RESUMO
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.
RESUMO
OBJECTIVE: As a measure of the quality of care provided to patients in the intensive care unit, comparison of nosocomial infection rates with those of the National Nosocomial Infection surveillance was completed during a 3-year observation period. DESIGN: The study design was a prospective study during 3 years between 1993 and 1995. During that period, patients at the medical/surgical and neurosurgical intensive care units and the high-risk nursery were surveyed for nosocomial infections. Device use, bloodstream infection, urinary tract infection, and ventilator-associated pneumonia nosocomial infection rates were calculated and compared with the National Nosocomial Infection Surveillance published rates for the same period. SETTING: The study setting was the medical/surgical intensive care unit, the neurosurgical intensive care unit, and the high-risk nursery at the Jordan University Hospital. RESULTS: Overall infection rates were 17.2 per 100 patients in the medical/surgical intensive care unit, 14.2 to 18.5 per 100 patients in the neurosurgical intensive care unit, and 13.4 to 73.5 per 100 patients in the high-risk nursery. When compared with the weight of the infants, these rates were 61.9 to 94 per 100 in infants weighing <1500 g, 26 to 30.8 per 100 patients in infants weighing >1500 g to 2500 g, and 11.7 to 14.4 per 100 in infants weighing >2500 g. Whereas device use was moderate, bloodstream infection and ventilator-associated pneumonia rates were >90th percentile for National Nosocomial Infection Surveillance in the high-risk nursery, and urinary tract infection was >90th percentile in the medical/surgical and neurosurgical intensive care units. Nosocomial infections at the intensive care units in developing countries need further investigation and control.