Size Of Neurons Research Articles

Nuclear PTEN deficiency and heterozygous PTEN loss have distinct impacts on brain and lymph node size

Defects in PTEN, a critical tumor suppressor, are associated with tumorigenesis and aberrant organ sizes. It has been shown that heterozygous PTEN loss increases brains and neuron size, while the specific loss of nuclear PTEN has the opposite effect. Here, we investigate the impact of a combination of heterozygous PTEN loss and nuclear PTEN loss on the size of various organs, including the brain, liver, thymus, spleen, and inguinal lymph node. We found that the effect of the combination varies among organs. Notably, the combination of heterozygous PTEN loss and nuclear PTEN loss restored the normal size of brains and neurons. In contrast, the liver’s size was unaffected by either single PTEN defects or their combination. Strikingly, the size of the inguinal lymph node was greatly increased due to lymphoma by the combination of the two PTEN defects. These data suggest that nuclear PTEN and non-nuclear PTEN function in an antagonistic manner in the brain while acting synergistically in the inguinal lymph node.

Unique scales preserve self-similar integrate-and-fire functionality of neuronal clusters

Brains demonstrate varying spatial scales of nested hierarchical clustering. Identifying the brain’s neuronal cluster size to be presented as nodes in a network computation is critical to both neuroscience and artificial intelligence, as these define the cognitive blocks capable of building intelligent computation. Experiments support various forms and sizes of neural clustering, from handfuls of dendrites to thousands of neurons, and hint at their behavior. Here, we use computational simulations with a brain-derived fMRI network to show that not only do brain networks remain structurally self-similar across scales but also neuron-like signal integration functionality (“integrate and fire”) is preserved at particular clustering scales. As such, we propose a coarse-graining of neuronal networks to ensemble-nodes, with multiple spikes making up its ensemble-spike and time re-scaling factor defining its ensemble-time step. This fractal-like spatiotemporal property, observed in both structure and function, permits strategic choice in bridging across experimental scales for computational modeling while also suggesting regulatory constraints on developmental and evolutionary “growth spurts” in brain size, as per punctuated equilibrium theories in evolutionary biology.

Neurotoxicity studies with a tropomyosin-related kinase A inhibitor, ASP7962, on the sympathetic and sensory nervous systems in rats

ASP7962 is a small molecule inhibitor for the nerve growth factor (NGF) receptor, tropomyosin-related kinase A (TrkA). NGF contributes to the survival of sensory and sympathetic neurons through TrkA receptor activation. Gross, microscopic, and quantitative effects to the nervous system were evaluated following oral ASP7962 administration to Sprague Dawley rats for 4 weeks and 13 weeks and after a recovery period. Histopathological findings included reversible neuronal atrophy but no neuronal death in the sympathetic ganglia (cervicothoracic ganglion, cranial mesenteric ganglion or superior [cranial] cervical ganglion). Stereological analysis showed reversible decreased ganglion volume and/or decreased neuron size in the superior (cranial) cervical ganglion in both the 4-week and the 13-week repeated dose studies. There were no test article related changes in the brain, dorsal root ganglia with spinal nerve roots or trigeminal ganglia and no functional deficits. ASP7962 did not cause any detectable dysfunction of the sympathetic and sensory nervous system in either study.

66108 Central Cholinergic Synapse Formation in Optimized Primary Septal “Hippocampal Co” cultures

ABSTRACT IMPACT: Optimization of primary septal-hippocampal co-cultures facilitates studying central cholinergic synapse formation and dysfunction OBJECTIVES/GOALS: Septal cholinergic innervation to the hippocampus is critical for normal learning and memory and is severely degenerated in Alzheimer’s disease. To understand the molecular events underlying this loss, we optimized a primary septal-hippocampal co-culture system that facilitates the study of central cholinergic synapses. METHODS/STUDY POPULATION: We developed an optimized in vitro septal-hippocampal co-culture system modified from previously published protocols. Briefly, hippocampal and septal tissue were harvested from embryonic day 19 (E19) Sprague-Dawley rats, digested with 0.1% trypsin, and an equal number of cells from each region plated onto coverslips coated with poly-D-lysine and laminin at a final density of 300 cells/mm2. We use immunostaining with validated primary antibodies and a fluorescent binding assay, together with confocal microscopy, to determine the structure of cholinergic synapses that are 1) native, 2) mammalian, 3) CNS derived, 4) comprised of physiological synaptic partners, and 5) developmentally mature. RESULTS/ANTICIPATED RESULTS: After DIV21, co-cultures maintained a healthy morphology. A subpopulation of neurons strongly expressed the cholinergic markers vesicular ACh transporter (vAChT), choline acetyltransferase (ChAT), and the high-affinity choline transporter (ChT1), whereas most neurons lacked vAChT expression and were presumably glutamatergic or GABAergic. The percentage of cholinergic neurons attained in the co-culture is ˜5-7%. The size of these cholinergic neurons is strikingly similar to that reported for BFCNs in the intact brain (mean 30μm, range 18-43μm). All sampled cholinergic neurons (28/28 neurons) also expressed molecular machinery necessary for GABA release. Staining for a cholinergic postsynaptic marker shows that 63% of the contacts made with are synaptic. DISCUSSION/SIGNIFICANCE OF FINDINGS: Primary septal-hippocampal co-cultured neurons have not been exploited extensively in the field, perhaps due to the difficulty in maintaining such cultures for extended periods. Here, we optimized an in vitro septal-hippocampal co-culture system, a powerful tool to comprehensively analyze central cholinergic synapse formation and dysfunction.

Aging-related alteration of trigeminal ganglion structures; A histologic study of Neuronal population, Satellite Ganglionic Cells and Vascular bed

Background: Aging is associated with signs that are similar to peripheral neuropathy and age-related decline in the peripheral sensory system and proprioceptive functions. Trigeminal ganglion (TG) is one of the sensory ganglion providing sensory information from the orofacial region. Ultrastruchral alteration in neuronal population of TG has been reported.Aim of work: Examine the effects of aging on neuronal population, distribution, and satellite ganglionic cells (SGCs) and compare with the TG of young animal. Materials and Methods: Old male Wistar rats (32 weeks old) (250±20g) and young male (4weeks old) (150±20g) were deeply anesthetized with chloroform. To avoid inadvertent mechanical dark neuron formation, each animal was transcardially perfused with 500ml of 4% paraformaldehyde in0.1 M phosphate-buffered saline. The skull cap was cut open and the TG was exposed and removed carefully. The sections were selected according to the systematic random sampling(SRS) and stained with H&E. From each section 10 fields(200×160µm) were selected randomly and the profile of neurons, neuronal shapes, SGCs, and the number of capillary profiles were studied. Results: The measured profile of neurons in the TG of young (17.11± 4.8) and old animals (15.69±4.4) showed a meaningful level of differences(p 0.05). The number of capillary profiles in the TG of young animals (7±2.73) showed a meaningful difference with those of old animals (3.8±0.83) (p < 0.05). Conclusion: With aging neuro-glial population and vascular bed of TG undergo a series of quantitative and qualitative alterations. Precisely aging is associated with decrease in neuronal size and vascular bed while the number of SGCs remains without significant changes. Aging leads to changes in neuronal distribution and likely morphologic alterations in SGCs subpopulation.

Neuroserpin Is Strongly Expressed in the Developing and Adult Mouse Neocortex but Its Absence Does Not Perturb Cortical Lamination and Synaptic Proteome

Neuroserpin is a serine protease inhibitor that regulates the activity of tissue-type plasminogen activator (tPA) in the nervous system. Neuroserpin is strongly expressed during nervous system development as well as during adulthood, when it is predominantly found in regions eliciting synaptic plasticity. In the hippocampus, neuroserpin regulates developmental neurogenesis, synaptic maturation and in adult mice it modulates synaptic plasticity and controls cognitive and social behavior. High expression levels of neuroserpin in the neocortex starting from prenatal stage and persisting during adulthood suggest an important role for the serpin in the formation of this brain region and in the maintenance of cortical functions. In order to uncover neuroserpin function in the murine neocortex, in this work we performed a comprehensive investigation of its expression pattern during development and in the adulthood. Moreover, we assessed the role of neuroserpin in cortex formation by comparing cortical lamination and neuronal maturation between neuroserpin-deficient and control mice. Finally, we evaluated a possible regulatory role of neuroserpin at cortical synapses in neuroserpin-deficient mice. We observed that neuroserpin is expressed starting from the beginning of corticogenesis until adulthood throughout the neocortex in several classes of glutamatergic projection neurons and GABA-ergic interneurons. However, in the absence of neuroserpin we did not detect any alteration either in cortical layer formation, or in neuronal soma size and dendritic length. Furthermore, no significant quantitative changes were observed in the proteome of cortical synapses upon neuroserpin deficiency. We conclude that, although strongly expressed in the neocortex, absence of neuroserpin does not lead to gross developmental abnormalities, and does not perturb the composition of the cortical synaptic proteome.

Diffractive Deep Neural Networks at Visible Wavelengths

• A general method that extends diffractive deep neural networks from terahertz spectrum to visible wavelengths is proposed. • An improved formula is proposed to solve contradictions between wavelength, neuron size and fabrication limitation. • The diffractive deep neural networks at visible wavelengths can implement covered and altered target classification. Optical deep learning based on diffractive optical elements offers unique advantages for parallel processing, computational speed, and power efficiency. One landmark method is the diffractive deep neural network (D 2 NN) based on three-dimensional printing technology operated in the terahertz spectral range. Since the terahertz bandwidth involves limited interparticle coupling and material losses, this paper extends D 2 NN to visible wavelengths. A general theory including a revised formula is proposed to solve any contradictions between wavelength, neuron size, and fabrication limitations. A novel visible light D 2 NN classifier is used to recognize unchanged targets (handwritten digits ranging from 0 to 9) and targets that have been changed (i.e., targets that have been covered or altered) at a visible wavelength of 632.8 nm. The obtained experimental classification accuracy (84%) and numerical classification accuracy (91.57%) quantify the match between the theoretical design and fabricated system performance. The presented framework can be used to apply a D 2 NN to various practical applications and design other new applications.

A novel genetic LSTM model for wind power forecast

Variations of produced power in windmills may influence the appropriate integration in power-driven grids which may disrupt the balance between electricity demand and its production. Consequently, accurate prediction is extremely preferred for planning reliable and effective execution of power systems and to guarantee the continuous supply. For this purpose, a novel genetic long short term memory (GLSTM) framework comprising of long short term memory and genetic algorithm (GA) is proposed to predict short-term wind power. In the proposed GLSTM model, the strength of LSTM is employed due to its capability of automatically learning features from sequential data, while the global optimization strategy of GA is exploited to optimize window size and number of neurons in LSTM layers. Prediction from GLSTM has been compared with actual power, predictions of support vector regressor, and with reported techniques in terms of standard performance indices. It can be evaluated from the comparison that GLSTM and its variants provide accurate, reliable, and robust predictions of wind power of seven wind farms in Europe. In terms of percentage improvement, GLSTM, on average, improves wind power predictions from 6% to 30% as opposed to existing techniques. Wilcoxon signed-rank test demonstrates that GLSTM is significantly different from standard LSTM.

Quantifying mitochondrial volume density in phrenic motor neurons

BackgroundPrevious assessments of mitochondrial volume density within motor neurons used electron microscopy (EM) to image mitochondria. However, adequate identification and sampling of motor neurons within a particular motor neuron pool is largely precluded using EM. Here, we present an alternative method for determining mitochondrial volume density in identified motor neurons within the phrenic motor neuron (PhMN) pool, with greatly increased sampling. New methodThis novel method for assessing mitochondrial volume density in PhMNs uses a combination of intrapleural injection of Alexa 488-conjugated cholera toxin B (CTB) to retrogradely label PhMNs, followed by intrathecal application of MitoTracker Red to label mitochondria. This technique was validated by comparison to 3D EM determination of mitochondrial volume density as a “gold standard”. ResultsA mean mitochondrial volume density of ∼11 % was observed across PhMNs using the new MitoTracker Red method. This compared favourably with mitochondrial volume density (∼11 %) measurements using EM. Comparison with existing methodThe range, mean and variance of mitochondrial volume density estimates in PhMNs were not different between EM and fluorescent imaging techniques. ConclusionsFluorescent imaging may be used to estimate mitochondrial volume density in a large sample of motor neurons, with results similar to EM, although EM did distinguish finer mitochondrion morphology compared to MitoTracker fluorescence. Compared to EM methods, the assessment of a larger sample size and unambiguous identification of motor neurons belonging to a specific motor neuron pool represent major advantages over previous methods.

Quantitative determination of neuronal size and density using flow cytometry

BackgroundRecent anthropomorphic disturbances are occurring at an increasing rate leading to organisms facing a variety of challenges. This change is testing the information processing capacity (IPC) of all animals. Brain function is widely accepted to be influenced by a variety of factors, including relative size, number of neurons and neuronal densities. Therefore, in order to understand what drives an animals IPC, a methodological approach to analyze these factors must be established. New methodHere we created a protocol that allowed for high-throughput, non-biased quantification of neuronal density and size across six regions of the brain. We used the Isotropic Fractionator method in combination with flow cytometry to identify neuronal and non-neuronal cells in the brains of adult rats. Comparison with existing methodsThe results obtained were comparable to those identified using stereological counting methods. ResultsBy employing this new method, the number of nuclei in a specific brain region can be compared between replicate animals within an experiment. By calibrating the forward scatter channel of the flow cytometer with size standard beads, neuronal and non-neuronal nuclear sizes can be estimated simultaneously with nuclei enumeration. These techniques for nuclear counting and size estimation are technically and biologically reproducible. ConclusionUse of flow cytometry provides a methodological approach that allows for consistency in research, so that information on brain morphology, and subsequent function, will become comparable across taxa.

Analysis of morphological and neurochemical changes in subthalamic nucleus neurons in response to a unilateral 6-OHDA lesion of the substantia nigra in adult rats.

BackgroundSubthalamic nucleus (STN) neurons undergo changes in their pattern of activity and morphology during the clinical course of Parkinson’s disease (PD). Striatal dopamine depletion and hyperactivity of neurons in the parafascicular nucleus (Pf) of the intralaminar thalamus are predicted to contribute to the STN changes.ObjectiveThis study investigated possible morphological and neurochemical changes in STN neurons in a rat model of unilateral, nigral dopamine neuron loss, in relation to previously documented alterations in Pf neurons.MethodsMale Sprague-Dawley rats received a unilateral injection of 6-hydroxydopamine (6-OHDA) into the substantia nigra pars compacta (SNpc). Rats were randomly divided into two groups (6/group) for study at 1 and 5 months by post-treatment. The extent of SNpc dopamine neuron damage was assessed in an amphetamine-induced rotation test and postmortem assessment of tyrosine hydroxylase mRNA levels using in situ hybridization histochemistry. Neural cross-sectional measurements and assessment of vesicular glutamate transporter-2 (vGlut2) mRNA levels were performed to measure the impact on neurons in the STN.ResultsA unilateral SNpc dopaminergic neuron lesion significantly decreased the cross-sectional area of STN neurons ipsilateral to the lesion, at 1 month (P < 0.05) and 5 months (P < 0.01) post-lesion, while bilateral vGlut2 mRNA levels in STN neurons were unaltered.ConclusionsDecreased size of STN neurons in the presence of sustained vGlut2 mRNA levels following a unilateral SNpc 6-OHDA lesion, indicate altered STN physiology. This study presents further details of changes within the STN, coincident with observed alterations in Pf neurons and behaviour.Data availabilityThe data associated with the findings of this study are available from the corresponding author upon request.

Arginine Vasopressin-Containing Neurons of the Suprachiasmatic Nucleus Project to CSF.

While it is well established that there are robust circadian rhythms of arginine vasopressin (AVP) in the cerebrospinal fluid (CSF), the route whereby the peptide reaches the CSF is not clear. A , AVP neurons constitute the largest fraction of the SCN neuronal population. Here, we show that processes of AVP-expressing SCN neurons cross the epithelium of the 3rd ventricular wall to reach the CSF (black arrows). Additionally, we report rostro-caudal differences in AVP neuron size and demonstrate that the localization of cells expressing the clock protein PER2 extend beyond the AVP population, thereby indicating that the size of this nucleus is somewhat larger than previously understood. B , Following lateral ventricle (LV) injection of cholera toxin β subunit (CTβ ; magenta) the retrograde tracer is seen in AVP neurons of the SCN, supporting the anatomical evidence that AVP neuronal processes directly contact the CSF.Arginine vasopressin (AVP) expressing neurons form the major population in the brain's circadian clock located in the hypothalamic suprachiasmatic nucleus (SCN). They participate in inter-neuronal coupling and provide an output signal for synchronizing daily rhythms. AVP is present at high concentrations in the cerebrospinal fluid (CSF) and fluctuates on a circadian timescale. While it is assumed that rhythms in CSF AVP are of SCN origin, a route of communication between these compartments has not been delineated. Using immunochemistry (ICC) and cell filling techniques, we determine the morphology and location of AVP neurons in mouse and delineate their axonal and dendritic processes. Cholera toxin β subunit (CTβ) tracer injected into the lateral ventricle tests whether AVP neurons communicate with CSF. Most importantly, the results indicate that AVP neurons lie in close proximity to the third ventricle, and their processes cross the ventricular wall into the CSF. We also report that contrary to widely held assumptions, AVP neurons do not fully delineate the SCN borders as PER2 expression extends beyond the AVP region. Also, AVP neurons form a rostral prong originating in the SCN medial-most and ventral-most aspect. AVP is lacking in the mid-dorsal shell but does occur at the base of the SCN just above the optic tract. Finally, neurons of the rostral SCN are smaller than those lying caudally. These findings extend our understanding of AVP signaling potential, demonstrate the heterogeneity of AVP neurons, and highlight limits in using this peptide to delineate the mouse SCN.

Neuregulin-4 Is Required for Maintaining Soma Size of Pyramidal Neurons in the Motor Cortex.

The regulation of neuronal soma size is essential for appropriate brain circuit function and its dysregulation is associated with several neurodevelopmental disorders. A defect in the dendritic growth and elaboration of motor neocortical pyramidal neurons in neonates lacking neuregulin-4 (NRG4) has previously been reported. In this study, we investigated whether the loss of NRG4 causes further morphologic defects that are specific to these neurons. We analyzed the soma size of pyramidal neurons of layer (L)2/3 and L5 of the motor cortex and a subpopulation of multipolar interneurons in this neocortical region in Nrg4+/+ and Nrg4−/− mice. There were significant decreases in pyramidal neuron soma size in Nrg4−/− mice compared with Nrg4+/+ littermates at all stages studied [postnatal day (P)10, P30, and P60]. The reduction was especially marked at P10 and in L5 pyramidal neurons. Soma size was not significantly different for multipolar interneurons at any age. This in vivo phenotype was replicated in pyramidal neurons cultured from Nrg4−/− mice and was rescued by NRG treatment. Analysis of a public single-cell RNA sequencing repository revealed discrete Nrg4 and Erbb4 expression in subpopulations of L5 pyramidal neurons, suggesting that the observed defects were due in part to loss of autocrine Nrg4/ErbB4 signaling. The pyramidal phenotype in the motor cortex of Nrg4−/− mice was associated with a lack of Rotarod test improvement in P60 mice, suggesting that absence of NRG4 causes alterations in motor performance.

Deep Neural Networks for Sensor-Based Human Activity Recognition Using Selective Kernel Convolution

Recently, the state-of-the-art performance in various sensor-based human activity recognition (HAR) tasks has been acquired by deep learning, which can extract automatically features from raw data. In standard convolutional neural networks (CNNs), there is usually the same receptive field (RF) size of artificial neurons within each feature layer. It is well known that the RF size of neurons is able to change adaptively according to the stimulus, which has rarely been exploited in HAR. In this article, a new multibranch CNN is introduced, which utilizes a selective kernel mechanism for HAR. To the best of our knowledge, it is for the first time to adopt an attention idea to perform kernel selection among multiple branches with different RFs in the HAR scenario. We perform extensive experiments on several benchmark HAR datasets, namely, UCI-HAR, UNIMIB SHAR, WISDM, PAMAP2, and OPPORTUNITY, as well as weakly labeled datasets. Ablation experiments show that the selective kernel convolution can adaptively choose an appropriate RF size among multiple branches for classifying numerous human activities. As a result, it can achieve a higher recognition accuracy under a similar computing budget.

Modulation of SETDB1 activity by APQ ameliorates heterochromatin condensation, motor function, and neuropathology in a Huntington’s disease mouse model

The present study describes evaluation of epigenetic regulation by a small molecule as the therapeutic potential for treatment of Huntington’s disease (HD). We identified 5-allyloxy-2-(pyrrolidin-1-yl)quinoline (APQ) as a novel SETDB1/ESET inhibitor using a combined in silico and in vitro cell based screening system. APQ reduced SETDB1 activity and H3K9me3 levels in a HD cell line model. In particular, not only APQ reduced H3K9me3 levels in the striatum but it also improved motor function and neuropathological symptoms such as neuronal size and activity in HD transgenic (YAC128) mice with minimal toxicity. Using H3K9me3-ChIP and genome-wide sequencing, we also confirmed that APQ modulates H3K9me3-landscaped epigenomes in YAC128 mice. These data provide that APQ, a novel small molecule SETDB1 inhibitor, coordinates H3K9me-dependent heterochromatin remodelling and can be an epigenetic drug for treating HD, leading with hope in clinical trials of HD.

Computational and theoretical insights into the homeostatic response to the decreased cell size of midbrain dopamine neurons.

Midbrain dopamine neurons communicate signals of reward anticipation and attribution of salience. This capacity is distorted in heroin or cocaine abuse or in conditions such as human mania. A shared characteristic among rodent models of these behavioral disorders is that dopamine neurons in these animals acquired a small size and manifest an augmented spontaneous and burst activity. The biophysical mechanism underlying this increased excitation is currently unknown, but is believed to primarily follow from a substantial drop in K+ conductance secondary to morphology reduction. This work uses a dopamine neuron mathematical model to show, surprisingly, that under size diminution a reduction in K+ conductance is an adaptation that attempts to decrease cell excitability. The homeostatic response that preserves the intrinsic activity is the conservation of the ion channel density for each conductance; a result that is analytically demonstrated and challenges the experimentalist tendency to reduce intrinsic excitation to K+ conductance expression level. Another unexpected mechanism that buffers the raise in intrinsic activity is the presence of the ether‐a‐go‐go‐related gen K+ channel since its activation is illustrated to increase with size reduction. Computational experiments finally demonstrate that size attenuation results in the paradoxical enhancement of afferent‐driven bursting as a reduced temporal summation indexed correlates with improved depolarization. This work illustrates, on the whole, that experimentation in the absence of mathematical models may lead to the erroneous interpretation of the counterintuitive aspects of empirical data.

Chapter 22 - Pleasure, addiction, and hypocretin (orexin)

The hypocretins/orexins were discovered in 1998. Within 2 years, this led to the discovery of the cause of human narcolepsy, a 90% loss of hypothalamic neurons containing these peptides. Further work demonstrated that these neurons were not simply linked to waking. Rather these neurons were active during pleasurable behaviors in waking and were silenced by aversive stimulation. This was seen in wild-type mice, rats, cats, and dogs. It was also evident in humans, with increased Hcrt release during pleasurable activities and decreased release, to the levels seen in sleep, during pain. We found that human heroin addicts have, on average, an increase of 54% in the number of detectable Hcrt neurons compared to "control" human brains and that these Hcrt neurons are substantially smaller than those in control brains. We found that in mice, chronic morphine administration induced the same changes in Hcrt neuron number and size. Our studies in the mouse allowed us to determine the specificity, dose response relations, time course of the change in the number of Hcrt neurons, and that the increased number of Hcrt neurons after opiates was not due to neurogenesis. Furthermore, we found that it took a month or longer for these anatomical changes in the mouse brain to return to baseline. Human narcoleptics, despite their prescribed use of several commonly addictive drugs, do not show significant evidence of dose escalation or substance use disorder. Similarly, mice in which the peptide has been eliminated are resistant to addiction. These findings are consistent with the concept that an increased number of Hcrt neurons may underlie and maintain opioid or cocaine use disorders.

Regulation of glial size by eicosapentaenoic acid through a novel Golgi apparatus mechanism.

Coordination of cell growth is essential for the development of the brain, but the molecular mechanisms underlying the regulation of glial and neuronal size are poorly understood. To investigate the mechanisms involved in glial size regulation, we used Caenorhabditis elegans amphid sheath (AMsh) glia as a model and show that a conserved cis-Golgi membrane protein eas-1/GOLT1B negatively regulates glial growth. We found that eas-1 inhibits a conserved E3 ubiquitin ligase rnf-145/RNF145, which, in turn, promotes nuclear activation of sbp-1/ SREBP, a key regulator of sterol and fatty acid synthesis, to restrict cell growth. At early developmental stages, rnf-145 in the cis-Golgi network inhibits sbp-1 activation to promote the growth of glia, and when animals reach the adult stage, this inhibition is released through an eas-1-dependent shuttling of rnf-145 from the cis-Golgi to the trans-Golgi network to stop glial growth. Furthermore, we identified long-chain polyunsaturated fatty acids (LC-PUFAs), especially eicosapentaenoic acid (EPA), as downstream products of the eas-1-rnf-145-sbp-1 pathway that functions to prevent the overgrowth of glia. Together, our findings reveal a novel and potentially conserved mechanism underlying glial size control.

Prediction of Surface Roughness of Mild Steel Alloy in CNC Milling Process Using ANN and GA Technique

In this paper, Analysis Of Variance (ANOVA), Artificial Neural Network (ANN), and Genetic Algorithm (GA) have been studied to predict the effect of milling parameters on the Surface Roughness (Ra) during machining of mild steel alloy. The milling experiments carried out based on the Taguchi design of experiments method using (L16) orthogonal array with 3 factors and 4 levels. The influence of three independent variables such as spindle speed (910, 930, 960, and 1000 rpm), feed rate (93, 95, 98, and 102 mm/min), and Tool Diameter (8, 10, 12, and 14 mm) on the Surface Roughness (Ra) were tested and analyzed with (ANOVA) to predict the response which indicates that spindle speed was the most significant factor effecting on Surface Roughness (Ra). Artificial Neural Network (ANN) and numerical methods are used widely for modeling and predict the performance of manufacturing technologies. Neural Network technique with 2 hidden layers, 10 neurons size, 1000 epochs, and Trainlm transfer function is used to predict the result. The Genetic Algorithm (GA) has been utilized to find optimal cutting conditions during a milling process. From the results, the optimal value of spindle speed is (930 rpm), feed-rate is (95 mm/min) and tool diameter is (8 mm). This network structure is capable of predicting the Surface Roughness (Ra) well to optimize the milling parameters. Artificial Neural Network (ANN) predicted results indicate good agreement between the experimental and the predicted values.

Diffusion kurtosis imaging of gray matter in young adults with autism spectrum disorder

Prior ex vivo histological postmortem studies of autism spectrum disorder (ASD) have shown gray matter microstructural abnormalities, however, in vivo examination of gray matter microstructure in ASD has remained scarce due to the relative lack of non-invasive methods to assess it. The aim of this work was to evaluate the feasibility of employing diffusional kurtosis imaging (DKI) to describe gray matter abnormalities in ASD in vivo. DKI data were examined for 16 male participants with a diagnosis of ASD and IQ>80 and 17 age- and IQ-matched male typically developing (TD) young adults 18–25 years old. Mean (MK), axial (AK), radial (RK) kurtosis and mean diffusivity (MD) metrics were calculated for lobar and sub-lobar regions of interest. Significantly decreased MK, RK, and MD were found in ASD compared to TD participants in the frontal and temporal lobes and several sub-lobar regions previously associated with ASD pathology. In ASD participants, decreased kurtosis in gray matter ROIs correlated with increased repetitive and restricted behaviors and poor social interaction symptoms. Decreased kurtosis in ASD may reflect a pathology associated with a less restrictive microstructural environment such as decreased neuronal density and size, atypically sized cortical columns, or limited dendritic arborizations.