bluuebunny/crossref_metadata_2025_split huggingface dataset:
Placental Transfer of IgG Antibodies Specific to Klebsiella and Pseudomonas LPS and to Group B Streptococcus in Twin Pregnancies
Authors: Stach S. C. L. , Brizot M. L. , Liao A. W. , Palmeira P. , Francisco R. P. V. , Carneiro‐Sampaio M. M. S. , Zugaib M. 
Published: November 2014

AbstractGroup B Streptococcus (GBS), Klebsiella spp. and Pseudomonas spp. are important aetiological agents of neonatal infections in Brazil. There is a lack of data in the literature regarding the specific transport of immunoglobulin G (IgG) against these pathogens in multiple pregnancies. Maternal (n = 55) and umbilical cord (n = 110) blood samples were prospectively collected at birth from 55 twin pregnancies. The factors associated with cord levels and transfer ratios of IgG against GBS, Klebsiella and Pseudomonas were examined. The IgG umbilical cord serum levels specific to GBS, Klebsiella LPS and Pseudomonas LPS were significantly associated with maternal‐specific IgG concentrations and the presence of diabetes. The anti‐Klebsiella IgG cord serum concentrations were also related to birthweight and the presence of hypertension. The transfer ratios against GBS and Pseudomonas LPS were associated with maternal‐specific IgG concentrations. The transfer ratios for GBS and Pseudomonas LPS were associated with gestational age at delivery and the presence of diabetes, respectively. None of the examined parameters were related to Klebsiella LPS transfer ratios. We conclude that in twin pregnancies, specific maternal IgG serum concentrations and diabetes were the parameters associated with umbilical cord serum IgG concentrations reactive with the three pathogens investigated. All the other parameters investigated showed different associations with neonatal‐specific IgG levels according to the antigen studied. There was no uniformity of the investigated parameters regarding association with placental IgG transfer ratios against the GBS, Pseudomonas LPS and Klebsiella LPS.
Narrating Sustainability in Canadian Health Care Reform Discourse
Authors: Bhatia Vandna , Orsini Michael 
Published: November 2014

AbstractIn Canada, as in other industrialized welfare states, definitions of health system sustainability reflect different goals and correspondingly diverse ways of understanding exactly what is to be sustained and how. In this article, we report on results from a survey of documents and groups involved in and/or concerned about sustainability of the healthcare system. We identify four broad narratives of sustainability in Canadian healthcare reform discourse, and explore what these different sustainability narratives tell us about the character and contours of these often‐fractious debates. We argue that sustainability itself may not be a paradigm shift, as has been suggested, but a plot device that helps to steer the story in a particular direction, ‘black‐boxing’ certain aspects of context and emphasizing others.
Quantitative polymerase chain reaction for detection of human herpesvirus‐7 infection in umbilical cord blood donors
Authors: Abedi E. , Kheirandish M. , Sharifi Z. , Samiee S. , Kokhaei P. , Pourpak Z. , Ashraf M.J. 
Published: November 2014

AbstractObjectiveUmbilical cord blood (UCB) has been a reasonable alternative to granulocyte colony‐stimulating factor‐mobilized peripheral blood or bone marrow, as a source of hematopoietic stem cells with a lower risk of graft‐versus‐host disease. In immunocompromised hosts after transplantation, the risk of viral infection in adults, especially with beta‐herpesviruses such as human herpesvirus‐7 (HHV‐7), may be increased. This virus in immunocompromised patients can be reactivated from latency and converted to an active phase. Therefore, light‐upon‐extension real‐time polymerase chain reaction (PCR) was developed to assess the prevalence and load of HHV‐7 in the plasma and buffy coat of donors.MethodsAbout 825 UCB samples under standard protocol from donors were collected. Then, DNA from plasma and buffy coat was extracted and quantitative real‐time PCR was performed with light‐upon‐extension primers.ResultsOverall, HHV‐7 was detected in 3.64% (30/825) of UCB donors. HHV‐7 DNA was detected in 26 (3.2%) buffy coat samples (latent infection), and only 4 (0.48%) of them were positive for HHV‐7 DNA in plasma samples (active infection); the mean HHV‐7 viral load was 1.31 × 101 copies/mL in latent infection, and 1.94 × 105 copies/mL in active infection.ConclusionsWe suggest that real‐time PCR in plasma and buffy coat could be a useful method to detect active and latent HHV‐7 infection in UCB donors and determine its role in subsequent transmission events.
Atorvastatin reduces T‐cell activation and exhaustion among HIV‐infected cART‐treated suboptimal immune responders in Uganda: a randomised crossover placebo‐controlled trial
Authors: Nakanjako Damalie , Ssinabulya Isaac , Nabatanzi Rose , Bayigga Lois , Kiragga Agnes , Joloba Moses , Kaleebu Pontiano , Kambugu Andrew D. , Kamya Moses R. , Sekaly Rafick , Elliott Alison , Mayanja‐Kizza Harriet 
Published: November 2014

AbstractObjectiveT‐cell activation independently predicts mortality, poor immune recovery and non‐AIDS illnesses during combination antiretroviral therapy (cART). Atorvastatin showed anti‐immune activation effects among HIV‐infected cART‐naïve individuals. We investigated whether adjunct atorvastatin therapy reduces T‐cell activation among cART‐treated adults with suboptimal immune recovery.MethodsA randomised double‐blind placebo‐controlled crossover trial, of atorvastatin 80 mg daily vs. placebo for 12 weeks, was conducted among individuals with CD4 increase <295 cells/μl after seven years of suppressive cART. Change in T‐cell activation (CD3 + CD4 + /CD8 + CD38 + HLADR+) and in T‐cell exhaustion (CD3 + CD4 + /CD8 + PD1 + ) was measured using flow cytometry.ResultsThirty patients were randomised, 15 to each arm. Atorvastatin resulted in a 28% greater reduction in CD4 T‐cell activation (60% reduction) than placebo (32% reduction); P = 0.001. Atorvastatin also resulted in a 35% greater reduction in CD8‐T‐cell activation than placebo (49% vs. 14%, P = 0.0009), CD4 T‐cell exhaustion (27% vs. 17% in placebo), P = 0.001 and CD8 T‐cell exhaustion (27% vs. 16%), P = 0.004. There was no carry‐over/period effect. Expected adverse events were comparable in both groups, and no serious adverse events were reported.ConclusionAtorvastatin reduced T‐cell immune activation and exhaustion among cART‐treated adults in a Ugandan cohort. Atorvastatin adjunct therapy should be explored as a strategy to improve HIV treatment outcomes among people living with HIV in sub‐Saharan Africa.
PRL1 modulates root stem cell niche activity and meristem size through WOX5 and PLTs in Arabidopsis
Authors: Ji Hongtao , Wang Shuangfeng , Li Kexue , Szakonyi Dóra , Koncz Csaba , Li Xia 
Published: November 2014

SummaryThe stem cell niche in the root meristem maintains pluripotent stem cells to ensure a constant supply of cells for root growth. Despite extensive progress, the molecular mechanisms through which root stem cell fates and stem cell niche activity are determined remain largely unknown. In Arabidopsis thaliana, the Pleiotropic Regulatory Locus 1 (PRL1) encodes a WD40‐repeat protein subunit of the spliceosome‐activating Nineteen Complex (NTC) that plays a role in multiple stress, hormone and developmental signaling pathways. Here, we show that PRL1 is involved in the control of root meristem size and root stem cell niche activity. PRL1 is strongly expressed in the root meristem and its loss of function mutation results in disorganization of the quiescent center (QC), premature stem cell differentiation, aberrant cell division, and reduced root meristem size. Our genetic studies indicate that PRL1 is required for confined expression of the homeodomain transcription factor WOX5 in the QC and acts upstream of the transcription factor PLETHORA (PLT) in modulating stem cell niche activity and root meristem size. These findings define a role for PRL1 as an important determinant of PLT signaling that modulates maintenance of the stem cell niche and root meristem size.
Peripheral chemoreceptors and cardiorespiratory coupling: a link to sympatho‐excitation
Authors: Zoccal Daniel B. 
Published: November 2014

New Findings
What is the topic of this review?
Chronic intermittent hypoxia (CIH), as observed in patients with obstructive sleep apnoea, is associated with the development of sympathetically mediated arterial hypertension. Nevertheless, the mechanisms underpinning the augmented sympathetic outflow in CIH still remain under investigation.
What advances does it highlight?
In this report, I present experimental evidence supporting the hypothesis that changes in the function of the respiratory network and coupling with the sympathetic nervous system may be considered as a novel and relevant mechanism for the increase in baseline sympathetic outflow in animals submitted to CIH.
Chronic intermittent hypoxia (CIH) has been identified as a relevant risk factor for the development of enhanced sympathetic outflow and arterial hypertension. Several studies have highlighted the importance of peripheral chemoreceptors for the cardiovascular changes elicited by CIH. However, the effects of CIH on the central mechanisms regulating sympathetic outflow are not fully elucidated. Our research group has explored the hypothesis that the enhanced sympathetic drive following CIH exposure is, at least in part, dependent on alterations in the respiratory network and its interaction with the sympathetic nervous system. In this report, I discuss the changes in the discharge profile of baseline sympathetic activity in rats exposed to CIH, their association with the generation of active expiration and the interactions between expiratory and sympathetic neurones after CIH conditioning. Together, these findings are consistent with the theory that mechanisms of central respiratory–sympathetic coupling are a novel factor in the development of neurogenic hypertension.
Short‐latency inhibitory reflex responses to inspiratory loading of the scalene muscles are impaired in spinal cord injury
Authors: McBain Rachel A. , Hudson Anna L. , Gandevia Simon C. , Butler Jane E. 
Published: November 2014

New Findings

What is the central question of this study?
The aim was to determine whether the reflex inhibition in the electromyographic activity of scalene muscles in response to inspiratory muscle loading is present in individuals with cervical spinal cord injury and to examine whether the intercostal muscle afferents are critical for genesis of the reflex.

What is the main finding and its importance?
The lack of reflex inhibition in response to inspiratory loading in individuals with complete cervical spinal cord injury suggests that the reflex critically requires input from intercostal afferents and/or an intact intersegmental neural network.
In healthy individuals, transient loading of inspiratory muscles with a brief inspiratory occlusion produces a short‐latency inhibitory response (IR) in the electromyographic activity of scalene muscles at ∼40 ms, followed by an excitatory response (ER). It has been argued that this reflex plays a protective role in neuromuscular control of the inspiratory muscles and that it is co‐ordinated by spinal segmental or supraspinal circuits. In this study, the reflex response to airway occlusion was recorded bilaterally from scalene muscles in 14 subjects and from the right costal diaphragm in seven subjects with spinal cord injury [SCI, C4–C6; American Spinal Injury Association (ASIA) Impairment Scale (AIS) A]. The incidence, latency and size of the reflex were compared with previously published data from able‐bodied subjects. Only two subjects with SCI showed an IR, and six subjects had an ER. Latencies to the onset and peak of the IR and ER were 5–50 ms longer than in able‐bodied subjects. However, when reflexes were identified, their size in individuals with SCI was similar to that of control subjects. We conclude that afferents from the scalene muscles and diaphragm are insufficient in most subjects with SCI to evoke the usual inhibition to airway occlusion and that input from chest wall afferents below the spinal cord lesion may be important for genesis of the short‐latency inhibition in the able‐bodied subjects.
The role of gastrointestinal vagal afferent fibres in obesity
Authors: Kentish Stephen J. , Page Amanda J. 
Published: November 2014

AbstractGastrointestinal (GI) vagal afferents are a key mediatory of food intake. Through a balance of responses to chemical and mechanical stimuli food intake can be tightly controlled via the ascending satiety signals initiated in the GI tract. However, vagal responses to both mechanical and chemical stimuli are modified in diet‐induced obesity (DIO). Much of the research to date whilst in relatively isolated/controlled circumstances indicates a shift between a balance of orexigenic and anorexigenic vagal signals to blunted anorexigenic and potentiated orexigenic capacity. Although the mechanism responsible for the DIO shift in GI vagal afferent signalling is unknown, one possible contributing factor is the gut microbiota. Nevertheless, whatever the mechanism, the observed changes in gastrointestinal vagal afferent signalling may underlie the pathophysiological changes in food consumption that are pivotal for the development and maintenance of obesity.
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Molecular mechanisms of temperature adaptation
Authors: Bagriantsev Sviatoslav N. , Gracheva Elena O. 
Published: November 2014

AbstractThermal perception is a fundamental physiological process pertaining to the vast majority of organisms. In vertebrates, environmental temperature is detected by the primary afferents of the somatosensory neurons in the skin, which express a ‘choir’ of ion channels tuned to detect particular temperatures. Nearly two decades of research have revealed a number of receptor ion channels that mediate the perception of several temperature ranges, but most still remain molecularly orphaned. Yet even within this well‐researched realm, most of our knowledge largely pertains to two closely related species of rodents, mice and rats. While these are standard biomedical research models, mice and rats provide a limited perspective to elucidate the general principles that drive somatosensory evolution. In recent years, significant advances have been made in understanding the molecular mechanism of temperature adaptation in evolutionarily distant vertebrates and in organisms with acute thermal sensitivity. These studies have revealed the remarkable versatility of the somatosensory system and highlighted adaptations at the molecular level, which often include changes in biophysical properties of ion channels from the transient receptor potential family. Exploiting non‐standard animal models has the potential to provide unexpected insights into general principles of thermosensation and thermoregulation, unachievable using the rodent model alone.
Short‐chain fatty acid sensing in rat duodenum
Authors: Akiba Yasutada , Inoue Takuya , Kaji Izumi , Higashiyama Masaaki , Narimatsu Kazuyuki , Iwamoto Ken‐ichi , Watanabe Masahiko , Guth Paul H. , Engel Eli , Kuwahara Atsukazu , Kaunitz Jonathan D 
Published: November 2014

Key points
Luminal lipid in the duodenum modulates gastroduodenal functions via the release of gut hormones and mediators such as cholecystokinin and 5‐HT.
The effects of luminal short‐chain fatty acids (SCFAs) in the foregut are unknown.
Free fatty acid receptors (FFARs) for long‐chain fatty acids (LCFAs) and SCFAs are expressed in enteroendocrine cells. SCFA receptors, termed FFA2 and FFA3, are expressed in duodenal enterochromaffin cells and L cells, respectively.
Activation of LCFA receptor (FFA1) and presumed FFA3 stimulates duodenal HCO3− secretion via a glucagon‐like peptide (GLP)‐2 pathway, whereas FFA2 activation induces HCO3− secretion via muscarinic and 5‐HT4 receptor activation.
The presence of SCFA sensing in the duodenum with GLP‐2 and 5‐HT signals further supports the hypothesis that luminal SCFA in the foregut may contribute towards the generation of functional symptoms.
AbstractIntraduodenal fatty acids (FA) and bacterial overgrowth, which generate short‐chain FAs (SCFAs), have been implicated in the generation of functional dyspepsia symptoms. We studied the mechanisms by which luminal SCFA perfusion affects duodenal HCO3− secretion (DBS), a measure of mucosal neurohumoral activation. Free fatty acid receptor (FFAR) 1 (FFA1), which binds long‐chain FA (LCFA), and SCFA receptors FFA2 and FFA3 were immunolocalised to duodenal enteroendocrine cells. FFA3 colocalised with glucagon‐like peptide (GLP)‐1, whereas FFA2 colocalised with 5‐HT. Luminal perfusion of the SCFA acetate or propionate increased DBS, enhanced by dipeptidyl peptidase‐IV (DPPIV) inhibition, at the same time as increasing GLP‐2 portal blood concentrations. Acetate‐induced DBS was partially inhibited by monocarboxylate/HCO3− exchanger inhibition without affecting GLP‐2 release, implicating acetate absorption in the partial mediation of DBS. A selective FFA2 agonist dose‐dependently increased DBS, unaffected by DPPIV inhibition or by cholecystokinin or 5‐HT3 receptor antagonists, but was inhibited by atropine and a 5‐HT4 antagonist. By contrast, a selective FFA1 agonist increased DBS accompanied by GLP‐2 release, enhanced by DPPIV inhibition and inhibited by a GLP‐2 receptor antagonist. Activation of FFA1 by LCFA and presumably FFA3 by SCFA increased DBS via GLP‐2 release, whereas FFA2 activation stimulated DBS via muscarinic and 5‐HT4 receptor activation. SCFA/HCO3− exchange also appears to be present in the duodenum. The presence of duodenal fatty acid sensing receptors that signal hormone release and possibly signal neural activation may be implicated in the pathogenesis of functional dyspepsia.
Silicon central pattern generators for cardiac diseases
Authors: Nogaret Alain , O'Callaghan Erin L. , Lataro Renata M. , Salgado Helio C. , Meliza C. Daniel , Duncan Edward , Abarbanel Henry D. I. , Paton Julian F. R. 
Published: November 2014

AbstractCardiac rhythm management devices provide therapies for both arrhythmias and resynchronisation but not heart failure, which affects millions of patients worldwide. This paper reviews recent advances in biophysics and mathematical engineering that provide a novel technological platform for addressing heart disease and enabling beat‐to‐beat adaptation of cardiac pacing in response to physiological feedback. The technology consists of silicon hardware central pattern generators (hCPGs) that may be trained to emulate accurately the dynamical response of biological central pattern generators (bCPGs). We discuss the limitations of present CPGs and appraise the advantages of analog over digital circuits for application in bioelectronic medicine. To test the system, we have focused on the cardio‐respiratory oscillators in the medulla oblongata that modulate heart rate in phase with respiration to induce respiratory sinus arrhythmia (RSA). We describe here a novel, scalable hCPG comprising physiologically realistic (Hodgkin–Huxley type) neurones and synapses. Our hCPG comprises two neurones that antagonise each other to provide rhythmic motor drive to the vagus nerve to slow the heart. We show how recent advances in modelling allow the motor output to adapt to physiological feedback such as respiration. In rats, we report on the restoration of RSA using an hCPG that receives diaphragmatic electromyography input and use it to stimulate the vagus nerve at specific time points of the respiratory cycle to slow the heart rate. We have validated the adaptation of stimulation to alterations in respiratory rate. We demonstrate that the hCPG is tuneable in terms of the depth and timing of the RSA relative to respiratory phase. These pioneering studies will now permit an analysis of the physiological role of RSA as well as its any potential therapeutic use in cardiac disease.
Protection of intestinal injury during heat stroke in mice by interleukin‐6 pretreatment
Authors: Phillips Neil A. , Welc Steven S. , Wallet Shannon M. , King Michelle A. , Clanton Thomas L. 
Published: November 2014

Key points
Heat stroke afflicts thousands of humans each year, worldwide.
The immune system responds to hyperthermia exposure resulting in heat stroke by producing an array of immunological proteins, such as interleukin‐6 (IL‐6). However, the physiological functions of IL‐6 and other cytokines in hyperthermia are poorly understood.
We hypothesized that IL‐6 plays a protective role in conditions of heat stroke. To test this, we gave small IL‐6 supplements to mice prior to exposing them to hot environments sufficient to induce conditions of heat stroke.
Pretreatment with IL‐6 resulted in improved ability to withstand heat exposure in anaesthetized mice, it protected the intestine from injury, reducing the permeability of the intestinal barrier, and it attenuated the release of other cytokines involved in inflammation.
The results support the hypothesis that IL‐6 is a ‘physiological stress hormone’ that plays an important role in survival during acute life‐threatening conditions such as heat stroke.
AbstractThe role of interleukin‐6 (IL‐6) in hyperthermia and heat stroke is poorly understood. Plasma IL‐6 is elevated following hyperthermia in animals and humans, and IL‐6 knockout mice are more intolerant of severe hyperthermia. We evaluated the effect of IL‐6 supplementation on organ injury following severe hyperthermia exposure in anaesthetized mice. Two hours prior to hyperthermia, mice were treated with 0.6 μg intraperitoneal IL‐6, or identical volumes of saline in controls. Mice were anaesthetized, gavaged with FITC–dextran for measures of gastrointestinal permeability, and exposed to incremental (0.5°C every 30 min) increases in temperature. Heating stopped when maximum core temperature (Tc) of 42.4°C was attained (Tc,max). The mice recovered at room temperature (≈22°C) for 30 or 120 min, at which time plasma and tissues were collected. IL‐6‐treated mice, on average, required ≈25 min longer to attain Tc,max. Injury and swelling of the villi in the duodenum was present in untreated mice after 30 min of recovery. These changes were blocked by IL‐6 treatment. IL‐6 also reduced gastrointestinal permeability, assayed by the accumulation of FITC–dextran in plasma. Plasma cytokines were also attenuated in IL‐6‐treated animals, including significant reductions in TNFα, MCP‐1 (CXCL2), RANTES (CCL5) and KC (CCL5). The results demonstrate that IL‐6 has a protective influence on the pattern of physiological responses to severe hyperthermia, suggesting that early endogenous expression of IL‐6 may provide a protection from the development of organ damage and inflammation.