Σάββατο 1 Δεκεμβρίου 2018
Examination of the enhanced recovery guidelines in thoracic surgery
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Neuromonitoring in the elderly
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Incremental value of noncerebral somatic tissue oxygenation monitoring for patients undergoing surgery
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Spinal cord perfusion protection for thoraco-abdominal aortic aneurysm surgery
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Prehabilitation is better than cure
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Extravascular lung water monitoring for thoracic and lung transplant surgeries
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Biomarkers and postoperative cognitive function: could it be that easy?
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Delayed recovery following thoracic surgery: persistent issues and potential interventions
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Amplification of endothelium‐dependent vasodilatation in contracting human skeletal muscle: role of KIR channels
Key points
In humans, the vasodilatory response to skeletal muscle contraction is mediated in part by activation of inwardly rectifying potassium (KIR) channels. Evidence from animal models suggest that KIR channels serve as electrical amplifiers of endothelium‐dependent hyperpolarization (EDH). We found that skeletal muscle contraction amplifies vasodilatation to the endothelium‐dependent agonist acetylcholine (ACh), whereas there was no change in the vasodilatory response to sodium nitroprusside, an endothelium‐independent nitric oxide donor. Blockade of KIR channels reduced the exercise‐induced amplification of ACh‐mediated vasodilatation. Conversely, pharmacological activation of KIR channels in quiescent muscle via intra‐arterial infusion of KCl independently amplified the vasodilatory response to ACh. This study is the first in humans to demonstrate that specific endothelium‐dependent vasodilatory signalling is amplified in the vasculature of contracting skeletal muscle and that KIR channels may serve as amplifiers of EDH‐like vasodilatory signalling in humans.
Abstract
The local vasodilatory response to muscle contraction is due in part to the activation of inwardly rectifying potassium (KIR) channels. Evidence from animal models suggest that KIR channels function as "amplifiers" of endothelium‐dependent vasodilators. We tested the hypothesis that contracting muscle selectively amplifies endothelium‐dependent vasodilatation via activation of KIR channels. We measured forearm blood flow (Doppler ultrasound) and calculated changes in vascular conductance (FVC) to local intra‐arterial infusion of ACh (endothelium‐dependent dilator) during resting conditions, handgrip exercise (5% maximum voluntary contraction), or sodium nitroprusside (SNP; endothelium‐independent dilator) which served as a high‐flow control condition (n = 7, young healthy men and women). Trials were performed before and after blockade of KIR channels via infusion of barium chloride. Exercise augmented peak ACh‐mediated vasodilatation (ΔFVC saline: 117 ± 14; exercise: 236 ± 21 ml (min)−1(100 mmHg)−1; P<0.05), whereas SNP did not impact ACh‐mediated vasodilatation. Blockade of KIR channels attenuated the exercise‐induced augmentation of ACh. In 8 additional subjects, SNP was administered as the experimental dilator. In contrast to ACh, exercise did not alter SNP‐mediated vasodilatation (ΔFVC saline: 158 ± 35; exercise: 121 ± 22 ml (min)−1(100 mmHg)−1; NS). Finally, in a subset 6 subjects, direct pharmacological activation of KIR channels in quiescent muscle via infusion of KCl amplified peak ACh‐mediated vasodilatation (ΔFVC saline: 97 ± 15, KCl: 142 ± 16 ml (min)−1(100 mmHg)−1; respectively; P<0.05). These findings indicate that skeletal muscle contractions selectively amplify endothelium‐dependent vasodilatory signalling via activation of KIR channels, and this may be an important mechanism contributing to the normal vasodilatory response to exercise in humans.
This article is protected by copyright. All rights reserved
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The impact of age and egg-laying cycle on female grasshoppers’ preference functions for acoustic signals
Abstract
Female responsiveness and the shape of preference functions for male signal traits are important determinants for male mating success. We observed the responsiveness and the selectivity of virgin grasshopper females (Chorthippus biguttulus L.) for different features of males' acoustic signals throughout their life span to detect possible influences of age on the females' preference functions. In particular, we explored the hypothesis that the females may become less selective with increasing age and, therefore, would start to accept songs that are normally rejected. Such an age effect could relieve the selection pressure on male signal traits. In the majority of animals tested, the general responsiveness decreased with age although a few individuals exhibited an opposite trend. Contrary to the above expectation, there was no indication of a loss of selectivity in older females or an increased acceptance of normally unattractive song models. The timing within the oviposition cycle had a strong effect on responsiveness: near oviposition the general responsiveness increased and with it also the half width of the preference functions. However, highly unattractive song models remained unattractive also near oviposition.
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Highlights from Gastro Update Europe – Prague, June 2018
Publication date: Available online 30 November 2018
Source: Arab Journal of Gastroenterology
Author(s): Guido N.J. Tytgat
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Correlation between expression of MMP-9 and MMP-3 in Helicobacter pylori infected patients with different gastroduodenal diseases
Publication date: Available online 30 November 2018
Source: Arab Journal of Gastroenterology
Author(s): Nader Bagheri, Marzieh Sadeghiani, Ghorbanali Rahimian, Majid Mahsa, Mohammedhadi Shafigh, Mahmoud Rafieian-kopaei, Hedayatollah Shirzad
Abstract
Background and study aims
Helicobacter pylori (H. pylori) has been implicated in the pathogenesis of most important gastro-duodenal diseases, such as gastritis, peptic ulcer disease (PUD) and gastric cancer. H. pylori upregulates the expression and activity of several matrix metalloproteinases (MMPs) in the gastric mucosa, but the role of MMP-3 and MMP-9 in infected patients with H. pylori have not been clearly defined yet. We examined mucosal MMP-3 and MMP-9 mRNA levels in gastric mucosa of H. pylori infected patients and evaluated the effects of virulence factors cagA and vacA allelic variants on these levels. We also determined correlation between mucosal MMP-3 and MMP-9 mRNA levels and types of disease.
Patients and methods
Total RNA was extracted from gastric biopsies of 50 H. pylori-infected patients and 50 H. pylori-negative patients. Mucosal MMP-3 and MMP-9 mRNA expression level in H. pylori-infected and non-infected gastric biopsies were determined by real time-polymerase chain reaction (PCR). Presence of vacA (vacuolating cytotoxin A) and cagA (cytotoxin associated gene A) virulence factors were evaluated using PCR.
Results
The levels of MMP-3 in gastric mucosa were not different between H. pylori-positive and H. pylori-negative patients. There was no correlation between MMP-3 mRNA expression and virulence factor (cagA and vacA allelic variants) and the different types of disease (gastritis and PUD) in infected patients. But MMP-9 mRNA expression was significantly higher in biopsies of H. pylori-infected patients compared to H. pylori-negative patients. Also mucosal MMP-9 mRNA expression in H. pylori-infected patients was significantly associated with cagA status PUD.
Conclusion
Our results suggest that MMP-9 might be involved in the pathogenesis of H. pylori. PUD could be associated with cag PAI-dependent MMP-9 upregulation.
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A positive feedback regulation of Heme oxygenase 1 by CELF1 in cardiac myoblast cells
Publication date: Available online 30 November 2018
Source: Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanisms
Author(s): Yang Liu, Huiwen Wang, Jun Wang, Bin Wei, Xinyi Zhang, Mengqi Zhang, Dong Cao, Jiang Dai, Zhen Wang, Eric Nyirimigabo, Guangju Ji
Abstract
As an RNA binding protein, CUG-BP Elav-like family (CELF) has been shown to be critical for heart biological functions. However, no reports have revealed the function of CELF1 in hypertrophic cardiomyopathy (HCM). Hinted by RNA immunoprecipitation-sequencing (RIP-seq) data, the influence of the CELF protein on heme oxygenase-1 (HO-1) expression was tested by modulating CELF1 levels. Cardiac hypertrophy is related to oxidative stress-induced damage. Hence, the cardiovascular system may be protected against further injury by upregulating the expression of antioxidant enzymes, such as HO-1. During the past two decades, research has demonstrated the central role of HO-1 in the protection against diseases. Thus, understanding the molecular mechanisms underlying the modulation of HO-1 expression is profoundly important for developing new strategies to prevent cardiac hypertrophy.
To elucidate the molecular mechanisms underlying HO-1 regulation by the CELF protein, we performed RNA immunoprecipitation (RIP), biotin pull-down analysis, luciferase reporter and mRNA stability assays. We found that the expression of HO-1 was downregulated by CELF1 through the conserved GU-rich elements (GREs) in HO-1 3′UTR transcripts. Correspondingly, CELF1 expression was regulated by controlling the release of carbon monoxide (CO) in H9C2 cells. The CELF1-HO-1-CO regulation axis constituted a novel positive feedback circuit. In addition, we detected the potential involvement of CELF1 and HO-1 in samples from HCM patients. We found that CELF1 and CELF2, but not HO-1, were highly expressed in HCM heart samples. Thus, a manipulation targeting CELF1 could be developed as a potential therapeutic option for cardiac hypertrophy.
Graphical abstract
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Acknowledgement to Reviewers
Publication date: December 2018
Source: Clinical Neurophysiology, Volume 129, Issue 12
Author(s):
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Contents
Publication date: December 2018
Source: Clinical Neurophysiology, Volume 129, Issue 12
Author(s):
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Editorial Board
Publication date: December 2018
Source: Clinical Neurophysiology, Volume 129, Issue 12
Author(s):
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Effects of deep brain stimulation on the primary motor cortex: Insights from transcranial magnetic stimulation studies
Publication date: Available online 30 November 2018
Source: Clinical Neurophysiology
Author(s): Zhen Ni, Kaviraja Udupa, Mark Hallett, Robert Chen
Abstract
Deep brain stimulation (DBS) implanted in different basal ganglia nuclei regulates the dysfunctional neuronal circuits and improves symptoms in movement disorders. However, the understanding of the neurophysiological mechanism of DBS is at an early stage. Transcranial magnetic stimulation (TMS) can be used safely in movement disorder patients with DBS, and can shed light on how DBS works. DBS at a therapeutic setting normalizes the abnormal motor cortical excitability measured with motor evoked potentials (MEP) produced by primary motor cortical TMS. Abnormal intracortical circuits in the motor cortex tested with paired-pulse TMS paradigm also show normalization with DBS. These changes are accompanied with improvements in symptoms after chronic DBS. Single-pulse DBS produces cortical evoked potentials recorded by electroencephalography at specific latencies and modulates motor cortical excitability at certain time intervals measured with MEP. Combination of basal ganglia DBS with motor cortical TMS at stimulus intervals consistent with the latency of cortical evoked potentials delivered in a repetitive mode produces plastic changes in the primary motor cortex. TMS can be used to examine the effects of open and closed loop DBS. Patterned DBS and TMS delivered in a repetitive mode may be developed as a new therapeutic method for movement disorder patients.
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