bluuebunny/crossref_metadata_2025_split huggingface dataset:
Intestinal adaptations in chronic kidney disease and the influence of gastric bypass surgery
Authors: Hatch Marguerite 
Published: June 2014

New Findings
What is the topic of this review?
This review primarily focuses on the compensatory adaptations in gastrointestinal oxalate transport that can impact urinary oxalate excretion in the context of hyperoxaluria, a major risk factor in kidney stone disease.
What advances does it highlight?
The intestine, which is generally considered an absorptive organ, contributes to oxalate homeostasis by playing a role in enteric elimination/excretion of oxalate that has beneficial effects, especially when renal function is compromised. Conversely, when enteric elimination of oxalate is promoted, urinary oxalate can be reduced even in hyperoxaluric conditions. This report highlights the physiological signalling between the kidney and the gut and vice versa.
Studies have shown that compensatory adaptations in gastrointestinal oxalate transport can impact the amount of oxalate excreted by the kidney. Hyperoxaluria is a major risk factor in the formation of kidney stones, and oxalate is derived from both the diet and the liver metabolism of glyoxylate. Although the intestine generally absorbs oxalate from dietary sources and can contribute as much as 50% of urinary oxalate, enteric oxalate elimination plays a significant role when renal function is compromised. While the mechanistic basis for these changes in the direction of intestinal oxalate movements in chronic renal failure involves an upregulation of angiotensin II receptors in the large intestine, enteric secretion/excretion of oxalate can also occur by mechanisms that are independent of angiotensin II. Most notably, the commensal bacterium Oxalobacter sp. interacts with the host enterocyte and promotes the movement of oxalate from the blood into the lumen, resulting in the beneficial effect of significantly lowering urinary oxalate excretion. Changes in the passive permeability of the intestine, such as in steatorrhoea and following gastric bypass, also promote oxalate absorption and hyperoxaluria. In summary, this report highlights the two‐way physiological signalling between the gut and the kidney, which may help to alleviate the consequences of certain kidney diseases.
Neuronal activation by mucosal biopsy supernatants from irritable bowel syndrome patients is linked to visceral sensitivity
Authors: Buhner Sabine , Braak Breg , Li Qin , Kugler Eva Maria , Klooker Tamira , Wouters Mira , Donovan Jemma , Vignali Sheila , Mazzuoli‐Weber Gemma , Grundy David , Boeckxstaens Guy , Schemann Michael 
Published: June 2014

New Findings
What is the central question of this study?
Supernatants from colonic mucosal biopsies from patients with irritable bowel syndrome (IBS) activate enteric and dorsal root ganglion (DRG) neurons. Based on the discomfort/pain threshold during rectal distension, IBS patients may be subtyped as normo‐ or hypersensitive. However, the link between neuronal activation and visceral sensitivity remains unknown.
What is the main finding and its importance?
We found that supernatants from hypersensitive IBS patients caused stronger activation of enteric and DRG neurons than supernatants from normosensitive IBS patients. The level of activation correlated with the individual discomfort/pain threshold pressure values. We therefore conclude that mucosal biopsy supernatants have biomarker potential and may, in the future, help to personalize treatment of IBS patients with different visceral sensitivities.
Based on the discomfort/pain threshold during rectal distension, irritable bowel syndrome (IBS) patients may be subtyped as normo‐ or hypersensitive. We previously showed that mucosal biopsy supernatants from IBS patients activated enteric and visceral afferent neurons. We tested the hypothesis that visceral sensitivity is linked to the degree of neuronal activation. Normo‐ and hypersensitive IBS patients were distinguished by their discomfort/pain threshold to rectal balloon distension with a barostat. Using potentiometric and Ca2+ dye imaging, we recorded the response of guinea‐pig enteric submucous and mouse dorsal root ganglion (DRG) neurons, respectively, to mucosal biopsy supernatants from normosensitive (n = 12 tested in enteric neurons, n = 9 tested in DRG) and hypersensitive IBS patients (n = 9, tested in both types of neurons). In addition, we analysed the association between neuronal activation and individual discomfort/pain pressure thresholds. The IBS supernatants evoked Ca2+ transients in DRG neurons and spike discharge in submucous neurons. Submucous and DRG neurons showed significantly stronger responses to supernatants from hypersensitive IBS patients as reflected by higher spike frequency or stronger [Ca2+]i transients in a larger proportion of neurons. The neuroindex as a product of spike frequency or [Ca2+]i transients and proportion of responding neurons correlated significantly with the individual discomfort/pain thresholds of the IBS patients. Supernatants from hypersensitive IBS patients caused stronger activation of enteric and DRG neurons. The level of activation correlated with the individual discomfort/pain threshold pressure values. These findings support our hypothesis that visceral sensitivity is linked to activation of peripheral neurons by biopsy supernatants.
Spatial organization and coordination of slow waves in the mouse anorectum
Authors: Hall K. A. , Ward S. M. , Cobine C. A. , Keef K. D. 
Published: June 2014

Key points
The internal anal sphincter (IAS) develops tone important for maintaining high anal pressure and continence whereas tone in the rectum is less.
To investigate tone generation, the electrical properties [membrane potential (Em) and slow waves (SWs)] and morphology of the mouse IAS and distal rectum were compared.
SWs were greatest in amplitude and frequency at the distal end of the IAS and declined toward the rectum. SWs were also coordinated to a greater degree in the circumferential than the oral direction.
The circular muscle was divided into ‘minibundles’ in the IAS but not rectum. Intramuscular interstitial cells of Cajal and platelet‐derived growth factor receptor alpha‐positive cells were present in each minibundle making each a possible candidate for SW generation.
The features that distinguish the IAS from rectum (i.e. depolarized Em, larger and higher frequency SWs and multiunit configuration) are all properties that are predicted to result in greater tone generation.
AbstractThe internal anal sphincter (IAS) develops tone and is important for maintaining a high anal pressure while tone in the rectum is less. The mechanisms responsible for tone generation in the IAS are still uncertain. The present study addressed this question by comparing the electrical properties and morphology of the mouse IAS and distal rectum. The amplitude of tone and the frequency of phasic contractions was greater in the IAS than in rectum while membrane potential (Em) was less negative in the IAS than in rectum. Slow waves (SWs) were of greatest amplitude and frequency at the distal end of the IAS, declining in the oral direction. Dual microelectrode recordings revealed that SWs were coordinated over a much greater distance in the circumferential direction than in the oral direction. The circular muscle layer of the IAS was divided into five to eight ‘minibundles’ separated by connective tissue septa whereas few septa were present in the rectum. The limited coordination of SWs in the oral direction suggests that the activity in adjacent minibundles is not coordinated. Intramuscular interstitial cells of Cajal and platelet‐derived growth factor receptor alpha‐positive cells were present in each minibundle suggesting a role for one or both of these cells in SW generation. In summary, three important properties distinguish the IAS from the distal rectum: (1) a more depolarized Em; (2) larger and higher frequency SWs; and (3) the multiunit configuration of the muscle. All of these characteristics may contribute to greater tone generation in the IAS than in the distal rectum.
Assessment of in vivo skeletal muscle mitochondrial respiratory capacity in humans by near‐infrared spectroscopy: a comparison with in situ measurements
Authors: Ryan Terence E. , Brophy Patricia , Lin Chien‐Te , Hickner Robert C. , Neufer P. Darrell 
Published: June 2014

Key points
In vivo skeletal muscle mitochondrial respiratory capacity was determined from the post‐exercise recovery kinetics of muscle oxygen consumption () measured using near‐infrared spectroscopy (NIRS) in humans.
NIRS recovery rates were compared with the in situ gold standard of high‐resolution respirometry measured in permeabilized muscle fibre bundles prepared from muscle biopsies taken from the same participants.
NIRS‐measured recovery kinetics of were well correlated with maximal ADP‐stimulated mitochondrial respiration in permeabilized fibre bundles.
NIRS provides a cost‐effective, non‐invasive means of assessing in vivo mitochondrial respiratory capacity.
AbstractThe present study aimed to compare in vivo measurements of skeletal muscle mitochondrial respiratory capacity made using near‐infrared spectroscopy (NIRS) with the current gold standard, namely in situ measurements of high‐resolution respirometry performed in permeabilized muscle fibres prepared from muscle biopsies. Mitochondrial respiratory capacity was determined in 21 healthy adults in vivo using NIRS to measure the recovery kinetics of muscle oxygen consumption following a ∼15 s isometric contraction of the vastus lateralis muscle. Maximal ADP‐stimulated (State 3) respiration was measured in permeabilized muscle fibres using high‐resolution respirometry with sequential titrations of saturating concentrations of metabolic substrates. Overall, the in vivo and in situ measurements were strongly correlated (Pearson's r = 0.61–0.74, all P < 0.01). Bland–Altman plots also showed good agreement with no indication of bias. The results indicate that in vivo NIRS corresponds well with the current gold standard, in situ high‐resolution respirometry, for assessing mitochondrial respiratory capacity.
Mitochondrial reactive oxygen species production and respiratory complex activity in rats with pressure overload‐induced heart failure
Authors: Schwarzer Michael , Osterholt Moritz , Lunkenbein Anne , Schrepper Andrea , Amorim Paulo , Doenst Torsten 
Published: June 2014

Key points
Pressure overload induces cardiac hypertrophy developing into heart failure.
During pressure overload‐induced heart failure development in the rat, mitochondrial capacity to produce reactive oxygen species (ROS) increased significantly with the onset of diastolic functional changes.
Treatment to reduce ROS production was able to diminish mitochondrial ROS production but was not able to prevent or delay heart failure development.
The results question a primary role of ROS in the mechanism causing contractile dysfunction under pressure overload.
AbstractWe investigated the impact of cardiac reactive oxygen species (ROS) during the development of pressure overload‐induced heart failure. We used our previously described rat model where transverse aortic constriction (TAC) induces compensated hypertrophy after 2 weeks, heart failure with preserved ejection fraction at 6 and 10 weeks, and heart failure with systolic dysfunction after 20 weeks. We measured mitochondrial ROS production rates, ROS damage and assessed the therapeutic potential of in vivo antioxidant therapies. In compensated hypertrophy (2 weeks of TAC) ROS production rates were normal at both mitochondrial ROS production sites (complexes I and III). Complex I ROS production rates increased with the appearance of diastolic dysfunction (6 weeks of TAC) and remained high thereafter. Surprisingly, maximal ROS production at complex III peaked at 6 weeks of pressure overload. Mitochondrial respiratory capacity (state 3 respiration) was elevated 2 and 6 weeks after TAC, decreased after this point and was significantly impaired at 20 weeks, when contractile function was also impaired and ROS damage was found with increased hydroxynonenal. Treatment with the ROS scavenger α‐phenyl‐N‐tert‐butyl nitrone or the uncoupling agent dinitrophenol significantly reduced ROS production rates at 6 weeks. Despite the decline in ROS production capacity, no differences in contractile function between treated and untreated animals were observed. Increased ROS production occurs early in the development of heart failure with a peak at the onset of diastolic dysfunction. However, ROS production may not be related to the onset of contractile dysfunction.
Hypometabolism and hypothermia in the rat model of endotoxic shock: independence of circulatory hypoxia
Authors: Corrigan Joshua J. , Fonseca Monique T. , Flatow Elizabeth A. , Lewis Kevin , Steiner Alexandre A. 
Published: June 2014

Key points
The hypometabolic, hypothermic response that often replaces fever in endotoxic shock might be consequential to hypoxia, but the available evidence is circumstantial.
Here, this hypothesis was tested in an unprecedented experimental preparation that provides simultaneous measurements of oxygen delivery and consumption in rats whose ability to regulate body temperature has not been disrupted by anaesthetics.
The results are striking for indicating that hypometabolism and hypothermia in endotoxic shock occur independently of global or tissue hypoxia.
The results also demonstrate that a switch in thermal response from fever to hypothermia serves as a pre‐emptive strategy to avoid hypoxia in endotoxic shock.
These findings are potentially relevant to critical care, as interventions aimed at elevating oxygen delivery in patients with septic shock are based on the (perhaps erroneous) premise that circulatory hypoxia is the cause of hypometabolism in this patient population.
AbstractWe tested the hypothesis that development of hypothermia instead of fever in endotoxic shock is consequential to hypoxia. Endotoxic shock was induced by bacterial lipopolysaccharide (LPS, 500 μg kg−1 i.v.) in rats at an ambient temperature of 22°C. A β3‐adrenergic agonist known to activate metabolic heat production, CL316,243, was employed to evaluate whether thermogenic capacity could be impaired by the fall in oxygen delivery () during endotoxic shock. This possibility was rejected as CL316,243 (0.15 mg kg−1 i.v.) evoked similar rises in oxygen consumption () in the presence and absence of endotoxic shock. Next, to investigate whether a less severe form of circulatory hypoxia could be triggering hypothermia, the circulating volume of LPS‐injected rats was expanded using 6% hetastarch with the intention of improving tissue perfusion and alleviating hypoxia. This intervention attenuated not only the fall in arterial pressure induced by LPS, but also the associated falls in and body temperature. These effects, however, occurred independently of hypoxia, as they were not accompanied by any detectable changes in NAD+/NADH ratios. Further experimentation revealed that even the earliest drops in cardiac output and during endotoxic shock did not precede the reduction in that brings about hypothermia. In fact, and fell in such a synchrony that the / ratio remained unaffected. Only when hypothermia was prevented by exposure to a warm environment (30°C) did an imbalance in the / ratio become evident, and such an imbalance was associated with reductions in the renal and hypothalamic NAD+/NADH ratios. In conclusion, hypometabolism and hypothermia in endotoxic shock are not consequential to hypoxia but serve as a pre‐emptive strategy to avoid hypoxia in this model.
The pH-Dependent Expression of the Urease Operon in Streptococcus salivarius Is Mediated by CodY
Authors: Huang Szu-Chuan , Burne Robert A. , Chen Yi-Ywan M. 
Published: June 2014

ABSTRACT

Urease gene expression in
Streptococcus salivarius
57.I, a strain of one of the major alkali producers in the mouth, is induced by acidic pH and excess amounts of carbohydrate. Expression is controlled primarily at the transcriptional level from a promoter, p

ureI

. Recent sequencing analysis revealed a CodY box located 2 bases 5′ to the −35 element of p

ureI

. Using continuous chemostat culture, transcription from p

ureI

was shown to be repressed by CodY, and at pH 7 the repression was more pronounced than that in cells grown at pH 5.5 under both 20 and 100 mM glucose. The direct binding of CodY to p

ureI

was demonstrated by electrophoretic mobility shift assay and chromatin immunoprecipitation (ChIP)–quantitative real-time PCR (qPCR). The result of ChIP-qPCR also confirmed that the regulation of CodY is indeed modulated by pH and the binding of CodY at neutral pH is further enhanced by a limited supply of glucose (20 mM). In the absence of CodY, the C-terminal domain of the RNA polymerase (RNAP) α subunit interacted with the AT tracks within the CodY box, indicating that CodY and RNAP compete for the same binding region. Such regulation could ensure optimal urease expression when the enzyme is most required, i.e., at an acidic growth pH with an excess amount of carbon nutrients.
Trichoderma atroviride Transcriptional Regulator Xyr1 Supports the Induction of Systemic Resistance in Plants
Authors: Reithner Barbara , Mach-Aigner Astrid R. , Herrera-Estrella Alfredo , Mach Robert L. 
Published: June 2014

ABSTRACT

As a result of a transcriptome-wide analysis of the ascomycete
Trichoderma atroviride
, mycoparasitism-related genes were identified; of these, 13 genes were further investigated for differential expression.
In silico
analysis of the upstream regulatory regions of these genes pointed to xylanase regulator 1 (Xyr1) as a putatively involved regulatory protein. Transcript analysis of the
xyr1
gene of
T. atroviride
in confrontation with other fungi allowed us to determine that
xyr1
levels increased during mycoparasitism. To gain knowledge about the precise role of Xyr1 in the mycoparasitic process, the corresponding gene was deleted from the
T. atroviride
genome. This resulted in strong reductions in the transcript levels of
axe1
and
swo1
, which encode accessory cell wall-degrading enzymes considered relevant for mycoparasitism. We also analyzed the role of Xyr1 in the
Trichoderma
-
Arabidopsis
interaction, finding that the plant response elicited by
T. atroviride
is delayed if Xyr1 is missing in the fungus.
Abundance and Diversity of Soybean-Nodulating Rhizobia in Black Soil Are Impacted by Land Use and Crop Management
Authors: Yan Jun , Han Xiao Zeng , Ji Zhao Jun , Li Yan , Wang En Tao , Xie Zhi Hong , Chen Wen Feng 
Published: June 2014

ABSTRACT

To investigate the effects of land use and crop management on soybean rhizobial communities, 280 nodule isolates were trapped from 7 fields with different land use and culture histories. Besides the known
Bradyrhizobium japonicum
, three novel genospecies were isolated from these fields. Grassland (GL) maintained a higher diversity of soybean bradyrhizobia than the other cultivation systems. Two genospecies (
Bradyrhizobium
spp. I and III) were distributed widely in all treatments, while
Bradyrhizobium
sp. II was found only in GL treatment. Cultivation with soybeans increased the rhizobial abundance and diversity, except for the soybean monoculture (S-S) treatment. In monoculture systems, soybeans favored
Bradyrhizobium
sp. I, while maize and wheat favored
Bradyrhizobium
sp. III. Fertilization decreased the rhizobial diversity indexes but did not change the species composition. The organic carbon (OC) and available phosphorus (AP) contents and pH were the main soil parameters positively correlated with the distribution of
Bradyrhizobium
spp. I and II and
Bradyrhizobium japonicum
and negatively correlated with
Bradyrhizobium
sp. III. These results revealed that different land uses and crop management could not only alter the diversity and abundance of soybean rhizobia, but also change interactions between rhizobia and legume or nonlegume plants, which offered novel information about the biogeography of rhizobia.
Optimization of Multilocus Sequence Analysis for Identification of Species in the Genus Vibrio
Authors: Gabriel Michael W. , Matsui George Y. , Friedman Robert , Lovell Charles R. 
Published: June 2014

ABSTRACT

Multilocus sequence analysis (MLSA) is an important method for identification of taxa that are not well differentiated by 16S rRNA gene sequences alone. In this procedure, concatenated sequences of selected genes are constructed and then analyzed. The effects that the number and the order of genes used in MLSA have on reconstruction of phylogenetic relationships were examined. The
recA
,
rpoA
,
gapA
, 16S rRNA gene,
gyrB
, and
ftsZ
sequences from 56 species of the genus
Vibrio
were used to construct molecular phylogenies, and these were evaluated individually and using various gene combinations. Phylogenies from two-gene sequences employing
recA
and
rpoA
in both possible gene orders were different. The addition of the
gapA
gene sequence, producing all six possible concatenated sequences, reduced the differences in phylogenies to degrees of statistical (bootstrap) support for some nodes. The overall statistical support for the phylogenetic tree, assayed on the basis of a reliability score (calculated from the number of nodes having bootstrap values of ≥80 divided by the total number of nodes) increased with increasing numbers of genes used, up to a maximum of four. No further improvement was observed from addition of the fifth gene sequence (
ftsZ
), and addition of the sixth gene (
gyrB
) resulted in lower proportions of strongly supported nodes. Reductions in the numbers of strongly supported nodes were also observed when maximum parsimony was employed for tree construction. Use of a small number of gene sequences in MLSA resulted in accurate identification of
Vibrio
species.
Microbial Community Degradation of Widely Used Quaternary Ammonium Disinfectants
Authors: Oh Seungdae , Kurt Zohre , Tsementzi Despina , Weigand Michael R. , Kim Minjae , Hatt Janet K. , Tandukar Madan , Pavlostathis Spyros G. , Spain Jim C. , Konstantinidis Konstantinos T. 
Published: June 2014

ABSTRACT

Benzalkonium chlorides (BACs) are disinfectants widely used in a variety of clinical and environmental settings to prevent microbial infections, and they are frequently detected in nontarget environments, such as aquatic and engineered biological systems, even at toxic levels. Therefore, microbial degradation of BACs has important ramifications for alleviating disinfectant toxicity in nontarget environments as well as compromising disinfectant efficacy in target environments. However, how natural microbial communities respond to BAC exposure and what genes underlie BAC biodegradation remain elusive. Our previous metagenomic analysis of a river sediment microbial community revealed that BAC exposure selected for a low-diversity community, dominated by several members of the
Pseudomonas
genus that quickly degraded BACs. To elucidate the genetic determinants of BAC degradation, we conducted time-series metatranscriptomic analysis of this microbial community during a complete feeding cycle with BACs as the sole carbon and energy source under aerobic conditions. Metatranscriptomic profiles revealed a candidate gene for BAC dealkylation, the first step in BAC biodegradation that results in a product 500 times less toxic. Subsequent biochemical assays and isolate characterization verified that the putative amine oxidase gene product was functionally capable of initiating BAC degradation. Our analysis also revealed cooperative interactions among community members to alleviate BAC toxicity, such as the further degradation of BAC dealkylation by-products by organisms not encoding amine oxidase. Collectively, our results advance the understanding of BAC aerobic biodegradation and provide genetic biomarkers to assess the critical first step of this process in nontarget environments.