humans. Growth of the Boulders colony was initially rapid, largely through immigration, but has since slowed, possibly as a result of density-dependent effects either on land (where there has been active management to limit the spread of the colony) or at sea. We test the latter hypothesis by comparing the foraging effort of Penguins feeding small chicks at island and mainland sites, and relate this to the foraging area available to birds. Three-dimensional foraging paths of African Penguins were reconstructed using GPS and time,depth loggers. There were no intercolony differences in the rate at which birds dived during the day (33 dives/h), in diving depths (mean 17 m, max. 69 m) or in travelling speeds. The maximum speed recorded was 2.85 m/s, with birds travelling faster when commuting (average 1.18 m/s) than when foraging (0.93 m/s) or resting at sea (0.66 m/s during the day, 0.41 m/s at night). There were strong correlations between foraging trip duration, foraging range and total distance travelled. Foraging effort was correlated with chick age at Robben Island, but not at Boulders. Contrary to Ashmole's hypothesis, birds from Boulders (c. 1000 pairs) travelled further (46,53 km) and foraged for longer (13.2 h) than did birds from Robben Island (c. 7000 pairs) and Dassen Island (c. 21 000 pairs) (33 km, 10.3 h). The mean foraging range also differed significantly between mainland (18,20 km) and island colonies (9 km). The area available to central-place-foraging seabirds breeding on the mainland is typically less than that for seabirds breeding on islands, but the greater foraging range of Boulders birds results in an absolute foraging area roughly twice that of island colonies, and the area per pair is an order of magnitude greater for the relatively small Boulders colony. Ashmole's hypothesis assumes relatively uniform prey availability among colonies, but our results suggest this does not apply in this case. The greater foraging effort of Boulders birds probably reflects reduced prey availability in False Bay, and thus the recent slowing in growth at the colony may be the result of differential immigration rather than management actions to limit the spatial growth of the colony. [source] | ||||||||||||||||||||||||||||||||||||||||||||||||||||