bluuebunny/crossref_metadata_2025_split huggingface dataset:
Hyperglycaemia and cardiovascular disease
Authors: Bartnik M. , Norhammar A. , Rydén L. 
Published: June 2007

Abstract.Coronary artery disease and type 2 diabetes are chronic diseases of substantial and growing prevalence. Their coincidence is common, markedly enhancing mortality and morbidity. The risk for cardiovascular disease increases along a spectrum of blood glucose concentrations already apparent at levels regarded as normal. Accordingly, strategies for the early detection of glucometabolic disturbances are needed to find ways to prevent the occurrence of cardiovascular complications or to treat them already at an early stage. More specifically, abnormal glucose tolerance is almost twice as common amongst patients with a myocardial infarction as in population‐based controls and a normal glucose regulation is indeed less common than abnormal glucose metabolism also amongst patients with stable coronary artery disease. Already an abnormal glucose tolerance is a strong risk factor for future cardiovascular events after an acute myocardial infarction. An oral glucose tolerance test should, therefore, be a part of the evaluation of total risk in all patients with coronary artery disease. As glucose disturbances are common and easy to detect, they may be suitable targets for novel secondary preventive efforts.
Regulatory T cells in health and disease
Authors: Rouse B. T. 
Published: June 2007

Abstract.The healthy host does not normally develop tissue destructive autoimmunity in part because of the presence of natural regulatory T cells. These cells are best identified by their expression of a unique transcription factor forkhead box transcription factor (Foxp3) that controls their regulatory function. Several other types of regulatory T cells also occur most of which are induced in response to antigen stimulation. Some of these express the Foxp3 transcription factor but many do not. The role of natural T‐regulatory cells as well as induceable regulatory cells in autoimmunity, cancer, allergy and infectious disease is described. The current status of therapeutic approaches that modulate regulatory T‐cell responses on the outcome of experimental animal and human disease is also discussed.
Coalescence methods reveal the impact of vicariance on the spatial genetic structure of Elephantulus edwardii (Afrotheria, Macroscelidea)
Authors: SMIT H. A. , ROBINSON T. J. , VAN VUUREN B. J. 
Published: June 2007

AbstractWithin the Macroscelidea 15 species of elephant‐shrews are recognized, of which nine occur in the southern African subregion. The Cape rock elephant‐shrew (Elephantulus edwardii) is the only strictly endemic South African elephant‐shrew species. Recent distribution data suggest that E. edwardii is continuously distributed from Namaqualand in the Western Cape Province to Port Elizabeth in the Eastern Cape Province. Molecular sequences from the mitochondrial cytochrome b gene and variable control region indicate significant substructure within the Cape rock elephant‐shrew across its distribution. Our data unequivocally showed the presence of a northern Namaqua and central Fynbos clade with four evolutionary lineages identified within the latter. The geographical delimitation of the northern and central clades corresponds closely with patterns reported for other rock‐dwelling vertebrate species, indicating a shared biogeographical history for these taxa in South Africa. A coalescent method revealed the effects of ancestral polymorphism in shaping the Namaqua and Fynbos populations since their divergence ~1.7 million years ago. Furthermore, our analyses uncovered a distinct Karoo lineage(s) that does not correspond to any of the previously described and/or currently recognized species, and we therefore argue for the possible recognition of a new sister taxon to E. edwardii. The taxonomic affinities of this clade were examined by sequencing corresponding regions from the type specimens of species described in the past, but which presently are synonimized within E. edwardii. Our results reveal the morphological misidentification of one of these types, accentuating the problems of field identification.
Effects of population succession on demographic and genetic processes: predictions and tests in the daylily Hemerocallis thunbergii (Liliaceae)
Authors: CHUNG MI YOON , NASON JOHN D. , CHUNG MYONG GI 
Published: June 2007

AbstractSpatial genetic structure within plant populations is influenced by variation in demographic processes through space and time, including a population's successional status. To determine how demographic structure and fine‐scale genetic structure (FSGS) change with stages in a population's successional history, we studied Hemerocallis thunbergii (Liliaceae), a nocturnal flowering and hawkmoth‐pollinated herbaceous perennial with rapid population turnover dynamics. We examined nine populations assigned to three successive stages of population succession: expansion, maturation, and senescence. We developed stage‐specific expectations for within‐population demographic and genetic structure, and then for each population quantified the spatial aggregation of individuals and genotypes using spatial autocorrelation methods (nonaccumulative O‐ring and kinship statistics, respectively), and at the landscape level measured inbreeding and genetic structure using Wright's F‐statistics. Analyses using the O‐ring statistic revealed significant aggregation of individuals at short spatial scales in expanding and senescing populations, in particular, which may reflect restricted seed dispersal around maternal individuals combined with relatively low local population densities at these stages. Significant FSGS was found for three of four expanding, no mature, and only one senescing population, a pattern generally consistent with expectations of successional processes. Although allozyme genetic diversity was high within populations (mean %P = 78.9 and HE = 0.281), landscape‐level differentiation among sites was also high (FST = 0.166) and all populations exhibited a significant deficit of heterozygotes relative to Hardy–Weinberg expectations (range F = 0.201–0.424, mean FIS = 0.321). Within populations, F was not correlated with the degree of FSGS, thus suggesting inbreeding due primarily to selfing as opposed to mating among close relatives in spatially structured populations. Our results demonstrate considerable variation in the spatial distribution of individuals and patterns and magnitude of FSGS in H. thunbergii populations across the landscape. This variation is generally consistent with succession‐stage‐specific differences in ecological processes operating within these populations.
Impact of Plio‐Pleistocene arid cycling on the population history of a southwestern Australian frog
Authors: EDWARDS DANIELLE L. , ROBERTS J. DALE , KEOGH J. SCOTT 
Published: June 2007

AbstractSouthwestern Australia is regarded as a global biodiversity hotspot. The region contains a high number of endemic species, ranging from Gondwanan relicts to much more recently evolved plant and animal species. Myobatrachid frogs are diverse in southwestern Australia, and while we know they have speciatedin situin the southwest, we know little about the temporal and geographical patterning of speciation events.Crinia georgianais an ideal subject to test hypotheses concerning the effect of climatic history on southwestern Australian anurans, as it is an old lineage with a broad distribution covering the entire region. We compiled an extensive phylogeographical data set based on 1085 bp of the mitochondrial gene ND2 for 68 individuals from 18 sites across the species’ range. Two major genetic clades were identified which were largely confined to the high rainfall and southeast coastal biogeographical zones, respectively. The clades appear to have diverged around the Plio‐Pleistocene border (1.26–1.72 million years ago), concordant with increasing intensity and frequency of arid climate cycles. Subsequent phylogeographical structure appears to have developed primarily during the Pleistocene climatic fluctuations that also have been integral in generating species diversity in the endemic southwestern Australian flora. Phylogeographical analyses identified several dispersal routes, possible refugial areas within the range of the species and also regions of secondary contact. Dispersal routes identified may now be closed to the species because of habitat destruction and salinity problems in inland regions, posing concerns about the evolutionary potential of the species in light of predicted climate change.
Rapid mixing between old and new C pools in the canopy of mature forest trees
Authors: KEEL SONJA G. , SIEGWOLF ROLF T.W. , JÄGGI MAYA , KÖRNER CHRISTIAN 
Published: June 2007

ABSTRACTStable C isotope signals in plant tissues became a key tool in explaining growth responses to the environment. The technique is based on the fundamental assumption that the isotopic composition of a given unit of tissue (e.g. a tree ring) reflects the specific C uptake conditions in the leaf at a given time. Beyond the methodological implications of any deviation from this assumption, it is of physiological interest whether new C is transferred directly from sources (a photosynthesizing leaf) to structural sinks (e.g. adjacent stem tissue), or inherently passes through existing (mobile) C pools, which may be of variable (older) age. Here, we explore the fate of 13C‐labelled photosynthates in the crowns of a 30–35 m tall, mixed forest using a canopy crane. In all nine study species labelled C reached woody tissue within 2–9 h after labelling. Four months later, very small signals were left in branch wood of Tilia suggesting that low mixing of new, labelled C with old C had taken place. In contrast, signals in Fagus and Quercus had increased, indicating more intense mixing. This species‐specific mixing of new with old C pools is likely to mask year‐ or season‐specific linkages between tree ring formation and climate and has considerable implications for climate reconstruction using stable isotopes as proxies for past climatic conditions.
Clinical application prospects of gastric pacing for treating postoperative gastric motility disorders
Authors: Li Fu‐Yu , Jiang Li‐Sheng , Cheng Jing‐Qiu , Mao Hui , Li Ning , Cheng Nan‐Sheng 
Published: June 2007

AbstractSimilar to the heartbeat, gastric peristalsis is regulated by an electrical rhythm generated by a pacemaker. Thus, electrical dysrhythmia of gastric slow waves will inevitably affect gastric peristalsis and emptying. The recurrence of postoperative gastroparesis is thereby closely related to the abnormalities of electrical dysrhythmia and ectopic pacemakers, resulting in postoperatively persistent gastric motility disorders in some severe cases, despite the use of prokinetic and antiemetic drugs. Recent studies have demonstrated that gastric pacing, analogous to pacing the human heart, is an attractive and promising therapy that is both feasible and safe. Gastric pacing has been shown to be strikingly effective in normalizing gastric dysrhythmia, increasing the activity of the gastric slow wave and thereby prompting gastric dynamia and emptying. Furthermore, the long‐term utilization of gastric pacing can (i) relieve patients from clinical symptoms, such as nausea and vomiting; (ii) release patients with severe postoperative gastroparesis from relying on prokinetic drugs and the jejunal feeding tube; (iii) return patients to normal oral nutritional intake and provide a more satisfactory nutritional status and most importantly; and (iv) give patients a better quality of life. Overall, research focused on gastric pacing has demonstrated excellent prospects for clinical application in the treatment of postoperative gastroparesis disorders, especially for those unresponsive to prokinetic drugs.
Polymorphisms in NFKBIA and ICAM‐1 genes in New Zealand Caucasian Crohn's disease patients
Authors: Hong Jiwon , Leung Euphemia , Fraser Alan G , Merriman Tony R , Vishnu Prakash , Krissansen Geoffrey W 
Published: June 2007

AbstractBackground and Aim:  Crohn's disease (CD) is a complex polygenetic inflammatory disease of the bowel. NFKBIA (IκBα) is a downstream regulator of NF‐κB, which is an effector of the major Crohn's susceptibility gene CARD15/NOD2. ICAM‐1 is an integrin ligand and vascular addressin, which contributes to the trafficking of pathogenic leukocytes into the inflamed bowel. Here we examined whether the NFKBIA 2758G/A and ICAM‐1 K469E variants, recently shown to be CD susceptibility genes in Caucasian populations in Germany and the United Kingdom, are associated with CD in Caucasian patients in New Zealand.Methods:  PCR‐RFLP analysis was used to examine the frequency of gene polymorphisms in 182 CD patients and 188 ethnically matched controls.Results:  There was no significant evidence of a difference in the allele frequency of either the 2758G/A polymorphism in NFKBIA (0.38 vs 0.35, P = 0.47) or the K469E polymorphism in ICAM‐1 (0.43 vs 0.37, P = 0.10) between CD patients and controls. Nevertheless, the ICAM‐1 469E allele significantly (P = 0.016, Pc = 0.047) influenced the age of diagnosis of CD. Meta‐analysis with five other studies confirmed a lack of association of the K469E polymorphism with Crohn's disease (P = 0.33; OR = 0.93; 95% CI, 0.82–1.07).Conclusion:  The NFKBIA 2758G/A and ICAM‐1 K469E polymorphisms are not significant risk factors for CD in New Zealand; however, there is evidence that the latter polymorphism influences the age of diagnosis.
A high‐threshold heat‐activated channel in cultured rat dorsal root ganglion neurons resembles TRPV2 and is blocked by gadolinium
Authors: Leffler Andreas , Linte Ramona Madalina , Nau Carla , Reeh Peter , Babes Alexandru 
Published: June 2007

AbstractHeat‐activated ion channels from the vanilloid‐type TRP group (TRPV1–4) seem to be central for heat‐sensitivity of nociceptive sensory neurons. Displaying a high‐threshold (> 52 °C) for activation, TRPV2 was proposed to act as a sensor for intense noxious heat in mammalian sensory neurons. However, although TRPV2 is expressed in a distinct population of thinly myelinated primary afferents, a widespread expression in a variety of neuronal and non‐neuronal tissues suggests a more diverse physiological role of TRPV2. In its role as a heat‐sensor, TRPV2 has not been thoroughly characterized in terms of biophysical and pharmacological properties. In the present study, we demonstrate that the features of heterologously expressed rat TRPV2 closely resemble those of high‐threshold heat‐evoked currents in medium‐ and large‐sized capsaicin‐insensitive rat dorsal root ganglion (DRG) neurons. Both in TRPV2‐expressing human embryonic kidney (HEK)293t cells and in DRGs, high‐threshold heat‐currents were sensitized by repeated activation and by the TRPV1–3 agonist, 2‐aminoethoxydiphenyl borate (2‐APB). In addition to a previously described block by ruthenium red, we identified the trivalent cations, lanthanum (La3+) and gadolinium (Gd3+) as potent blockers of TRPV2. Thus, we present a new pharmacological tool to distinguish between heat responses of TRPV2 and the closely related capsaicin‐receptor, TRPV1, which is strongly sensitized by trivalent cations. We demonstrate that self‐sensitization of heat‐evoked currents through TRPV2 does not require extracellular calcium and that TRPV2 can be activated in cell‐free membrane patches in the outside‐out configuration. Taken together our results provide new evidence for a role of TRPV2 in mediating high‐threshold heat responses in a subpopulation of mammalian sensory neurons.
Neurosteroid modulation of neuronal excitability and synaptic transmission in the rat medial vestibular nuclei
Authors: Grassi Silvarosa , Frondaroli Adele , Dieni Cristina , Dutia Mayank B. , Pettorossi Vito E. 
Published: June 2007

AbstractIn rat brainstem slices, we investigated the influence of the neurosteroids tetrahydrodeoxycorticosterone (THDOC) and allopregnanolone (ALLO) on the synaptically driven and spontaneous activity of vestibular neurons, by analysing their effects on the amplitude of the field potentials evoked in the medial vestibular nuclei (MVN) by vestibular afferent stimulation and on the spontaneous firing rate of MVN neurons. Furthermore, the interaction with γ‐aminobutyric acid (GABA) and glutamate receptors was analysed by using specific antagonists for GABAA (bicuculline), α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionic acid (AMPA)/ kainate [2,3‐dioxo‐6‐nitro‐1,2,3,4‐tetrahydrobenzo(f)quinoxaline‐7‐sulphonamide disodium salt (NBQX)], N‐methyl‐d‐aspartate (NMDA) [d‐(–)‐2‐amino‐5‐phosphonopentanoic acid (AP‐5)] and group I metabotropic glutamate receptors (mGlu‐I) [(R,S)‐1‐aminoindan‐1,5‐dicarboxylic acid (AIDA)] receptors. THDOC and ALLO evoked two opposite long‐lasting effects, consisting of either a potentiation or a reduction of field potential and firing rate, which showed early and late components, occurring in conjunction or separately after neurosteroid application. The depressions depended on GABAA receptors, as they were abolished by bicuculline, while early potentiation involved glutamate AMPA/kainate receptors, as NBQX markedly reduced the incidence of early firing rate enhancement and, in the case of ALLO, even provoked depression. This suggests that THDOC and ALLO enhance the GABAA inhibitory influence on the MVN neurons and facilitate the AMPA/kainate facilitatory one. Conversely, a late potentiation effect, which was still induced after glutamate and GABAA receptor blockade, might involve a different mechanism. We conclude that the modulation of neuronal activity in the MVN by THDOC and ALLO, through their actions on GABAA and AMPA/kainate receptors, may have a physiological role in regulating the vestibular system function under normal conditions and during the stress response that accompanies many forms of vestibular dysfunction.
Identification of genes differentially expressed in SH‐SY5Y neuroblastoma cells exposed to the prion peptide 106–126
Authors: Martínez Tamara , Pascual Angel 
Published: June 2007

AbstractPrion diseases are a group of neurodegenerative disorders characterized by astrocytosis and progressive neuronal degeneration. As a causative agent, prions have been intensely investigated in different experimental models. However, the mechanisms and pathways involved in the prion‐induced neurological dysfunction are poorly understood. In this work we have investigated the influence of prion infection on the gene expression profile in a human neuroblastoma cell line. Using a DNA microarray and quantitative reverse transcriptase‐polymerase chain reaction methods, we have analysed in SH‐SY5Y cells the effects of a synthetic peptide corresponding to the 106–126 neurotoxic region of the cellular human prion protein. Our results show that addition of this peptide to the neuronal culture specifically changes the expression of a relative high number of genes, and causes a progressive neuronal death even in the absence of microglia.
Effects of pilocarpine on the cortical and hippocampal theta rhythm in different vigilance states in rats
Authors: Tejada S. , Rial R. V. , Coenen A. M. L. , Gamundi A. , Esteban S. 
Published: June 2007

AbstractIt has been suggested that theta rhythm gates the flow of information between the hippocampus and cortex during memory processes. The cholinergic system plays an important role in regulating vigilance states and in generating theta rhythm. This study aims to analyse the effects of the muscarinic agonist pilocarpine (120 and 360 µg, i.c.v.) on hippocampal and frontal cortical theta rhythm during several vigilance states in rats. Pilocarpine injection increased the duration and number of episodes with theta activity, particularly when theta rhythm appeared during waking states in the cortex and hippocampus simultaneously. It seems that the effects of pilocarpine are related to the appearance of cortical theta activity in waking states, and suggest that pilocarpine could modify the transference rate of information from the hippocampus to cortex in rats during wakefulness states, in relation to the postulated effect of cholinergic system modulating memory consolidation.
Trophic effects of keratinocytes on the axonal development of sensory neurons in a coculture model
Authors: Ulmann Lauriane , Rodeau Jean‐Luc , Danoux Louis , Contet‐Audonneau Jean‐Luc , Pauly Gilles , Schlichter Rémy 
Published: June 2007

AbstractThe epidermis, the outermost structure of the skin, fulfils important roles as a physical barrier between the organism and its environment and as a neuroendocrine, immune and sensory organ. It is innervated by unmyelinated sensory fibres conveying nociceptive and thermoceptive information. Little is known concerning the functional interactions between these sensory fibres and the keratinocytes, which constitute 95% of the epidermal cells. We have developed a coculture model of primary rat sensory neurons and keratinocytes, as well as of equivalent cell‐lines: ND7‐23 neurons and A431 keratinocytes. We show that primary dorsal root ganglion neurons survive well in a standard keratinocyte reference medium containing a low concentration of calcium, but fail to extend axons. However, when neurons are cocultured with keratinocytes, axonal outgrowth is strongly stimulated. The use of a Transwell culture system indicated that the stimulation of axonal growth depends on a soluble factor secreted by keratinocytes. Axon outgrowth was also induced by nerve growth factor or brain‐derived neurotrophic factor, but not by neurotrophin 3 or glial cell‐derived neurotrophic factor. Neurons cocultured with keratinocytes did not change their responses to ATP, capsaicin or high potassium solution, as measured by calcium imaging. The trophic effect of keratinocytes concerned essentially a population of medium‐sized (17–25 µm) neurons, some of which expressed substance P‐like immunoreactivity and responded to capsaicin. Our preparation, in which cells are maintained at low external calcium concentration, could represent a useful in vitro model for characterizing the effect of skin‐derived guidance and trophic factors.
Insulin glulisine: a faster onset of action compared with insulin lispro
Authors: Heise T. , Nosek L. , Spitzer H. , Heinemann L. , Niemöller E. , Frick A. D. , Becker R. H. A. 
Published: June 2007

Aim:  This randomized, single‐centre, double‐blind, crossover study compared the pharmacodynamic and pharmacokinetic properties of two different doses of insulin glulisine (glulisine) and insulin lispro (lispro) in lean to obese subjects.Methods:  Eighty subjects without diabetes, stratified into four body mass index (BMI) classes (<25, ≥25 to <30, ≥30 to <35 and ≥35 kg/m2), were randomized to receive single injections of glulisine and lispro (0.2 and 0.4 U/kg) on four study days under glucose clamp conditions. Glucose infusion rates (GIR) and insulin (INS) concentrations were assessed for 10 h postdose.Results:  Glulisine showed a greater early metabolic action than lispro [GIR‐area under the curve (GIR‐AUC) between 0 and 1 h (0.2 U/kg: 102.3 ± 75.1 vs. 83.1 ± 72.8 mg/kg, p < 0.05; 0.4 U/kg: 158.0 ± 100.0 vs. 112.3 ± 70.8 mg/kg, p < 0.001)], with an earlier time to 10% of total GIR‐AUC (0.2 U/kg: 1.4 ± 0.4 vs. 1.5 ± 0.4 h; 0.4 U/kg: 1.4 ± 0.3 vs. 1.5 ± 0.3 h, p < 0.05). The total metabolic effect was not different between the two insulins. In accordance with these findings, the time to 10% of total INS‐AUC was faster with glulisine compared with lispro at either dose (0.2 U/kg: 0.7 ± 0.2 vs. 0.8 ± 0.2 h; 0.4 U/kg: 0.8 ± 0.2 vs. 0.9 ± 0.2 h, p < 0.001). The faster rise in insulin concentrations and the earlier onset of activity of glulisine vs. lispro was consistently observed in each individual BMI class.Conclusions:  Glulisine shows a faster onset of action than lispro, independent of BMI and dose.