bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cardiovascular risk levels in general practice patients with type 2 diabetes in rural and urban areas
Authors: Wan Qing , Harris Mark F. , Powell‐Davies Gawaine , Jayasinghe Upali W. , Flack Jeff , Georgiou Andrew , Burns Joan R. , Penn Danielle L. 
Published: September 2007

AbstractObjective:  To investigate the change of cardiovascular risk factor from 2000 to 2002 in general practice patients with type 2 diabetes in urban and rural areas, and the association between cardiovascular risk (both single risk factors and coronary heart disease absolute risk (CHDAR)) and rurality in three years. Methods:  In total, 6305 patients were extracted from 16 Divisions (250 practices). Multivariate regression at Division, practice and patient levels was conducted with adjustment for age and gender. Results:  In each of the three years, most single individual risk factors and CHDAR were high. Comparing 2002 with 2000: for urban patients in 2002 total cholesterol (OR 0.85) and low‐density lipoprotein (OR 0.81) significantly decreased, and high‐density lipoprotein (HDL) (OR 1.16) significantly increased; for rural patients in 2002 HbA1c (OR 0.85) significantly decreased and HDL (OR 1.22) significantly increased; and CHDAR significantly improved only in urban patients (OR 0.93) in 2002. In 2002 rural patients were still more likely to be overweight/obese (OR 1.16), be current smokers (OR 1.36), and have worse HDL (OR 0.84) and triglycerides (OR 1.23) than their urban counterparts.Conclusion:  Some key individual risk factors and CHDAR did not improve in rural patients with type 2 diabetes despite a number of programs designed to provide comprehensive care to rural patients with diabetes. More emphasis is needed on supporting access to lifestyle changes (such as smoking, diet and physical activity) in rural primary health care.
Disturbed colocalization of multidrug resistance protein 2 and radixin in human cholestatic liver diseases
Authors: Kojima Hideyuki , Sakurai Shinya , Uemura Masahito , Kitamura Kensuke , Kanno Hiroki , Nakai Yoshiyuki , Fukui Hiroshi 
Published: September 2007

AbstractBackground and Aim:  Endocytic retrieval of multidrug resistance protein 2 (MRP2) is closely associated with cholestasis and may be attributed to the disturbed linking of MRP2 and radixin, a cross‐linker between actin filaments and membrane proteins. This study aimed to investigate the role of radixin in the altered localization of MRP2 in various human cholestatic liver diseases.Methods:  Using immunofluorescence microscopy, we investigated the localization and expression of MRP2 and radixin in various cholestatic liver diseases, such as drug‐induced liver injury, obstructive jaundice, primary sclerosing cholangitis and autoimmune hepatitis. Changes in localization and expression were analyzed using Scion Image (software).Results:  In the icteric drug‐induced liver injury, MRP2 was localized outside as well as inside of ZO‐1 staining, indicating endocytic retrieval from the canalicular membrane into the pericanalicular compartments of the hepatocytes. The colocalization of MRP2 and radixin observed in the controls was disturbed, and MRP2 fluorescence disappeared in the canaliculi with disrupted radixin staining. Disturbed colocalization of MRP2 and radixin as well as endocytic retrieval of MRP2 was found in the poorly drained obstructive jaundice. When drainage was good, MRP2 was exclusively colocalized with radixin. Similar findings were observed in autoimmune hepatitis and primary sclerosing cholangitis. In the controls, the immunostaining intensity curves for MRP2 and radixin were steeply elevated in the canaliculi. The intensity curves for MRP2 and radixin were broadened in the icteric drug‐induced liver injury and poorly drained obstructive jaundice, indicating endocytic retrieval into the hepatocytes. The peak fluorescence intensities for MRP2 and radixin decreased in the icteric liver.Conclusion:  Disturbed colocalization of MRP2 and radixin was common in various cholestatic liver diseases, which may be associated with endocytic retrieval of MRP2 due to failure in anchoring MRP2 in the canalicular membrane.
Taxonomic investigation using DNA fingerprinting in Geitlerinema species (Oscillatoriales, Cyanobacteria)
Authors: Bittencourt‐Oliveira Maria do Carmo , Massola Nelson Sidnei , Hernandez‐Marine Mariona , Romo Susana , Moura Ariadne do Nascimento 
Published: September 2007

SUMMARYThe taxonomic study of 14 strains of Geitlerinema amphibium (Ag. ex Gom.) Anagnostidis and Geitlerinema unigranulatum (R.N. Singh) Komárek and Azevedo, coming from several localities was undertaken. Use was made of morphological data and molecular data were obtained by means of the DNA fingerprinting technique using highly iterated palindrome (HIP1) sequences. The employed morphological characteristics were those used for species taxonomic identification belonging to the Geitlerinema genus, namely, cell dimensions, shape of the apical cell, motility, number and localization of cyanophycin granules in the cell. The two species revealed as polymorphic were discriminated only by means of the average cellular diameters. In spite of this, minima and maxima values of the cellular diameters overlapped. It was found from molecular analysis that a high genetic diversity and the formation of two clusters consisted of G. amphibium and G. unigranulatum, plus a sole strain keeping itself isolated from the remaining. Also, these clusters were not related to the geographic location; they encompassed strains from water bodies distant from each other by as much as 3500 km, or Brazilian and Spanish strains. Molecular and morphological data support the possibility that G. unigranulatum could be considered a synonym for G. amphibium. HIP1 fingerprinting is a powerful tool for the study of genetic of cyanobacteria closely related taxa. This study points to the necessity of using other than morphological data in the taxonomic revision of cyanobacteria, as well as in the proposition of new taxons.
Impairment of hippocampal gamma (γ)‐frequency oscillations in vitro in mice overexpressing human amyloid precursor protein (APP)
Authors: Driver Joanne E. , Racca Claudia , Cunningham Mark O. , Towers Stephen K. , Davies Ceri H. , Whittington Miles A. , LeBeau Fiona E. N. 
Published: September 2007

AbstractAlzheimer's disease is associated with a dramatic decline in cognitive performance including hippocampal‐dependent memory. We have investigated one feature of hippocampal activity related to memory, the γ (30–80 Hz)‐frequency rhythm. Hippocampal slices from mice overexpressing the human amyloid precursor protein (APP)SWE mutation (TAS10) were compared at 8 and 16 months of age with wild‐type littermates. In slices obtained from TAS10 mice aged 8 months the γ‐frequency activity evoked with bath application of 200 nm kainate was significantly (P < 0.05; n = 8 slices, five animals) impaired (area power, 5956 ± 2487 µV2) compared to slices from wild‐type animals (area power, 18 256 ± 7880 µV2). At 16 months of age there was no longer a significant difference (P > 0.05; n = 11 slices from five animals) between slices from TAS10 and wild‐type control mice as the wild‐type mice now exhibited a marked age‐dependent reduction in γ‐frequency activity (TAS10 area power, 5751 ± 1573 µV2; wild‐type area power = 5379 ± 1454 µV2). Although no dense‐core plaques were evident at 8 months there was detectable amyloid labelling in the TAS10 mice which might account for the deficits in γ activity observed at this age. Dense plaques were clearly evident in the TAS10, but not wild‐type, mice at 16 months of age but no further reductions in γ‐frequency activity were seen in the TAS10 mice. These data suggest that deficits in network function in Alzheimer's disease occur early and are not directly correlated to amyloid load.
Laser capture microdissection and microarray analysis of dividing neural progenitor cells from the adult rat hippocampus
Authors: Gurok Ulf , Loebbert Ralf W. , Meyer Axel H. , Mueller Reinhold , Schoemaker Hans , Gross Gerhard , Behl Berthold 
Published: September 2007

AbstractNeural progenitor cells reside in the hippocampus of adult rodents and humans and generate granule neurons throughout life. Knowledge about the molecular processes regulating these neurogenic cells is fragmentary. In order to identify genes with a role in the proliferation of adult neural progenitor cells, a protocol was elaborated to enable the staining and isolation of such cells under RNA‐preserving conditions with a combination of immunohistochemistry and laser capture microdissection. We increased proliferation of neural progenitor cells by electroconvulsive treatment, one of the most effective antidepressant treatments, and isolated Ki‐67‐positive cells using this new protocol. RNA amplification viain vitrotranscription and subsequent microarray analysis revealed over 100 genes that were differentially expressed in neural progenitor cells due to electroconvulsive treatment compared to untreated control animals. Some of these genes have already been implicated in the functioning of neural progenitor cells or have been induced by electroconvulsive treatment; these include brain‐derived neurotrophic factor (Bdnf), PDZ‐binding kinase (Pbk) and abnormal spindle‐like microcephaly‐associated (Aspm). In addition, genes were identified for which no role in the proliferation of neurogenic progenitors has been described so far, such as enhancer of zeste homolog 2 (Ezh2).
Estrogen modulates neuronal movements within the developing preoptic area–anterior hypothalamus
Authors: Knoll John Gabriel , Wolfe Cory A. , Tobet Stuart A. 
Published: September 2007

AbstractThe preoptic area–anterior hypothalamus (POA‐AH) is characterized by sexually dimorphic features in a number of vertebrates and is a key region of the forebrain for regulating physiological responses and sexual behaviours. Using live‐cell fluorescence video microscopy with organotypic brain slices, the current study examined sex differences in the movement characteristics of neurons expressing yellow fluorescent protein (YFP) driven by the Thy‐1 promoter. Cells in slices from embryonic day 14 (E14), but not E13, mice displayed significant sex differences in their basal neuronal movement characteristics. Exposure to 10 nm estradiol‐17β (E2), but not 100 nm dihydrotestosterone, significantly altered cell movement characteristics within minutes of exposure, in a location‐specific manner. E2 treatment decreased the rate of motion of cells located in the dorsal POA‐AH but increased the frequency of movement in cells located more ventrally. These effects were consistent across age and sex. To further determine whether early‐developing sex differences in the POA‐AH depend upon gonadal steroids, we examined cell positions in mice with a disruption of the steroidogenic factor‐1 gene, in which gonads do not form. An early‐born cohort of cells were labelled with the mitotic indicator bromodeoxyuridine (BrdU) on E11. More cells were found in the POA‐AH of females than males on the day of birth (P0) regardless of gonadal status. These results support the hypothesis that estrogen partially contributes to brain sexual dimorphism through its influence on cell movements during development. Estrogen's influence may be superimposed upon a pre‐existing genetic bias.
Distinct changes in evoked and resting globus pallidus activity in early and late Parkinson's disease experimental models
Authors: Zold Camila L. , Larramendy Celia , Riquelme Luis A. , Murer M. Gustavo 
Published: September 2007

AbstractThe main clinical manifestations of Parkinson's disease are caused by alterations of basal ganglia activity that are tied in with the progressive loss of mesencephalic dopaminergic neurons. Recent theoretical and modeling studies have suggested that changes in resting neuronal activity occurred later in the course of the disease than those evoked by phasic cortical input. However, there is no empirical support for this proposal. Here we report a marked increase in the responsiveness of globus pallidus neurons to electrical motor cortex stimulation, in the absence of noticeable changes in resting activity, in anesthetized rats that had consistently shown a deficit in forelimb use during behavioral testing before the experiments, and had ∼45% dopamine neurons spared in the substantia nigra. Pallidal neurons were also over‐responsive to motor cortex stimulation and lost spatial selectivity for cortical inputs in rats with extensive nigrostriatal damage. After partial lesions, over‐responsiveness was mainly due to an increased proportion of neurons showing excitatory responses, while extensive lesions led to an increased likelihood of inhibitory responding neurons. Changes in resting neuronal activity, comprising pauses disrupting tonic discharge, occurred across different global brain states, including an activated condition which shares similarities with natural patterns of cortical activity seen in awake states and rapid eye‐movement sleep, but only after massive nigrostriatal degeneration. These results suggest that a loss of functional segregation and an abnormal temporal encoding of phasic cortical inputs by globus pallidus neurons may contribute to inducing early motor impairment in Parkinson's disease.
Inhibitory control of the human dorsolateral prefrontal cortex during the anti‐saccade paradigm − a transcranial magnetic stimulation study
Authors: Nyffeler Thomas , Müri René M. , Bucher‐Ottiger Y. , Pierrot‐Deseilligny Charles , Gaymard Bertrand , Rivaud‐Pechoux Sophie 
Published: September 2007

AbstractIn the anti‐saccade paradigm, subjects are instructed not to make a reflexive saccade to an appearing lateral target but to make an intentional saccade to the opposite side instead. The inhibition of reflexive saccade triggering is under the control of the dorsolateral prefrontal cortex (DLPFC). The critical time interval at which this inhibition takes place during the paradigm, however, is not exactly known. In the present study, we used single‐pulse transcranial magnetic stimulation (TMS) to interfere with DLPFC function in 15 healthy subjects. TMS was applied over the right DLPFC either 100 ms before the onset of the visual target (i.e. −100 ms), at target onset (i.e. 0 ms) or 100 ms after target onset (i.e. +100 ms). Stimulation 100 ms before target onset significantly increased the percentage of anti‐saccade errors to both sides, while stimulation at, or after, target onset had no significant effect. All three stimulation conditions had no significant influence on saccade latency of correct or erroneous anti‐saccades. These findings show that the critical time interval at which the DLPFC controls the suppression of a reflexive saccade in the anti‐saccade paradigm is before target onset. In addition, the results suggest the view that the triggering of correct anti‐saccades is not under direct control of the DLPFC.
Facilitation of spinal reflexes assists performing but not learning an obstacle‐avoidance locomotor task
Authors: Michel J. , Van Hedel H.J.A. , Dietz V. 
Published: September 2007

AbstractThe aim of this study was to investigate spinal reflex (SR) modulation during the performance and learning of a precision locomotor task. Healthy subjects had to minimize foot clearance when repeatedly stepping on a treadmill over a randomly approaching obstacle. The subjects walked with reduced vision and were informed about the approaching obstacle and task performance by acoustic warning and feedback signals, respectively. SRs were randomly evoked by tibial nerve stimulation (with non‐nociceptive and nociceptive stimulus intensity) during the mid‐stance phase in both normal and pre‐obstacle stepping. Foot clearance and electromyographic activity of the tibialis anterior and biceps femoris muscles of the right leg were analysed. Only if a delay was introduced between warning signal and nerve stimulation, was the SR amplitude in both muscles enhanced prior to obstacle steps compared with normal steps for both stimulus intensities. Thus, the reflex enhancement depended on the subject's awareness of the approaching obstacle. Improved performance was reflected in a decreased foot clearance, but did not correlate with the course of SR amplitude. It is concluded that obstacle stepping is associated with a facilitation of SR pathways, probably by supraspinal drive. This facilitation might provide assistance in safe obstacle stepping, e.g. to compensate quickly if resistance is encountered.
Early necrosis and apoptosis of Schwann cells transplanted into the injured rat spinal cord
Authors: Hill Caitlin E. , Hurtado Andres , Blits Bas , Bahr Ben A. , Wood Patrick M. , Bartlett Bunge Mary , Oudega Martin 
Published: September 2007

AbstractPoor survival of cells transplanted into the CNS is a widespread problem and limits their therapeutic potential. Whereas substantial loss of transplanted cells has been described, the extent of acute cell loss has not been quantified previously. To assess the extent and temporal profile of transplanted cell death, and the contributions of necrosis and apoptosis to this cell death following spinal cord injury, different concentrations of Schwann cells (SCs), lentivirally transduced to express green fluorescent protein (GFP), were transplanted into a 1‐week‐old moderate contusion of the adult rat thoracic spinal cord. In all cases, transplanted cells were present from 10 min to 28 days. There was a 78% reduction in SC number within the first week, with no significant decrease thereafter. Real‐time polymerase chain reaction showed a similar 80% reduction in GFP‐DNA within the first week, confirming that the decrease in SC number was due to death rather than decreased GFP transgene expression. Cells undergoing necrosis and apoptosis were identified using antibodies against the calpain‐mediated fodrin breakdown product and activated caspase 3, respectively, as well as ultrastructurally. Six times more SCs died during the first week after transplantation by necrosis than apoptosis, with the majority of cell death occurring within the first 24 h. The early death of transplanted SCs indicates that factors present, even 1 week after a moderate contusion, are capable of inducing substantial transplanted cell death. Intervention by strategies that limit necrosis and/or apoptosis should be considered for enhancing acute survival of transplanted cells.
Cocaine‐ and amphetamine‐regulated transcript peptide (CART) is present in peptidergic C primary afferents and axons of excitatory interneurons with a possible role in nociception in the superficial laminae of the rat spinal cord
Authors: Kozsurek Márk , Lukácsi Erika , Fekete Csaba , Wittmann Gábor , Réthelyi Miklós , Puskár Zita 
Published: September 2007

AbstractCocaine‐ and amphetamine‐regulated transcript peptides (CART) have been implicated in the regulation of several physiological functions, including pain transmission. A dense plexus of CART‐immunoreactive fibres has been described in the superficial laminae of the spinal cord, which are key areas in sensory information and pain processing. In this study, we used antibody against CART peptide, together with markers for various types of primary afferents, interneurons and descending systems to determine the origin of the CART‐immunoreactive axons in the superficial laminae of the rat spinal cord. Calcitonin gene‐related peptide (CGRP), a marker for peptidergic primary afferents in the dorsal horn, was present in 72.6% and 34.8% of CART‐immunoreactive axons in lamina I and II, respectively. The majority of these fibres also contained substance P (SP), while a few were somatostatin (SOM)‐positive. The other subpopulation of CART‐immunoreactive boutons in lamina I and II also expressed SP and/or SOM without CGRP, but contained vesicular glutamate transporter 2, which is present mainly in excitatory interneuronal terminals. Our data demonstrate that the majority of CART‐immunoreactive axons in the spinal dorsal horn originate from peptidergic nociceptive primary afferents, while the rest arise from excitatory interneurons that contain SP or SOM. This strongly suggests that CART peptide can affect glutamatergic neurotransmission as well as the release and effects of SP and SOM in nociception and other sensory processes.
CNS‐irrelevant T‐cells enter the brain, cause blood–brain barrier disruption but no glial pathology
Authors: Smorodchenko Alina , Wuerfel Jens , Pohl Elena E. , Vogt Johannes , Tysiak Eva , Glumm Robert , Hendrix Sven , Nitsch Robert , Zipp Frauke , Infante‐Duarte Carmen 
Published: September 2007

AbstractInvasion of autoreactive T‐cells and alterations of the blood–brain barrier (BBB) represent early pathological manifestations of multiple sclerosis and its animal model experimental autoimmune encephalomyelitis (EAE). Non‐CNS‐specific T‐cells are also capable of entering the CNS. However, studies investigating the spatial pattern of BBB alterations as well as the exact localization and neuropathological consequences of transferred non‐CNS‐specific cells have been thus far lacking. Here, we used magnetic resonance imaging and multiphoton microscopy, as well as histochemical and high‐precision unbiased stereological analyses to compare T‐cell transmigration, localization, persistence, relation to BBB disruption and subsequent effects on CNS tissue in a model of T‐cell transfer of ovalbumin (OVA)‐ and proteolipid protein (PLP)‐specific T‐cells. BBB alterations were present in both EAE‐mice and mice transferred with OVA‐specific T‐cells. In the latter case, BBB alterations were less pronounced, but the pattern of initial cell migration into the CNS was similar for both PLP‐ and OVA‐specific cells [mean (SEM), 95 × 103 (7.6 × 103) and 88 × 103 (18 × 103), respectively]. Increased microglial cell density, astrogliosis and demyelination were, however, observed exclusively in the brain of EAE‐mice. While mice transferred with non‐neural‐specific cells showed similar levels of rhodamine‐dextran extravasation in susceptible brain regions, EAE‐mice presented huge BBB disruption in brainstem and moderate leakage in cerebellum. This suggests that antigen specificity and not the absolute number of infiltrating cells determine the magnitude of BBB disruption and glial pathology.
Relationship between age and spontaneous ventilation during intravenous anesthesia in children
Authors: BARKER NIGEL , LIM JOANNE , AMARI ERICA , MALHERBE STEPHAN , ANSERMINO J. MARK 
Published: September 2007

SummaryBackground:  Maintaining spontaneous ventilation in children, using total intravenous anesthesia (TIVA), is often desirable, particularly for airway endoscopy. The aim of this study was to evaluate the effect of age on the dose of remifentanil tolerated during spontaneous ventilation under anesthesia maintained with infusions of propofol and remifentanil and to provide guidelines for the administration of remifentanil and propofol to maintain spontaneous ventilation in children.Methods:  Forty‐five children scheduled for strabismus surgery were divided by age into three groups (group I: 6 months–3 years, group II: 3 years–6 years, and group III: 6 years–9 years). The propofol infusion was titrated using State Entropy as a pharmacodynamic endpoint and remifentanil infused, using a modified up‐and‐down method, with respiratory rate depression as a pharmacodynamic endpoint. A respiratory rate of just greater than 10, stable for 10 min, determined the final remifentanil infusion rate. The group mean was estimated from the final remifentanil infusion rate tolerated (RD50).Results:  The RD50 of groups I, II, and III were 0.192 (0.08), 0.095 (0.04), and 0.075 (0.03) μg·kg−1·min−1 respectively. Pair‐wise comparisons between the groups for the rate of remifentanil tolerated revealed a statistically significant increase in the RD50 in children less than 3 years of age compared with older children in groups II and III (P < 0.001). The relationship between remifentanil dose and age, weight or height was not linear.Conclusions:  Younger children, especially those aged less than 3 years, tolerate a higher dose of remifentanil while still maintaining spontaneous respiration. TIVA with spontaneous ventilation is readily achieved in younger children and infants.