Introduction Lower third molar impaction surgery is one of the most common minor oral surgical procedures done. Trismus has been one of the most common and disturbing postoperative sequelae for patients. The study aimed to evaluate the electrical activity of the masseter and temporalis muscles after mandibular third molar surgery. Materials and methods The research was conducted at Saveetha Dental College and hospitals in the Department of Oral and Maxillofacial Surgery. The study consisted of 20 individuals. The EMG (electromyography) activities of both masseter muscles in each patient were measured before the tooth extraction surgery, postoperatively after 72 hours, and after seven days. The inter-incisal distance was also measured at similar follow-up intervals. Data were analyzed using IBM Corp. Released 2015. IBM SPSS Statistics for Windows, Version 23.0. Armonk, NY: IBM Corp., with p-values less than 0.05 considered statistically significant. The Mann-Whitney U test was used for the comparison of electrical activity between masseter and temporalis on both the operated and non-operated sides during preoperative, postoperative, 72-hour, and postoperative seven-day periods. Results It has been found that the electrical activity of the temporalis is higher than that of the masseter muscle measured at all the intervals of the follow-up period, with statistically significant values (p=0.001). It was noted that all the patients have reduced mouth opening when compared with preoperative (mean mouth opening = 45.6 mm), postoperative 72 hours (mean mouth opening = 31.2 mm), and postoperative seven days (mean mouth opening =35.6 mm). When a comparison was done between temporalis and masseter, the masseter took longer to return to pre-operative electrical activity, which might also imply that for prolonged trismus seen in patients after lower third molar surgery, it is the masseter that is affected and needs recovery for trismus to be resolved.  Conclusion  Based on the results obtained, it can be concluded that there was a reduction in the electrical activity of both the masseter and temporalis post-third molar impaction surgery. It was also found that there was a reduction in mouth opening in patients who underwent lower third molar extraction surgery. Masseter muscle took longer to return to its preoperative electrical activity than temporalis muscle, implying that targeted therapies to accelerate the healing of masseter muscle may prevent prolonged trismus in patients who undergo lower third molar impaction surgery.

Pancreatic β-cells are equipped with the molecular machinery allowing them to respond to high glucose levels in the form of electrical activity and Ca2+ oscillations. These oscillations drive insulin secretion. Two key ionic mechanisms involved in this response are the Store-Operated Current and the current through ATP-dependent K+ channels. Both currents have been shown to be regulated by the protein STIM1, but this dual regulation by STIM1 has not been studied before. In this paper, we use mathematical modelling to gain insight into the role of STIM1 in the β-cell response. We extended a previous β-cell model to include the dynamics of STIM1 and described the dependence of the ATP-dependent K+ current on STIM1. Our simulations suggest that the total concentration of STIM1 modifies the bursting frequency, the burst duration and the intracellular Ca2+ levels. These results are in good agreement with experimental reports, and the contribution of the studied currents to electrical activity and Ca2+ dynamics is discussed. The model predicts that in the absence of STIM1 the excitability of the plasma membrane increases and that the glucose threshold for electrical activity is shifted to lower concentrations. These computational predictions may be related to impaired insulin secretion under conditions of reduced STIM1 in the diabetic state.

UNASSIGNED: The physiological and prognostical significance of accessory and expiratory muscles activation is unknown during a spontaneous breathing trial (SBT). We hypothesized that, in patients experiencing weaning failure, accessory and expiratory muscles are activated to cope with an increased respiratory workload.
UNASSIGNED: To describe accessory and expiratory muscle activation non-invasively by surface electromyography (sEMG) during an SBT and to assess differences in electrical activity (EA) of the inspiratory and expiratory muscles in successful vs. failing weaning patients.
UNASSIGNED: Intubated patients on mechanical ventilation for more than 48 h undergoing an SBT were enrolled in a medical and surgical third-level ICU of the University Teaching Hospital. Baseline characteristics and physiological variables were recorded in a crossover physiologic prospective clinical study.
UNASSIGNED: Of 37 critically ill mechanically ventilated patients, 29 (78%) patients successfully passed the SBT. Rapid shallow breathing index (RSBI) was higher in patients who failed SBT compared with the successfully weaned patients at baseline and over time (group-by-time interaction p < 0.001). EA of both the diaphragm (EAdisurf) and of accessory muscles (ACCsurf) was higher in failure patients compared with success (group-by-time interaction p = 0.0174 and p < 0.001, respectively). EA of expiratory muscles (ESPsurf) during SBT increased more in failure than in weaned patients (group-by-time interaction p < 0.0001).
UNASSIGNED: Non-invasive respiratory muscle monitoring by sEMG was feasible during SBT. Respiratory muscles EA increased during SBT, regardless of SBT outcome, and patients who failed the SBT had a higher increase of all the inspiratory muscles EA compared with the patients who passed the SBT. Recruitment of expiratory muscles-as quantified by sEMG-is associated with SBT failure.

Investigating the pathophysiological mechanisms underlying brain disorders is a priority if novel therapeutic strategies are to be developed. In vivo studies of animal models and in vitro studies of cell lines/primary cell cultures may provide useful tools to study certain aspects of brain disorders. However, discrepancies among these studies or unsuccessful translation from animal/cell studies to human/clinical studies often occur, because these models generally represent only some symptoms of a neuropsychiatric disorder rather than the complete disorder. Human brain slice cultures from postmortem tissue or resected tissue from operations have shown that, in vitro, neurons and glia can stay alive for long periods of time, while their morphological and physiological characteristics, and their ability to respond to experimental manipulations are maintained. Human brain slices can thus provide a close representation of neuronal networks in vivo, be a valuable tool for investigation of the basis of neuropsychiatric disorders, and provide a platform for the evaluation of novel pharmacological treatments of human brain diseases. A brain bank needs to provide the necessary infrastructure to bring together donors, hospitals, and researchers who want to investigate human brain slices in cultures of clinically and neuropathologically well-documented material.

The TRPM5 channels are transient receptor potential channels whose presence in the human pancreatic β-cell has been confirmed. The sensitivity of these channels to membrane voltage, temperature and intracellular calcium concentration and their possible role in insulin secretion has made them a focal point in research in the past decade. While experimental researches have confirmed the role of the TRPM5 channels in insulin secretion, but the underlying mechanism is still unclear. In this study, based on the experimental results of other studies, a mathematical description of the TRPM5 channel activity has been proposed which correlates the TRPM5 electrical activity to the voltage and intracellular calcium concentration. The resulting expression has been added to the existing mathematical model of the human β-cell and the enhanced model has been used for investigating the effect of the TRPM5 channel on the β-cell electrical activity. The results of our study show that the TRPM5 influences other ion channel activities through speeding up membrane depolarization. In addition, we have shown that the TRPM5 increases the amplitude and firing rate of action potentials by possibly affecting the Na+ and gamma-Aminobutyric acid related currents. The results also confirm the prominent effect of the TRPM5 channels in glucose-stimulated condition.

Botulinum neurotoxins are metalloproteases that specifically cleave N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) proteins in synaptic terminals, resulting in a potent inhibition of vesicle fusion and transmitter release. The family comprises different serotypes (BoNT/A to BoNT/G). The natural target of these toxins is represented by the neuromuscular junction, where BoNTs block acetylcholine release. In this review, we describe the actions of botulinum toxins after direct delivery to the central nervous system (CNS), where BoNTs block exocytosis of several transmitters, with near-complete silencing of neural networks. The use of clostridial neurotoxins in the CNS has allowed us to investigate specifically the role of synaptic activity in different physiological and pathological processes. The silencing properties of BoNTs can be exploited for therapeutic purposes, for example to counteract pathological hyperactivity and seizures in epileptogenic brain foci, or to investigate the role of activity in degenerative diseases like prion disease. Altogether, clostridial neurotoxins and their derivatives hold promise as powerful tools for both the basic understanding of brain function and the dissection and treatment of activity-dependent pathogenic pathways.

The serosal slow waves in the human colon are complex, since their amplitude and frequency vary over time. Therefore, this study employed a simulation to investigate the consistency between serosal slow waves and cutaneous electrical activity by evaluating whether changes of the cutaneous waveform features due to anatomical and physiological parameters are detectable in the cutaneous electrical activity. The simulation results indicated that (a) changes in the dipole moment involve detectable changes in the amplitude of the cutaneous electrical activity; (b) changes in the annular band velocity induce modifications in the cutaneous signal frequency; and (c) changes in the anatomical factors affect both the amplitude and the frequency of the cutaneous signal. Therefore, we observed that there is consistency between serosal slow waves and cutaneous electrical activity. On these bases, we think that modifications in the cutaneous electrical activity observed in our study could represent the marker of specific physiological motor activity of the colon, and such information can improve the recording of the experimental measurements of the cutaneous electrical activity of the colon in humans.

Endocrine cells of the pituitary gland secrete a number of hormones, and the amount of hormone released by a cell is controlled in large part by the cell\'s electrical activity and subsequent Ca(2+) influx. Typical electrical behaviors of pituitary cells include continuous spiking and so-called pseudo-plateau bursting. It has been shown that the amplitude of Ca(2+) fluctuations is greater in bursting cells, leading to the hypothesis that bursting cells release more hormone than spiking cells. In this work, we apply computer simulations to test this hypothesis. We use experimental recordings of electrical activity as input to mathematical models of Ca(2+) channel activity, buffered Ca(2+) diffusion, and Ca(2+)-driven exocytosis. To compare the efficacy of spiking and bursting on the same cell, we pharmacologically block the large-conductance potassium (BK) current from a bursting cell or add a BK current to a spiking cell via dynamic clamp. We find that bursting is generally at least as effective as spiking at evoking hormone release and is often considerably more effective, even when normalizing to Ca(2+) influx. Our hybrid experimental/modeling approach confirms that adding a BK-type K(+) current, which is typically associated with decreased cell activity and reduced secretion, can actually produce an increase in hormone secretion, as suggested earlier.

The integrative properties of cortical pyramidal dendrites are essential to the neural basis of cognitive function, but the impact of amyloid beta protein (abeta) on these properties in early Alzheimer\'s is poorly understood. In animal models, electrophysiological studies of proximal dendrites have shown that abeta induces hyperexcitability by blocking A-type K+ currents (I(A)), disrupting signal integration. The present study uses a computational approach to analyze the hyperexcitability induced in distal dendrites beyond the experimental recording sites. The results show that back-propagating action potentials in the dendrites induce hyperexcitability and excessive calcium concentrations not only in the main apical trunk of pyramidal cell dendrites, but also in their oblique dendrites. Evidence is provided that these thin branches are particularly sensitive to local reductions in I(A). The results suggest the hypothesis that the oblique branches may be most vulnerable to disruptions of I(A) by early exposure to abeta, and point the way to further experimental analysis of these actions as factors in the neural basis of the early decline of cognitive function in Alzheimer\'s.