A Novel Design of Morlet Wavelet to Solve the Dynamics of Nervous Stomach Nonlinear Model

The present study introduces a novel design of Morlet wavelet neural network (MWNN) models to solve a class of a nonlinear nervous stomach system represented with governing ODEs systems via three categories, tension, food and medicine, i.e., TFM model. The comprehensive detail of each category is designated together with the sleep factor, food rate, tension rate, medicine factor and death rate are also provided. The computational structure of MWNNs along with the global search ability of genetic algorithm (GA) and local search competence of active-set algorithms (ASAs), i.e., MWNN-GA-ASAs is applied to solve the TFM model. The optimization of an error function, for nonlinear TFM model and its related boundary conditions, is performed using the hybrid heuristics of GA-ASAs. The performance of the obtained outcomes through MWNN-GA-ASAs for solving the nonlinear TFM model is compared with the results of state of the article numerical computing paradigm via Adams methods to validate the precision of the MWNN-GA-ASAs. Moreover, statistical assessments studies for 50 independent trials with 10 neuron-based networks further authenticate the efficacy, reliability and consistent convergence of the proposed MWNN-GA-ASAs.

Analytical and Approximate Solutions of a Novel Nervous Stomach Mathematical Model

The stomach is usually considered as a hollow muscular sac, which initiates the second segment of digestion. It is the most sophisticated endocrine structure having unique biochemistry, physiology, microbiology, and immunology. The pivotal aim of the present study is to propose the nonlinear mathematical model of the nervous stomach system based on three compartments namely, tension (T), food (F), and medicine (M). The detailed description of each compartment is provided along with the mathematical form and different rates/factors, such as sleep factor, food rate, tension rate, medicine term, and death rate. The solution of the designed model is presented numerically by using the well-known differential transformation technique. The behavior of the obtained solution has been captured with respect to time as well as presentations of the numerical simulations.

A-24 Influence of Biopsychosocial Factors on First-Appointment Presentation After Sport Related Concussion (SRC)

Objective To examine the influence of biopsychosocial factors on clinical outcomes and recovery time following SRC Method 59 athletes with SRC (51% male) aged 14.42, SD= 1.65 years from two concussion specialty clinics between May 2019 and January 2020. Patients completed the Behavioral Regulation Assessment for Concussion (BRAC) inventory measuring sleep, diet, hydration, physical activity and stress; on a 4-point Likert scale, ImPACT, and PCSS. Analyses included one-way ANOVAs with Tukey’s post-hoc test and chi-square analyses. Results Verbal memory scores were higher F(3,55)= 2.85, p<.05 in participants reporting 8-10hrs of sleep “most of the time” (M= 85.12, SD = 10.58) vs. “some of the time “ (M= 75.65, SD= 11.91). Verbal memory differed when engaged in stress regulation F(4,54)= 2.65, p<.05; “MOT” (M=81.38, SD= 10.95); “SOT” (M=82.33, SD= 12.64) and “never” (M= 84.05, SD= 13.07). PCSS sleep factor scores increased when individuals obtained 8-10hrs of sleep “MOT” (M=.30, SD=.423) “SOT” (M= 1.40, SD= 1.54) and “seldom/rarely” (M= 1.95, SD= 1.58). PCSS somatic scores were associated with decreased sleep X2(1, N=57) = 37.68; p= .001, and hydration X2(1, N=57) = 60.70 p< .001. Sleep and recovery time X2(1, N=55) = 120.82 p= .028. Conclusions Findings suggest that biopsychosocial factors including sleep, stress, and hydration are associated with symptoms, cognitive function, and recovery time following SRC and should be monitored by clinicians.

Adenosine inhibits glutamatergic input to basal forebrain cholinergic neurons

Adenosine has been proposed as an endogenous homeostatic sleep factor that accumulates during waking and inhibits wake-active neurons to promote sleep. It has been specifically hypothesized that adenosine decreases wakefulness and promotes sleep recovery by directly inhibiting wake-active neurons of the basal forebrain (BF), particularly BF cholinergic neurons. We previously showed that adenosine directly inhibits BF cholinergic neurons. Here, we investigated 1) how adenosine modulates glutamatergic input to BF cholinergic neurons and 2) how adenosine uptake and adenosine metabolism are involved in regulating extracellular levels of adenosine. Our experiments were conducted using whole cell patch-clamp recordings in mouse brain slices. We found that in BF cholinergic neurons, adenosine reduced the amplitude of AMPA-mediated evoked glutamatergic excitatory postsynaptic currents (EPSCs) and decreased the frequency of spontaneous and miniature EPSCs through presynaptic A1 receptors. Thus we have demonstrated that in addition to directly inhibiting BF cholinergic neurons, adenosine depresses excitatory inputs to these neurons. It is therefore possible that both direct and indirect inhibition may synergistically contribute to the sleep-promoting effects of adenosine in the BF. We also found that blocking the influx of adenosine through the equilibrative nucleoside transporters or inhibiting adenosine kinase and adenosine deaminase increased endogenous adenosine inhibitory tone, suggesting a possible mechanism through which adenosine extracellular levels in the basal forebrain are regulated.

Comparative effects of pregabalin on anxiety and sleep disturbance: Results of a path analysis

IntroductionSleep disturbance is one of the key DSM-IV criteria for generalized anxiety disorder (GAD), and represents the chief complaint in approximately one-third of patients presenting in the primary care setting.Objectives/aimsTo evaluate the extent to which improvement in anxiety is a direct effect of treatment with pregabalin, or is an indirect effect mediated by improvement in sleep disturbance, and vice-versa.MethodsData were pooled from 4 double-blind, placebo-controlled (n = 406) short-term trials of pregabalin (all doses combined; n = 853) in the treatment of generalized anxiety disorder (GAD). The effect of treatment on anxiety was measured using the Hamilton Anxiety Rating Scale (HAM-A), effect of treatment on sleep disturbance was measured using the 3-item Hamilton Depression Rating Scale (HAM-D) sleep factor. Path analyses, using a set of multivariate regression models, were used to evaluate the reciprocal effects of pregabalin on improvement in anxiety in the presence of improvement in sleep disturbance, and vice-versa.ResultsSleep disturbance was common in this GAD sample, with 51.2% (placebo) and 52.2% (pregabalin) of patients, respectively, reporting moderate-to-severe insomnia (HAM-D sleep factor score ≥3). The results of the path analysis indicated that 91.7% (P < 0.0001) of improvement in anxiety was a direct effect of treatment with pregabalin, while 8.3% of improvement in anxiety was an indirect effect, mediated by improvement in sleep disturbance.ConclusionsIn this pooled 4-study data set, the anxiolytic efficacy of pregabalin appears to be primarily a direct effect, with only a small (8.3%) indirect effect, mediated by improvement in sleep disturbance.

Effects on sleep of microdialysis of adenosine A1 and A2a receptor analogs into the lateral preoptic area of rats

Evidence suggests that adenosine (AD) is an endogenous sleep factor. The hypnogenic action of AD is mediated through its inhibitory A1 and excitatory A2A receptors. Although AD is thought to be predominantly active in the wake-active region of the basal forebrain (BF), a hypnogenic action of AD has been demonstrated in several other brain areas, including the preoptic area. We hypothesized that in lateral preoptic area (LPOA), a region with an abundance of sleep-active neurons, AD acting via A1 receptors would induce waking by inhibition of sleep-active neurons and that AD acting via A2A receptors would promote sleep by stimulating the sleep-active neurons. To this end, we studied the effects on sleep of an AD transport inhibitor, nitrobenzyl-thio-inosine (NBTI) and A1 and A2A receptor agonists/antagonists by microdialyzing them into the LPOA. The results showed that, in the sleep-promoting area of LPOA: 1) A1 receptor stimulation or inhibition of AD transport by NBTI induced waking and 2) A2A receptor stimulation induced sleep. We also confirmed that NBTI administration in the wake promoting area of the BF increased sleep. The effects of AD could be mediated either directly or indirectly via interaction with other neurotransmitter systems. These observations support a hypothesis that AD mediated effects on sleep-wake cycles are site and receptor dependent.