bluuebunny/crossref_metadata_2025_split huggingface dataset:
Wind‐controlled linear patterning and cyclic succession in Tasmanian Sphagnum mires
Authors: Morgan Sam W. , Kirkpatrick James B. , Di Folco Maj‐Britt 
Published: January 2010

Summary 1. We investigated the characteristics and causes of striped patterning in minerotrophic Sphagnum cristatum mires on the western Central Plateau in Tasmania by surveying the mire vegetation, surface and subsurface topography, analysing their topographic exposure to the prevailing strong winds relative to non‐striped mires, stratigraphic analysis, measurements of wind speed and direction across and along ridges and swales in typical synoptic conditions, and measurement of growth rates and asymmetry of shrubs. 2. The stripes were orientated south‐west–north‐east, independent of the aspect of the general slope. The shrub Richea scoparia was dominant on the north‐west‐facing slopes of the low ridges that formed the stripes. Sphagnum cristatum was dominant on the south‐east‐facing ridge slopes and the restiad, Baloskion australe was dominant in the swales. The stripes were independent of the topography of the underlying block stream. Striped mires were more exposed to both north‐westerly and south‐westerly winds than non‐striped mires. 3. Strong north‐westerly winds formed rotors behind each ridge, with wind speed being highest on the north‐west‐facing ridge slope and lowest on the south‐east‐facing ridge slope. The annual growth of R. scoparia inversely reflected this variation in wind speed. South‐westerly winds were stronger in the swales than on the ridges and stronger on the south‐west extremity of the ridges than further to the north‐east. Asymmetry in R. scoparia on the ridges reflected this variation in wind speed. 4. We infer that the ridges slowly migrate in a cyclic successional pattern as the result of differential growth rates of R. scoparia in response to variation in the speed of drying north‐westerly winds. The stripes appear to result from training of shrubs by strong, cold south‐westerly winds, which also inhibit the growth of R. scoparia in the swales. 5.
Synthesis. There are no other documented cases of wind‐controlled patterning and cyclic succession in mires, and no case of exposure to two distinct wind directions being responsible for patterning in any vegetation type. The distinctiveness of the process and the form merit recognition of these striped mires as outstanding in their universal value under the world heritage area criteria.
A high protein low fat meal does not influence glucose and insulin responses in obese individuals with or without type 2 diabetes
Authors: Papakonstantinou E. , Triantafillidou D. , Panagiotakos D. B. , Iraklianou S. , Berdanier C. D. , Zampelas A. 
Published: January 2010

AbstractBackground:  When substituted for carbohydrate in a meal, dietary protein enhances glycaemic control in subjects with type 2 diabetes (DM2). It is unknown whether the effect is a result of increased protein or reduced carbohydrate. The present study aimed to compare the effects of two meals differing in protein to fat ratios on post‐prandial glucose and insulin responses.Methods:  This was a crossover, blind study in which obese subjects with (n = 23) and without (n = 26) DM2 consumed two meals in random order with equal amounts of energy (3.1 MJ, 741 kcal), fibre and carbohydrates and a 1‐week washout period. Meals were a high protein, low fat (30% protein, 51% carbohydrates, 19% fat) meal and a low protein, high fat (15% protein, 51% carbohydrates, 34% fat) meal. Subjects were matched for age and body mass index. Plasma glucose and insulin were measured at fasting, 30, 60, 90, 120 min post‐prandially. Insulin resistance and insulin sensitivity were assessed.Results:  There was no significant meal effect on glucose and insulin responses within groups. Glucose response was higher in diabetic (120 min 11 ± 0.7 mmol L−1) compared to nondiabetic (120 min 5 ± 0.2; P < 0.001) subjects. Diabetic subjects had significantly higher insulin resistance (P < 0.001) and lower insulin sensitivity (P < 0.001) than nondiabetics. Although peak insulin levels, 60 min post‐prandially, did not differ between groups (81 ± 9 pmol L−1 for diabetic versus 79 ± 7 pmol L−1 for nondiabetic subjects), they were achieved much later, 90 min post‐prandially, in diabetic, (99 ± 8 pmol L−1) compared to nondiabetic (63 ± 7 pmol L−1, P = 0.002) subjects.Conclusions:  Manipulating protein to fat ratio in meals does not affect post‐prandial plasma blood glucose or insulin responses in obese people with and without DM2.
The influence of alcohol consumed with a meal on endothelial function in healthy individuals
Authors: Hampton S. M. , Isherwood C. , Kirkpatrick V. J. E. , Lynne‐Smith A. C. , Griffin B. A. 
Published: January 2010

AbstractBackground:  Alcohol and polyphenols in wine and fruit juices have been strongly implicated in the favourable effects on of these beverages on vascular function. Despite a wealth of information on the metabolic and vascular effects of alcohol and polyphenols, the combined influences of these substances on vascular function, especially when consumed with food, is poorly understood. A study was designed to determine the effects of a phenolic‐rich grape juice, with or without alcohol, on vascular endothelial function in the postprandial state.Methods:  Ten subjects consumed a standard meal with a test drink on three separate occasions. On each occasion, the test drink accompanying the meal was either red grape juice, red grape juice plus alcohol (12% v/v), or water. Endothelial function was measured by flow mediated dilatation (FMD) prior to then 30 and 60 minutes after consuming the meal. Blood samples were taken for the determination of plasma glucose, triacylglycerol (TAG) and non esterified fatty acids (NEFA) at regular intervals.Results:  There was a significant effect of the three treatments (P = 0.0026) and time (P = 0.021) on percentage FMD. The meals with the grape juice and grape juice plus alcohol produced similar FMD responses but were both significantly greater than the meal with water. The concentration of plasma glucose, TAG and NEFA were similar after each treatment.Conclusion:  Alcohol had no effect on vascular function in the early postprandial phase. These findings provide new evidence to support the potential benefit of non‐alcoholic components within alcoholic beverages on vascular function in the fed state.
Nutritional vitamin A status in northeast Brazilian lactating mothers
Authors: Da Silva Ribeiro K. D. , De Araújo K. F. , De Souza H. H. B. , Soares F. B. , Da Costa Pereira M. , Dimenstein R. 
Published: January 2010

AbstractBackground:  Vitamin A deficiency is the major cause of morbidity and mortality among children and in women of reproductive age in developing countries. The present study aimed to assess maternal nutritional vitamin A status, as well as analyse the association of preformed vitamin A and pro‐vitamin A consumption on the nutritional status of nursing mothers, based on serum retinol and retinol colostrum concentrations coupled with dietary intake.Methods:  Serum and colostrums were collected from 86 healthy parturients, recruited within 16 h postpartum. Blood samples were obtained, the morning after an overnight fast. Retinol was analysed by high‐performance liquid chromatography. Dietary vitamin A was assessed using a food frequency questionnaire and the women were separated into two groups according to the predominant dietary source of vitamin A: group A, >50% preformed vitamin A (n = 37); and group B >50% pro‐vitamin A carotenoids, (n = 49).Results:  Serum retinol and total vitamin A ingestion (mean ± SD) were higher in group A than in group B (1.4 ± 0.4 μmol L−1 and 2072.0 ± 1465.9 μg retinol activity equivalent (RAE) day−1 versus 1.2 ± 0.6 μmol L−1 and 1051.6 ± 920.4 μg RAE day−1, respectively (P < 0.05), but colostrum retinol (3.4 ± 1.7 μmol L−1 and 3.6 ± 1.9 μmol L−1) was similar in both groups. In group B, 36.7% (n = 18) of the nursing mothers presented a risk of developing vitamin A deficiency, based on their dietary intake.Conclusions:  On the basis of the intake of the pro‐vitamin A carotenoids, some women may be at risk of vitamin A deficiency. However, their status is currently normal, as indicated by serum and milk retinol concentrations.
Plasmodium pyruvate dehydrogenase activity is only essential for the parasite's progression from liver infection to blood infection
Authors: Pei Ying , Tarun Alice S. , Vaughan Ashley M. , Herman Rob W. , Soliman Joanne M. B. , Erickson‐Wayman Alyssa , Kappe Stefan H. I. 
Published: January 2010

Summary Plasmodium parasites possess a single pyruvate dehydrogenase (PDH) enzyme complex that is localized to the plastid‐like organelle known as the apicoplast. Unlike most eukaryotes, Plasmodium parasites lack a mitochondrial PDH. The PDH complex catalyses the conversion of pyruvate to acetyl‐CoA, an important precursor for the tricarboxylic acid cycle and type II fatty acid synthesis (FAS II). In this study, using a rodent malaria model, we show that the PDH E1α and E3 subunits colocalize with the FAS II enzyme FabI in the apicoplast of liver stages but are not significantly expressed in blood stages. Deletion of the E1α or E3 subunit genes of Plasmodium yoelii PDH caused no defect in blood stage development, mosquito stage development or early liver stage development. However, the gene deletions completely blocked the ability of the e1α‐ and e3‐ parasites to form exo‐erythrocytic merozoites during late liver stage development, thus preventing the initiation of a blood stage infection. This phenotype is similar to that observed for deletions of genes involved in FAS II elongation. The data strongly support the hypothesis that the sole role of PDH is to provide acetyl‐CoA for FAS II.
Effects of ocean acidification and high temperatures on the bryozoan Myriapora truncata at natural CO2 vents
Authors: Rodolfo‐Metalpa Riccardo , Lombardi Chiara , Cocito Silvia , Hall‐Spencer Jason M. , Gambi Maria Cristina 
Published: January 2010

AbstractThere are serious concerns that ocean acidification will combine with the effects of global warming to cause major shifts in marine ecosystems, but there is a lack of field data on the combined ecological effects of these changes due to the difficulty of creating large‐scale, long‐term exposures to elevated CO2 and temperature. Here we report the first coastal transplant experiment designed to investigate the effects of naturally acidified seawater on the rates of net calcification and dissolution of the branched calcitic bryozoan Myriapora truncata (Pallas, 1766). Colonies were transplanted to normal (pH 8.1), high (mean pH 7.66, minimum value 7.33) and extremely high CO2 conditions (mean pH 7.43, minimum value 6.83) at gas vents off Ischia Island (Tyrrhenian Sea, Italy). The net calcification rates of live colonies and the dissolution rates of dead colonies were estimated by weighing after 45 days (May–June 2008) and after 128 days (July–October) to examine the hypothesis that high CO2 levels affect bryozoan growth and survival differently during moderate and warm water conditions. In the first observation period, seawater temperatures ranged from 19 to 24 °C; dead M. truncata colonies dissolved at high CO2 levels (pH 7.66), whereas live specimens maintained the same net calcification rate as those growing at normal pH. In extremely high CO2 conditions (mean pH 7.43), the live bryozoans calcified significantly less than those at normal pH. Therefore, established colonies of M. truncata seem well able to withstand the levels of ocean acidification predicted in the next 200 years, possibly because the soft tissues protect the skeleton from an external decrease in pH. However, during the second period of observation a prolonged period of high seawater temperatures (25–28 °C) halted calcification both in controls and at high CO2, and all transplants died when high temperatures were combined with extremely high CO2 levels. Clearly, attempts to predict the future response of organisms to ocean acidification need to consider the effects of concurrent changes such as the Mediterranean trend for increased summer temperatures in surface waters. Although M. truncata was resilient to short‐term exposure to high levels of ocean acidification at normal temperatures, our field transplants showed that its ability to calcify at higher temperatures was compromised, adding it to the growing list of species now potentially threatened by global warming.
Attenuated familial adenomatous polyposis: results from an international collaborative study
Authors: Knudsen A. L. , Bülow S. , Tomlinson I. , Möslein G. , Heinimann K. , Christensen I. J. ,   The AFAP Study Group
Published: January 2010

AbstractAim  The study aimed to describe genetical and clinical features of attenuated familial adenomatous polyposis (AFAP) and to propose clinical criteria and guidelines for treatment and surveillance.Method  A questionnaire study was carried out of polyposis registries with data on patients with presumed AFAP, defined as having ≤100 colorectal adenomas at age ≥25.Results  One hundred and ninety‐six patients were included. The median number of adenomas was 25 (0–100) with a uniform distribution of colorectal adenomas and carcinomas (CRC). Age at CRC diagnosis was delayed by 15 years compared with classic FAP. Eighty‐two patients had a colectomy and an ileorectal anastomosis and 5/82 (6%) had a secondary proctectomy. The location of the mutation in the APC gene was known in 69/171 (40%) tested patients. Only 15/29 (52%) of mutations in APC were found in parts of the gene usually associated with AFAP (the 5′ end, exon 9 and 3′ end).Conclusions  A subset of FAP patients with a milder phenotype does exist and treatment and surveillance had to be modified accordingly. The mutation detection rate is lower than in classic FAP and mutations in AFAP patients are located throughout the APC gene. We propose the following clinical diagnostic criteria for AFAP: a dominant mode of inheritance of colorectal adenomatosis and <100 colorectal adenomas at age 25 or older. Colonoscopy had to be preferred to sigmoidoscopy and surveillance had to be life‐long. In the majority of patients, prophylactic colectomy and ileorectal anastomosis are recommended at the age of 20–25 years.
Symptoms and signs in patients with colorectal cancer
Authors: John S. K. P. , George S. , Primrose J. N. , Fozard J. B. J. 
Published: January 2010

AbstractThe symptoms and signs of colorectal cancer vary from the general population to primary care and in the referred population to secondary care. This review aims to address the diverse symptoms, signs and combinations with relevance to colorectal cancer at various points in the diagnostic pathway and tries to shed light on this complex and confusing area. A move towards a lower threshold for referral and increased use of diagnostics might be a more reliable option for early diagnosis.
Periictal heart rate variability analysis suggests long‐term postictal autonomic disturbance in epilepsy
Authors: Toth V. , Hejjel L. , Fogarasi A. , Gyimesi C. , Orsi G. , Szucs A. , Kovacs N. , Komoly S. , Ebner A. , Janszky J. 
Published: January 2010

Background:  One of the possible pathomechanisms of sudden death in epilepsy (SUDEP) is a postictal dysregulation of autonomic nervous system. We performed a heart rate variability (HRV) analysis of the periictal state to analyze whether a cardiac autonomic disturbance exists after an epileptic seizure.Methods:  We included 31 periictal video–EEG–ECG recordings of 31 patients with epilepsy who had consecutively undergone pre‐surgical evaluation. Nine generalized tonic‐clonic (GTCS), 15 complex partial, and seven simple motor seizures were included. HRV was evaluated by analyzing 5‐min‐long ECG epochs, sampling from baseline, direct preictal, early‐postictal (<15 min after the seizure), and late‐postictal (5–6 h after the seizure) periods.Results:  The heart rate was elevated immediately after the seizures, but 5–6 h postictally returned to the baseline level. Time‐domain components of HRV decreased after the seizure and this decrease lasted for 5–6 h. Low‐frequency power decreased in the early‐postictal phase and high‐frequency power of HRV dropped in the late‐postictal phase. GTCS had an impact on short‐term but not on long‐term postictal HRV decrease.Conclusions:  We found decreased HRV immediately after the seizures, which lasted at least 5–6 h postictally, indicating a long‐term postictal disturbance of the autonomous nervous system. GTCS were accompanied by a more decreased HRV than other seizures. Our results may have relevance in explaining pathomechanism of SUDEP.
Sp proteins play a critical role in histone deacetylase inhibitor‐mediated derepression of CYP46A1 gene transcription
Authors: Nunes Maria João , Milagre Inês , Schnekenburger Michael , Gama Maria João , Diederich Marc , Rodrigues Elsa 
Published: January 2010

J. Neurochem. (2010) 113, 418–431.AbstractWe investigated whether the CYP46A1 gene, a neuronal‐specific cytochrome P450, responsible for the majority of brain cholesterol turnover, is subject to transcriptional modulation through modifications in histone acetylation. We demonstrated that inhibition of histone deacetylase activity by trichostatin A (TSA), valproic acid and sodium butyrate caused a potent induction of both CYP46A1 promoter activity and endogenous expression. Silencing of Sp transcription factors through specific small interfering RNAs, or impairing Sp binding to the proximal promoter, by site‐directed mutagenesis, led to a significant decrease in TSA‐mediated induction of CYP46A1 expression/promoter activity. Electrophoretic mobility shift assay, DNA affinity precipitation assays and chromatin immunoprecipitation assays were used to determine the multiprotein complex recruited to the CYP46A1 promoter, upon TSA treatment. Our data showed that a decrease in Sp3 binding at particular responsive elements, can shift the Sp1/Sp3/Sp4 ratio, and favor the detachment of histone deacetylase (HDAC) 1 and HDAC2 and the recruitment of p300/CBP. Moreover, we observed a dynamic change in the chromatin structure upon TSA treatment, characterized by an increase in the local recruitment of euchromatic markers and RNA polymerase II. Our results show the critical participation of an epigenetic program in the control of CYP46A1 gene transcription, and suggest that brain cholesterol catabolism may be affected upon treatment with HDAC inhibitors.
Altered brain phospholipid and acylcarnitine profiles in propionic acid infused rodents: further development of a potential model of autism spectrum disorders
Authors: Thomas Raymond H. , Foley Kelly A. , Mepham Jennifer R. , Tichenoff Lisa J. , Possmayer Fred , MacFabe Derrick F. 
Published: January 2010

J. Neurochem. (2010) 113, 515–529.AbstractRecent studies have demonstrated intraventricular infusions of propionic acid (PPA) a dietary and enteric short‐chain fatty acid can produce brain and behavioral changes similar to those observed in autism spectrum disorder (ASD). The effects of PPA were further evaluated to determine if there are any alterations in brain lipids associated with the ASD‐like behavioral changes observed following intermittent intraventricular infusions of PPA, the related enteric metabolite butyric acid (BUT) or phosphate‐buffered saline vehicle. Both PPA and BUT produced significant increases (p < 0.001) in locomotor activity (total distance travelled and stereotypy). PPA and to a lesser extent BUT infusions decreased the levels of total monounsaturates, total ω6 fatty acids, total phosphatidylethanolamine plasmalogens, the ratio of ω6 : ω3 and elevated the levels of total saturates in separated phospholipid species. In addition, total acylcarnitines, total long‐chain (C12–C24) acylcarnitines, total short‐chain (C2 to C9) acylcarnitines, and the ratio of bound to free carnitine were increased following infusions with PPA and BUT. These results provide evidence of a relationship between changes in brain lipid profiles and the occurrence of ASD‐like behaviors using the autism rodent model. We propose that altered brain fatty acid metabolism may contribute to ASD.
The amyloid precursor protein intracellular domain (AICD) disrupts actin dynamics and mitochondrial bioenergetics
Authors: Ward Manus W. , Concannon Caoimhín G. , Whyte Jacqueline , Walsh Ciara M. , Corley Brian , Prehn Jochen H. M. 
Published: January 2010

J. Neurochem. (2010) 10.1111/j.1471‐4159.2010.06615.xAbstractThe amyloid precursor protein (APP) is critically involved in the pathogenesis of Alzheimer’s disease, and is strongly up‐regulated in response to traumatic, metabolic, or toxic insults to the nervous system. The processing of APP by γ/ε‐secretase activity results in the generation of the APP intracellular domain (AICD). Previously, we have shown that AICD induces the expression of genes (transgelin, α2‐actin) with functional roles in actin organization and dynamics and demonstrated that the induction of AICD and its co‐activator Fe65 (AICD/Fe65) resulted in a loss of organized filamentous actin structures within the cell. As mitochondrial function is thought to be reliant on ordered actin dynamics, we examined mitochondrial function in human SHEP neuroblastoma cells inducibly expressing AICD/Fe65. Confocal analysis of the mitochondrial membrane potential (Δψm) identified a significant decrease in the Δψm in the AICD50/Fe65 over‐expressing cells. This was paralleled by significantly reduced ATP levels and decreased basal superoxide production. Over‐expression of the proposed AICD target gene transgelin in SHEP‐SF parental cells and primary neurons was sufficient to destabilize actin filaments, depolarize Δψm, and significantly alter mitochondrial disrtibution and morphology. Our data demonstrate that the induction of AICD/Fe65 or transgelin significantly alters actin dynamics and mitochondrial function in neuronal cells.
Protein modification and replicative senescence of WI‐38 human embryonic fibroblasts
Authors: Ahmed Emad K. , Rogowska‐Wrzesinska Adelina , Roepstorff Peter , Bulteau Anne‐Laure , Friguet Bertrand 
Published: January 2010

SummaryOxidized proteins as well as proteins modified by the lipid peroxidation product 4‐hydroxy‐2‐nonenal (HNE) and by glycation (AGE) have been shown to accumulate with aging in vivo and during replicative senescence in vitro. To better understand the mechanisms by which these damaged proteins build up and potentially affect cellular function during replicative senescence of WI‐38 fibroblasts, proteins targeted by these modifications have been identified using a bidimensional gel electrophoresis‐based proteomic approach coupled with immunodetection of HNE‐, AGE‐modified and carbonylated proteins. Thirty‐seven proteins targeted for either one of these modifications were identified by mass spectrometry and are involved in different cellular functions such as protein quality control, energy metabolism and cytoskeleton. Almost half of the identified proteins were found to be mitochondrial, which reflects a preferential accumulation of damaged proteins within the mitochondria during cellular senescence. Accumulation of AGE‐modified proteins could be explained by the senescence‐associated decreased activity of glyoxalase‐I, the major enzyme involved in the detoxification of the glycating agents methylglyoxal and glyoxal, in both cytosol and mitochondria. This finding suggests a role of detoxification systems in the age‐related build‐up of damaged proteins. Moreover, the oxidized protein repair system methionine sulfoxide reductase was more affected in the mitochondria than in the cytosol during cellular senescence. Finally, in contrast to the proteasome, the activity of which is decreased in senescent fibroblasts, the mitochondrial matrix ATP‐stimulated Lon‐like proteolytic activity is increased in senescent cells but does not seem to be sufficient to cope with the increased load of modified mitochondrial proteins.