Publications by authors named "George Ghali"

Background: Predicting hemolysis numerically based on the power-law model using idealized coefficients obtained from simplified devices yields a large variability in hemolysis index predictions. A computational fluid dynamics (CFD)-based Kriging surrogate modeling approach, developed by Craven et al. at the US Food & Drug Administration (FDA), was applied to a Fontan cavopulmonary assist device (CPAD) to generate device-specific hemolysis power-law coefficients.

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The respiratory rhythm and pattern and sympathetic and parasympathetic outflows are generated by distinct, though overlapping, propriobulbar arrays of neuronal microcircuit oscillators constituting networks utilizing mutual excitatory and inhibitory neuronal interactions, residing principally within the metencephalon and myelencephalon, and modulated by synaptic influences from the cerebrum, thalamus, hypothalamus, cerebellum, and mesencephalon and ascending influences deriving from peripheral stimuli relayed by cranial nerve afferent axons. Though the respiratory and cardiovascular regulatory effector mechanisms utilize distinct generators, there exists significant overlap and interconnectivity amongst and between these oscillators and pathways, evidenced reciprocally by breathing modulation of sympathetic oscillations and sympathetic modulation of neural breathing. These coupling mechanisms are well-demonstrated coordinately in sympathetic- and respiratory-related central neuronal and efferent neurogram recordings and quantified by the findings of cross-correlation, spectra, and coherence analyses, combined with empirical interventions including lesioning and pharmacological agonist and antagonist microinjection studies, baroloading, barounloading, and hypoxic and/or hypercapnic peripheral and/or central chemoreceptor stimulation.

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Mayer waves may synchronize overlapping propriobulbar interneuronal microcircuits constituting the respiratory rhythm and pattern generator, sympathetic oscillators, and cardiac vagal preganglionic neurons. Initially described by Sir Sigmund Mayer in the year 1876 in the arterial pressure waveform of anesthetized rabbits, authors have since extensively observed these oscillations in recordings of hemodynamic variables, including arterial pressure waveform, peripheral resistance, and blood flow. Authors would later reveal the presence of these oscillations in sympathetic neural efferent discharge and brainstem and spinal zones corresponding with sympathetic oscillators.

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We, the Editors and Publisher of Acta Cardiologica, have retracted the following article:Michael George Zaki Ghali, Rebecca Stewart, George Zaki Ghali & Wolf Blitzer (2020) Two dimensional speckle tracking echocardiography detects cardiac allograft stage III vasculopathy in recipients of heart transplants with preserved systolic function, Acta Cardiologica, DOI: 10.1080/00015385.2020.

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Blood dynamically and richly supplies the cerebral tissue via microvessels invested in pia matter perforating the cerebral substance. Arteries penetrating the cerebral substance derive an investment from one or two successive layers of pia mater, luminally apposed to the pial-glial basal lamina of the microvasculature and abluminally apposed to a series of aquaporin IV-studded astrocytic end feet constituting the soi-disant glia limitans. The full investment of successive layers forms the variably continuous walls of the periarteriolar, pericapillary, and perivenular divisions of the perivascular fluid compartment.

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Nafamostat mesylate, an apparent soi-disant panacea of sorts, is widely used to anticoagulate patients undergoing hemodialysis or cardiopulmonary bypass, mitigate the inflammatory response in patients diagnosed with acute pancreatitis, and reverse the coagulopathy of patients experiencing the commonly preterminal disseminated intravascular coagulation in the Far East. The serine protease inhibitor nafamostat mesylate exhibits significant neuroprotective effects in the setting of neurovascular ischemia. Nafamostat mesylate generates neuroprotective effects by attenuating the enzymatic activity of serine proteases, neuroinflammatory signaling cascades, and the endoplasmic reticulum stress responses, downregulating excitotoxic transient receptor membrane channel subfamily 7 cationic currents, modulating the activity of intracellular signal transduction pathways, and supporting neuronal survival (brain-derived neurotrophic factor/TrkB/ERK1/2/CREB, nuclear factor kappa B.

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Background: The potent inhalational anesthetic isoflurane has widespread use in experimental investigations. Intratracheal administration of the agent attenuates breathing, blood pressure, heart rate, and baroreflex control of heart rate. Concurrent effects of potent inhalational anesthetics on hemodynamic waves and neural respiratory output have yet to be systematically interrogated.

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Neoplastically transformed astrocytes express functionally active cell surface β adrenergic receptors (βARs). Treatment of glioma models in vitro and in vivo with β adrenergic agonists variably amplifies or attenuates cellular proliferation. In the majority of in vivo models, β adrenergic agonists generally reduce cellular proliferation.

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Decerebration permits neurophysiological experimentation absent the confounding effects of anesthesia. Use of the unanesthetized decerebrate preparation in vivo offers several advantages compared with recordings performed in reduced slice preparations, providing the capacity to perform extracellular and intracellular neuronal recordings in the presence of an intact brainstem network. The decerebration procedure typically generates variable degrees of blood loss, which often compromises the hemodynamic stability of the preparation.

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Variability in cardiovascular spectra was first described by Stephan Hales in 1733. Traube and Hering initially noted respirophasic variation of the arterial pressure waveform in 1865 and Sigmund Mayer noted a lower frequency oscillation of the same in anesthetized rabbits in 1876. Very low frequency oscillations were noted by Barcroft and Nisimaru in 1932, likely representing vasogenic autorhythmicity.

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This article has been withdrawn at the request of the author(s) and/or editor. The Publisher apologizes for any inconvenience this may cause. The full Elsevier Policy on Article Withdrawal can be found at https://www.

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This article has been withdrawn at the request of the author(s) and/or editor. The Publisher apologizes for any inconvenience this may cause. The full Elsevier Policy on Article Withdrawal can be found at https://www.

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Patients with complex, multisutural, and syndromic craniosynostosis (CSO) frequently exhibit intracranial hypertension. The intracranial hypertension cannot be entirely attributed to the craniocephalic disproportion with calvarial restriction because cranial vault expansion has not consistently alleviated elevated intracranial pressure. Evidence has most strongly supported a multifactorial interaction, including venous hypertension along with other pathogenic processes.

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