bluuebunny/crossref_metadata_2025 huggingface dataset:
Anaerobic ammonia oxidation in a fertilized paddy soil
Authors: Zhu Guibing , Wang Shanyun , Wang Yu , Wang Chaoxu , Risgaard-Petersen Nils , Jetten Mike SM , Yin Chengqing
Published: May 2011

Evidence for anaerobic ammonium oxidation in a paddy field was obtained in Southern China using an isotope-pairing technique, quantitative PCR assays and 16S rRNA gene clone libraries, along with nutrient profiles of soil cores. A paddy field with a high load of slurry manure as fertilizer was selected for this study and was shown to contain a high amount of ammonium (6.2–178.8 mg kg−1). The anaerobic oxidation of ammonium (anammox) rates in this paddy soil ranged between 0.5 and 2.9 nmolN per gram of soil per hour in different depths of the soil core, and the specific cellular anammox activity observed in batch tests ranged from 2.9 to 21 fmol per cell per day. Anammox contributed 4–37% to soil N2 production, the remainder being due to denitrification. The 16S rRNA gene sequences of surface soil were closely related to the anammox bacteria ‘Kuenenia’, ‘Anammoxoglobus’ and ‘Jettenia’. Most of the anammox 16S rRNA genes retrieved from the deeper soil were affiliated to ‘Brocadia’. The retrieval of mainly bacterial amoA sequences in the upper part of the paddy soil indicated that nitrifying bacteria may be the major source of nitrite for anammox bacteria in the cultivated horizon. In the deeper oxygen-limited parts, only archaeal amoA sequences were found, indicating that archaea may produce nitrite in this part of the soil. It is estimated that a total loss of 76 g N m−2 per year is linked to anammox in the paddy field.
Inhibition of Tyrosine Phosphorylation Prevents Delayed Neuronal Death following Cerebral Ischemia
Authors: Kindy Mark S.
Published: May 2011

Protein tyrosine phosphorylation plays an important role in the regulation of neuronal function. We examined the effects of inhibition of tyrosine phosphorylation on ischemic neuronal damage in the CA1 region of the hippocampus. In the gerbil hippocampus, genistein and lavendustin A, tyrosine kinase inhibitors, were administered 30 min before initiation of 5-min ischemia and reperfusion. Both genistein and lavendustin A blocked tyrosine phosphorylation and prevented delayed neuronal death (DND). However, genistin, an inactive analogue of genistein, did not block DND. Genistein was dose-dependent in the inhibition of DND after ischemia and reperfusion. Administration of genistein 5 to 10 min after ischemia and reperfusion was ineffective in blocking DND in the CA1 region of the hippocampus. The tyrosine kinase inhibitors selectively blocked the phosphorylation of microtubule-associated protein (MAP)-2 kinase following ischemia and reperfusion injury. These results suggest that tyrosine phosphorylation in the ischemic brain is important for neuronal injury and that MAP-2 kinase may play a role in the onset of delayed neuronal death.
Basic FGF, NGF, and IGFs Protect Hippocampal and Cortical Neurons against Iron-Induced Degeneration
Authors: Zhang Ying , Tatsuno Tohru , Carney John M. , Mattson Mark P.
Published: May 2011

Iron is believed to contribute to the process of cell damage and death resulting from ischemic and traumatic insults by catalyzing the oxidation of protein and lipids. Exposure of cultured rat hippocampal neurons to iron (FeSO4) caused a dose-dependent reduction in neuronal survival, which was potentiated by ascorbate. Damage to neurons was associated with a significant level of oxygen radical in the culture medium. The iron chelator desferal prevented both the neuronal degeneration caused by FeSO4 and the production of oxygen radical, demonstrating that ionic iron was responsible for the cell damage. Iron neurotoxicity was associated with an elevation of [Ca2+]i and was attenuated by NMDA receptor antagonists. Since recent findings demonstrated neuroprotective effects of growth factors in cell culture and in vivo models of ischemia, we examined the effects of growth factors on iron-induced damage. Basic fibroblast growth factor (bFGF), nerve growth factor (NGF), and insulinlike growth factors (IGF-I and IGF-II) each protected neurons against iron-induced damage. Both rat hippocampal and human cortical neurons were protected by these growth factors. Taken together, the data suggest that the neuroprotective effects of growth factors against excitotoxic/ischemic insults may result, in part, from a prevention or attenuation of oxidative damage.
Temperature Modulation of Cerebral Depolarization during Focal Cerebral Ischemia in Rats: Correlation with Ischemic Injury
Authors: Chen Qun , Chopp Michael , Bodzin Gordon , Chen Hua
Published: May 2011

The role of cerebral depolarizations in focal cerebral ischemia is unknown. We therefore measured the direct current (DC) electrical activity in the cortex of Wistar rats subjected to transient occlusion of the middle cerebral artery (MCA). Focal ischemia was induced for 90 min by insertion of an intraluminal filament to occlude the MCA. To modulate cell damage, we subjected the rats to hypothermic (30°C, n = 4), normothermic (37°C, n = 4), and hyperthermic (40°C, n = 6) ischemia. Controlled temperatures were also maintained during 1 h of reperfusion. Continuous cortical DC potential changes were measured using two active Ag–AgCl electrodes placed in the cortical lesion. Animals were killed 1 week after ischemia. The brains were sectioned and stained with hematoxylin and eosin, for evaluation of neuronal damage, and calculation of infarct volume. All animals exhibited an initial depolarization within 30 min of ischemia, followed by a single depolarization event in hypothermic animals, and multiple periodic depolarization events in both normothermic and hyperthermic animals. Hyperthermic animals exhibited significantly more (p < 0.05) DC potential deflections (n = 6.17 ± 0.67) than normothermic animals (n = 2.75 ± 0.96). The ischemic infarct volume (% of hemisphere) was significantly different for the various groups; hypothermic animals exhibited no measurable infarct volume, while the ischemic infarct volume was 10.2 ± 12.3% in normothermic animals and 36.5 ± 3.4% in hyperthermic animals (p < 0.05). A significant correlation was detected between the volume of infarct and number of depolarization events ( r = 0.90, p < 0.001). Our data indicate that body temperature has a profound effect on the number of ischemic depolarization events, and ischemic cell damage after transient MCA occlusion, and suggest a role for ischemic depolarizations in mediating ischemic cell damage.
Alterations of a 200 kDa Neurofilament in the Rat Hippocampus after Forebrain Ischemia
Authors: Kaku Yasuhiko , Yonekawa Yasuhiro , Tsukahara Tetsuya , Ogata Nobuyoshi , Kimura Tetsuya , Taniguchi Takashi
Published: May 2011

Alteration in the concentration of a 200 kDa neurofilament (NF200) in the rat hippocampus after forebrain ischemia and its relationship to hippocampal neuronal death were studied with an anti-200 kDa neurofilament antibody, using immunohistochemical and immunoblotting techniques. In rats subjected to 8 min of transient forebrain ischemia, hematoxylin-eosin staining showed survival of most of the neurons in the hippocampal CA1 region at 1 day and loss of more than 75% of the neurons at 7 days after ischemia. Immunoblotting showed that the concentration of NF200 in the hippocampal homogenate tended to decrease after ischemia, to 69% of that of control at 1 day and to 60% of the control value at 7 days after 8 min of forebrain ischemia. Following 5 min of ischemia as well, the decrease in the concentration of neurofilaments in the hippocampal region preceded histological confirmation of neuronal cell death. These results suggest that degradation of neurofilament triplet proteins occurred even after ischemia of minimal duration and preceded neuronal death. Degradation of cytoskeletal proteins may play an important role in the mechanism of delayed neuronal death after cerebral ischemia.
Alterations in Protein Kinase C Activity and Membrane Lipid Metabolism in Cerebral Vasospasm after Subarachnoid Hemorrhage
Authors: Takuwa Yoh , Matsui Toru , Abe Yoichiro , Nagafuji Toshiaki , Yamashita Kamejiro , Asano Takao
Published: May 2011

Changes in protein kinase C (PKC) activity, membrane lipid metabolism, and the extent of 20-kDa myosin light chain (MLC) phosphorylation in spastic cerebral basilar arteries were examined by using the beagle “two-hemorrhage” model of subarachnoid hemorrhage. In spastic arteries at days 4 and 7, cytosolic PKC activity showed a decrease of 40–45% with no significant changes in membrane PKC activity as compared with nonspastic control arteries. Cytosolic PKC activity of the day 14 arteries returned toward the normal control level with the remission of vasospasm. Western blot analysis of the PKC isoforms revealed that the amounts of PKCα and PKCε but not PKCζ were decreased in spastic arteries. As compared with nonspastic arteries, spastic arteries showed higher rates of incorporation of [3H]choline into phosphatidylcholine (PC) and [14C]ethanolamine into phosphatidylethanolamine (PE), but not of [3H]myoinositol into phosphoinositides, suggesting the stimulated turnover of PC and PE. The extent of 20-kDa MLC phosphorylation was not increased in the spastic arteries at days 4 or 7 as compared with that in the nonspastic control arteries. These results demonstrate that PKC activity and related membrane lipid metabolism are altered in spastic basilar arteries after subarachnoid hemorrhage.
PET Study of Changes in Local Brain Hemodynamics and Oxygen Metabolism after Unilateral Middle Cerebral Artery Occlusion in Baboons
Authors: Pappata S. , Fiorelli M. , Rommel T. , Hartmann A. , Dettmers C. , Yamaguchi T. , Chabriat H. , Poline J. B. , Crouzel C. , Di Giamberardino L. , Baron J. C.
Published: May 2011

Local cerebral hemodynamics and oxygen metabolism were measured by positron emission tomography (PET) with the oxygen-15 (15O) steady-state method in baboons, immediately before (TO), 1 (T1), and 3–4 (T2) h after permanent middle cerebral artery occlusion (MCAO). At T1, there was a marked fall in both cerebral blood flow (CBF) and the CBF/cerebral blood volume (CBV) ratio in the occluded territory; these changes were sustained at T2, indicating stable reduction in cerebral perfusion pressure and lack of spontaneous reperfusion within this time range. Compared with preocclusion conditions, the oxygen extraction fraction (OEF) in the occluded territory was elevated at both T1 and T2, indicative of a persistent oligemia/ischemia for up to 3 h after MCAO. At T2, however, this OEF increase had lessened, concomitantly with a decline in cerebral metabolic rate of oxygen (CMRO2). This impairment of oxidative metabolism occurred earlier in the deep, compared with the cortical, MCA territories; in the latter, the CMRO2 was essentially preserved at T1 and only moderately reduced at T2, possibly suggesting prolonged viability. Finally, no significant changes in CBF or CMRO2 were observed in the contralateral MCA territory in this time range after MCAO. Despite methodological limitations (mainly partial volume effects related to PET imaging, which may have resulted in an underestimation of true changes and an overlooking of heterogeneous changes) our study demonstrates the feasibility of the combined PET-MCAO paradigm in baboons; this experimental approach should be valuable in investigating the pathophysiology and therapy of acute stroke.
Modeling Analysis of [11C]Flumazenil Kinetics Studied by PET: Application to a Critical Study of the Equilibrium Approaches
Authors: Delforge Jacques , Syrota André , Bottlaender Michel , Varastet Marina , Loc'h Christian , Bendriem Bernard , Crouzel Christian , Brouillet Emmanuel , Maziere Mariannick
Published: May 2011

The multi-injection modeling approach was used for the in vivo quantitation of benzodiazepine receptors in baboon brain using positron emission tomography (PET) and [11C]flumazenil (RO 15-1788) as a specific ligand. The model included three compartments (plasma, free, and bound ligand) and five parameters (including the benzodiazepine receptor concentration). The plasma concentration after correction for the metabolites was used as the input function. The experimental protocol consisted of four injections of labeled and/or unlabeled ligand. This protocol allows the evaluation, from a single experiment, of the five model parameters in various regions of interest. For example, in the temporal cortex, the concentration of receptor sites available for binding ( B′max) and the equilibrium dissociation constant ( Kd) were estimated to be 70 ± 15 pmol/ml and 15.8 ± 2.2 n M, respectively. The validity of the equilibrium approach, which is the most often used quantitation method, has been studied from simulated data calculated using these model parameters. The equilibrium approaches consist of reproducing in PET studies the experimental conditions that permit the use of the usual in vitro methods such as Scatchard analysis. These approaches are often open to criticism because of the difficulty of defining the notion of equilibrium in in vivo studies. However, it appears that the basic relation of Scatchard analysis is valid over a broader range of conditions than those normally used, such as the requirement of a constant bound/free ratio. Simulations showed that the values of the receptor concentration ( B′max) and the equilibrium dissociation constant ( Kd) found using Scatchard analysis are always underestimated. These simulations also suggest an explanation concerning the dependency of B′max and Kd on the time point employed for the Scatchard analysis, a phenomenon found by several authors. To conclude, we propose new protocols that allow the estimation of the B′max and Kd parameters using a Scatchard analysis but based on a protocol including only one or two injections. These protocols being entirely noninvasive, it thus becomes possible to investigate possible changes in receptor density and/or affinity in patients.
Defective Brain Energy Metabolism Shown by in vivo 31P MR Spectroscopy in 28 Patients with Mitochondrial Cytopathies
Authors: Barbiroli Bruno , Montagna Pasquale , Martinelli Paolo , Lodi Raffaele , Iotti Stefano , Cortelli Pietro , Funicello Rosanna , Zaniol Paolo
Published: May 2011

We studied brain energy metabolism by phosphorus magnetic resonance spectroscopy (31P MRS) in 28 patients with mitochondrial cytopathies, and 20 normal control subjects. Fourteen patients had myopathy alone, six had only mild brain symptoms, and eight showed different degrees of brain involvement. Brain 31P MRS showed a low phosphocreatine content in all patients, accompanied by a high inorganic phosphate in 14 of 28 patients. The average value of the Pi concentration in the patient group was significantly (p = 0.009) different from the control group. The cytosolic pH was normal. From these data were derived a high concentration of ADP (calculated from the creatine kinase equilibrium), a high percent value of V/Vmax for ATP biosynthesis, and a low phosphorylation potential, all features showing a derangement of brain energy metabolism, in all patients with mitochondrial cytopathies. 31P MRS proved to be sensitive enough to disclose a deficit of mitochondrial functionality not only in the affected patients, but also in those without clinically evident brain symptoms.
Hypoxia Increases Velocity of Blood Flow through Parenchymal Microvascular Systems in Rat Brain
Authors: Bereczki Daniel , Wei Ling , Otsuka Tadahiro , Acuff Virgil , Pettigrew Karen , Patlak Clifford , Fenstermacher Joseph
Published: May 2011

The postulation that hypoxia increases local cerebral blood flow (lCBF) mainly by perfusing more capillaries (the capillary recruitment hypothesis) was tested in awake adult male Sprague–Dawley rats exposed to 10% O2 and control rats. The [14C]iodoantipyrine technique was used to measure lCBF. Local cerebral blood volume was determined by measuring plasma and red cell distribution spaces within the brain parenchyma with 125I-labeled serum albumin (RISA) and 55Fe-labeled red cells (RBC), respectively. Tissue radioactivity in 44 brain areas was estimated by quantitative autoradiography. Hypoxia raised lCBF by 25–90% in all brain areas. In about one-quarter of the brain areas, the rise in blood flow was associated with a small increase in microvascular plasma and blood volumes. This change in blood volume, which could be the result of perfusing more parenchymal microvessels and/or increasing parenchymal microvessel diameter, is not sufficient to account for the observed rise in lCBF. In the remaining areas the RISA, RBC, and blood spaces were either unchanged or only marginally increased by hypoxia. For this hypoxic perturbation, the major mechanism of raising blood flow appears to be increased velocity of microvessel perfusion and not perfusion of more capillaries. These findings provide only limited support for the capillary recruitment hypothesis.
The Velocities of Red Cell and Plasma Flows through Parenchymal Microvessels of Rat Brain are Decreased by Pentobarbital
Authors: Wei Ling , Otsuka Tadahiro , Acuff Virgil , Bereczki Daniel , Pettigrew Karen , Patlak Clifford , Fenstermacher Joseph
Published: May 2011

Local cerebral blood flow is lowered in many brain areas of the rat by high-dose pentobarbital (50 mg/kg). In the present study, the mechanism of this flow change was examined by measuring the distribution of radiolabeled red blood cells (RBCs) and albumin (RISA) in small parenchymal microvessels and calculating the microvascular distribution spaces and mean transit times of RBCs, RISA, and blood. In most brain areas, pentobarbital slightly decreased the RISA space, modestly increased the RBC space, and did not alter the blood space. The mean transit times of RBCs, RISA, and blood through the perfused microvessels were considerably greater in treated rats than in controls. These findings indicate that the mechanism by which high-dose pentobarbital diminishes local cerebral blood flow in rat brain is, in the main, a lowered linear velocity of plasma and RBC flow through small parenchymal microvessels and not decreased percentage of perfused capillaries (capillary retirement). This response is probably driven mainly by lowered local metabolism and may well entail a slight increase in the number of small microvessels that are perfused by RBCs.
Redistribution of Glutamate and Glutamine in Slices of Human Neocortex Exposed to Combined Hypoxia and Glucose Deprivation in vitro
Authors: Aas Jan-Erik , Berg-Johnsen Jon , Hegstad Elisabeth , Laake Jon H. , Langmoen Iver A. , Ottersen Ole P.
Published: May 2011

This study was undertaken to elucidate the roles of neurons and glial cells in the handling of glutamate and glutamine, a glutamate precursor, during cerebral ischemia. Slices (400–600 μm) from human neocortex obtained during surgery for epilepsy or brain tumors were incubated in artificial cerebrospinal fluid and subjected to 30 min of combined hypoxia and glucose deprivation (an in vitro model of brain ischemia). These slices, and control slices that had not been subjected to “ischemic” conditions, were then fixed and embedded. Ultrathin sections were processed according to a postembedding immunocytochemical method with polyclonal antibodies raised against glutamate or glutamine, followed by colloidal gold-labeled secondary antibodies. The gold particle densities over various tissue profiles were calculated from electron micrographs using a specially designed computer program. Combined hypoxia and glucose deprivation caused a reduced glutamate immunolabeling in neuronal somata, while that of glial processes increased. Following 1 h of recovery, the glutamate labeling of neuronal somata declined further to very low values, compared to control slices. The glutamate labeling of glial cells returned to normal levels following recovery. In axon terminals, no consistent change in the level of glutamate immunolabeling was observed. Immunolabeling of glutamine was low in both nerve terminals and neuronal somata in normal slices and was reduced to nondetectable levels in nerve terminals upon hypoxia and glucose deprivation. This treatment was also associated with a reduced glutamine immunolabeling in glial cells. Reversed glutamate uptake due to perturbations of the transmembrane ion concentrations and membrane potential probably contributes to the loss of neuronal glutamate under “ischemic” conditions. The increased glutamate labeling of glial cells under the same conditions can best be explained by assuming that glial cells resist a reversal of glutamate uptake, and that their ability to convert glutamate into glutamine is compromised due to the energy failure. The persistence of a nerve terminal pool of glutamate is compatible with recent biochemical data indicating that the exocytotic glutamate release is contingent on an adequate energy supply and therefore impeded during ischemia.
Transforming Growth Factor-β1 Prevents Glutamate Neurotoxicity in Rat Neocortical Cultures and Protects Mouse Neocortex from Ischemic Injury in vivo
Authors: Prehn Jochen H. M. , Backhauß Cord , Krieglstein Josef
Published: May 2011

Transforming growth factor-β1 (TGF-β1) has been shown to be an injury-related peptide growth factor within the mammalian central nervous system. We tested whether TGF-β1 has the capacity to protect rat neocortical neurons against excitotoxic damage in vitro and mouse neocortex against ischemic injury in vivo. After 14 days in vitro, cultured neurons from rat cerebral cortex were exposed to 1 m M l-glutamate in serum-free culture medium. The cultures received TGF-β1 immediately after the addition of glutamate. Eighteen hours later, the cell viability of the cultures was determined using trypan blue exclusion. TGF-β1 (1–10 ng/ml) significantly reduced the excitotoxic neuronal damage in a concentration-dependent manner. In vivo, male NMRI mice were subjected to a permanent occlusion of the left middle cerebral artery by microbipolar electrocoagulation. After 48 h, the animals received a transcardiac injection of carbon black. The area of ischemia (devoid of carbon) was restricted to the neocortex and its size was determined planimetrically by means of an image-analyzing system. The treatment with TGF-β1 (1 μg/kg i.c.v.) at 6, 4, or 2 h prior to vessel occlusion reduced the area of ischemia by 5.3, 10.0, and 9.6%, respectively. The effect of the treatment with TGF-β1 was statistically significant (p < 0.05 by two-way ANOVA). The present in vitro and in vivo data suggest that TGF-β1 has the capacity to diminish the deleterious consequences of an excitotoxic or ischemic insult.
Effect of Propentofylline on Regional Cerebral Glucose Metabolism in Acute Ischemic Stroke
Authors: Huber M. , Kittner B. , Hojer C. , Fink G. R. , Neveling M. , Heiss W.-D.
Published: May 2011

In a randomized double-blind placebo-controlled study in 30 patients with acute ischemic stroke, the effect of the adenosine uptake blocker propentofylline on regional brain glucose metabolism (rCMRglu) was investigated using repeated positron emission tomography (PET) with 2-[18F]fluoro-2-deoxy-d-glucose (FDG). Treatment was initiated within 48 h after onset of symptoms. The clinical course was followed for 3 months. In the propentofylline group, after 14 days rCMRglu was increased in the infarct by 37.3% and was practically unchanged in other brain regions, whereas in the control group glucose metabolism had decreased in all regions (1.4–13.4%). These differences were significant between the two groups [Analysis of variance (ANOVA) p = 0.005]. Although there was a trend toward greater clinical improvement in the propentofylline-treated patients, this did not reach statistical significance. The results correspond to experimental data showing that propentofylline improves energy metabolism in cerebral ischemia. A clinical trial is needed to determine whether this new therapeutic principle can be successfully used in acute human stroke.
Trends in the Prevalence of Abdominal Obesity and Overweight in English Adults (1993–2008)
Authors: Howel Denise
Published: May 2011

The rising prevalence of generalized obesity is well documented, but less is known about trends in abdominal obesity. Levels of abdominal obesity and overweight are reported for adults in the Health Survey for England (HSE) by survey year and age for 1993–2008. HSE is a nationally representative cross‐sectional population survey using an interviewer‐administered questionnaire and measurement of waist circumference (WC) by nurse, allowing calculation of abdominal overweight and obesity (≥94 cm and ≥102 cm in men, and ≥80 cm and ≥88 cm in women). A total of 40,001 men and 46,397 women aged 18–67 provided data on WC in this period. Between 1993 and 2008 abdominal overweight rose from 44.9% to 62.3% in men, and from 46.6% to 66.8% in women, while abdominal obesity rose from 19.2% to 35.7% in men, and from 23.8% to 43.9% women. However, the rates of increase over time in England appear to be slowing down: curves with a less than linear increase each year were a better fit to the data than a linear trend. There was some variation across the age range in the time trend in abdominal obesity and overweight, in that the absolute increases over time were slightly less for younger adults.
Interaction of FTO and Physical Activity Level on Adiposity in African‐American and European‐American Adults: The ARIC Study
Authors: Demerath Ellen W. , Lutsey Pam L. , Monda Keri L. , Linda‐Kao Wen Hong , Bressler Jan , Pankow James S. , North Kari E. , Folsom Aaron R.
Published: May 2011

Physical inactivity accentuates the association of variants in the FTO locus with obesity‐related traits but evidence is largely lacking in non‐European populations. Here we tested the hypothesis that physical activity (PA) modifies the association of the FTO single‐nucleotide polymorphism (SNP) rs9939609 with adiposity traits in 2,656 African Americans (AA) (1,626 women and 1,030 men) and 9,867 European Americans (EA) (5,286 women and 4,581 men) aged 45–66 years in the Atherosclerosis Risk in Communities (ARIC) study. Individuals in the lowest quintile of the sport activity index of the Baecke questionnaire were categorized as low PA. Baseline BMI, waist circumference (WC), and skinfold measures were dependent variables in regression models testing the additive effect of the SNP, low PA, and their interaction, adjusting for age, alcohol use, cigarette use, educational attainment, and percent European ancestry in AA adults, stratified by sex and race/ethnicity. rs9939609 was associated with adiposity in all groups other than AA women. The SNP × PA interaction was significant in AA men (P ≤ 0.002 for all traits) and EA men (P ≤ 0.04 for all traits). For each additional copy of the A (risk) allele, WC in AA men was higher in those with low PA (βlowPA: 5.1 cm, 95% confidence interval (CI): 2.6–7.5) than high PA (βhighPA: 0.7 cm, 95% CI: −0.4 to 1.9); P (interaction) = 0.002). The interaction effect was not observed in EA or AA women. FTO SNP × PA interactions on adiposity were observed for AA as well as EA men. Differences by sex require further examination.
Comparison of Glucostatic Parameters After Hypocaloric Diet or Bariatric Surgery and Equivalent Weight Loss
Authors: Plum Leona , Ahmed Leaque , Febres Gerardo , Bessler Marc , Inabnet William , Kunreuther Elizabeth , McMahon Donald J. , Korner Judith
Published: May 2011

Weight‐loss independent mechanisms may play an important role in the improvement of glucose homeostasis after Roux‐en‐Y gastric bypass (RYGB). The objective of this analysis was to determine whether RYGB causes greater improvement in glucostatic parameters as compared with laparoscopic adjustable gastric banding (LAGB) or low calorie diet (LCD) after equivalent weight loss and independent of enteral nutrient passage. Study 1 recruited participants without type 2 diabetes mellitus (T2DM) who underwent LAGB (n = 8) or RYGB (n = 9). Study 2 recruited subjects with T2DM who underwent LCD (n = 7) or RYGB (n = 7). Insulin‐supplemented frequently‐sampled intravenous glucose tolerance test (fsIVGTT) was performed before and after equivalent weight reduction. MINMOD analysis of insulin sensitivity (Si), acute insulin response to glucose (AIRg) and C‐peptide (ACPRg) response to glucose, and insulin secretion normalized to the degree of insulin resistance (disposition index (DI)) were analyzed. Weight loss was comparable in all groups (7.8 ± 0.4%). In Study 1, significant improvement of Si, ACPRg, and DI were observed only after LAGB. In Study 2, Si, ACPRg, and plasma adiponectin increased significantly in the RYGB‐DM group but not in LCD. DI improved in both T2DM groups, but the absolute increase was greater after RYGB (258.2 ± 86.6 vs. 55.9 ± 19.9; P < 0.05). Antidiabetic medications were discontinued after RYGB contrasting with 55% reduction in the number of medications after LCD. No intervention affected fasting glucagon‐like peptide (GLP)‐1, peptide YY (PYY) or ghrelin levels. In conclusion, RYGB produced greater improvement in Si and DI compared with diet at equivalent weight loss in T2DM subjects. Such a beneficial effect was not observed in nondiabetic subjects at this early time‐point.
Teaching Children With Hearing Impairment To Listen and Speak When the Home Language is Not English
Authors: Douglas Michael
Published: May 2011

Many speech-language pathologists (SLPs), deaf educators, and audiologists (AuDs) are finding themselves serving increasing numbers of children with hearing impairment (HI) who come from families that do not speak English. The majority of these families are likely to select listening and spoken language (LSL) as the primary method of communication for their children. This paper will present issues that need to be considered to support develop of LSL in more than one language for an ever-growing population of children with HI in the United States. Specific areas discussed include bilingual capabilities of some children with hearing loss, achievements of children with HI at a few institutions in North America, determining the language(s) of intervention, understanding current models of intervention, and implementing strategies that facilitate successful multilingual learning.
Development of Differential Sensitivity for Shape Changes Resulting from Linear and Nonlinear Planar Transformations
Authors: Ons Bart , Wagemans Johan
Published: May 2011

A shape bias for extending names to objects that look visually similar has been commonly accepted but it is hard to define which kind of shape dissimilarities are diagnostic for the identity of an object. Here, we present a transformational approach to describe shape differences that can incorporate many significant shape features. We introduce two kinds of transformations: one kind concerns linear transformations of the image plane (affine transformations), generally limiting shape variations within the borders of basic-level categories; the other kind concerns nonlinear continuous transformations of the image plane (topological transformations), allowing all kinds of shape variation crossing and not crossing the borders of basic-level categories. We administered stimulus pairs differing in these shape transformations to children of 3 years to 7 years old in a delayed match-to-sample task. With increasing age, especially between 5 years and 6 years, children became more sensitive to the topological deformations that are relevant for between-category distinctions, indicating that acquired categorical knowledge in early years induces perceptual learning of the relevant generic shape differences between categories.
Paradoxical Perception of Surfaces in the Shepard Tabletop Illusion
Authors: Tyler Christopher W
Published: May 2011

The Shepard tabletop illusion, consisting of different perspective embeddings of two identical parallelograms as tabletops, affords a profound difference in their perceived surface shapes. My analysis reveals three further paradoxical aspects of this illusion, in addition to its susceptibility to the ‘inverse perspective illusion’ of the implied orthographic perspective of the table images. These novel aspects of the illusion are: a paradoxical slant of the tabletops, a paradoxical lack of perceived depth, and a paradoxical distortion of the length of the rear legs. The construction of the illusion resembles scenes found in ancient Chinese scroll paintings, and an analysis of the source of the third effect shows that the interpretation in terms of surfaces can account for the difference in treatment of the filled-in versus open forms in the Chinese painting from more than 1000 years ago.
Soluble phosphate in fluctuating groundwater under cropping in the north-eastern wet tropics of Australia
Authors: Rasiah V. , Moody P. W. , Armour J. D.
Published: May 2011

Soluble reactive phosphorus (SP) present in groundwater (GW) is generally considered insignificant, and therefore of little consequence to the quality of waters receiving base-flow discharges. In this study we investigated whether: (i) significant quantities of SP were present in GW (GW-SP); (ii) potential existed for GW-SP to be exported to streams via base-flow discharge; and (iii) the exports are a health risk to ecosystems receiving base-flow discharges. Investigations were carried out at two sites in the Tully River Catchment (TRC) during three consecutive rainy seasons, and 24 wells in the Johnstone River Catchment (JRC) were also monitored during one rainy season, in the north-eastern wet tropics of Australia. In the TRC, the GW-SP varied temporally, within and between rainy seasons, from 2 to 158 μg P/L at Site 1 and from 3 to 31 μg P/L at Site 2. The temporal variations in GW-SP were driven by fluctuating water-table at Site 2, but no such trend was observed at Site 1. The SP in drain-water (DW-SP) varied temporally from 0.6 to 110 μg P/L at Site 1, compared with 2–83 μg P/L at Site 2. The positive association between DW-SP and GW-SP at Site 2 indicated an export of SP from GW to a drain via base-flow discharge. In the JRC, the GW-SP in the 24 wells varied temporally from 0 to 300 μg P/L with the means across the wells ranging from 5 to 190 μg P/L, with the variations driven by fluctuating water-tables. More than 50% of the GW-SP or DW-SP concentrations in TRC were significantly higher than the P trigger values, 2–5 μg P/L, proposed to sustain the health of aquatic ecosystems in this region; a similar result was observed in the JRC. Speciation analysis via filtering (i.e. P passing through a 0.45-μm filter) for selected GW samples indicated substantial quantities of soluble organic P in some wells, ranging from 5 to 89% (mean 38%) of the total soluble P (SP plus soluble organic P). Because the soluble organic P was not included in GW-SP determinations, the hazard/risk mentioned above is an underestimate. The GW-SP exported during rainy seasons, from both catchments, ranged from 0.16 to 0.43 kg P/ha. Our findings indicate there were significant quantities of SP and soluble organic P in GW, it was exported to streams, and there is a health risk to receiving surface water bodies.
A new model for dung decomposition and phosphorus transformations and loss in runoff
Authors: Vadas P. A. , Aarons S. R. , Butler D. M. , Dougherty W. J.
Published: May 2011

Non point-source pollution of fresh waters by agricultural phosphorus (P) can accelerate eutrophication of surface waters and limit their use for drinking, recreation, and industry. An important pathway of agricultural P transport is surface runoff, to which unincorporated dung from grazing cattle can be a significant contributor. Computer models commonly used to identify agricultural areas with a high potential for P export do not adequately simulate dung application to the soil surface, dung disappearance, and dung P loss to runoff. We developed a new model to simulate these processes for grazing cattle dung. The model simulates dung organic matter decomposition and assimilation into soil by bioturbation as a function of air temperature and dung moisture. We validated that the model can accurately predict rates of dung disappearance, using data from 12 published studies. The model also simulates four pools of inorganic and organic P, P mineralisation to water-extractable P, leaching of dung water-extractable P into soil by rain, and loss of dissolved inorganic P in runoff. We validated the ability of the model to reliably simulate these P processes, using data from six published dung P transformation studies and six runoff studies. Overall, the model represents a novel approach for assessing the environmental impact of grazing dairy and beef cattle. Research should investigate the impact of dung deposition rate as a function of time and animal diet and type, where deposition occurs relative to runoff movement, weather conditions, and the ability of dung pad crusting to reduce P release to runoff.
Deep drainage through Vertosols in irrigated fields measured with drainage lysimeters
Authors: Gunawardena T. A. , McGarry D. , Robinson J. B. , Silburn D. M.
Published: May 2011

Rising groundwater and salinity are potential risks across irrigated agricultural landscapes. Water is scarce in many areas that will benefit from efficient water use. Excessive deep drainage (DD, mm) beneath irrigated crops is undesirable because it may cause salinity and decrease water-use efficiency. Nine irrigated, commercial cotton fields (eight furrow-irrigated and one spray, lateral-move irrigated) were selected in the upper Murray–Darling Basin, on Vertosols with a wide range of clay contents (38–75%). The lysimeters used, described as ‘confined, undisturbed, constant tension, non-weighing’, were installed to capture water passing 1.5 m depth at three in-field positions: (i) near the head ditch, (ii) mid-way between head and tail ditches, and (iii) close to the tail ditch. At two sites, infiltration along the length of the field was monitored in two seasons using furrow advance-SIRMOD methods.
Seasonal DD values of up to 235 mm (2.4 ML/ha.season) were measured (range 1–235 mm), equivalent to 27% of the irrigation applied at that location in that season. Individual DD events >90 mm accounted for 15 of 66 measured values from 26 furrow irrigations. DD varied strongly along the length of each field, with DD commonly reducing from the head ditch to the tail ditch. SIRMOD simulation mirrored this trend, with large decreases in infiltration amounts from head to tail. Greater DD at head locations was attributed to long periods of inundation, especially early in the season when siphons (in-flows) were allowed to run for up to 24 h. Most of the DD occurred during pre-irrigation and the first two or three in-crop irrigations. Inter-season variation in DD was large; limited water supply in drought years led to fewer irrigations with smaller volumes, resulting in little or no DD. The DD under lateral-move, spray irrigation was almost zero; only one irrigation event in 4 years resulted in DD. Control of DD under furrow irrigation can be achieved by changing irrigation management to lateral-move, spray irrigation, which minimises DD and greatly increases water-use efficiency with no yield (cotton) penalty. Across all of the lysimetry sites, high salinities of the DD leachate indicated that large amounts of salt were being mobilised. The fate and impacts of this mobilised and leached salt are uncertain.
Soil microbial biomass—Interpretation and consideration for soil monitoring
Authors: Gonzalez-Quiñones V. , Stockdale E. A. , Banning N. C. , Hoyle F. C. , Sawada Y. , Wherrett A. D. , Jones D. L. , Murphy D. V.
Published: May 2011

Since 1970, measurement of the soil microbial biomass (SMB) has been widely adopted as a relatively simple means of assessing the impact of environmental and anthropogenic change on soil microorganisms. The SMB is living and dynamic, and its activity is responsible for the regulation of organic matter transformations and associated energy and nutrient cycling in soil. At a gross level, an increase in SMB is considered beneficial, while a decline in SMB may be considered detrimental if this leads to a decline in biological function. However, absolute SMB values are more difficult to interpret. Target or reference values of SMB are needed for soil quality assessments and to allow ameliorative action to be taken at an appropriate time. However, critical values have not yet been successfully identified for SMB. This paper provides a conceptual framework which outlines how SMB values could be interpreted and measured, with examples provided within an Australian context.
Active multistage coarsening of actin networks driven by myosin motors
Authors: Soares e Silva Marina , Depken Martin , Stuhrmann Björn , Korsten Marijn , MacKintosh Fred C. , Koenderink Gijsje H.
Published: May 2011

In cells, many vital processes involve myosin-driven motility that actively remodels the actin cytoskeleton and changes cell shape. Here we study how the collective action of myosin motors organizes actin filaments into contractile structures in a simplified model system devoid of biochemical regulation. We show that this self-organization occurs through an active multistage coarsening process. First, motors form dense foci by moving along the actin network structure followed by coalescence. Then the foci accumulate actin filaments in a shell around them. These actomyosin condensates eventually cluster due to motor-driven coalescence. We propose that the physical origin of this multistage aggregation is the highly asymmetric load response of actin filaments: they can support large tensions but buckle easily under piconewton compressive loads. Because the motor-generated forces well exceed this threshold, buckling is induced on the connected actin network that resists motor-driven filament sliding. We show how this buckling can give rise to the accumulation of actin shells around myosin foci and subsequent coalescence of foci into superaggregates. This new physical mechanism provides an explanation for the formation and contractile dynamics of disordered condensed actomyosin states observed in vivo.
Key role for IL-21 in experimental autoimmune uveitis
Authors: Wang Lu , Yu Cheng-Rong , Kim Hyoung-Pyo , Liao Wei , Telford William G. , Egwuagu Charles E. , Leonard Warren J.
Published: May 2011

IL-21 is a pleiotropic type 1 cytokine that shares the common cytokine receptor γ-chain, γ
c
, with IL-2, IL-4, IL-7, IL-9, and IL-15. IL-21 is most homologous to IL-2. These cytokines are encoded by adjacent genes, but they are functionally distinct. Whereas IL-2 promotes development of regulatory T cells and confers protection from autoimmune disease, IL-21 promotes differentiation of Th17 cells and is implicated in several autoimmune diseases, including type 1 diabetes and systemic lupus erythematosus. However, the roles of IL-21 and IL-2 in CNS autoimmune diseases such as multiple sclerosis and uveitis have been controversial. Here, we generated
Il21
-mCherry/
Il2
-emGFP dual-reporter transgenic mice and showed that development of experimental autoimmune uveitis (EAU) correlated with the presence of T cells coexpressing IL-21 and IL-2 into the retina. Furthermore,
Il21r
−/−
mice were more resistant to EAU development than wild-type mice, and adoptive transfer of

Il21r
−/−

T cells induced much less severe EAU, underscoring the need for IL-21 in the development of this disease and suggesting that blocking IL-21/γ
c
–signaling pathways may provide a means for controlling CNS auto-inflammatory diseases.
Apoptosis regulator through modulating IAP expression (ARIA) controls the PI3K/Akt pathway in endothelial and endothelial progenitor cells
Authors: Koide Masahiro , Ikeda Koji , Akakabe Yoshiki , Kitamura Youhei , Ueyama Tomomi , Matoba Satoaki , Yamada Hiroyuki , Okigaki Mitsuhiko , Matsubara Hiroaki
Published: May 2011

Endothelial and endothelial progenitor cells (ECs and EPCs) play a fundamental role in angiogenesis that is essential for numerous physiological and pathological processes. The phosphatase and tensin homolog (PTEN)/ phosphoinositide 3-kinase (PI3K) pathway has been implicated in angiogenesis, but the mechanism in the regulation of this pathway in ECs and EPCs is poorly understood. Here we show that ARIA (apoptosis regulator through modulating IAP expression), a transmembrane protein that we recently identified, regulates the PTEN/PI3K pathway in ECs and EPCs and controls developmental and postnatal angiogenesis in vivo. We found that ARIA is abundantly expressed in EPCs and regulates their angiogenic functions by modulating PI3K/Akt/endothelial nitric oxide synthase (eNOS) signaling. Genetic deletion of ARIA caused nonfatal bleeding during embryogenesis, in association with increased small vessel density and altered expression of various vascular growth factors including angiopoietins and VEGF receptors. Postnatal neovascularization induced by critical limb ischemia was substantially enhanced in ARIA-null mice, in conjunction with more bone marrow (BM)-derived ECs detected in ischemic muscles. Administration of PI3K or NO synthase inhibitor completely abolished the enhanced neovascularization in ARIA
−/−
mice. Mechanistically, we identified that ARIA interacts with PTEN at the intracellular domain independently of the PTEN phosphorylation in its C-terminal tail. Overexpressed ARIA increased PTEN in the membrane fraction, whereas ARIA-silencing reduced the membrane-associated PTEN, resulting in modified PI3K/Akt signaling. Taken together, our findings establish a previously undescribed mode of regulation of the PTEN/PI3K/Akt pathway by ARIA, and reveal a unique mechanism in the control of angiogenesis. These functions of ARIA might offer a unique therapeutic potential.
Crystal structure of lactose permease in complex with an affinity inactivator yields unique insight into sugar recognition
Authors: Chaptal Vincent , Kwon Seunghyug , Sawaya Michael R. , Guan Lan , Kaback H. Ronald , Abramson Jeff
Published: May 2011

Lactose permease of
Escherichia coli
(LacY) with a single-Cys residue in place of A122 (helix IV) transports galactopyranosides and is specifically inactivated by methanethiosulfonyl-galactopyranosides (MTS-gal), which behave as unique suicide substrates. In order to study the mechanism of inactivation more precisely, we solved the structure of single-Cys122 LacY in complex with covalently bound MTS-gal. This structure exhibits an inward-facing conformation similar to that observed previously with a slight narrowing of the cytoplasmic cavity. MTS-gal is bound covalently, forming a disulfide bond with C122 and positioned between R144 and W151. E269, a residue essential for binding, coordinates the C-4 hydroxyl of the galactopyranoside moiety. The location of the sugar is in accord with many biochemical studies.
Integrin activation and internalization on soft ECM as a mechanism of induction of stem cell differentiation by ECM elasticity
Authors: Du Jing , Chen Xiaofei , Liang Xudong , Zhang Guangyao , Xu Jia , He Linrong , Zhan Qingyuan , Feng Xi-Qiao , Chien Shu , Yang Chun
Published: May 2011

The mechanism by which ECM elasticity induces lineage specification of stem cells has not been clearly understood. Integrins are well-documented mechanosensors that are positioned at the beginning of the sensing pathway. By using an antibody specifically recognizing the active conformation of β1 integrin, we observed that β1 integrin activation in bone marrow mesenchymal stem cells (BMMSCs) was induced by soft substrate to a significantly greater degree than by stiff substrate. In contrast, however, the level of cell surface integrin on soft substrate was significantly lower than that on stiff substrate. Soft substrate markedly enhanced the internalization of integrin, and this internalization was mediated mainly through caveolae/raft-dependent endocytosis. The inhibition of integrin internalization blocked the neural lineage specification of BMMSCs on soft substrate. Furthermore, soft substrate also repressed the bone morphogenetic protein (BMP)/Smad pathway at least partially through integrin-regulated BMP receptor endocytosis. A theoretical analysis based on atomic force microscopy (AFM) data indicated that integrin–ligand complexes are more easily ruptured on soft substrate; this outcome may contribute to the enhancement of integrin internalization on soft substrate. Taken together, our results suggest that ECM elasticity affects integrin activity and trafficking to modulate integrin BMP receptor internalization, thus contributing to stem cell lineage specification.