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Symmetrically Dependent Observations
Published in Marlos A. G. Viana, Vasudevan Lakshminarayanan, Symmetry in Optics and Vision Studies, 2019
Marlos A. G. Viana, Vasudevan Lakshminarayanan
In the study described by [97], intraocular pressure (IOP) quantifications at pre-treatment (Y1) and post-treatment (Y2) conditions were obtained from fellow glaucomatous eyes of N = 15 subjects on topical beta-blocker therapy. We want to estimate the covariance structure between pre- and post-treatment ordered IOP. This is important to assess and linearly predict the best (worst) post-treatment IOP from pre-treatment ocular pressure quantifications. The observed covariance matrices for IOP between fellow eyes are S11=[12.4107.0197.01912.924],S22=[17.02915.37115.37117.352],
Treatment of acute contrast reactions
Published in William H. Bush, Karl N. Krecke, Bernard F. King, Michael A. Bettmann, Radiology Life Support (Rad-LS), 2017
Epinephrine is an excellent, if not the best, drug for treating many serious contrast reactions. Its use necessitates careful attention and specific application. For example, in individuals with a fragile intracerebral or coronary circulation, the vasoconstrictive alpha-agonist effects of a large dose of epinephrine may invoke a hypertensive crisis or myocardial ischemia.44 Beta-receptor sites ordinarily respond to lower doses of epinephrine than alpha-sites, but if a patient is on beta-blockers, the refractory response that may occur could encourage the radiologist to increase the dose of epinephrine to the point where unwanted alpha-effects would be generated. Patients with chronic asthma may simulate patients receiving beta-blockers, since a systemic beta-adrenergic hyporesponsiveness has long been documented in this group of patients.
Drug-induced bronchospasm
Published in Philippe Camus, Edward C Rosenow, Drug-induced and Iatrogenic Respiratory Disease, 2010
K Suresh Babu, Jaymin Morjaria
Beta-blockers have a significant impact on the prognosis of patients with cardiovascular disease, especially those with hypertension, coronary artery disease and chronic heart failure.143 A number of studies have shown that cardioselective (β1) beta-blockers are not only safe but are beneficial in patients with coexisting airways and coronary disease.144 Although theoretically cardioselective, beta-blockers should abolish the incidence of bronchospasm, but there are reports of alteration in pulmonary function with β1-selective blockers.145 A meta-analysis by Salpeter et al. evaluated data from 29 clinical trials to observe the pulmonary effects of a single dose and chronic use of oral β1-selective blockers in patients who had reversible airways disease.146 Although β1-selective blockers have low affinity to β2-receptors, the selectivity is incomplete. Long-term dosing did not change the forced expiratory volume in 1 second (FEV1) or symptoms, or rescue medication used from placebo in patients who had mild-to-moderate airways disease. However, a single administration of a β1-selective blocker decreased FEV1 by just under 8 per cent more than placebo. There was a greater than 13 per cent increase in FEV1 with β-agonist response.
Multi-model Markov decision processes
Published in IISE Transactions, 2021
Lauren N. Steimle, David L. Kaufman, Brian T. Denton
The first goal, glycemic control, is typically achieved quickly following diagnosis of diabetes using oral medications and/or insulin. Management of cardiovascular risk, the focus of this case study, is a longer term challenge, with a complex trade-off between the harms of medication and the risk of future CHD and stroke events. Patients with diabetes are at much higher risk of stroke and CHD events than the general population. Well-known risk factors include Total Cholesterol (TC), High Density Lipids (HDL – often referred to as “good cholesterol”), and Systolic Blood Pressure (SBP). Like blood glucose, the risk factors of TC, HDL, and SBP are also controllable with medical treatment. Medications, such as statins and fibrates, can reduce TC and increase HDL. Similarly, there are a number of medications that can be used to reduce blood pressure including ACE inhibitors, ARBs, beta blockers, thiazide, and calcium channel blockers. All of these medications have side effects that must be weighed against the long-term benefits of lower risk of CHD and stroke. An added challenge to deciding when and in what sequence to initiate medication is due to the conflicting risk estimates provided by two well known clinical studies: the FHS (Wolf et al., 1991; Wilson et al., 1998) and the ACC/AHA assessment of cardiovascular risk (Goff et al., 2014).
The Neurostructure of Morality and the Hubris of Memory Manipulation
Published in The New Bioethics, 2018
The primary pharmacological agent examined for treatment of PTSD is propranolol, a beta-adrenergic receptor antagonist (Donovan 2010, p. 64). Propranolol suppresses noradrenergic activation by blocking beta 1 and beta 2 adrenoreceptors, located in target areas of the peripheral sympathetic nervous system, as well as in various brain regions, including the amygdala. Multiple studies have indicated that single doses of propranolol influence emotional processing and reduce physiological markers of acute arousal following exposure to emotionally evocative stimuli (Terbeck et al. 2013, pp. 323–28). Additionally, fMRI studies have demonstrated that propranolol effects a reduction in amygdala responses to highly emotional pictures or emotional facial expressions (Hurlemann et al. 2010, pp. 1–10). Due to its ability to reduce heart rate and inhibit arterial vasoconstriction, beta-blockers have been administered for decades to treat hypertension and other cardiovascular diseases (Donovan 2010, p. 64). However, its inhibitory effect on the physiological aspects of emotional stimulation also makes it an effective and thus widely employed treatment for stress, acute anxiety, and performance anxiety. By virtue of its capacity to reduce emotional memory consolidation, propranolol has been proposed as a promising safeguard again PTSD if effectively administered prior to or immediately following a traumatic event.18 Since the beta-adrenergic system is involved not only with response and memory formation, but also with the conditioning of emotional responses tied to memory, propranolol serves to both blunt memory formation and disassociate memory from an emotional response thereto (Donovan 2013, p. 64).