bluuebunny/crossref_metadata_2025_split huggingface dataset:
Anopheles culicifacies sibling species in Odisha, eastern India: First appearance of Anopheles culicifacies E and its vectorial role in malaria transmission
Authors: Das Mumani , Das Biswadeep , Patra Aparna P. , Tripathy Hare K. , Mohapatra Namita , Kar Santanu K. , Hazra Rupenangshu K. 
Published: April 2013

AbstractObjectiveTo identify the Anopheles culicifacies sibling species complex and study their vectorial role in malaria endemic regions of Odisha.MethodsMosquitoes were collected from 6 malaria endemic districts using standard entomological collection methods. An. culicifacies sibling species were identified by multiplex polymerase chain reaction (PCR) using cytochrome oxidase subunit II (COII) region of mitochondrial DNA. Plasmodium falciparum (Pf) sporozoite rate and human blood fed percentage (HBF) were estimated by PCR using Pf‐ and human‐specific primers. Sequencing and phylogenetic analysis were performed to confirm the type of sibling species of An. culicifacies found in Odisha.ResultsMultiplex PCR detected An. culicifacies sibling species A, B, C, D and E in the malaria endemic regions of Odisha. An. culicifacies E was detected for the first time in Odisha, which was further confirmed by molecular phylogenetics. Highest sporozoite rate and HBF percentage were observed in An. culicifacies E in comparison with other sibling species. An. culicifacies E collected from Nawarangapur, Nuapara and Keonjhar district showed high HBF percentage and sporozoite rates.ConclusionAn. culicifacies B was the most abundant species, followed by An. culicifacies C and E. High sporozoite rate and HBF of An. culicifacies E indicated that it plays an important role in malaria transmission in Odisha. Appropriate control measures against An. culicifacies E at an early stage are needed to prevent further malaria transmission in Odisha.
SPL8 and miR156‐targeted SPL genes redundantly regulate Arabidopsis gynoecium differential patterning
Authors: Xing Shuping , Salinas María , Garcia‐Molina Antoni , Höhmann Susanne , Berndtgen Rita , Huijser Peter 
Published: April 2013

SummarySPL8 and miR156‐targeted SPL genes are known to play an essential role in Arabidopsis anther development. Here we show that these SPL genes are also expressed within the developing gynoecium, where they redundantly control development of the female reproductive tract. Whereas the gynoecium morphology in the spl8 single mutant is largely normal, additional down‐regulation of miR156‐targeted SPL genes results in a shortened style and an apically swollen ovary narrowing onto an elongated gynophore. In particular, the septum does not form properly and lacks a transmitting tract. Loss of SPL8 function enhances the mutant phenotypes of ett, crc and spt, indicating a functional overlap between SPL8 and these genes in regulating gynoecium development. Furthermore, gynoecium development of 35S:MIR156b spl8–1 double mutants shows enhanced sensitivity to a polar auxin transport inhibitor, and the expression pattern of the auxin biosynthesis gene YUCCA4 is altered compared to wild‐type. Our observations imply that SPL8 and miR156‐targeted SPL genes control gynoecium patterning through interference with auxin homeostasis and signalling.
Requirement for the plastidial oxidative pentose phosphate pathway for nitrate assimilation in Arabidopsis
Authors: Bussell John D. , Keech Olivier , Fenske Ricarda , Smith Steven M. 
Published: April 2013

SummarySugar metabolism and the oxidative pentose phosphate pathway (OPPP) are strongly implicated in N assimilation, although the relationship between them and the roles of the plastidial and cytosolic OPPP have not been established genetically. We studied a knock‐down mutant of the plastid‐localized OPPP enzyme 6‐phosphogluconolactonase 3 (PGL3). pgl3‐1 plants exhibited relatively greater resource allocation to roots but were smaller than the wild type. They had a lower content of amino acids and free in leaves than the wild type, despite exhibiting comparable photosynthetic rates and efficiency, and normal levels of many other primary metabolites. When N‐deprived plants were fed via the roots with , pgl3‐1 exhibited normal induction of OPPP and nitrate assimilation genes in roots, and amino acids in roots and shoots were labeled with 15N at least as rapidly as in the wild type. However, when N‐replete plants were fed via the roots with sucrose, expression of specific OPPP and N assimilation genes in roots increased in the wild type but not in pgl3‐1. Thus, sugar‐dependent expression of N assimilation genes requires OPPP activity and the specificity of the effect of the pgl3‐1 mutation on N assimilation genes establishes that it is not the result of general energy deficiency or accumulation of toxic intermediates. We conclude that expression of specific nitrate assimilation genes in the nucleus of root cells is positively regulated by a signal emanating from OPPP activity in the plastid.
Pulmonary hypertension and the right ventricle in hypoxia
Authors: Naeije Robert , Dedobbeleer Chantal 
Published: April 2013

New Findings
What is the topic of this review?Studies a,contabs,longabsre reviewed showing that hypoxic pulmonary vasoconstriction and subsequent remodelling expose the right ventricle to increased afterload, and that this is occasionally a cause of high‐altitude right heart failure.
What advances does it highlight?Non‐invasive field studies have shown that hypoxic pulmonary hypertension limits exercise capacity in relationship to increased pulmonary artery pressures in high‐altitude newcomers. This is compensated for by increased lung diffusing capacity, decreased ventilator response and polycythaemia in high‐altitude inhabitants. There is recently reported echocardiographic evidence of altered right ventricular function at high altitudes at rest. These data need to be confirmed with measurements during exercise.
Hypoxia causes pulmonary vasoconstriction. Regional hypoxic vasoconstriction improves the matching of perfusion to alveolar ventilation. Global hypoxic vasoconstriction increases right ventricular afterload. The hypoxic pulmonary pressor response is universal in mammals and in birds, but with considerable interspecies and interindividual variability. Chronic hypoxia induces pulmonary hypertension in proportion to initial vasoconstriction. Prolonged hypoxic exposure is also associated with an increase in red blood cell mass, which aggravates pulmonary hypertension by an increase in blood viscosity. Hypoxic pulmonary hypertension in humans is usually mild to moderate, but pulmonary vascular pressure–flow relationships are steep, which corresponds to a substantial afterload on the right ventricle during exercise. A partial recovery of 10–25% of the hypoxia‐induced decrease in maximal oxygen uptake has been reported with intake‐specific pulmonary vasodilating interventions. Hypoxia has been reported to decrease myocardial fibre contractility in vitro. However, the acutely hypoxic right ventricle remains able to preserve the coupling of its contractility to increased afterload in intact animals. Echocardiographic studies of the right ventricle in healthy hypoxic human subjects show altered diastolic function, but systolic function that is preserved or even increased acutely and slightly depressed chronically. These findings are more pronounced in patients with chronic mountain sickness. Their clinical significance remains incompletely understood. Almost no imaging studies of right ventricular function have been reported in a minority of subjects who develop severe pulmonary hypertension and clinical right ventricular failure in hypoxia. No imaging studies of right ventricular function during hypoxic exercise in normal subjects are yet available. Thus, while it is plausible that the right ventricle limits exercise capacity in hypoxia, this still needs to be firmly established.
The influence of gender on the development of pulmonary arterial hypertension
Authors: Dempsie Yvonne , MacLean Margaret R. 
Published: April 2013

New Findings
What is the topic of this review?Pulmonary arterial hypertension (PAH) in its idiopathic and familial forms occurs more frequently in females than in males (>2:1 incidence ratio). Experimentally, however, female gender and oestrogens can both protect against and exacerbate PAH. This review will discuss our current understanding of the influence of sex hormones on the development of PAH.
What advances does it highlight?Findings from recently described female gender‐specific murine models of PAH will be highlighted. Specifically, the role of oestrogen metabolism and the oestrogen‐metabolizing enzyme CYP1B1 in the development of PAH are discussed. Recent evidence suggesting that sex hormones have direct effects on the right ventricle is also discussed.
Pulmonary arterial hypertension (PAH) is a progressive disease in which increased pulmonary arterial pressure and remodelling eventually lead to right heart failure and death. Idiopathic and familial PAH occur far more frequently in women than in men. Historically, investigations into this gender bias have been impeded because female gender and oestrogens paradoxically protect against PAH in commonly used rodent models. However, recent descriptions of female gender‐specific murine models of PAH have led to an increased understanding of the role of oestrogens in disease development. Specifically, oestrogen metabolism has been highlighted as playing an important role in disease development, and the oestrogen‐metabolizing enzyme CYP1B1 may represent a novel therapeutic target. In addition, emerging evidence suggests that sex hormones may have direct effects on the right ventricle independent of haemodynamic effects. This review discusses our current understanding of the role of sex hormones in the development of PAH.
Cardiorespiratory coupling of sympathetic outflow in humans: a comparison of respiratory and cardiac modulation of sympathetic nerve activity to skin and muscle
Authors: Fatouleh Rania , Macefield Vaughan G. 
Published: April 2013

New FindingsWhat is the central question of this study?Muscle sympathetic nerve activity (MSNA) is well known to be modulated by the arterial baroreceptors and respiration, but what are the magnitudes of cardiac and respiratory modulation of skin sympathetic nerve activity (SSNA), which primarily subserves thermoregulation?What is the main finding and what is its importance?Using direct microelectrode recordings of MSNA and SSNA in awake humans, we show that the magnitude of respiratory modulation of SSNA is identical to that of MSNA, the primary difference between the two sources of sympathetic outflow being the greater cardiac modulation of MSNA. This emphasises the role of the baroreceptors in entraining sympathetic outflow to muscle.It is well known that microelectrode recordings of skin sympathetic nerve activity (SSNA) in awake human subjects reveal spontaneous bursts of activity with no overt modulation by changes in blood pressure or respiration, in contrast to the clear cardiac and respiratory modulation of muscle sympathetic nerve activity (MSNA). However, cross‐correlation analysis has revealed that, like individual muscle vasoconstrictor neurones, the firing of individual cutaneous vasoconstrictor neurones is temporally coupled to both the cardiac and respiratory rhythms during cold‐induced cutaneous vasoconstriction, and the same is true of single sudomotor neurones during heat‐induced sweating. Here, we used cross‐correlation analysis to determine whether SSNA exhibits cardiac and respiratory modulation in thermoneutral conditions and to compare respiratory and cardiac modulation of SSNA with that of MSNA. Oligounitary recordings of spontaneous SSNA (n= 20) and MSNA (n= 18) were obtained during quiet, unrestrained breathing. Respiration was recorded by a strain‐gauge transducer around the chest and ECG recorded by surface electrodes. Respiratory and cardiac modulation of SSNA and MSNA were quantified by fitting polynomial equations to the cross‐correlation histograms constructed between the sympathetic spikes and respiration or ECG. The amplitude of the respiratory modulation (52.5 ± 3.4%) of SSNA was not significantly different from the amplitude of the cardiac modulation (46.6 ± 3.2%). Both were comparable to the respiratory modulation of MSNA (47.7 ± 4.2%), while cardiac modulation of MSNA was significantly higher (89.8 ± 1.5%). We conclude that SSNA and MSNA share similar levels of respiratory modulation, the primary difference between the two sources of sympathetic outflow being the marked cardiac modulation of MSNA provided by the baroreceptors.
Mitochondrial dysfunction and therapeutic approaches in respiratory and limb muscles of cancer cachectic mice
Authors: Fermoselle Clara , García‐Arumí Elena , Puig‐Vilanova Ester , Andreu Antoni L. , Urtreger Alejandro J. , de Kier Joffé Elisa D. Bal , Tejedor Alberto , Puente‐Maestu Luís , Barreiro Esther 
Published: April 2013

New Findings
What is the central question of this study?We explored whether experimental cancer‐induced cachexia may alter mitochondrial respiratory chain (MRC) complexes and oxygen uptake in respiratory and peripheral muscles, and whether signalling pathways, proteasome and oxidative stress influence that process.
What is the main finding and what is its importance?In cancer cachectic mice, MRC complexes and oxygen consumption were decreased in the diaphragm and gastrocnemius. Blockade of nuclear factor‐κB and mitogen‐activated protein kinase actions partly restored the muscle mass and force and corrected the MRC dysfunction, while concomitantly reducing tumour burden. Antioxidants improved mitochondrial oxygen consumption without eliciting effects on the loss of muscle mass and force or the tumour size, whereas bortezomib reduced tumour burden without influencing muscle mass and strength or MRC function.
Abnormalities in mitochondrial content, morphology and function have been reported in several muscle‐wasting conditions. We specifically explored whether experimental cancer‐induced cachexia may alter mitochondrial respiratory chain (MRC) complexes and oxygen uptake in respiratory and peripheral muscles, and whether signalling pathways, proteasomes and oxidative stress may influence that process. We evaluated complex I, II and IV enzyme activities (specific activity assays) and MRC oxygen consumption (polarographic measurements) in diaphragm and gastrocnemius of cachectic mice bearing the LP07 lung tumour, with and without treatment with N‐acetylcysteine, bortezomib and nuclear factor‐κB (sulfasalazine) and mitogen‐activated protein kinases (MAPK, U0126) inhibitors (n= 10 per group for all groups). Whole‐body and muscle weights and limb muscle force were also assessed in all rodents at baseline and after 1 month. Compared with control animals, cancer cachectic mice showed a significant reduction in body weight gain, smaller sizes of the diaphragm and gastrocnemius, lower muscle strength, decreased activity of complexes I, II and IV and decreased oxygen consumption in both muscles. Blockade of nuclear factor‐κB and MAPK actions restored muscle mass and force and corrected the MRC dysfunction in both muscles, while partly reducing tumour burden. Antioxidants improved mitochondrial oxygen uptake without eliciting significant effects on the loss of muscle mass and force or tumour size, whereas the proteasome inhibitor reduced tumour burden without significantly influencing muscle mass and strength or mitochondrial function. In conclusion, nuclear factor‐κB and MAPK signalling pathways modulate muscle mass and performance and MRC function of respiratory and limb muscles in this model of experimental cancer cachexia, thus offering targets for therapeutic intervention.
Evidence of Microbial Regulation of Biogeochemical Cycles from a Study on Methane Flux and Land Use Change
Authors: Nazaries Loïc , Pan Yao , Bodrossy Levente , Baggs Elizabeth M. , Millard Peter , Murrell J. Colin , Singh Brajesh K. 
Published: April 2013

ABSTRACT
Microbes play an essential role in ecosystem functions, including carrying out biogeochemical cycles, but are currently considered a black box in predictive models and all global biodiversity debates. This is due to (i) perceived temporal and spatial variations in microbial communities and (ii) lack of ecological theory explaining how microbes regulate ecosystem functions. Providing evidence of the microbial regulation of biogeochemical cycles is key for predicting ecosystem functions, including greenhouse gas fluxes, under current and future climate scenarios. Using functional measures, stable-isotope probing, and molecular methods, we show that microbial (community diversity and function) response to land use change is stable over time. We investigated the change in net methane flux and associated microbial communities due to afforestation of bog, grassland, and moorland. Afforestation resulted in the stable and consistent enhancement in sink of atmospheric methane at all sites. This change in function was linked to a niche-specific separation of microbial communities (methanotrophs). The results suggest that ecological theories developed for macroecology may explain the microbial regulation of the methane cycle. Our findings provide support for the explicit consideration of microbial data in ecosystem/climate models to improve predictions of biogeochemical cycles.
U(VI) Reduction in Sulfate-Reducing Subsurface Sediments Amended with Ethanol or Acetate
Authors: Converse Brandon J. , Wu Tao , Findlay Robert H. , Roden Eric E. 
Published: April 2013

ABSTRACT
An experiment was conducted with subsurface sediments from Oak Ridge National Laboratory to determine the potential for reduction of U(VI) under sulfate-reducing conditions with either ethanol or acetate as the electron donor. The results showed extensive U(VI) reduction in sediments supplied with either electron donor, where geochemical and microbiological analyses demonstrated active sulfate reduction.
Improving the Thermostability and Catalytic Efficiency of Bacillus deramificans Pullulanase by Site-Directed Mutagenesis
Authors: Duan Xuguo , Chen Jian , Wu Jing 
Published: April 2013

ABSTRACT

Pullulanase (EC 3.2.1.41) is a well-known starch-debranching enzyme. Its instability and low catalytic efficiency are the major factors preventing its widespread application. To address these issues, Asp437 and Asp503 of the pullulanase from
Bacillus deramificans
were selected in this study as targets for site-directed mutagenesis based on a structure-guided consensus approach. Four mutants (carrying the mutations D503F, D437H, D503Y, and D437H/D503Y) were generated and characterized in detail. The results showed that the D503F, D437H, and D503Y mutants had an optimum temperature of 55°C and a pH optimum of 4.5, similar to that of the wild-type enzyme. However, the half-lives of the mutants at 60°C were twice as long as that of the wild-type enzyme. In addition, the D437H/D503Y double mutant displayed a larger shift in thermostability, with an optimal temperature of 60°C and a half-life at 60°C of more than 4.3-fold that of the wild-type enzyme. Kinetic studies showed that the

K
m

values for the D503F, D437H, D503Y, and D437H/D503Y mutants decreased by 7.1%, 11.4%, 41.4%, and 45.7% and the
K
cat
/

K
m

values increased by 10%, 20%, 140%, and 100%, respectively, compared to those of the wild-type enzyme. Mechanisms that could account for these enhancements were explored. Moreover, in conjunction with the enzyme glucoamylase, the D503Y and D437H/D503Y mutants exhibited an improved reaction rate and glucose yield during starch hydrolysis compared to those of the wild-type enzyme, confirming the enhanced properties of the mutants. The mutants generated in this study have potential applications in the starch industry.
Effect of Pressure-Induced Changes in the Ionization Equilibria of Buffers on Inactivation of Escherichia coli and Staphylococcus aureus by High Hydrostatic Pressure
Authors: Gayán Elisa , Condón Santiago , Álvarez Ignacio , Nabakabaya Maria , Mackey Bernard 
Published: April 2013

ABSTRACT

Survival rates of
Escherichia coli
and
Staphylococcus aureus
after high-pressure treatment in buffers that had large or small reaction volumes (Δ
V
°), and which therefore underwent large or small changes in pH under pressure, were compared. At a low buffer concentration of 0.005 M, survival was, as expected, better in MOPS (morpholinepropanesulfonic acid), HEPES, and Tris, whose Δ
V
° values are approximately 5.0 to 7.0 cm
3
mol
−1
, than in phosphate or dimethyl glutarate (DMG), whose Δ
V
° values are about −25 cm
3
mol
−1
. However, at a concentration of 0.1 M, survival was unexpectedly better in phosphate and DMG than in MOPS, HEPES, or Tris. This was because the baroprotective effect of phosphate and DMG increased much more rapidly with increasing concentration than it did with MOPS, HEPES, or Tris. Further comparisons of survival in solutions of salts expected to cause large electrostriction effects (Na
2
SO
4
and CaCl
2
) and those causing lower electrostriction (NaCl and KCl) were made. The salts with divalent ions were protective at much lower concentrations than salts with monovalent ions. Buffers and salts both protected against transient membrane disruption in
E. coli
, but the molar concentrations necessary for membrane protection were much lower for phosphate and Na
2
SO
4
than for HEPES and NaCl. Possible protective mechanisms discussed include effects of electrolytes on water compressibility and kosmotropic and specific ion effects. The results of this systematic study will be of considerable practical significance in studies of pressure inactivation of microbes under defined conditions but also raise important fundamental questions regarding the mechanisms of baroprotection by ionic solutes.
Inactivation of Ca
2+
/H
+
Exchanger in Synechocystis sp. Strain PCC 6803 Promotes Cyanobacterial Calcification by Upregulating CO
2
-Concentrating Mechanisms
Authors: Jiang Hai-Bo , Cheng Hui-Min , Gao Kun-Shan , Qiu Bao-Sheng 
Published: April 2013

ABSTRACT

Cyanobacteria are important players in the global carbon cycle, accounting for approximately 25% of global CO
2
fixation. Their CO
2
-concentrating mechanisms (CCMs) are thought to play a key role in cyanobacterial calcification, but the mechanisms are not completely understood. In
Synechocystis
sp. strain PCC 6803, a single Ca
2+
/H
+
exchanger (Slr1336) controls the Ca
2+
/H
+
exchange reaction. We knocked out the exchanger and investigated the effects on cyanobacterial calcification and CCMs. Inactivation of
slr1336
significantly increased the calcification rate and decreased the zeta potential, indicating a relatively stronger Ca
2+
-binding ability. Some genes encoding CCM-related components showed increased expression levels, including the
cmpA
gene, which encodes the Ca
2+
-dependent HCO
3
−
transporter BCT1. The transcript level of
cmpA
in the mutant was 30 times that in wild type. A Western blot analysis further confirmed that protein levels of CmpA were higher in the mutant than the wild type. Measurements of inorganic carbon fluxes and O
2
evolution proved that both the net HCO
3
−
uptake rate and the BCT1 transporter supported photosynthetic rate in the
slr1336
mutant were significantly higher than in the wild type. This would cause the mutant cells to liberate more OH
−
ions out of the cell and stimulate CaCO
3
precipitation in the microenvironment. We conclude that the mutation of the Ca
2+
/H
+
exchanger in
Synechocystis
promoted the cyanobacterial calcification process by upregulating CCMs, especially the BCT1 HCO
3
−
transporter. These results shed new light on the mechanism by which CCM-facilitated photosynthesis promotes cyanobacterial calcification.