bluuebunny/crossref_metadata_2025_split huggingface dataset:
Recovery of consciousness following acute symptomatic seizures due to central nervous system infections in children
Authors: KING ELEANOR J , FERRIE COLIN D , LIVINGSTON JOHN H , TAYLOR JOHN C 
Published: February 2012

Aim  The aim of this study was to assess whether acute symptomatic epileptic seizures associated with central nervous system infections (ASinf) have a different ictal and postictal course to seizures of other aetiologies.Method  A case note analysis of 81 children (47 males; 34 females; age range 1mo–15y 6mo; median age 12mo) with central nervous system infections was undertaken. Seizure type, duration, aetiology, and timing were recorded. Recovery time to full consciousness in those not intubated was determined. Intubation rates and recovery times were compared with those from previous studies.Results  Of the 81 children, 40 (49.4%) had one or more ASinf. The different aetiologies were bacterial meningitis, aseptic meningitis, abscess/empyema, encephalitis, and postoperative infection. Twenty‐two had status epilepticus. The intubation rate in children with ASinf was higher than that in children with seizures of other aetiologies (21/40 [52.5%] vs 4/124 [3.23%]; p < 0.0001). Median postictal recovery time was 4.33 hours (0–207h). Children with ASinf took 4.3 (p<0.01), 3.0 (p=0.004), and 8.8 (p<0.001) times longer to recover than children who had seizures from all causes, remote symptomatic seizures, and febrile seizures respectively.Interpretation  ASinf in children are often longer, more likely to be associated with status epilepticus, more likely to necessitate intubation, and take longer to recover from than seizures of other aetiologies. This may help in the early diagnosis of central nervous system infection in children presenting with seizures.
Oxytocin hyperpolarizes cultured duodenum myenteric intrinsic primary afferent neurons by opening BKCa channels through IP3 pathway
Authors: Che Tongtong , Sun Hui , Li Jingxin , Yu Xiao , Zhu Dexiao , Xue Bing , Liu Kejing , Zhang Min , Kunze Wolfgang , Liu Chuanyong 
Published: February 2012

J. Neurochem. (2012) 121, 516–525.AbstractOxytocin (OT) is clinically important in gut motility and constitutively reduces duodenum contractility. Intrinsic primary afferent neurons (IPANs), whose physiological classification is as AH cells, are the 1st neurons of the peristaltic reflex pathway. We set out to investigate if this inhibitory effect is mediated by IPANs and to identify the ion channel(s) and intracellular signal transduction pathway that are involved in this effect. Myenteric neurons were isolated from the longitudinal muscle myenteric plexus (LMMP) preparation of rat duodenum and cultured for 16–24 h before electrophysiological recording in whole cell mode and AH cells identified by their electrophysiological characteristics. The cytoplasmic Ca2+ concentration ([Ca2+]i) of isolated neurons was measured using calcium imaging. The concentration of IP3 in the LMMP and the OT secreted from the LMMP were measured using ELISA. The oxytocin receptor (OTR) and large‐conductance calcium‐activated potassium (BKCa) channels, as well as the expression of OT and the IPAN marker calbindin 28 K, on the myenteric plexus neurons were localized using double‐immunostaining techniques. We found that administration of OT (10−7 to 10−5 M) dose dependently hyperpolarized the resting membrane potential and increased the total outward current. The OTR antagonist atosiban or the BKCa channel blocker iberiotoxin (IbTX) blocked the effects of OT suggesting that the increased outward current resulted from BKCa channel opening. OTR and the BKCaα subunit were co‐expressed on a subset of myenteric neurons at the LMMP. NS1619 (10−5 M, a BKCa channel activator) increased the outward current similar to the effect of OT. OT administration also increased [Ca2+]i and the OT‐evoked outward current was significantly attenuated by thapsigargin (10−6 M) or CdCl2. The effect of OT on the BKCa current was also blocked by pre‐treatment with the IP3 receptor antagonist 2‐APB (10−4 M) or the PLC inhibitor U73122 (10−5 M). OT (10−6 M) also increased the IP3 concentration within the LMMP. Both of the spontaneous and KCl‐induced secretion of OT was enhanced by atosiban. Most of OT‐immunoreactive cells are also immunoreactive for calbindin 28 K. In summary, we concluded that OT hyperpolarized myenteric IPANs by activating BKCa channels via the OTR‐PLC‐IP3‐Ca2+ signal pathway. OT might modulate IPANs mediated ENS reflex by an autocrine and negative feedback manner.
Inhibitory effects of sevoflurane on pacemaking activity of sinoatrial node cells in guinea‐pig heart
Authors: Kojima Akiko , Kitagawa Hirotoshi , Omatsu‐Kanbe Mariko , Matsuura Hiroshi , Nosaka Shuichi 
Published: February 2012

BACKGROUND AND PURPOSEThe volatile anaesthetic sevoflurane affects heart rate in clinical settings. The present study investigated the effect of sevoflurane on sinoatrial (SA) node automaticity and its underlying ionic mechanisms.EXPERIMENTAL APPROACHSpontaneous action potentials and four ionic currents fundamental for pacemaking, namely, the hyperpolarization‐activated cation current (If), T‐type and L‐type Ca2+ currents (ICa,T and ICa,L, respectively), and slowly activating delayed rectifier K+ current (IKs), were recorded in isolated guinea‐pig SA node cells using perforated and conventional whole‐cell patch‐clamp techniques. Heart rate in guinea‐pigs was recorded ex vivo in Langendorff mode and in vivo during sevoflurane inhalation.KEY RESULTSIn isolated SA node cells, sevoflurane (0.12–0.71 mM) reduced the firing rate of spontaneous action potentials and its electrical basis, diastolic depolarization rate, in a qualitatively similar concentration‐dependent manner. Sevoflurane (0.44 mM) reduced spontaneous firing rate by approximately 25% and decreased If, ICa,T, ICa,L and IKs by 14.4, 31.3, 30.3 and 37.1%, respectively, without significantly affecting voltage dependence of current activation. The negative chronotropic effect of sevoflurane was partly reproduced by a computer simulation of SA node cell electrophysiology. Sevoflurane reduced heart rate in Langendorff‐perfused hearts, but not in vivo during sevoflurane inhalation in guinea‐pigs.CONCLUSIONS AND IMPLICATIONSSevoflurane at clinically relevant concentrations slowed diastolic depolarization and thereby reduced pacemaking activity in SA node cells, at least partly due to its inhibitory effect on If, ICa,T and ICa,L. These findings provide an important electrophysiological basis of alterations in heart rate during sevoflurane anaesthesia in clinical settings.
Computational Flow Dynamics and Preclinical Assessment of a Novel Hemodialysis Catheter
Authors: Clark Timothy W.I. , Van Canneyt Koen , Verdonck Pascal 
Published: February 2012

AbstractWe examined flow characteristics and recirculation of a novel dialysis catheter with helically contoured lumens, which optimize the vectors of blood entering and leaving the device. Computational flow dynamics were used to measure shear stress, residence time (RT), Platelet Lysis Index (PLI), and recirculation of the study catheter, termed the VectorFlow catheter, compared with the Palindrome catheter. Bench and animal models were used to measure recirculation compared with other dialysis catheter designs. The VectorFlow catheter was associated with an 18% reduction in mean shear stress compared with the Palindrome catheter, at 13.6 and 16.6 Pa, respectively. Low PLI was seen with the VectorFlow (PLI = 0.019) and Palindrome (PLI = 0.015) catheters. The VectorFlow catheter was associated with a % RT >0.030  seconds of 1.2%, compared to 0.9% for the Palindrome. Calculated recirculation of the VectorFlow, Palindrome, and step‐tip catheter designs in reversed position were 1.2 × 10−4%, 0.039%, and 13.6%, respectively. In vitro, the VectorFlow catheter had no detectable recirculation (0%) compared to 7.3–9.5% with the Palindrome at flow rates of 400–600  ml/minute. In vivo, the VectorFlow catheter had no detectable recirculation, compared to 6.7–12% for the Palindrome. The VectorFlow catheter was associated with an absence of detectable recirculation with favorable flow dynamics.
Are there Neurological Consequences of Recurrent Intradialytic Hypotension?
Authors: Eldehni Mohamed Tarek , McIntyre Christopher W 
Published: February 2012

AbstractStructural abnormalities of the brain are common in hemodialysis (HD) patients, as are a wide range of severe functional deficiencies of cerebral function. Both depression and increasing dependency are highly prevalent in HD patients and worsen severely within the first 12 months of dialysis initiation. HD, as it is commonly practiced, is associated with significant recurrent episodes of circulatory stress. This results in acute injury to the heart, skin, kidney and gut, and drives longer term end‐organ chronic injury. This article aims to explore the hypothesis that the cerebral microcirculation is also sensitive to dialysis‐based circulatory stress (and other multiorgan consequences of recurrent dialysis‐induced ischemia), and that this may drive specific patterns of brain injury with resultant psychiatric and functional consequences.
Allergy influences the inflammatory status of the brain and enhances tau‐phosphorylation
Authors: Sarlus Heela , Höglund Caroline Olgart , Karshikoff Bianka , Wang Xiuzhe , Lekander Mats , Schultzberg Marianne , Oprica Mircea 
Published: February 2012

AbstractDespite the existing knowledge regarding the neuropathology of Alzheimer's disease (AD), the cause of sporadic forms of the disease is unknown. It has been suggested that systemic inflammation may have a role, but the exact mechanisms through which inflammatory processes influence the pathogenesis and progress of AD are not obvious. Allergy is a chronic inflammatory disease affecting more than 20% of the Western population, but the effects of allergic conditions on brain functions are largely unknown. The aim of this study was to investigate whether or not chronic peripheral inflammation associated with allergy affects the expression of AD‐related proteins and inflammatory markers in the brain. On the basis of previously described models for allergy in mice we developed a model of chronic airway allergy in mouse, with ovalbumin as allergen. The validity of the chronic allergy model was confirmed by a consistent and reproducible eosinophilia in the bronchoalveolar lavage (BAL) fluid of allergic animals. Allergic mice were shown to have increased brain levels of both immunoglobulin (Ig) G and IgE with a widespread distribution. Allergy was also found to increase phosphorylation of tau protein in the brain. The present data support the notion that allergy‐dependent chronic peripheral inflammation modifies the brain inflammatory status, and influences phosphorylation of an AD‐related protein, indicating that allergy may be yet another factor to be considered for the development and/or progression of neurodegenerative diseases such as AD.
The effect of cost surface parameterization on landscape resistance estimates
Authors: KOEN ERIN L. , BOWMAN JEFF , WALPOLE AARON A. 
Published: February 2012

AbstractA cost or resistance surface is a representation of a landscape’s permeability to animal movement or gene flow and is a tool for measuring functional connectivity in landscape ecology and genetics studies. Parameterizing cost surfaces by assigning weights to different landscape elements has been challenging however, because true costs are rarely known; thus, expert opinion is often used to derive relative weights. Assigning weights would be made easier if the sensitivity of different landscape resistance estimates to relative costs was known. We carried out a sensitivity analysis of three methods to parameterize a cost surface and two models of landscape permeability: least cost path and effective resistance. We found two qualitatively different responses to varying cost weights: linear and asymptotic changes. The most sensitive models (i.e. those leading to linear change) were accumulated least cost and effective resistance estimates on a surface coded as resistance (i.e. where high‐quality elements were held constant at a low‐value, and low‐quality elements were varied at higher values). All other cost surface scenarios led to asymptotic change. Developing a cost surface that produces a linear response of landscape resistance estimates to cost weight variation will improve the accuracy of functional connectivity estimates, especially when cost weights are selected through statistical model fitting procedures. On the other hand, for studies where cost weights are unknown and model selection is not being used, methods where resistance estimates vary asymptotically with cost weights may be more appropriate, because of their relative insensitivity to parameterization.
Conducting a meta‐analysis: basics and good practices
Authors: Cheung Mike W.‐L. , Ho Roger C. M. , Lim Yonghao , Mak Anselm 
Published: February 2012

AbstractMeta‐analysis is a statistical method to compare and combine effect sizes from a pool of relevant empirical studies. It is now a standard approach to synthesize research findings in many disciplines, including medical and healthcare research. This paper is the third paper of a mini‐series introducing systematic review and meta‐analysis. First, common effect sizes used in meta‐analysis are presented. Fixed‐, random‐ and mixed‐effects models are then introduced. Next, a real data set from a published meta‐analysis will be used to illustrate the procedures and interpretations. Last, software packages that may be used to conduct meta‐analyses will be highlighted.
In Vitro
Activity of the New Fluoroketolide Solithromycin (CEM-101) against a Large Collection of Clinical Neisseria gonorrhoeae Isolates and International Reference Strains, Including Those with High-Level Antimicrobial Resistance: Potential Treatment Option for Gonorrhea?
Authors: Golparian Daniel , Fernandes Prabhavathi , Ohnishi Makoto , Jensen Jörgen S. , Unemo Magnus 
Published: February 2012

ABSTRACT

Gonorrhea may become untreatable, and new treatment options are essential. We investigated the
in vitro
activity of the first fluoroketolide, solithromycin. Clinical
Neisseria gonorrhoeae
isolates and reference strains (
n
= 246), including the two extensively drug-resistant strains H041 and F89 and additional isolates with clinical cephalosporin resistance and multidrug resistance, were examined. The activity of solithromycin was mainly superior to that of other antimicrobials (
n
= 10) currently or previously recommended for gonorrhea treatment. Solithromycin might be an effective treatment option for gonorrhea.
Molecular Characterization of Extended-Spectrum-β-Lactamase-Producing and Plasmid-Mediated AmpC β-Lactamase-Producing Escherichia coli Isolated from Stray Dogs in South Korea
Authors: Tamang Migma Dorji , Nam Hyang-Mi , Jang Geum-Chan , Kim Su-Ran , Chae Myung Hwa , Jung Suk-Chan , Byun Jae-Won , Park Yong Ho , Lim Suk-Kyung 
Published: February 2012

ABSTRACT

A total of 47 extended-spectrum-cephalosporin-resistant
Escherichia coli
strains isolated from stray dogs in 2006 and 2007 in the Republic of Korea were investigated using molecular methods. Extended-spectrum β-lactamase (ESBL) and AmpC β-lactamase phenotypes were identified in 12 and 23
E. coli
isolates, respectively. All 12 ESBL-producing isolates carried
bla
CTX-M
genes. The most common CTX-M types were CTX-M-14 (
n
= 5) and CTX-M-24 (
n
= 3). Isolates producing CTX-M-3, CTX-M-55, CTX-M-27, and CTX-M-65 were also identified. Twenty-one of 23 AmpC β-lactamase-producing isolates were found to carry
bla
CMY-2
genes. TEM-1 was associated with CTX-M and CMY-2 β-lactamases in 4 and 15 isolates, respectively. In addition to
bla
TEM-1
, two isolates carried
bla
DHA-1
, and one of them cocarried
bla
CMY-2
. Both CTX-M and CMY-2 genes were located on large (40 to 170 kb) conjugative plasmids that contained the insertion sequence IS
Ecp1
upstream of the
bla
genes. Only in the case of CTX-M genes was there an IS
903
sequence downstream of the gene. The spread of ESBLs and AmpC β-lactamases occurred via both horizontal gene transfer, accounting for much of the CTX-M gene dissemination, and clonal spread, accounting for CMY-2 gene dissemination. The horizontal dissemination of
bla
CTX-M
and
bla
CMY-2
genes was mediated by IncF and IncI1-Iγ plasmids, respectively. The clonal spread of
bla
CMY-2
was driven mainly by
E. coli
strains of virulent phylogroup D lineage ST648. To our knowledge, this is the first report of
bla
DHA-1
in
E. coli
strains isolated from companion animals. This study also represents the first report of CMY-2 β-lactamase-producing
E. coli
isolates from dogs in the Republic of Korea.
The Staphylococcus aureus Alpha-Toxin Perturbs the Barrier Function in Caco-2 Epithelial Cell Monolayers by Altering Junctional Integrity
Authors: Kwak Young-Keun , Vikström Elena , Magnusson Karl-Eric , Vécsey-Semjén Beatrix , Colque-Navarro Patricia , Möllby Roland 
Published: February 2012

ABSTRACT

Increased microvascular permeability is a hallmark of sepsis and septic shock. Intestinal mucosal dysfunction may allow translocation of bacteria and their products, thereby promoting sepsis and inflammation. Although
Staphylococcus aureus
alpha-toxin significantly contributes to sepsis and perturbs the endothelial barrier function, little is known about possible effects of
S. aureus
alpha-toxin on human epithelial barrier functions. We hypothesize that
S. aureus
alpha-toxin in the blood can impair the intestinal epithelial barrier and thereby facilitate the translocation of luminal bacteria into the blood, which may in turn aggravate a septic condition. Here, we showed that staphylococcal alpha-toxin disrupts the barrier integrity of human intestinal epithelial Caco-2 cells as evidenced by decreased transepithelial electrical resistance (TER) and reduced cellular levels of junctional proteins, such as ZO-1, ZO-3, and E-cadherin. The Caco-2 cells also responded to alpha-toxin with an elevated cytosolic calcium ion concentration ([Ca
2+
]
i
), elicited primarily by calcium influx from the extracellular environment, as well as with a significant reduction in TER, which was modulated by intracellular calcium chelation. Moreover, a significantly larger reduction in TER and amounts of the junctional proteins,
viz
., ZO-3 and occludin, was achieved by basolateral than by apical application of the alpha-toxin. These experimental findings thus support the hypothesis that free staphylococcal alpha-toxin in the bloodstream may cause intestinal epithelial barrier dysfunction and further aggravate the septic condition by promoting the release of intestinal bacteria into the underlying tissues and the blood.
Different Patterns of Toll-Like Receptor 2 Polymorphisms in Populations of Various Ethnic and Geographic Origins
Authors: Ioana M. , Ferwerda B. , Plantinga T. S. , Stappers M. , Oosting M. , McCall M. , Cimpoeru A. , Burada F. , Panduru N. , Sauerwein R. , Doumbo O. , van der Meer J. W. M. , van Crevel R. , Joosten L. A. B. , Netea M. G. 
Published: February 2012

ABSTRACT

Upon the invasion of the host by microorganisms, innate immunity is triggered through pathogen recognition by pattern recognition receptors (PRRs). Toll-like receptors (TLRs) are the best-studied class of PRRs, and they recognize specific pathogen-associated molecular patterns (PAMPs) from various microorganisms. A large number of studies have shown that genetic variation in TLRs may influence susceptibility to infections. We assessed the genetic variation of
TLR2
, which encodes one of the most important TLRs, in various populations around the globe and correlated it with changes in the function of the molecule. The three best-known nonsynonymous
TLR2
polymorphisms (1892C>A, 2029C>T, and 2258G>A) were assessed in different populations from the main continental masses: Romanians, Vlax-Roma, Dutch (European populations), Han Chinese (East Asia), Dogon, Fulani (Africa), and Trio Indians (America). The 2029C>T polymorphism was absent in both European and non-European populations, with the exception of the Vlax-Roma, suggesting that this polymorphism most likely arose in Indo-Aryan people after migration into South Asia. The 1892C>A polymorphism that was found exclusively in European populations, but not in Asian, African, or American volunteers, probably occurred in proto-Indo-Europeans. Interestingly, 2258G>A was present only in Europeans, including Vlax-Roma, but at a very low frequency. The differential pattern of the
TLR2
polymorphisms in various populations may explain some of the differences in susceptibility to infections between these populations.
Regulation of Subtilase Cytotoxin-Induced Cell Death by an RNA-Dependent Protein Kinase-Like Endoplasmic Reticulum Kinase-Dependent Proteasome Pathway in HeLa Cells
Authors: Yahiro Kinnosuke , Tsutsuki Hiroyasu , Ogura Kohei , Nagasawa Sayaka , Moss Joel , Noda Masatoshi 
Published: February 2012

ABSTRACT

Shiga-toxigenic
Escherichia coli
(STEC) produces subtilase cytotoxin (SubAB), which cleaves the molecular chaperone BiP in the endoplasmic reticulum (ER), leading to an ER stress response and then activation of apoptotic signaling pathways. Here, we show that an early event in SubAB-induced apoptosis in HeLa cells is mediated by RNA-dependent protein kinase (PKR)-like ER kinase (PERK), not activating transcription factor 6 (ATF6) or inositol-requiring enzyme 1(Ire1), two other ER stress sensors. PERK knockdown suppressed SubAB-induced eIF2α phosphorylation, activating transcription factor 4 (ATF4) expression, caspase activation, and cytotoxicity. Knockdown of eIF2α by small interfering RNA (siRNA) or inhibition of eIF2α dephosphorylation by Sal003 enhanced SubAB-induced caspase activation. Treatment with proteasome inhibitors (i.e., MG132 and lactacystin), but not a general caspase inhibitor (Z-VAD) or a lysosome inhibitor (chloroquine), suppressed SubAB-induced caspase activation and poly(ADP-ribose) polymerase (PARP) cleavage, suggesting that the ubiquitin-proteasome system controls events leading to caspase activation, i.e., Bax/Bak conformational changes, followed by cytochrome
c
release from mitochondria. Levels of ubiquitinated proteins in HeLa cells were significantly decreased by SubAB treatment. Further, in an early event, some antiapoptotic proteins, which normally turn over rapidly, have their synthesis inhibited, and show enhanced degradation via the proteasome, resulting in apoptosis. In PERK knockdown cells, SubAB-induced loss of ubiquitinated proteins was inhibited. Thus, SubAB-induced ER stress is caused by BiP cleavage, leading to PERK activation, not by accumulation of ubiquitinated proteins, which undergo PERK-dependent degradation via the ubiquitin-proteasome system.