Amplitude Slope Research Articles

Effect of ceftriaxone on paired-pulse response and long-term potentiation of hippocampal dentate gyrus neurons in rats with Alzheimer-like disease

AimsGlutamatergic dysfunction is posed as a main stage in neurodegenerative disorders such as Alzheimer's disease (AD). Glutamate-mediated excitotoxicity contributes to cognitive dysfunction and cell death in AD. Ceftriaxone (CFT), a well-known upregulator of GLT-1, selectively induces the expression of glutamate transporter-1 (GLT-1) in different brain regions and therefore can be posed as a potential candidate for elimination of glutamate-induced excitotoxicity which is an early prominent event in AD brains. This study was designed to investigate the electrophysiological and behavioral effects of the β-lactam antibiotic ceftriaxone in okadaic acid (OKA)-induced model of AD. Materials and methodsMale Wistar rats divided into four control, ceftriaxone (CFT), OKA, and OKA plus ceftriaxone (OKA + CFT) groups. OKA was injected intracerebroventricularly (i.c.v., 200 ng/5 μl) into lateral ventricles and after two weeks the evoked field potential recorded from hippocampal perforant path-DG synapses in order to evaluate the effect of ceftriaxone treatment (200 mg/kg/day, i.p.) on long-term potentiation (LTP) and paired-pulse responses. Key findingsResults of this study revealed that ceftriaxone treatment significantly ameliorates the OKA-induced attenuation of field excitatory post-synaptic potential (fEPSP) slope and population spike (PS) amplitude following high-frequency stimulation and paired-pulse paradigm indicating its beneficial effects on both short-term and long-term plasticity in these neurons. Ceftriaxone also has an improving effect on OKA-induced impairment in short- and long-term memories evaluated by alternation behavior and passive avoidance tasks in rats. SignificanceTherefore, this study suggests that GLT-1 might be a promising therapeutic target for treatment of neurodegenerative disorders such as AD in the future.

The effects of hyperbilirubinaemia on synaptic plasticity in the dentate gyrus region of the rat hippocampus in vivo.

IntroductionThe aim of our study is to investigate the effect of hyperbilirubinaemia on synaptic plasticity in the dentate gyrus (DG) region of the rat hippocampus.Material and methodsSeven-day-old healthy Sprague Dawley (SD) rats were randomly divided into a control group and an experiment group (n = 20 in each group). The input/output (I/O) functions, paired-pulse reactions (PPR), excitatory postsynaptic potential (EPSP), and population spike (PS) amplitude were measured in the DG area of both groups of rats in response to stimulation applied to the lateral perforant path.ResultsCompared with that in the control rats, the current-voltage curves of both EPSP slope and PS amplitude in the experimental rats were significantly depressed. The average peak facilitation was 187 ±16% in the control and 164 ±18% in the experiment group (F = 21.054, p < 0.01). The facilitation period duration of PS was 155 ms in the experimental rats, which was less than that of the controls (235 ms). In the control group, the long-term potentiation (LTP) amplitudes were 140 ±3.5% and 242 ±6%, when estimated from the EPSP slope and PS amplitude, respectively, which were significantly depressed to 124 ±3.4% (EPSP slope, F = 70.489, p < 0.01) and 138 ±8.6% (PS amplitude, F = 253.46, p < 0.01), respectively, in the experiment group.ConclusionsThese findings suggest that hyperbilirubinaemia could induce impairment of synaptic plasticity in the rat DG area in vivo, including I/O function, paired-pulse ratio (PPR), and LTP, which may be closely related to cognitive impairment.

Changes over time in the electrically evoked compound action potential (ECAP) interphase gap (IPG) effect following cochlear implantation in Guinea pigs

The electrically-evoked compound action potential (ECAP) is correlated with spiral ganglion neuron (SGN) density in cochlear implanted animals. In a previous study, we showed that ECAP amplitude growth function (AGF) linear slopes for stimuli with a constant interphase gap (IPG) changed significantly over time following implantation. Related studies have also shown that 1) IPG sensitivity for ECAP measures (“IPG Effect”) is related to SGN density in animals and 2) the ECAP IPG Effect is related to speech recognition performance in humans with cochlear implants. The current study examined how the ECAP IPG Effect changed following cochlear implantation in four non-deafened guinea pigs with residual inner hair cells (IHCs) and 5 deafened, neurotrophin-treated guinea pigs. Simple impedances were measured on the same days as the ECAP measures. Generally, non-deafened implanted animals with higher SGN survival demonstrated higher ECAP AGF linear slope and peak amplitude values than the deafened, implanted guinea pigs. The ECAP IPG Effect for the AGF slopes and peak amplitudes was also larger in the hearing animals. The N1 latencies for a constant IPG were not different between groups, but the N1 latency IPG Effect was smaller in the non-deafened, implanted animals. Similar to previously reported results, ECAP measures using a fixed or changing IPG required as many as three months after implantation before a stable point could be calculated, but this was dependent on the animal and condition. For all ECAP measures most animals showed greater variance in the first 30 days post-implantation. Post-implantation changes in ECAPs and impedances were not correlated with one another. Results from this study are helpful for estimating the mechanisms underlying ECAP characteristics and have implications for clinical application of the ECAP measures in long-term human cochlear implant recipients. Specifically, these measures could help to monitor neural health over a period of time, or during a time of stability these measures could be used to help select electrode sites for activation in clinical programming.

Coenzyme Q10 supplementation reverses diabetes-related impairments in long-term potentiation induction in hippocampal dentate gyrus granular cells: An in vivo study

Diabetes mellitus (DM) is associated with impaired hippocampal synaptic plasticity. Coenzyme Q10 (CoQ10) acts as an antioxidant and exerts neuroprotective effects. Accordingly, this study aimed at evaluating the effects of CoQ10 on hippocampal long-term potentiation (LTP) and paired-pulse facilitation (PPF) in streptozotocin (STZ)-induced diabetic rats. Male Wistar rats were randomly divided into six groups (n = 8 per group) as follows and treated for 90 days: the control, control + low dose of CoQ10 (100 mg/kg), control + high dose of CoQ10 (600 mg/kg), diabetic, diabetic + low dose of CoQ10, and diabetic + high dose of CoQ10 groups. Diabetes was induced by a single intraperitoneal injection of 50 mg/kg STZ. The population spike (PS) amplitude and slope of excitatory post synaptic potentials (EPSPs) were measured in dentate gyrus (DG) area in response to the stimulation applied to the perforant path (PP). The results showed that the STZ-induced diabetes impaired LTP induction in the PP-DG synapses. This finding is supported by the decreased EPSP slope and PS amplitude of LTP (P < 0.05). Both low- and high-dose CoQ10 supplementation in the control and diabetic animals enhanced EPSP slope and PS amplitude of LTP in the granular cells of DG (P < 0.05). PPF was affected by LTP induction in diabetic animals receiving the high dose of CoQ10 (P < 0.05). It is suggested that CoQ10 administration could attenuate deteriorative effect of STZ-induced diabetes on in vivo LTP in the DG. The enhanced transmitter release can be partly one of the possible underlying mechanism(s) responsible for the LTP induction in the diabetic animals treated with CoQ10.

Aerobic Interval Training Impacts Muscle and Brain Oxygenation Responses to Incremental Exercise

The purpose of the present study was to assess the effects of aerobic interval training on muscle and brain oxygenation to incremental ramp exercise. Eleven physically active subjects performed a 6-week interval training period, proceeded and followed by an incremental ramp exercise to exhaustion (25 W min–1). Throughout the tests pulmonary gas exchange and muscle (Vastus Lateralis) and brain (prefrontal cortex) oxygenation [concentration of deoxygenated and oxygenated hemoglobin, HHb and O2Hb, and tissue oxygenation index (TOI)] were continuously recorded. Following the training intervention peak had increased with 7.8 ± 5.0% (P < 0.001). The slope of the decrease in muscle TOI had decreased (P = 0.017) 16.6 ± 6.4% and the amplitude of muscle HHb and totHb had increased (P < 0.001) 40.4 ± 15.8 and 125.3 ± 43.1%, respectively. The amplitude of brain O2Hb and totHb had increased (P < 0.05) 40.1 ± 18.7 and 26.8 ± 13.6%, respectively. The training intervention shifted breakpoints in muscle HHb, totHb and TOI, and brain O2Hb, HHb, totHb and TOI to a higher absolute work rate and (P < 0.05). The relative (in %) change in peak was significantly correlated to relative (in %) change slope of muscle TOI (r = 0.69, P = 0.011) and amplitude of muscle HHb (r = 0.72, P = 0.003) and totHb (r = 0.52, P = 0.021), but not to changes in brain oxygenation. These results indicate that interval training affects both muscle and brain oxygenation, coinciding with an increase in aerobic fitness (i.e., peak). The relation between the change in peak and muscle but not brain oxygenation suggests that brain oxygenation per se is not a primary factor limiting exercise tolerance during incremental exercise.

Hearing complaints in HIV infection originate in the brain not the ear.

Evidence suggests damage to brain auditory pathways, rather than inner ear damage, underlies the hearing difficulties HIV+ individuals report. But, antiretroviral therapy (ART) may affect the hearing system and also lead to hearing complaints. Longitudinal study of HIV+ and HIV- individuals in Dar es Salaam Tanzania. A subset of this cohort started ART while in the study allowing the effects of ART to be studied directly. The ability to hear quiet sounds (pure-tone audiometry), cochlear outer hair cell function [distortion-product otoacoustic emissions (DPOAEs)], and gaps-in-noise detection thresholds (a central auditory processing test) were assessed at each visit. Visits were scheduled for 6-month intervals, but the number and spacing of visits varied. In the group that started ART while in the study, 107 HIV+ individuals had audiometric thresholds, 98 had DPOAEs, and 98 had gap measurements suitable for analysis. Data were analyzed using a linear mixed model with time and starting ART as fixed effects and individual participant repeated measures as random effects. Starting ART did not affect audiometric or gap detection thresholds. The slope of the DPOAE amplitude vs. time relationship was more negative after starting ART but did not differ from the HIV- group. Gap thresholds were higher in the HIV+ group. ART did not affect audiometric thresholds significantly suggesting common ART drugs are not major ototoxins. The gap detection results from the study show effects on central auditory processing in HIV+ individuals, supporting the origin of HIV-related hearing complaints in the central auditory system.

Effect of Riluzole, a Glutamate Release Inhibitor, on Synaptic Plasticity in the Intrahippocampal Aβ Rat Model of Alzheimer’s Disease

Alzheimer’s disease (AD) is associated with cognitive deficits of varying degrees and with impairment of the synaptic transmission-related tasks. Pathologically, AD is highlighted with accumulation of extracellular β-amyloid plaques and of neurofibrillary tangles. Glutamate-mediated neurotoxicity plays a pivotal role in the pathogenesis of AD. Deficits of long-term potentiation (LTP) and neuronal synaptic plasticity as an essential mechanism of the learning and memory disorders in AD has been ascribed to over-activation of glutamate receptors. We examined the effect of riluzole, a glutamate release inhibitor, on LTP impairment in the dentate gyrus (DG) in a rat model of AD provided by bilateral intrahippocampal amyloid β (Aβ 25-35) injections; riluzole was administered at a dose of 10 mg/kg. The LTP in perforant path-DG synapses was evaluated using measurements of the field excitatory postsynaptic potential (fEPSP) slope and population spike (PS) amplitude. We found that Aβ (25–34) significantly decreased the fEPSP slope and PS amplitude, as compared to those in the sham group; riluzole pretreatment in the Aβ-microinjected group significantly increased these parameters. Taken together, it is concluded that riluzole could noticeably improve synaptic plasticity and enhan ce LTP in the rat model of AD.

Photoplethysmographic Waveform in Hyperbaric Environment.

The objective of this work is the identification of significant variations of morphological parameters of the photoplethysmographic (PPG) signal when the subjects are exposed to an increase in atmospheric pressure. To achieve this goal, the PPG signal of 26 subjects, exposed to a hyperbaric environment whose pressure increases up to 5 atm, has been recorded. From this record, segments of 4 minutes have been processed at 1 atm, 3 atm and 5 atm, both in the descending (D) and ascending (A) periods of the immersion. In total, four states (3D, 5, 3A and 1A) normalized to the basal state (1D) have been considered. In these segments, six morphological parameters of the PPG signal were studied. The width, the amplitude, the widths of the anacrotic and catacrotic phases, and the upward and downward slopes of each PPG pulse were extracted. The results showed significant increases in the three parameters related to the pulse width. This increase is significant in the four states analysed for the anacrotic phase width. Furthermore, a significant decrease in the amplitude and in both slopes (in the states 1A) was observed. These results show that the PPG width responds rapidly to the increase in pressure, indicating an activation of the sympathetic system, while amplitude and pulse slopes are decreased when the subjects are exposed to the hyperbaric environment for a considerable period of time.

Stator current model for detecting rolling bearing faults in induction motors using magnetic equivalent circuits

Stator current modeling for defective induction motor rolling bearings (IMRBs) based on magnetic equivalent circuits (MEC) is carried out. A dynamic model of rotor system supported by defective IMRBs is established to numerically obtain the non-uniform time-varying air gap length. MEC modeling of a induction motor (IM) is then conducted and a magnetic equivalent network is formed by connecting the flux tubes with nodes. After considering the nonlinear air gap permeance, nonlinear iron material and magnetic saturation, an iterative numerical integration method is proposed to solve the stator current model. Finite element analysis and dynamic tests on a typical IM are carried out for verification. Based on these, the fault characteristic frequencies in stator current spectra are, respectively, identified for outer race spall, inner race spall and ball spall. Fault-related frequencies are basically represented by the combinations between the passing frequency (outer race, inner race or ball), its harmonics and power supply frequency. Due to the modulation of rotor (or cage) rotation, higher harmonics of rotor frequency (or cage frequency) participate in the fault-related frequencies of the inner race (or ball) spall. Some fault-related frequencies, which might be more suitable for condition monitoring of induction motors, are recommended by comparing the slope of each spectral amplitude varying with spall width.

Revised Global Wave Number Spectra From Recent Altimeter Observations

AbstractGlobal sea surface height wave number spectra are revisited using the most recent, lower‐noise satellite altimeter missions from Saral/AltiKa and Sentinel‐3 and compared to Jason‐2 wave number spectra. Spectral preprocessing is configured to minimize the spectral slope distortion in the mesoscale wavelength range. A geographically variable wavelength range is used to calculate the spectral slopes, taking into account the regional eddy length scales based on the local Rossby radius. This dynamical wavelength range increases the spectral slope by 0.5 in middle to high latitudes, compared to a fixed wavelength range, and by ‐1.0 to 1.0 in different regions of the intertropical band. Using this dynamical wavelength range, mean sea surface height wave number spectra for these lower‐noise missions exhibit low slope values (k‐2) in the intertropical band, values of k‐11/3 in the midlatitudes, and reaches k‐5 in the subpolar regions and the Antarctic circumpolar current. An important seasonality is also revealed, with mesoscale spectral slope amplitudes decreasing in winter by 0.5 to 1.5 compared to summer, for the middle‐ to high‐energy regions. A phase‐locked internal tide correction is tested but has only a small impact on the spectral slope estimates when using the dynamical wavelength range.

How Well Does Diadochokinetic Task Performance Predict Articulatory Imprecision? Differentiating Individuals with Parkinson’s Disease from Control Subjects

Objective: To investigate whether syllables produced in an oral diadochokinetic (DDK) task may be quantified so that persons with Parkinson’s disease (PD) perceived to have reduced articulatory precision when reading may be correctly identified using that quantification. Patients and Methods: Syllable sequences from 38 speakers with PD and 38 gender- and age-matched control speakers (normal controls [NC]) were quantified acoustically and evaluated in terms of (1) the speakers’ ability to accurately predict speaker group membership (PD or NC) and (2) their ability to predict reduced/non-reduced articulatory precision. Results: A balanced accuracy of 80–93% in predicting speaker group membership was achieved. The best measures were related to the proportion of a syllable made up of a vowel, amplitude slope and syllable-to-syllable variation in duration and amplitude. The best material was that based on /ka/. Reduced articulatory precision was accurately predicted from DDK measures in 89% of the samples. Release-transient prominence and voicing during the onset of plosives were particularly strong predictors. Conclusions: DDK sequences can predict articulatory imprecision as observed in another speech task. The linking of performance across speech tasks probably requires measures of stability in syllable durations and amplitudes, as well as measures of subsyllabic acoustic features.

Adult-Onset Hypothyroidism Alters the Metaplastic Properties of Dentate Granule Cells by Decreasing Akt Phosphorylation.

The expression of homosynaptic long-term depression (LTD) governs the subsequent induction of long-term potentiation (LTP) at hippocampal synapses. This process, called metaplasticity, is associated with a transient increase in the levels of several kinases, such as extracellular signal-regulated protein kinases 1/2 (ERK1/2), c-Jun N-terminal kinase (JNK), and Akt kinase. It has been increasingly realized that the chemical changes in the hippocampus caused by hypothyroidism may be the key underlying causes of the learning deficits, memory loss, and impaired LTP associated with this disease. However, the functional role of thyroid hormones in the "plasticity of synaptic plasticity" has only begun to be elucidated. To address this issue, we sought to determine whether the administration of 6-n-propyl-2-thiouracil (PTU) alters the relationship between priming and the induction of subsequent LTP and related signaling molecules. The activation of ERK1/2, JNK, and Akt was measured in the hippocampus at least 95min after priming onset. We found that priming stimulation at 5Hz for 3s negatively impacted the induction of LTP by subsequent tetanic stimulation in hypothyroid animals, as manifested by a more rapid decrease in the fEPSP slope and population spike amplitude. This phenomenon was accompanied by lower levels of phosphorylated Akt in the surgically removed hippocampus of the hypothyroid rats compared to the euthyroid rats. The metaplastic response and the expression of these proteins in the 1-Hz-primed hippocampus were not different between the two groups. These observations suggest that decreased PI3K/Akt signaling may be involved in the compromised metaplastic regulation of LTP observed in hypothyroidism, which may account for the learning difficulties/cognitive impairments associated with this condition.

Nonlinear two-layer model for photocarrier radiometry of ion-implanted silicon wafers

A nonlinear two-layer model was developed to describe and analyze Photocarrier Radiometric (PCR) signals of ion-implanted Si wafers which are intrinsically nonlinear with excitation laser power. The thickness of the implantation layer and the optical/electronic damage threshold for different implantation doses were estimated using the Monte Carlo method and the effective medium approximation theory, respectively, which can provide key parameter values for the model to calculate the nonlinearity coefficient, defined as the slope of PCR amplitude versus excitation power in log-log scale. Experimentally, the nonlinearity coefficients of seven c-Si wafers with implantation doses from 1011 to 1016 cm-2 were measured at two different excitation wavelengths (830 and 405 nm), and good agreement between theory and experiment was found. Results show that the nonlinearity coefficient has a negative correlation with the implantation dose, and the coefficient measured at 405 nm is consistently smaller than that measured at 830 nm for each sample. Compared with the conventional PCR models, the nonlinear two-layer model proposed here is more coincident with experimental facts, thus enabling PCR to provide more accurate quantitative characterization of the carrier recombination and transport properties of ion-implanted semiconductor wafers.

An increase in sleep slow waves predicts better working memory performance in healthy individuals

Sleep is imperative for brain health and well-being, and restorative sleep is associated with better cognitive functioning. Increasing evidence indicates that electrophysiological measures of sleep, especially slow wave activity (SWA), regulate the consolidation of motor and perceptual procedural memory. In contrast, the role of sleep EEG and SWA in modulating executive functions, including working memory (WM), has been far less characterized. Here, we investigated across-night changes in sleep EEG that may ameliorate WM performance. Participants (N = 25, M = 100%) underwent two consecutive nights with high-density EEG, along with N-back tasks, which were administered at three time points the day before and after the second night of sleep. Non-rapid eye movement sleep EEG power spectra, power topography, as well as several slow-wave parameters were computed and compared across nights. Improvers on the 1-back, but not non-improvers, showed a significant increase in SWA as well as in down slope and negative peak amplitude, in a fronto-parietal region, and these parameters increases predicted better WM performance. Overall, these findings show that slow-wave sleep has a beneficial effect on WM and that it can occur in the adult brain even after minimal training. This is especially relevant, when considering that WM and other executive function cognitive deficits are present in several neuropsychiatric disorders, and that slow-wave enhancing interventions can improve cognition, thus providing novel insights and treatment strategies for these patients.

Investigation of protective effects of coenzyme Q10 on impaired synaptic plasticity in a male rat model of Alzheimer’s disease

Oxidative stress plays a key role in contributing to β-amyloid (Aβ) deposition in Alzheimer’s disease (AD). Coenzyme Q10 (Q10) is a powerful antioxidant that buffers the potential adverse consequences of free radicals. In this study, we investigated the neuroprotective effects of Q10 on Aβ-induced impairment in hippocampal long-term potentiation (LTP), a widely researched model of synaptic plasticity, which occurs during learning and memory, in a rat model of AD. In this study, 50 adult male Wistar rats were assigned to five groups: control group (saline); sham group; intraventricular PBS injection, Aβ group; intraventricular Aβ injection, Q10 group; and Q10 via oral gavage and Q10 + Aβ group. Q10 was administered via oral gavage, once a day, for 3 weeks before and 3 weeks after the Aβ injection. After the treatment period, in vivo electrophysiological recordings were performed to quantify the excitatory postsynaptic potential (EPSP) slope and population spike (PS) amplitude in the hippocampal dentate gyrus. LTP was created by a high-frequency stimulation of the perforant pathway. Following LTP induction, the EPSP slope and PS amplitude were significantly diminished in Aβ-injected rats, compared with sham and control rats. Q10 treatment of Aβ-injected rats significantly attenuated these decreases, suggesting that Q10 reduces the effects of Aβ on LTP. Aβ significantly increased serum malondialdehyde levels and total oxidant levels, whereas Q10 supplementation significantly reversed these parameters and increased total antioxidant capacity levels. The present findings suggested that Q10 treatment offers neuroprotection against the detrimental effects of Aβ on hippocampal synaptic plasticity via its antioxidant activity.

Okadaic acid attenuates short-term and long-term synaptic plasticity of hippocampal dentate gyrus neurons in rats.

Protein phosphorylation states have a pivotal role in regulation of synaptic plasticity and long-term modulation of synaptic transmission. Serine/threonine protein phosphatase 1 (PP1) and 2A (PP2A) have a critical effect on various regulatory mechanisms involved in synaptic plasticity, learning and memory. Okadaic acid (OKA), a potent inhibitor of PP1 and PP2A, reportedly leads to cognitive decline and Alzheimer's disease (AD)-like pathology. The aim of this study was to examine the effect of OKA on electrophysiological characteristics of hippocampal dentate gyrus (DG) neurons in vivo. Male Wistar rats were divided into two control and OKA groups. OKA was injected intracerebroventricularly (i.c.v.) into lateral ventricles and after two weeks the long-term potentiation (LTP) and paired-pulse responses recorded from hippocampal perforant path-DG synapses in order to assess short-term and long-term synaptic plasticity. Results of this study revealed that OKA-induced inhibition of PP1 and PP2A activity drastically attenuates the field excitatory postsynaptic potential (fEPSP) slope and population spike (PS) amplitude following paired pulse and high frequency stimulation (HFS) of hippocampal DG neurons indicating pre- and post-synaptic involvement in electrical activity of these neurons. Administration of OKA impaired the short-term and long-term spatial memories conducted by Y-maze and passive avoidance tests, respectively. OKA-induced attenuation in electrophysiological activity and consequent memory deficits also provide a beneficial tool for studying neurodegenerative disorders such as AD.

Functional Change of Brain Serotonergic Activity and Free Tryptophan in the Plasma of Depressed Women

The main objective was to show the decrement of serotoninergic brain activity in depressed women, through the analyses of the slope amplitude of N1/P2 components of the auditory-evoked potentials (AEP), and the measurement of the L-tryptophan free fraction in plasma (FFT). This cross-sectional study was carried out in 60 women, 30 depressed and 30 normal controls. Both groups were measured FFT, glucose, and neutral amino acids (NAA) levels; besides performing AEP to analyses the N1/P2 slope amplitude. It was found a lengthening in the slope amplitude of N1/P2 components of AEP in the group of depressed women, and despite that the level of FFT was low, there were no changes between bound fraction and the total L-Trp. The former suggests a decrease in serotonergic brain activity in the group of depressed women. Otherwise, since the auditory cortex response to sound is regulated by serotonergic innervation, it was expected a change in the behavior of AEP in the group of depressed patients. Thus, the slope amplitude of N1/P2 components of the AEP and the measurement of FFT have proved to be a good clinical indicators of the serotonergic neurotransmission state in the brain of depressed patients, and in another clinical conditions where brain serotonin is involved.

Quantitative Evaluation of the Relationship between T-Wave-Based Features and Serum Potassium Level in Real-World Clinical Practice.

Background Proper management of hyperkalemia that leads to fatal cardiac arrhythmia has become more important because of the increased prevalence of hyperkalemia-prone diseases. Although T-wave changes in hyperkalemia are well known, their usefulness is debatable. We evaluated how well T-wave-based features of electrocardiograms (ECGs) are correlated with estimated serum potassium levels using ECG data from real-world clinical practice. Methods We collected ECGs from a local ECG repository (MUSE™) from 1994 to 2017 and extracted the ECG waveforms. Of about 1 million reports, 124,238 were conducted within 5 minutes before or after blood collection for serum potassium estimation. We randomly selected 500 ECGs and two evaluators measured the amplitude (T-amp) and right slope of the T-wave (T-right slope) on five lead waveforms (V3, V4, V5, V6, and II). Linear correlations of T-amp, T-right slope, and their normalized feature (T-norm) with serum potassium levels were evaluated using Pearson correlation coefficient analysis. Results Pearson correlation coefficients for T-wave-based features with serum potassium between the two evaluators were 0.99 for T-amp and 0.97 for T-right slope. The coefficient for the association between T-amp, T-right slope, and T-norm, and serum potassium ranged from -0.22 to 0.02. In the normal ECG subgroup (normal ECG or otherwise normal ECG), there was no correlation between T-wave-based features and serum potassium level. Conclusions T-wave-based features were not correlated with serum potassium level, and their use in real clinical practice is currently limited.

Depotentiation of Long-Term Potentiation Is Associated with Epitope-Specific Tau Hyper-/Hypophosphorylation in the Hippocampus of Adult Rats.

It is well-known that some kinases which are involved in the induction of synaptic plasticity probably modulate tau phosphorylation. However, how depression of potentiated synaptic strength contributes to tau phosphorylation is unclear because of the lack of experiments in which depotentiation of LTP was induced. Field excitatory postsynaptic potential (fEPSP) and population spike (PS) were recorded from the dentate gyrus in response to the perforant pathway stimulation. To induce LTP, high-frequency stimulation (HFS) was used, while, for depotentiation of LTP, low-frequency stimulation (LFS) consisting of 900 pulses at 1Hz was applied 5min after tetanization. In some experiments, a neutral protocol at 0.033Hz was applied throughout the experiment without any induction of synaptic plasticity. One-hertz depotentiation protocol was able to decrease fEPSP slope which was previously increased by HFS, whereas no significant change in fEPSP slope and PS amplitude was observed in neutral protocol experiments. Relative to saline infusion, LTP was lower in magnitude and was more reversed by subsequent LFS in the presence of ERK1/2 inhibitor. Western blot experiments indicated that tau protein was hyperphosphorylated at ser416 epitope but rather hypophosphorylated at thr231 epitope in the whole hippocampus upon depotentiation of LTP. These changes concomitantly occurred with a notable increase in the levels of total tau and in the levels of phosphorylated form of the extracellular signal-regulated protein kinases 1 and 2 (ERK1/2). ERK1/2 inhibition resulted in a decrease in phosphorylation of tau at p416Tau when ERK1/2 was inhibited. These findings indicate that some forms of long-term plastic changes might be related with epitope-specific tau phosphorylation and ERK1/2 activation in the hippocampus. Therefore, we emphasize that tau may be crucial for physiological learning as well as Alzheimer's disease pathology.

Simple method for the determination of the effective infrared absorption coefficient of semiconductor wafer using modulated photothermal infrared radiometry

A simple method for the estimation the infrared absorption coefficient of semiconductor wafers is proposed which is based on the photothermal infrared radiometry (PTR) measurement technique. Applying the method on Si and GaAs wafers which have been studied recently it is shown that information about the infrared absorption coefficient can be deduced from the slope of the PTR amplitudes. The obtained results are in a good agreement with values obtained using computational method reported recently.