[Microanatomical Investigation of the Subtemporal Transtentorial Approach]. / é¢žä¸‹ç»å°è„‘å¹•å ¥è·¯çš„æ˜¾å¾®è§£å‰–å­¦ç ”ç©¶.

Objective: To study the microanatomic structure of the subtemporal transtentorial approach to the lateral side of the brainstem, and to provide anatomical information that will assist clinicians to perform surgeries on the lateral, circumferential, and petroclival regions of the brainstem. Methods: Anatomical investigations were conducted on 8 cadaveric head specimens (16 sides) using the infratemporal transtentorial approach. The heads were tilted to one side, with the zygomatic arch at its highest point. Then, a horseshoe incision was made above the auricle. The incision extended from the midpoint of the zygomatic arch to one third of the mesolateral length of the transverse sinus, with the flap turned towards the temporal part. After removing the bone, the arachnoid and the soft meninges were carefully stripped under the microscope. The exposure range of the surgical approach was observed and the positional relationships of relevant nerves and blood vessels in the approach were clarified. Important structures were photographed and the relevant parameters were measured. Results: The upper edge of the zygomatic arch root could be used to accurately locate the base of the middle cranial fossa. The average distances of the star point to the apex of mastoid, the star point to the superior ridge of external auditory canal, the anterior angle of parietomastoid suture to the superior ridge of external auditory canal, and the anterior angle of parietomastoid suture to the star point of the 10 adult skull specimens were 47.23 mm, 45.27 mm, 26.16 mm, and 23.08 mm, respectively. The subtemporal approach could fully expose the area from as high as the posterior clinoid process to as low as the petrous ridge and the arcuate protuberance after cutting through the cerebellar tentorium. The approach makes it possible to handle lesions on the ventral or lateral sides of the middle clivus, the cistern ambiens, the midbrain, midbrain, and pons. In addition, the approach can significantly expand the exposure area of the upper part of the tentorium cerebelli through cheekbone excision and expand the exposure range of the lower part of the tentorium cerebelli through rock bone grinding technology. The total length of the trochlear nerve, distance of the trochlear nerve to the tentorial edge of cerebellum, length of its shape in the tentorial mezzanine, and its lower part of entering into the tentorium cerebelli to the petrosal ridge were (16.95±4.74) mm, (1.27±0.73) mm, (5.72±1.37) mm, and (4.51±0.39) mm, respectively. The cerebellar tentorium could be safely opened through the posterior clinoid process or arcuate protrusion for localization. The oculomotor nerve could serve as an anatomical landmark to locate the posterior cerebral artery and superior cerebellar artery. Conclusion: Through microanatomic investigation, the exposure range and intraoperative difficulties of the infratemporal transtentorial approach can be clarified, which facilitates clinicians to accurately and safely plan surgical methods and reduce surgical complications.

Role of dietary tea polyphenols on growth performance and gut health benefits in juvenile hybrid sturgeon (Acipenser baerii ♀ × A. schrenckii ♂).

The present study aimed to evaluate the effects of dietary TPs on growth performance, intestinal digestion, microflora and immunity in juvenile hybrid sturgeon. A total of 450 fish (97.20 ± 0.18 g) were randomly divided into a standard diet (TP-0) or four treatments consisting of a standard diet supplemented with four concentrations of TPs (mg/kg): 100 (TP-100), 300 (TP-300), 500 (TP-500), and 1000 (TP-1000) for 56 days. The TP-300 significantly increased weight gain rate (WGR) and specific growth rate (SGR) (p < 0.05), and TP-1000 significantly increased the feed conversion ratio (FCR) (p < 0.05). TP-300 and TP-500 significantly increased intestinal trypsin, amylase, and lipase activities (p < 0.05). Besides, TP-300 significantly enhanced total antioxidant capacity (T-AOC) and the levels of superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH) and decreased malondialdehyde (MDA) content (p < 0.05). Moreover, TP-300 decreased the expression levels of tumor necrosis factor-alpha (TNF-α), interleukin 8 (IL-8), and interleukin 1ß(IL-1ß) compared with TP-0 and TP-1000 (p < 0.05). In addition, the intestinal microbiota diversity in the TP-300 group was observably higher, the dominant microbiota was Bacteroidota, Cyanobacteria, Proteobacteria and Firmicutes at the phylum level, Enterobacteriaceae, Nostocaceae and Clostridiaceae at the family level. The relative abundances of potential probiotics including Rhodobacteraceae and potential pathogens especially Clostridiaceae were the highest, and lowest, respectively. In conclusion, TP-300 altered the abundance of microbial taxa, resulting in enhancing the intestinal digestion, antioxidant status and non-specific immunity to improve the growth performance in juvenile hybrid sturgeon.

Calcium-Activated Calpain Specifically Cleaves Glutamate Receptor IIA But Not IIB at the Drosophila Neuromuscular Junction.

Calpains are calcium-dependent, cytosolic proteinases active at neutral pH. They do not degrade but cleave substrates at limited sites. Calpains are implicated in various pathologies, such as ischemia, injuries, muscular dystrophy, and neurodegeneration. Despite so, the physiological function of calpains remains to be clearly defined. Using the neuromuscular junction of Drosophila of both sexes as a model, we performed RNAi screening and uncovered that calpains negatively regulated protein levels of the glutamate receptor GluRIIA but not GluRIIB. We then showed that calpains enrich at the postsynaptic area, and the calcium-dependent activation of calpains induced cleavage of GluRIIA at Q788 of its C terminus. Further genetic and biochemical experiments revealed that different calpains genetically and physically interact to form a protein complex. The protein complex was required for the proteinase activation to downregulate GluRIIA. Our data provide a novel insight into the mechanisms by which different calpains act together as a complex to specifically control GluRIIA levels and consequently synaptic function.SIGNIFICANCE STATEMENT Calpain has been implicated in neural insults and neurodegeneration. However, the physiological function of calpains in the nervous system remains to be defined. Here, we show that calpain enriches at the postsynaptic area and negatively and specifically regulates GluRIIA, but not IIB, level during development. Calcium-dependent activation of calpain cleaves GluRIIA at Q788 of its C terminus. Different calpains constitute an active protease complex to cleave its target. This study reveals a critical role of calpains during development to specifically cleave GluRIIA at synapses and consequently regulate synaptic function.

TNF-α-induced p53 activation induces apoptosis in neurological injury.

It was previously confirmed that the apoptotic and necrotic neurons are found during the acute post-traumatic period, suggesting the induction of apoptosis after traumatic brain injury (TBI). To further explore the involvement of apoptotic factors in TBI, an apoptosis antibody array was conducted to measure the alterations of apoptotic factors in rat brain cortex after TBI. As a result, the Neurological Severity Scale (NSS) scores after TBI were increased, and the cell morphology of the brain cortex was destructed with increased neuronal apoptosis. Furthermore, the caspase-3 activity was increased, and the apoptotic-related factors TNF-α and p53 were up-regulated in the brain cortex. More importantly, in vitro experiments demonstrated that down-regulation of TNF-α in oxygen-glucose deprivation/reoxygenation (OGD/R) cells increased cell viability and decreased apoptosis and the p53 expression. These results suggested the involvement of TNF-α-induced apoptotic signalling pathway by activating p53 in the molecular mechanism of neurological injury.

Comparative Study of Micro-Bone Window and Conventional Bone Window Microsurgery for Hypertensive Intracerebral Hemorrhage.

OBJECTIVE: To compare and analyze the efficacy and safety of traditional craniotomy and small bone window craniotomy in the treatment of hypertensive cerebral hemorrhage (HICH). PATIENTS AND METHODS: Fifty-four patients with HICH treated with traditional craniotomy and small bone window craniotomy were retrospectively analyzed. The operation time, hospitalization time, preoperative, and postoperative CT analysis, Glasgow coma scale (GCS) score and Glasgow outcome scale (GOS) scores were analyzed. RESULTS: There were no significant differences in gender, age, hematoma volume, GCS score and pre-operative time between the 2 groups (P > 0.05). The operation time and hospitalization time of the micro-bone window group were shorter than those of the traditional operation group (P < 0.05). The GCS and GOS scores of the small bone window group after 3 days and 6 months were higher than those of the traditional operation group (P < 0.05). However, there was no significant difference in hematoma clearance rate, re-bleeding rate and infection rate between the two groups (P > 0.05). CONCLUSION: For patients with GCS 8-12 HICH, micro-bone window not only has the same effect as traditional bone window, but also has the advantages of shorter operation time and less trauma.

Lentivirus mediated γ-interferon-inducible lysosomal thiol reductase (GILT) knockdown suppresses human glioma U373MG cell proliferation.

BACKGROUND: Glioma is the most common malignancy in brain carcinoma with poor prognosis due to the lack of understanding of the mechanism underlying the disease. γ-interferon-inducible lysosomal thiol reductase (GILT) plays a critical role in the process of antigen processing. However, the role of GILT in the tumorigenesis of glioma remains unknown. MATERIALS AND METHODS: The expression of GILT was analyzed by bioinformatics using the public database and by qPCR in three human glioma cell lines. Cell growth and viability were determined by Celigo and MTT assays, while cell cycle arrest and apoptosis were determined using flow cytometry. Giemsa staining was used to analyze the colony formation, while cell motility was assessed using transwell migration and invasion assays, as well as, using tumor growth in nude mice. RESULTS: GILT was highly expressed as observed in the public database on human gliomas and two human glioma cell lines, U373MG and U87MG cells. The downregulation of GILT by lentiviral-mediated silencing inhibits the cell growth, colony formation, and migration but promotes apoptosis and results in cell cycle arrest at the G0/G1 phase in the U373MG cells. Also, the knockdown of GILT inhibits tumor growth in vivo. CONCLUSION: Elevated GILT is positively associated with glioma progression. GILT silencing suppresses cell proliferation, colony formation, migration, and tumor growth, and induces apoptosis and cell cycle arrest. GILT may serve as a potential target for the treatment of glioma.

Angelman Syndrome Protein Ube3a Regulates Synaptic Growth and Endocytosis by Inhibiting BMP Signaling in Drosophila.

Altered expression of the E3 ubiquitin ligase UBE3A, which is involved in protein degradation through the proteasome-mediated pathway, is associated with neurodevelopmental and behavioral defects observed in Angelman syndrome (AS) and autism. However, little is known about the neuronal function of UBE3A and the pathogenesis of UBE3A-associated disorders. To understand the in vivo function of UBE3A in the nervous system, we generated multiple mutations of ube3a, the Drosophila ortholog of UBE3A. We found a significantly increased number of total boutons and satellite boutons in conjunction with compromised endocytosis in the neuromuscular junctions (NMJs) of ube3a mutants compared to the wild type. Genetic and biochemical analysis showed upregulation of bone morphogenetic protein (BMP) signaling in the nervous system of ube3a mutants. An immunochemical study revealed a specific increase in the protein level of Thickveins (Tkv), a type I BMP receptor, but not other BMP receptors Wishful thinking (Wit) and Saxophone (Sax), in ube3a mutants. Ube3a was associated with and specifically ubiquitinated lysine 227 within the cytoplasmic tail of Tkv, and promoted its proteasomal degradation in Schneider 2 cells. Negative regulation of Tkv by Ube3a was conserved in mammalian cells. These results reveal a critical role for Ube3a in regulating NMJ synapse development by repressing BMP signaling. This study sheds new light onto the neuronal functions of UBE3A and provides novel perspectives for understanding the pathogenesis of UBE3A-associated disorders.

Treatment of Traumatic Depressed Compound Skull Fractures.

BACKGROUND: A skull fracture widely occurs in patients with traumatic brain injury, leading to intracranial hematoma, brain contusion, and intracranial infection. It also influences the prognosis and death of patients. This study aimed to discuss cases of patients with comminuted skull fractures. METHODS: From October 2015 to December 2018, 38 patients with comminuted skull fractures were admitted to the hospital. All patients underwent three-dimensional reconstruction of computed tomography scan images. Digital subtraction angiography or magnetic resonance venography was performed to find out the venous sinus. The clinical findings of the patients were significant regarding gender, age, injury mechanism, location, admission Glasgow Coma Scale (GCS), combined epidural, subdural, cerebral contusion, intracranial pneumatosis, maximum depth of depression, admission to surgery, dural tear, post-operative cerebrospinal fluid leakage, post-operative infection, and Glasgow Outcome Scale (GOS) 3 months after surgery. RESULTS: The incidence of traffic accidents, fall from a height, railway accidents, fall of an object, and chop injury was 60.5%, 18.4%, 13.2%, 5.3%, and 2.6%, respectively. Intra-operative dural trar negatively correlated with epidural hematoma, cerebral contusion, and subdural hematoma. Also, post-operative infection negatively correlated with intracranial pneumatosis, depth of fracture depression, and pre-operative cerebrospinal fluid leakage. No correlation was found between contusion, subdural hematoma, intracranial pneumatosis, depth of fracture depression, and post-operative infection. The GOS score positively correlated with age, pre-operative cerebrospinal fluid leakage, and admission GCS score. CONCLUSIONS: A perfect pre-operative examination is a key to successful surgery. Further studies should be conducted to find out more effective treatments for traumatic comminuted skull fractures.

A Handy Flexible Micro-Thermocouple Using Low-Melting-Point Metal Alloys.

A handy, flexible micro-thermocouple using low-melting-point metal alloys is proposed in this paper. The thermocouple has the advantages of simple fabrication and convenient integration. Bismuth/gallium-based mixed alloys are used as thermocouple materials. To precisely inject the metal alloys to the location of the sensing area, a micro-polydimethylsiloxane post is designed within the sensing area to prevent outflow of the metal alloy to another thermocouple pole during the metal-alloy injection. Experimental results showed that the Seebeck coefficient of this thermocouple reached -10.54 µV/K, which was much higher than the previously reported 0.1 µV/K. The thermocouple was also be bent at 90° more than 200 times without any damage when the mass ratio of the bismuth-based alloy was <60% in the metal-alloy mixture. This technology mitigated the difficulty of depositing traditional thin⁻film thermocouples on soft substrates. Therefore, the thermocouple demonstrated its potential for use in microfluidic chips, which are usually flexible devices.

A Presynaptic Function of Shank Protein in Drosophila.

Human genetic studies support that loss-of-function mutations in the SH3 domain and ankyrin repeat containing family proteins (SHANK1-3), the large synaptic scaffolding proteins enriched at the postsynaptic density of excitatory synapses, are causative for autism spectrum disorder and other neuropsychiatric disorders in humans. To better understand the in vivo functions of Shank and facilitate dissection of neuropathology associated with SHANK mutations in human, we generated multiple mutations in the Shank gene, the only member of the SHANK family in Drosophila melanogaster Both male and female Shank null mutants were fully viable and fertile with no apparent morphological or developmental defects. Expression analysis revealed apparent enrichment of Shank in the neuropils of the CNS. Specifically, Shank coexpressed with another PSD scaffold protein, Homer, in the calyx of mushroom bodies in the brain. Consistent with high expression in mushroom body calyces, Shank mutants show an abnormal calyx structure and reduced olfactory acuity. These morphological and functional phenotypes were fully rescued by pan-neuronal reexpression of Shank, and only partially rescued by presynaptic but no rescue by postsynaptic reexpression of Shank. Our findings thus establish a previously unappreciated presynaptic function of Shank.SIGNIFICANCE STATEMENT Mutations in SHANK family genes are causative for idiopathic autism spectrum disorder. To understand the neural function of Shank, a large scaffolding protein enriched at the postsynaptic densities, we examined the role of Drosophila Shank in synapse development at the peripheral neuromuscular junctions and the central mushroom body calyx. Our results demonstrate that, in addition to its conventional postsynaptic function, Shank also acts presynaptically in synapse development in the brain. This study offers novel insights into the synaptic role of Shank.

Drosophila S6 Kinase like inhibits neuromuscular junction growth by downregulating the BMP receptor thickveins.

Synaptic connections must be precisely controlled to ensure proper neural circuit formation. In Drosophila melanogaster, bone morphogenetic protein (BMP) promotes growth of the neuromuscular junction (NMJ) by binding and activating the BMP ligand receptors wishful thinking (Wit) and thickveins (Tkv) expressed in motor neurons. We report here that an evolutionally conserved, previously uncharacterized member of the S6 kinase (S6K) family S6K like (S6KL) acts as a negative regulator of BMP signaling. S6KL null mutants were viable and fertile but exhibited more satellite boutons, fewer and larger synaptic vesicles, larger spontaneous miniature excitatory junctional potential (mEJP) amplitudes, and reduced synaptic endocytosis at the NMJ terminals. Reducing the gene dose by half of tkv in S6KL mutant background reversed the NMJ overgrowth phenotype. The NMJ phenotypes of S6KL mutants were accompanied by an elevated level of Tkv protein and phosphorylated Mad, an effector of the BMP signaling pathway, in the nervous system. In addition, Tkv physically interacted with S6KL in cultured S2 cells. Furthermore, knockdown of S6KL enhanced Tkv expression, while S6KL overexpression downregulated Tkv in cultured S2 cells. This latter effect was blocked by the proteasome inhibitor MG132. Our results together demonstrate for the first time that S6KL regulates synaptic development and function by facilitating proteasomal degradation of the BMP receptor Tkv.

Microtubule-severing protein Katanin regulates neuromuscular junction development and dendritic elaboration in Drosophila.

Microtubules (MTs) are crucial for diverse biological processes including cell division, cell growth and motility, intracellular transport and the maintenance of cell shape. MT abnormalities are associated with neurodevelopmental and neurodegenerative diseases such as hereditary spastic paraplegia. Among many MT regulators, katanin was the first identified MT-severing protein, but its neuronal functions have not yet been examined in a multicellular organism. Katanin consists of two subunits; the catalytic subunit katanin 60 contains an AAA (ATPases associated with a variety of cellular activities) domain and breaks MT fibers while hydrolyzing ATP, whereas katanin 80 is a targeting and regulatory subunit. To dissect the in vivo functions of Katanin, we generated mutations in Drosophila Katanin 60 and manipulated its expression in a tissue-specific manner. Null mutants of Katanin 60 are pupal lethal, demonstrating that it is essential for viability. Loss-of-function mutants of Katanin 60 showed excess satellite boutons, reduced neurotransmission efficacy, and more enlarged cisternae at neuromuscular junctions. In peripheral sensory neurons, loss of Katanin 60 led to increased elaboration of dendrites, whereas overexpression of Katanin 60 resulted in the opposite. Genetic interaction analyses indicated that increased levels of MT acetylation increase its susceptibility to Katanin-mediated severing in neuronal and non-neuronal systems. Taken together, our results demonstrate for the first time that Katanin 60 is required for the normal development of neuromuscular synapses and dendrites.

Low p21 level is necessary for the suppressive effects of micoRNA-31 on glioma cell migration and invasion.

MicroRNAs (miRNAs), a kind of endogenous non-coding RNAs, regulate gene expression through binding to the 3'-untranslational region (UTR) of target messenger RNAs (mRNAs) and act as endogenous agents of RNA interference, resulting in either mRNA degradation or translational repression. MiR-31 has been demonstrated to be associated with the development and progression of glioma. However, the underlying molecular mechanism remains largely unclear. In the present study, we demonstrated that miR-31 only inhibited the cell migration and invasion, as well as the expression of a known miR-31 target oncogene radixin, in U251 glioma cells that expressed low level of p21; however, miR-31 showed no above effects on glioma SHG44 cells that highly expressed p21. Moreover, upregulation of p21 in U251 cells reversed the suppressive effects of miR-31 on the cell migration and invasion, suggesting that low p21 level is necessary for the miR-31-mediated inhibitory effects on glioma. Furthermore, analysis for 35 glioma specimens showed that the expression of radixin was negatively correlated with the miR-31 level in glioma tissues with low p21 expression; however, no such correlation was found in glioma tissues with high p21 level, further supporting that the low p21 level is necessary for the suppressive effect of miR-31 on the expression of its target oncogenes. In summary, our study demonstrates that the suppressive effect of miR-31 on glioma cell migration and invasion is p21-dependent, and suggests that miR-31 may be used for the treatment of patients with p21-deficent glioma.

Drosophila cyfip regulates synaptic development and endocytosis by suppressing filamentous actin assembly.

The formation of synapses and the proper construction of neural circuits depend on signaling pathways that regulate cytoskeletal structure and dynamics. After the mutual recognition of a growing axon and its target, multiple signaling pathways are activated that regulate cytoskeletal dynamics to determine the morphology and strength of the connection. By analyzing Drosophila mutations in the cytoplasmic FMRP interacting protein Cyfip, we demonstrate that this component of the WAVE complex inhibits the assembly of filamentous actin (F-actin) and thereby regulates key aspects of synaptogenesis. Cyfip regulates the distribution of F-actin filaments in presynaptic neuromuscular junction (NMJ) terminals. At cyfip mutant NMJs, F-actin assembly was accelerated, resulting in shorter NMJs, more numerous satellite boutons, and reduced quantal content. Increased synaptic vesicle size and failure to maintain excitatory junctional potential amplitudes under high-frequency stimulation in cyfip mutants indicated an endocytic defect. cyfip mutants exhibited upregulated bone morphogenetic protein (BMP) signaling, a major growth-promoting pathway known to be attenuated by endocytosis at the Drosophila NMJ. We propose that Cyfip regulates synapse development and endocytosis by inhibiting actin assembly.

dAcsl, the Drosophila ortholog of acyl-CoA synthetase long-chain family member 3 and 4, inhibits synapse growth by attenuating bone morphogenetic protein signaling via endocytic recycling.

Fatty acid metabolism plays an important role in brain development and function. Mutations in acyl-CoA synthetase long-chain family member 4 (ACSL4), which converts long-chain fatty acids to acyl-CoAs, result in nonsyndromic X-linked mental retardation. ACSL4 is highly expressed in the hippocampus, a structure critical for learning and memory. However, the underlying mechanism by which mutations of ACSL4 lead to mental retardation remains poorly understood. We report here that dAcsl, the Drosophila ortholog of ACSL4 and ACSL3, inhibits synaptic growth by attenuating BMP signaling, a major growth-promoting pathway at neuromuscular junction (NMJ) synapses. Specifically, dAcsl mutants exhibited NMJ overgrowth that was suppressed by reducing the doses of the BMP pathway components, accompanied by increased levels of activated BMP receptor Thickveins (Tkv) and phosphorylated mothers against decapentaplegic (Mad), the effector of the BMP signaling at NMJ terminals. In addition, Rab11, a small GTPase involved in endosomal recycling, was mislocalized in dAcsl mutant NMJs, and the membrane association of Rab11 was reduced in dAcsl mutant brains. Consistently, the BMP receptor Tkv accumulated in early endosomes but reduced in recycling endosomes in dAcsl mutant NMJs. dAcsl was also required for the recycling of photoreceptor rhodopsin in the eyes, implying a general role for dAcsl in regulating endocytic recycling of membrane receptors. Importantly, expression of human ACSL4 rescued the endocytic trafficking and NMJ phenotypes of dAcsl mutants. Together, our results reveal a novel mechanism whereby dAcsl facilitates Rab11-dependent receptor recycling and provide insights into the pathogenesis of ACSL4-related mental retardation.

Identification of Buried Objects in GPR Using Amplitude Modulated Signals Extracted from Multiresolution Monogenic Signal Analysis.

It is necessary to detect the target reflections in ground penetrating radar (GPR) images, so that surface metal targets can be identified successfully. In order to accurately locate buried metal objects, a novel method called the Multiresolution Monogenic Signal Analysis (MMSA) system is applied in ground penetrating radar (GPR) images. This process includes four steps. First the image is decomposed by the MMSA to extract the amplitude component of the B-scan image. The amplitude component enhances the target reflection and suppresses the direct wave and reflective wave to a large extent. Then we use the region of interest extraction method to locate the genuine target reflections from spurious reflections by calculating the normalized variance of the amplitude component. To find the apexes of the targets, a Hough transform is used in the restricted area. Finally, we estimate the horizontal and vertical position of the target. In terms of buried object detection, the proposed system exhibits promising performance, as shown in the experimental results.

Brain tumor regulates neuromuscular synapse growth and endocytosis in Drosophila by suppressing mad expression.

The precise regulation of synaptic growth is critical for the proper formation and plasticity of functional neural circuits. Identification and characterization of factors that regulate synaptic growth and function have been under intensive investigation. Here we report that brain tumor (brat), which was identified as a translational repressor in multiple biological processes, plays a crucial role at Drosophila neuromuscular junction (NMJ) synapses. Immunohistochemical analysis demonstrated that brat mutants exhibited synaptic overgrowth characterized by excess satellite boutons at NMJ terminals, whereas electron microscopy revealed increased synaptic vesicle size but reduced density at active zones compared with wild-types. Spontaneous miniature excitatory junctional potential amplitudes were larger and evoked quantal content was lower at brat mutant NMJs. In agreement with the morphological and physiological phenotypes, loss of Brat resulted in reduced FM1-43 uptake at the NMJ terminals, indicating that brat regulates synaptic endocytosis. Genetic analysis revealed that the actions of Brat at synapses are mediated through mothers against decapentaplegic (Mad), the signal transduction effector of the bone morphogenetic protein (BMP) signaling pathway. Furthermore, biochemical analyses showed upregulated levels of Mad protein but normal mRNA levels in the larval brains of brat mutants, suggesting that Brat suppresses Mad translation. Consistently, knockdown of brat by RNA interference in Drosophila S2 cells also increased Mad protein level. These results together reveal an important and previously unidentified role for Brat in synaptic development and endocytosis mediated by suppression of BMP signaling.

Analysis of the lncRNA-miRNA-mRNA network to explore the regulation mechanism in human traumatic brain injury.

Traumatic brain injury (TBI) refers to brain dysfunction with or without traumatic structural injury induced by an external force. Nevertheless, the molecular mechanism of TBI remains undefined. Differentially expressed (DE) lncRNAs, DEmRNAs and DEmiRNAs were selected between human TBI tissues and the adjacent histologically normal tissue by high-throughput sequencing. Gene ontology enrichment analysis and Kyoto Encyclopedia of Genes and Genomes pathway analysis of overlapping DEmRNAs between predicted mRNAs of DEmiRNAs and DEmRNAs. The competitive endogenous RNA (ceRNA) network of lncRNA-miRNA-mRNA was established in light of the ceRNA theory. In the ceRNA network, the key lncRNAs were screened out. Then key lncRNAs related ceRNA subnetwork was constructed. After that, qRT-PCR was applied to validate the expression levels of hub genes. 114 DElncRNAs, 1807 DEmRNAs and 6 DEmiRNAs were DE in TBI. The TBI-related ceRNA network was built with 73 lncRNA nodes, 81 mRNA nodes and 6 miRNAs. According to topological analysis, two hub lncRNAs (ENST00000562897 and ENST00000640877) were selected to construct the ceRNA subnetwork. Subsequently, key lncRNA-miRNA-mRNA regulatory axes constructed by two lncRNAs including ENST00000562897 and ENST00000640877, two miRNAs including miR-6721-5p and miR-129-1-3p, two mRNAs including ketohexokinase (KHK) and cyclic nucleotide-gated channel beta1 (CNGB1), were identified. Furthermore, qRT-PCR results displayed that the expression of ENST00000562897, KHK and CNGB1 were significantly decreased in TBI, while the miR-6721-5p expression levels were markedly increased in TBI. The results of our study reveal a new insight into understanding the ceRNA regulation mechanism in TBI and select key lncRNA-miRNA-mRNA axes for prevention and treatment of TBI.

A Prediction Model Analysis of Behavior Recognition Based on Genetic Algorithm and Neural Network.

With the extensive application of virtual technology and simulation algorithm, motion behavior recognition is widely used in various fields. The original neural network algorithm cannot solve the problem of data redundancy in behavior recognition, and the global search ability is weak. Based on the above reasons, this paper proposes an algorithm based on genetic algorithm and neural network to build a prediction model of behavior recognition. Firstly, genetic algorithm is used to cluster the redundant data, so that the data are in fragment order, and then it is used to reduce the data redundancy of different behaviors and weaken the influence of dimension on behavior recognition. Then, the genetic algorithm clusters the data to form subgenetic particles with different dimensions and carries out coevolution and optimal location sharing for subgenetic particles with different dimensions. Through simulation test, the algorithm constructed in this paper is better than genetic algorithm and neural network algorithm in terms of calculation accuracy and convergence speed. Finally, the prediction model is constructed by setting the initial value and threshold to predict the behavior recognition, and the results show that the accuracy of the model constructed in this paper is improved in the analysis of behavior recognition.

Design and optimization of three-dimensional composite multilayer cylindrical pentamode metamaterials for controlling low frequency acoustic waves.

For three-dimensional pentamode metamaterials, it is of great significance to realize underwater low frequency acoustic wave control. Therefore, in order to compare with traditional double-cone pentamode metamaterials, two multilayer composite cylindrical three-dimensional pentamode metamaterials with low frequency and broad band gaps are proposed in this paper. By using pentamode metamaterials with lattice constants on the order of centimeters, the phononic band gaps below 60 Hz and the single-mode area below 30 Hz can be obtained. In addition, compared with asymmetrical double-cone locally resonant pentamode metamaterials, the lower edge frequency, relative bandwidth and figure of merit of the first phononic band gap can be reduced by up to 61.4%, 10.3% and 40.6%, respectively. It will provide reference and guidance for the engineering application of pentamode metamaterials in controlling the ultra-low frequency broadband acoustic waves, vibration and noise reduction.