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Tinnitus is a well-known pathological entity in clinical practice. However, the pathophysiological mechanisms behind tinnitus seem to be elusive and cannot provide a comprehensive understanding of its pathogenesis and clinical manifestations. Hence, in the present study, we explore the mathematical model of ions' quantum tunneling to propose an original pathophysiological mechanism for the sensation of tinnitus. The present model focuses on two major aspects: The first aspect is the ability of ions, including sodium, potassium, and calcium, to depolarize the membrane potential of inner hair cells and the neurons of the auditory pathway. This membrane depolarization is induced via the quantum tunneling of ions through closed voltage-gated channels. The state of membrane depolarization can be a state of hyper-excitability or hypo-excitability, depending on the degree of depolarization. Both of these states aid in understanding the pathophysiology of tinnitus. The second aspect is the quantum tunneling signals between the demyelinated neurons of the auditory pathway. These signals are mediated via the quantum tunneling of potassium ions, which exit to the extracellular fluid during an action potential event. These quantum signals can be viewed as a "quantum synapse" between neurons. The formation of quantum synapses results in hyper-excitability among the demyelinated neurons of the auditory pathway. Both of these aspects augment and amplify the electrical signals in the auditory pathway and result in a loss of the spatiotemporal fidelity of sound signals going to the brain centers. The brain interprets this hyper-excitability and loss of spatiotemporal fidelity as tinnitus. Herein, we show mathematically that the quantum tunneling of ions can depolarize the membrane potential of the inner hair cells and neurons of the auditory pathway. Moreover, we calculate the probability of action potential induction in the neurons of the auditory pathway generated by the quantum tunneling signals of potassium ions.
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INTRODUCTION: Approximately 15 to 33% of all dialysis treatments are complicated by intradialytic hypotension (IDH). In this study, we tested the hypothesis that the intravenous administration of hydrocortisone prior to HD treatment could prevent IDH or at least decrease the drop in the blood pressure resulting from IDH. METHODS: This study was approved by our local ethics committee/IRB (2017/87) and by the Jordan Food and Drug Administration (7/clinical/18). Additionally, it is registered on ClinicalTrials.gov (NCT03465007). In this preliminary investigational study, we screened all chronic hemodialysis patients at our clinic who were 18 years of age or older (n = 82) for IDH. There were 14 patients included in the interventional part of this study; patients were given IV hydrocortisone for 3 consecutive HD sessions, followed or preceded by 3 intervention-free sessions where they were given 5 ml of saline as a placebo. RESULTS: The initial total sample size was 82 patients. The frequency of IDH at our clinic was 24.4%. Fourteen out of the 20 patients who were diagnosed with IDH agreed to enroll in the interventional part of our study. The mean age of the patients in the interventional part of our study was 53.5 years (±10.3). These patients included 5 (35.7%) men and 9 (64.3%) women. Upon comparing the number of hypotensive attacks with and without the hydrocortisone administration, we found a significant difference (p = 0.003) between the hydrocortisone and placebo treatments in which 12 (85.7%) patients had fewer IDH episodes with the hydrocortisone treatment than with placebo. CONCLUSION: This preliminary investigational study found that the administration of a stress dose of hydrocortisone prior to hemodialysis could be an effective measure for preventing or minimizing the risk of IDH episodes. Additional prospective studies on this subject are needed. Ruling out adrenal insufficiency in patients diagnosed with IDH is also crucial.
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BACKGROUND AND OBJECTIVE: Xerostomia is a subjective measure of dry mouth, while hyposalivation is an objective measure of reduced saliva flow rate. In this study, we aim to assess the association between commonly used xerostomia scoring systems, with different hyposalivation measures among Sjogren Syndrome (SS) patients. METHODS: In a cohort of SS patients, we assessed xerostomia using Xerostomia index, clinical oral dryness scale (CODS), and the European League Against Rheumatism SS Patient-Reported Index (ESSPRI), and we assessed hyposalivation using unstimulated whole saliva flow (UWS), stimulated whole saliva flow (SWS), and stimulated parotid flow (SPF). We analyzed the association between xerostomia and hyposalivation using association tests in SPSS. RESULTS: We included a total of 49 patients in this study, of which 34 (68%) had primary SS, and 15 (32%) had secondary. CODS was significantly correlated with SWS (P=0.048), with a negative correlation coefficient of 0.216, and with SPF (P=0.009), with a negative correlation coefficient of 0.291. The dryness domain of ESSPRI was significantly correlated with UWS (P=0.031) with a negative correlation coefficient of 0.233. CONCLUSION: CODS is the scoring system with the highest correlation with hyposalivation, particularly SWS and SPF, followed by ESSPRI dry domain, which is correlated with UWS. Xerostomia index is not correlated with hyposalivation.
