Subjects -> ENGINEERING (Total: 2918 journals)
    - CHEMICAL ENGINEERING (259 journals)
    - CIVIL ENGINEERING (255 journals)
    - ELECTRICAL ENGINEERING (182 journals)
    - ENGINEERING (1464 journals)
    - ENGINEERING MECHANICS AND MATERIALS (476 journals)
    - HYDRAULIC ENGINEERING (60 journals)
    - INDUSTRIAL ENGINEERING (101 journals)
    - MECHANICAL ENGINEERING (121 journals)

ENGINEERING (1464 journals)                  1 2 3 4 5 6 7 8 | Last

Showing 1 - 200 of 1205 Journals sorted alphabetically
3 Biotech     Open Access   (Followers: 9)
3D Research     Hybrid Journal   (Followers: 22)
AAPG Bulletin     Hybrid Journal   (Followers: 11)
Abstract and Applied Analysis     Open Access   (Followers: 4)
Aceh International Journal of Science and Technology     Open Access   (Followers: 9)
ACS Nano     Hybrid Journal   (Followers: 448)
Acta Geotechnica     Hybrid Journal   (Followers: 7)
Acta Metallurgica Sinica (English Letters)     Hybrid Journal   (Followers: 10)
Acta Nova     Open Access   (Followers: 1)
Acta Polytechnica : Journal of Advanced Engineering     Open Access   (Followers: 4)
Acta Scientiarum. Technology     Open Access   (Followers: 3)
Acta Universitatis Cibiniensis. Technical Series     Open Access   (Followers: 1)
Active and Passive Electronic Components     Open Access   (Followers: 8)
Adaptive Behavior     Hybrid Journal   (Followers: 9)
Adsorption     Hybrid Journal   (Followers: 5)
Advanced Energy and Sustainability Research     Open Access   (Followers: 7)
Advanced Engineering Forum     Full-text available via subscription   (Followers: 14)
Advanced Engineering Research     Open Access  
Advanced Journal of Graduate Research     Open Access   (Followers: 4)
Advanced Quantum Technologies     Hybrid Journal   (Followers: 1)
Advanced Science     Open Access   (Followers: 13)
Advanced Science Focus     Free   (Followers: 7)
Advanced Science Letters     Full-text available via subscription   (Followers: 13)
Advanced Science, Engineering and Medicine     Partially Free   (Followers: 11)
Advanced Synthesis & Catalysis     Hybrid Journal   (Followers: 20)
Advanced Theory and Simulations     Hybrid Journal   (Followers: 5)
Advances in Catalysis     Full-text available via subscription   (Followers: 8)
Advances in Complex Systems     Hybrid Journal   (Followers: 12)
Advances in Engineering Software     Hybrid Journal   (Followers: 31)
Advances in Fuel Cells     Full-text available via subscription   (Followers: 20)
Advances in Fuzzy Systems     Open Access   (Followers: 5)
Advances in Geosciences (ADGEO)     Open Access   (Followers: 22)
Advances in Heat Transfer     Full-text available via subscription   (Followers: 30)
Advances in Human Factors/Ergonomics     Full-text available via subscription   (Followers: 27)
Advances in Magnetic and Optical Resonance     Full-text available via subscription   (Followers: 10)
Advances in Natural Sciences : Nanoscience and Nanotechnology     Open Access   (Followers: 36)
Advances in Operations Research     Open Access   (Followers: 14)
Advances in OptoElectronics     Open Access   (Followers: 6)
Advances in Physics Theories and Applications     Open Access   (Followers: 21)
Advances in Polymer Science     Hybrid Journal   (Followers: 53)
Advances in Porous Media     Full-text available via subscription   (Followers: 6)
Advances in Remote Sensing     Open Access   (Followers: 58)
Advances in Science and Research (ASR)     Open Access   (Followers: 8)
Aerobiologia     Hybrid Journal   (Followers: 4)
Aerospace Systems     Hybrid Journal   (Followers: 10)
African Journal of Science, Technology, Innovation and Development     Hybrid Journal   (Followers: 8)
AIChE Journal     Hybrid Journal   (Followers: 38)
Ain Shams Engineering Journal     Open Access   (Followers: 7)
Al-Nahrain Journal for Engineering Sciences     Open Access  
Al-Qadisiya Journal for Engineering Sciences     Open Access   (Followers: 2)
AL-Rafdain Engineering Journal     Open Access   (Followers: 3)
Alexandria Engineering Journal     Open Access   (Followers: 3)
AMB Express     Open Access   (Followers: 1)
American Journal of Applied Sciences     Open Access   (Followers: 27)
American Journal of Engineering and Applied Sciences     Open Access   (Followers: 12)
American Journal of Engineering Education     Open Access   (Followers: 20)
American Journal of Environmental Engineering     Open Access   (Followers: 16)
American Journal of Industrial and Business Management     Open Access   (Followers: 31)
Annals of Civil and Environmental Engineering     Open Access   (Followers: 3)
Annals of Combinatorics     Hybrid Journal   (Followers: 3)
Annals of Pure and Applied Logic     Open Access   (Followers: 6)
Annals of Regional Science     Hybrid Journal   (Followers: 10)
Annals of Science     Hybrid Journal   (Followers: 10)
Annual Journal of Technical University of Varna     Open Access   (Followers: 1)
Antarctic Science     Hybrid Journal   (Followers: 1)
Applicable Algebra in Engineering, Communication and Computing     Hybrid Journal   (Followers: 3)
Applicable Analysis: An International Journal     Hybrid Journal   (Followers: 2)
Applications in Energy and Combustion Science     Open Access   (Followers: 2)
Applications in Engineering Science     Open Access   (Followers: 1)
Applied Catalysis A: General     Hybrid Journal   (Followers: 8)
Applied Catalysis B: Environmental     Hybrid Journal   (Followers: 22)
Applied Clay Science     Hybrid Journal   (Followers: 6)
Applied Computational Intelligence and Soft Computing     Open Access   (Followers: 16)
Applied Engineering Letters     Open Access   (Followers: 4)
Applied Magnetic Resonance     Hybrid Journal   (Followers: 4)
Applied Nanoscience     Open Access   (Followers: 11)
Applied Network Science     Open Access   (Followers: 3)
Applied Numerical Mathematics     Hybrid Journal   (Followers: 6)
Applied Physics Research     Open Access   (Followers: 7)
Applied Sciences     Open Access   (Followers: 6)
Applied Spatial Analysis and Policy     Hybrid Journal   (Followers: 6)
Arab Journal of Basic and Applied Sciences     Open Access  
Arabian Journal for Science and Engineering     Hybrid Journal   (Followers: 5)
Archives of Computational Methods in Engineering     Hybrid Journal   (Followers: 6)
Archives of Thermodynamics     Open Access   (Followers: 13)
Arctic     Open Access   (Followers: 7)
Arid Zone Journal of Engineering, Technology and Environment     Open Access   (Followers: 2)
Arkiv för Matematik     Hybrid Journal   (Followers: 1)
ArtefaCToS : Revista de estudios sobre la ciencia y la tecnología     Open Access   (Followers: 1)
Asia-Pacific Journal of Science and Technology     Open Access  
Asian Engineering Review     Open Access  
Asian Journal of Applied Science and Engineering     Open Access   (Followers: 2)
Asian Journal of Applied Sciences     Open Access   (Followers: 2)
Asian Journal of Biotechnology     Open Access   (Followers: 9)
Asian Journal of Control     Hybrid Journal  
Asian Journal of Technology Innovation     Hybrid Journal   (Followers: 7)
Assembly Automation     Hybrid Journal   (Followers: 2)
ATZagenda     Hybrid Journal  
ATZextra worldwide     Hybrid Journal  
AURUM : Mühendislik Sistemleri ve Mimarlık Dergisi = Aurum Journal of Engineering Systems and Architecture     Open Access   (Followers: 1)
Australasian Journal of Engineering Education     Hybrid Journal   (Followers: 3)
Australasian Physical & Engineering Sciences in Medicine     Hybrid Journal   (Followers: 1)
Australian Journal of Multi-Disciplinary Engineering     Hybrid Journal   (Followers: 2)
Autocracy : Jurnal Otomasi, Kendali, dan Aplikasi Industri     Open Access  
Automotive and Engine Technology     Hybrid Journal  
Automotive Experiences     Open Access  
Automotive Innovation     Hybrid Journal   (Followers: 1)
Avances en Ciencias e Ingenierías     Open Access  
Avances: Investigación en Ingeniería     Open Access   (Followers: 6)
Balkan Region Conference on Engineering and Business Education     Open Access   (Followers: 2)
Bangladesh Journal of Scientific and Industrial Research     Open Access  
Basin Research     Hybrid Journal   (Followers: 6)
Batteries     Open Access   (Followers: 11)
Batteries & Supercaps     Hybrid Journal   (Followers: 7)
Bautechnik     Hybrid Journal   (Followers: 3)
Bell Labs Technical Journal     Hybrid Journal   (Followers: 29)
Beni-Suef University Journal of Basic and Applied Sciences     Open Access   (Followers: 3)
Beyond : Undergraduate Research Journal     Open Access  
Bhakti Persada : Jurnal Aplikasi IPTEKS     Open Access  
Bharatiya Vaigyanik evam Audyogik Anusandhan Patrika (BVAAP)     Open Access   (Followers: 1)
Bilge International Journal of Science and Technology Research     Open Access   (Followers: 1)
Biointerphases     Open Access   (Followers: 1)
Biomaterials Science     Full-text available via subscription   (Followers: 14)
Biomedical Engineering     Hybrid Journal   (Followers: 15)
Biomedical Engineering and Computational Biology     Open Access   (Followers: 13)
Biomedical Engineering Letters     Hybrid Journal   (Followers: 5)
Biomedical Engineering: Applications, Basis and Communications     Hybrid Journal   (Followers: 5)
Biomedical Microdevices     Hybrid Journal   (Followers: 8)
Biomedical Science and Engineering     Open Access   (Followers: 7)
Biomicrofluidics     Open Access   (Followers: 7)
Biotechnology Progress     Hybrid Journal   (Followers: 44)
Black Sea Journal of Engineering and Science     Open Access  
Botswana Journal of Technology     Full-text available via subscription   (Followers: 1)
Boundary Value Problems     Open Access   (Followers: 1)
Brazilian Journal of Science and Technology     Open Access   (Followers: 2)
Bulletin of Canadian Petroleum Geology     Full-text available via subscription   (Followers: 13)
Bulletin of Engineering Geology and the Environment     Hybrid Journal   (Followers: 15)
Bulletin of the Crimean Astrophysical Observatory     Hybrid Journal  
Cahiers Droit, Sciences & Technologies     Open Access   (Followers: 1)
Calphad     Hybrid Journal   (Followers: 2)
Canadian Geotechnical Journal     Hybrid Journal   (Followers: 30)
Canadian Journal of Remote Sensing     Full-text available via subscription   (Followers: 50)
Carbon Resources Conversion     Open Access   (Followers: 3)
Carpathian Journal of Electronic and Computer Engineering     Open Access  
Case Studies in Engineering Failure Analysis     Open Access   (Followers: 6)
Case Studies in Thermal Engineering     Open Access   (Followers: 8)
Catalysis Communications     Hybrid Journal   (Followers: 7)
Catalysis Letters     Hybrid Journal   (Followers: 3)
Catalysis Reviews: Science and Engineering     Hybrid Journal   (Followers: 9)
Catalysis Science and Technology     Hybrid Journal   (Followers: 13)
Catalysis Surveys from Asia     Hybrid Journal   (Followers: 4)
Catalysis Today     Hybrid Journal   (Followers: 8)
CEAS Space Journal     Hybrid Journal   (Followers: 6)
Cell Reports Physical Science     Open Access  
Cellular and Molecular Neurobiology     Hybrid Journal   (Followers: 2)
Central European Journal of Engineering     Hybrid Journal  
Chaos : An Interdisciplinary Journal of Nonlinear Science     Hybrid Journal   (Followers: 3)
Chaos, Solitons & Fractals     Hybrid Journal   (Followers: 3)
Chaos, Solitons & Fractals : X     Open Access   (Followers: 1)
Chinese Journal of Catalysis     Full-text available via subscription   (Followers: 3)
Chinese Journal of Engineering     Open Access   (Followers: 2)
Chinese Journal of Population, Resources and Environment     Open Access  
Chinese Science Bulletin     Open Access   (Followers: 1)
Ciencia e Ingenieria Neogranadina     Open Access  
Ciencia en su PC     Open Access   (Followers: 1)
Ciencia y Tecnología     Open Access  
Ciencias Holguin     Open Access   (Followers: 2)
CienciaUAT     Open Access   (Followers: 1)
Cientifica     Open Access  
CIRP Annals - Manufacturing Technology     Hybrid Journal   (Followers: 11)
CIRP Journal of Manufacturing Science and Technology     Hybrid Journal   (Followers: 14)
City, Culture and Society     Hybrid Journal   (Followers: 27)
Clay Minerals     Hybrid Journal   (Followers: 9)
Coal Science and Technology     Full-text available via subscription   (Followers: 4)
Coastal Engineering     Hybrid Journal   (Followers: 14)
Coastal Engineering Journal     Hybrid Journal   (Followers: 9)
Coastal Engineering Proceedings : Proceedings of the International Conference on Coastal Engineering     Open Access   (Followers: 2)
Coastal Management     Hybrid Journal   (Followers: 30)
Coatings     Open Access   (Followers: 4)
Cogent Engineering     Open Access   (Followers: 3)
Cognitive Computation     Hybrid Journal   (Followers: 3)
Color Research & Application     Hybrid Journal   (Followers: 4)
COMBINATORICA     Hybrid Journal  
Combustion Theory and Modelling     Hybrid Journal   (Followers: 17)
Combustion, Explosion, and Shock Waves     Hybrid Journal   (Followers: 20)
Communications Faculty of Sciences University of Ankara Series A2-A3 Physical Sciences and Engineering     Open Access  
Communications in Numerical Methods in Engineering     Hybrid Journal   (Followers: 2)
Components, Packaging and Manufacturing Technology, IEEE Transactions on     Hybrid Journal   (Followers: 28)
Composite Interfaces     Hybrid Journal   (Followers: 10)
Composite Structures     Hybrid Journal   (Followers: 334)
Composites Part A : Applied Science and Manufacturing     Hybrid Journal   (Followers: 276)
Composites Part B : Engineering     Hybrid Journal   (Followers: 311)
Composites Part C : Open Access     Open Access   (Followers: 3)
Composites Science and Technology     Hybrid Journal   (Followers: 245)
Comptes Rendus : Mécanique     Open Access   (Followers: 2)
Computation     Open Access   (Followers: 1)
Computational Geosciences     Hybrid Journal   (Followers: 20)
Computational Optimization and Applications     Hybrid Journal   (Followers: 11)
Computer Applications in Engineering Education     Hybrid Journal   (Followers: 6)
Computer Science and Engineering     Open Access   (Followers: 20)

        1 2 3 4 5 6 7 8 | Last

Similar Journals
Journal Cover
Cellular and Molecular Neurobiology
Journal Prestige (SJR): 1.283
Citation Impact (citeScore): 3
Number of Followers: 2  
 
  Hybrid Journal Hybrid journal (It can contain Open Access articles)
ISSN (Print) 1573-6830 - ISSN (Online) 0272-4340
Published by Springer-Verlag Homepage  [2658 journals]
  • Correction to: Opposite Roles of NT-3 and BDNF in Synaptic Remodeling of
           the Inner Ear Induced by Electrical Stimulation

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      Abstract: The original version of this article unfortunately contained an error in Figure 9.
      PubDate: 2021-11-01
       
  • Necroptotic–Apoptotic Regulation in an Endothelin-1 Model of
           Cerebral Ischemia

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      Abstract: The primary forms of cell death seen in ischemic stroke are of two major types: a necrotic/necroptotic form, and an apoptotic form that is frequently seen in penumbral regions of injury. Typically apoptotic versus necroptotic programmed cell death is described as competitive in nature, where necroptosis is often described as playing a backup role to apoptosis. In the present study, we examined the relationship between these two forms of cell death in a murine endothelin-1 model of ischemia–reperfusion injury in wildtype and caspase-3 null mice with and without addition of the pharmacologic RIPK1 phosphorylation inhibitor necrostatin-1. Analyses of ischemic brain injury were performed via both cellular and volumetric assessments, electron microscopy, TUNEL staining, activated caspase-3 and caspase-7 staining, as well as CD11b and F4/80 staining. Inhibition of caspase-3 or RIPK1 phosphorylation demonstrates significant neural protective effects which are non-additive and exhibit significant overlap in protected regions. Interestingly, morphologic analysis of the cortex demonstrates reduced apoptosis following RIPK1 inhibition. Consistent with this, RIPK1 inhibition reduces the levels of both caspase-3 and caspase-7 activation. Additionally, this protection appears independent of secondary inflammatory mediators. Together, these observations demonstrate that the necroptotic protein RIPK1 modifies caspase-3/-7 activity, ultimately resulting in decreased neuronal apoptosis. These findings thus modify the traditional exclusionary view of apoptotic/necroptotic signaling, revealing a new form of interaction between these dominant forms of cell death.
      PubDate: 2021-11-01
       
  • Neuroprotective Effects of Early Brain Injury after Subarachnoid
           Hemorrhage in Rats by Calcium Channel Mediating Hydrogen Sulfide

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      Abstract: The present study explored the modulating apoptosis effect of hydrogen sulfide (H2S) in subarachnoid hemorrhage (SAH) rats and its exact mechanism. A rat SAH model established by intravascular puncturing was used for the present study. After giving NaHS (donor of H2S), an L-type calcium channel opener (Bay K8644), or a calcium channel agonist (nifedipine), the neurological function of the rats, associated pathological changes, and expression of apoptosis-related proteins (Bcl-2, Bax, and caspase-3) and microtubule-associated protein (MAP-2) were examined. The concentration of H2S and expression of cystathionine beta synthase in the hippocampus changed upon early brain injury (EBI) after SAH. Compared with the SAH group, the neurological function of the rats and microstructure observed by electron microscopy were better in the SAH + NaHS group and SAH + Bay K8644 group. It was observed that apoptosis was more obvious in the SAH group than in the control group and was alleviated in the SAH + NaHS group. Furthermore, the alleviating effect of NaHS was partially weakened by nifedipine, indicating that the effect of anti-apoptosis in H2S might be correlated with the calcium channel. The expression of Bax and caspase-3 was elevated, while the expression of Bcl-2 decreased in the SAH group but improved in the SAH + NaHS and SAH + Bay K8644 group. Compared with the SAH + NaHS group, the expression of pro-apoptotic proteins was higher in the SAH + NaHS + nifedipine group. Therefore, upon EBI following SAH, the H2S system plays an important neurological protective effect by modulating the function of the L-type calcium channel and inhibiting apoptosis.
      PubDate: 2021-11-01
       
  • MMP-9 Inhibitor GM6001 Prevents the Development of ssTBI-Induced
           Parkinson’s Disease via the Autophagy Pathway

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      Abstract: Concussion is a widely recognized environmental risk factor for neurodegenerative diseases, including Parkinson’s disease (PD). Small-vessel disease of the brain has been reported to contribute to neurodegenerative diseases. In this study, we observed BBB disruption in wild-type (WT) mice, but not in matrix metalloproteinase 9 (MMP-9) knockout mice, subjected to single severe traumatic brain injury (ssTBI). Furthermore, treating ssTBI mice with the MMP-9 inhibitor GM6001 effectively maintained BBB integrity, promoted the elimination of damaged mitochondria via mitophagy, and then prevented neuronal death and progressive neurodegeneration. However, we did not observe this neuroprotective effect of MMP-9 inhibition in beclin-1−/+ mice. Collectively, these findings revealed that concussion led to BBB disruption via MMP-9, and that GM6001 prevented the development of PD via the autophagy pathway.
      PubDate: 2021-11-01
       
  • Time-Dependent Changes in the Serum Levels of Neurobiochemical Factors
           After Acute Methadone Overdose in Adolescent Male Rat

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      Abstract: Acute methadone toxicity is a major public health concern which has adverse effects on brain tissue and results in recurrent or delayed respiratory arrest. Our study aimed to investigate the time-dependent changes in several serum biochemical markers of brain damage, spatial working memory, and the brain tissue following acute methadone overdose. Adolescent male rats underwent an intraperitoneal (i.p.) injection of 15 mg/kg methadone. In case of apnea occurrence, resuscitation was performed by a ventilatory pump and administrating naloxone (2 mg/kg; i.p.). The animals were classified into groups of treated rats; methadone and naloxone-Apnea (M/N-Apnea), M/N-Sedate, Methadone, Naloxone, and control (saline) groups. The serum levels of S100B, neuron-specific enolase (NSE), myelin basic protein factors, and (Lactate/Pyruvate) L/P ratio were evaluated at the time-points of 6, 24, and 48 h (h). We found that the alterations of S100B and L/P ratio were considerable in the M/N-Apnea and Methadone groups from the early hours post-methadone overdose, while NSE serum levels elevation was observed only in M/N-Apnea group with a delay at 48 h. Further, we assessed the spatial working memory (Y-maze test), morphological changes, and neuronal loss. The impaired spontaneous alternation behavior was detected in the M/N-Apnea groups on days 5 and 10 post-methadone overdose. The morphological changes of neurons and the neuronal loss were detectable in the CA1, striatum, and cerebellum regions, which were pronounced in both M/N-Apnea and Methadone groups. Together, our findings suggest that alterations in the serum levels of S100B and NSE factors as well as L/P ratio could be induced by methadone overdose with the presence or absence of apnea before the memory impairment and tissue injury in adolescent male rats.
      PubDate: 2021-11-01
       
  • Elevated miR-29a Contributes to Axonal Outgrowth and Neurological Recovery
           After Intracerebral Hemorrhage via Targeting PTEN/PI3K/Akt Pathway

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      Abstract: Spontaneous intracerebral hemorrhage (ICH) is a clinical challenge with high disability and lacks an effective treatment. miR-29a strongly expressed in the brain has been implicated in various neurological disorders. In this study, we investigated the biological roles of miR-29a in axonal outgrowth and neurological outcomes after ICH and relevant molecular mechanism. The rat model of ICH was established by injection of autologous whole blood into the right basal ganglia. First, a significant decrease in miR-29a level was found in perihematomal brain tissues and cerebrospinal fluid (CSF) after ICH in vivo and hemin-treated neurons in vitro. Further study documented that lentivirus-mediated miR-29a overexpression could remarkably attenuate hemorrhagic brain injury, promoted regenerative outgrowth of injured axons and improved neurobehavioral and cognitive impairments after ICH in rats. In addition, we also identified that overexpression of miR-29a obviously alleviated neuronal damage and mitochondrial dysfunctions, and facilitated neurite outgrowth in cultured neurons exposed to hemin in vitro. Furthermore, luciferase reporter assay showed that miR-29a directly targeted the 3′-UTR region of phosphatase and tensin homolog (PTEN) mRNA and negatively regulated its expression. More importantly, pharmacological inhibition of PTEN has similar neuroprotective effects as miR-29a overexpression involving activation of the PI3K/Akt pathway after hemorrhagic stroke. Collectively, these results suggested that elevated miR-29a could contribute to axonal outgrowth and neurological recovery through targeting PTEN/PI3K/Akt pathway after ICH, thereby providing a potential therapeutic target for patients with ICH.
      PubDate: 2021-11-01
       
  • Ryanodine Receptors: A Potential Treatment Target in Various
           Neurodegenerative Disease

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      Abstract: Progressive neuronal demise is a key contributor to the key pathogenic event implicated in many different neurodegenerative disorders (NDDs). There are several therapeutic strategies available; however, none of them are particularly effective. Targeted neuroprotective therapy is one such therapy, which seems a compelling option, yet remains challenging due to the internal heterogeneity of the mechanisms underlying various NDDs. An alternative method to treat NDDs is to exploit common modalities involving molecularly distinct subtypes and thus develop specialized drugs with broad-spectrum characteristics. There is mounting evidence which supports for the theory that dysfunctional ryanodine receptors (RyRs) disrupt intracellular Ca2+ homeostasis, contributing to NDDs significantly. This review aims to provide direct and indirect evidence on the intersection of NDDs and RyRs malfunction, and to shed light on novel strategies to treat RyRs-mediated disease, modifying pharmacological therapies such as the potential therapeutic role of dantrolene, a RyRs antagonist.
      PubDate: 2021-11-01
       
  • Central Cholinergic Synapse Formation in Optimized Primary
           Septal-Hippocampal Co-cultures

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      Abstract: Septal innervation of basal forebrain cholinergic neurons to the hippocampus is critical for normal learning and memory and is severely degenerated in Alzheimer’s disease. To understand the molecular events underlying physiological cholinergic synaptogenesis and remodeling, as well as pathological loss, we developed an optimized primary septal-hippocampal co-culture system. Hippocampal and septal tissue were harvested from embryonic Sprague–Dawley rat brain and cultured together at varying densities, cell ratios, and in the presence of different growth factors. We identified conditions that produced robust septal-hippocampal synapse formation. We used confocal microscopy with primary antibodies and fluorescent ligands to validate that this system was capable of generating developmentally mature cholinergic synapses. Such synapses were comprised of physiological synaptic partners and mimicked the molecular composition of in vivo counterparts. This co-culture system will facilitate the study of the formation, plasticity, and dysfunction of central mammalian cholinergic synapses.
      PubDate: 2021-11-01
       
  • Involvement of SNARE Protein Interaction for Non-classical Release of
           DAMPs/Alarmins Proteins, Prothymosin Alpha and S100A13

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      Abstract: Prothymosin alpha (ProTα) is involved in multiple cellular processes. Upon serum-free stress, ProTα lacking a signal peptide sequence is non-classically released from C6 glioma cells as a complex with Ca2+-binding cargo protein S100A13. Thus, ProTα and S100A13 are conceived to be members of damage-associated molecular patterns (DAMPs)/alarmins. However, it remains to be determined whether stress-induced release of ProTα and S100A13 involves SNARE proteins in the mechanisms underlying membrane tethering of the multiprotein complex. In the present study, we used C6 glioma cells as a model of ProTα release. In pull-down assay, p40 synaptotagmin-1 (Syt-1), a vesicular SNARE, formed a hetero-oligomeric complex with homodimeric S100A13 in a Ca2+-dependent manner. The interaction between p40 Syt-1 and S100A13 was also Ca2+-dependent in surface plasmon resonance (SPR). Immunoprecipitation using conditioned medium (CM) revealed that p40 Syt-1 was co-released with ProTα and S100A13 upon serum-free stress. In in situ proximity ligation assay (PLA), Syt-1 interacted with S100A13 upon serum-free stress in C6 glioma cells. The intracellular delivery of anti-Syt-1 IgG blocked serum free-induced release of ProTα and S100A13. Serum free-induced ProTα-EGFP release was significantly blocked by botulinum neurotoxin/C1 (BoNT/C1), which cleaves target SNARE syntaxin-1 (Stx-1). In immunocytochemistry, the cellular loss of ProTα-EGFP, S100A13, and Syt-1 was also blocked by BoNT/C1. Furthermore, the intracellular delivery of anti-Stx-1 IgG or Stx-1 siRNA treatment blocked Syt-1, S100A13 and ProTα release from C6 glioma cells. All these findings suggest that SNARE proteins play roles in stress-induced non-classical release of DAMPs/alarmins proteins, ProTα and S100A13 from C6 glioma cells.
      PubDate: 2021-11-01
       
  • STAT3 Contributes to Intracranial Aneurysm Formation and Rupture by
           Modulating Inflammatory Response

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      Abstract: Intracranial aneurysm (IA) is a common type of refractory cerebrovascular diseases. Inflammatory responses have been reported to be associated with the pathogenesis of IA. We aimed to study the role of STAT3 on IA formation and inflammatory response. STAT3 expression and clinicopathological factors were analyzed in IA and normal cerebral arteries. mRNA level of STAT3 was detected in normal, unruptured, and ruptured IA tissues by RT-PCR and Western blot. Inflammatory cytokines were examined by ELISA in unruptured, ruptured IA tissues, as well as cells with STAT3 overexpression or knockdown. mRNA of phenotypic modulation-related factors was tested by RT-PCR in STAT3 overexpressing or knockdown VSMCs. STAT3 expression was upregulated in ruptured IA tissues and highly associated with IA diameter and IA type. Inflammatory cytokine secretion was increased in ruptured IA samples and positively correlated with STAT3 expression. STAT3 overexpression led to enhanced expression of SM-α actin, SM-MHC, MMP2, and MMP9, and increased secretion of inflammatory cytokines. Our findings have demonstrated that STAT3 is a key regulator in IA formation by modulating inflammatory cytokine expression.
      PubDate: 2021-11-01
       
  • LncRNA HOTAIR Promotes Neuronal Damage Through Facilitating NLRP3
           Mediated-Pyroptosis Activation in Parkinson’s Disease via Regulation of
           miR-326/ELAVL1 Axis

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      Abstract: Parkinson’s disease (PD) seriously threatens human’s health. Researches have shown a close correlation between long non-coding RNAs (lncRNAs) and PD. However, the biological function of lncRNA homeobox transcript antisense RNA (HOTAIR) in PD remains largely unknown. In this study, we established PD models in vivo and in vitro by using 1-methyl-4-phenyl-2, 3, 6-tetrahydropyridine (MPTP) and 1-methyl-4-phenylpyridinium (MPP+) to assess the role of HOTAIR in pyroptotic cell death and neuronal damage. RNA immunoprecipitation (RIP) and dual luciferase reporter assay were used to verify the interaction between miR-326 and HOTAIR or ELAV like RNA binding protein 1 (ELAVL1). LncRNA HOTAIR was upregulated in PD mice and MPP+ induced SH-SY5Y cells. Additionally, knockdown of HOTAIR notably attenuated the symptom of PD in vivo. Downregulation of HOTAIR could obviously promoted cell viability and suppressed NLR family pyrin domain containing 3 (NLRP3) mediated pyroptotic cell death of SH-SY5Y cells in the presence of MPP+. Further, lncRNA HOTAIR positively regulated ELAVL1 expression by targeting miR-326, and downregulation of HOTAIR or ELAVL1 notably suppressed promotive effects of miR-326 inhibitor on MPP+ induced pyroptosis via activation of NLRP3 inflammasome. Collectively, HOTAIR silencing significantly inhibits neuronal damage through repressing NLRP3 mediated pyroptosis activation via regulation of miR-326/ELAVL1 axis in PD, which may contribute to a better understanding of PD pathogenesis and provide new treatment strategies for this disease.
      PubDate: 2021-11-01
       
  • The Laminin-Induced Phosphorylation of PKCδ Regulates AQP4 Distribution
           and Water Permeability in Rat Astrocytes

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      Abstract: In astrocytes, the water-permeable channel aquaporin-4 (AQP4) is concentrated at the endfeet that abut the blood vessels of the brain. The asymmetric distribution of this channel is dependent on the function of dystroglycan (DG), a co-expressed laminin receptor, and its associated protein complex. We have demonstrated that the addition of laminin to astrocytes in culture causes the clustering of AQP4, DG, and lipid rafts. The last, in particular, have been associated with the initiation of cell signaling. As laminin binding to DG in muscle cells can induce the tyrosine phosphorylation of syntrophin and laminin requires tyrosine kinases for acetylcholine receptor clustering in myotubes, we asked if signal transduction might also be involved in AQP4 clustering in astrocytes. We analyzed the timecourse of AQP4, DG, and monosialotetrahexosylganglioside (GM1) clustering in primary cultures of rat astrocytes following the addition of laminin, and determined that the clustering of DG precedes that of AQP4 and GM1. We also showed that laminin induces the formation of phosphotyrosine-rich clusters and that the tyrosine kinase inhibitor, genistein, disrupts the laminin-induced clustering of both β-DG and AQP4. Using the Kinexus antibody microarray chip, we then identified protein-serine kinase C delta (PKCδ) as one of the main proteins exhibiting high levels of tyrosine phosphorylation upon laminin treatment. Selective inhibitors of PKC and siRNA against PKCδ disrupted β-DG and AQP4 clustering, and also caused water transport to increase in astrocytes treated with laminin. Our results demonstrate that the effects of laminin on AQP4 localization and function are relayed, at least in part, through PKC signaling.
      PubDate: 2021-11-01
       
  • Sevoflurane Post-Conditioning Ameliorates Neuronal Deficits and Axon
           Demyelination After Neonatal Hypoxic Ischemic Brain Injury: Role of
           Microglia/Macrophage

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      Abstract: Microglia/macrophages have been identified to be highly polarized after ischemia. Interestingly, the polarization of these microglia/macrophages varies immensely under differing disease conditions. Post-conditioning using sevoflurane, a volatile anesthetic, could provide long-term neuroprotection to neonatal rats after hypoxic-ischemic brain injury (HIBI). Thus, the current study aimed at investigating the effects of sevoflurane post-conditioning (SPC) on microglia/macrophage polarization after HIBI induction in neonatal rats. Additionally, we aimed at identifying the underpinning mechanisms specifically related to autophagy and lysosomal protease enzyme, cathepsin B. To develop a HIBI model, 7-day-old Sprague–Dawley rats underwent left common carotid artery ligation followed by 2 h of hypoxia. The role of microglia/macrophages in the neuroprotection conferred by SPC was examined by left-side intra-cerebroventricular injection with adenovirus vector carrying catB-GFP or rapamycin. The number of interleukin (IL)-1β+ cells, cathepsin B+ cells, light chain 3B positive (LC3B+) cells among ionized calcium binding adaptor molecule 1(Iba1+)cells to investigate microglia polarization, neuronal apoptosis to assess neuronal death in the acute phase were tested at 24 h after HIBI. Behavioral tests including suspension test, Morris water maze tests were performed to investigate the long-term effects of SPC, at 21 to 34 days post HIBI. Nissl staining and myelin basic protein (MBP) immunostaining to assess the long-term neuronal and myelin damage were performed at 34 days after HIBI. Based on the obtained results post HIBI, we observed the cells that were positive for IL-1β, cathepsin B, and LC3B among Iba1 positive cell population in the hippocampus were significantly decreased after SPC treatment. SPC significantly attenuated the HIBI-induced increase in neuronal apoptosis, improved long-term cognitive function, and attenuated HI-induced decrease of Nissl-positive cells and MBP expression. However, these trends were reversed by injection of adenovirus vector carrying catB-GFP and rapamycin. SPC attenuated microglia polarization towards neurotoxic phenotypes, alleviates neuronal death and axon demyelination after HIBI in neonatal rats by regulating microglia autophagy and cathepsin B expression, and therefore provided long-term cognitive, learning and memory protection.
      PubDate: 2021-11-01
       
  • Real-Time Noninvasive Bioluminescence, Ultrasound and Photoacoustic
           Imaging in NFκB-RE-Luc Transgenic Mice Reveal Glia Maturation
           Factor-Mediated Immediate and Sustained Spatio-Temporal Activation of
           NFκB Signaling Post-Traumatic Brain Injury in a Gender-Specific Manner

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      Abstract: Neurotrauma especially traumatic brain injury (TBI) is the leading cause of death and disability worldwide. To improve upon the early diagnosis and develop precision-targeted therapies for TBI, it is critical to understand the underlying molecular mechanisms and signaling pathways. The transcription factor, nuclear factor kappa B (NFκB), which is ubiquitously expressed, plays a crucial role in the normal cell survival, proliferation, differentiation, function, as well as in disease states like neuroinflammation and neurodegeneration. Here, we hypothesized that real-time noninvasive bioluminescence molecular imaging allows rapid and precise monitoring of TBI-induced immediate and rapid spatio-temporal activation of NFκB signaling pathway in response to Glia maturation factor (GMF) upregulation which in turn leads to neuroinflammation and neurodegeneration post-TBI. To test and validate our hypothesis and to gain novel mechanistic insights, we subjected NFκB-RE-Luc transgenic male and female mice to TBI and performed real-time noninvasive bioluminescence imaging (BLI) as well as photoacoustic and ultrasound imaging (PAI). Our BLI data revealed that TBI leads to an immediate and sustained activation of NFκB signaling. Further, our BLI data suggest that especially in male NFκB-RE-Luc transgenic mice subjected to TBI, in addition to brain, there is widespread activation of NFκB signaling in multiple organs. However, in the case of the female NFκB-RE-Luc transgenic mice, TBI induces a very specific and localized activation of NFκB signaling in the brain. Further, our microRNA data suggest that TBI induces significant upregulation of mir-9-5p, mir-21a-5p, mir-34a-5p, mir-16-3p, as well as mir-155-5p within 24 h and these microRNAs can be successfully used as TBI-specific biomarkers. To the best of our knowledge, this is one of the first and unique study of its kind to report immediate and sustained activation of NFκB signaling post-TBI in a gender-specific manner by utilizing real-time non-invasive BLI and PAI in NFκB-RE-Luc transgenic mice. Our study will prove immensely beneficial to gain novel mechanistic insights underlying TBI, unravel novel therapeutic targets, as well as enable us to monitor in real-time the response to innovative TBI-specific precision-targeted gene and stem cell-based precision medicine.
      PubDate: 2021-11-01
       
  • Valproic Acid Sensitizes Glioma Cells to Luteolin Through Induction of
           Apoptosis and Autophagy via Akt Signaling

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      Abstract: Glioma is a highly malignant type of intracranial tumor with a poor prognosis resulting from traditional chemo-resistance with temozolomide (TMZ). Luteolin has been detected to exert limited anti-tumor effects on gliomas, while valproic acid (VPA) is a common chemotherapy sensitizer in the treatment of tumors. In this study, three glioma cell lines including U251, LN229 and SNB19 were selected for evaluation of combined anti-tumor effects of VPA and luteolin via Cell Counting Kit-8 (CCK-8) assay, colony formation assay, wound-healing assay, flow cytometry and western blot assay. The results disclosed that VPA sensitized glioma cells to luteolin by repressing cell viability, colony formation and migration. Mechanically, VPA boosted cellular apoptosis and cell-cycle arrest by increased level of cleaved caspase-3/caspase-3, cleaved PARP/PARP and Bax/Bcl-2. In addition, VPA also facilitated cellular autophagy via the decline of p62, p-Akt/Akt and the accumulation of LC3-II. These findings suggested that VPA enhanced the anticancer effects of luteolin by strengthening apoptosis and autophagy via Akt signaling, which could be adopted as a novel therapy for glioma.
      PubDate: 2021-11-01
       
  • Opposite Roles of NT-3 and BDNF in Synaptic Remodeling of the Inner Ear
           Induced by Electrical Stimulation

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      Abstract: With the development of neural prostheses, neural plasticity including synaptic remodeling under electrical stimulation is drawing more and more attention. Indeed, intracochlear electrical stimulation used to restore hearing in deaf can induce the loss of residual hearing and synapses of the inner hair cells (IHCs). However, the mechanism under this process is largely unknown. Considering that the guinea pig is always a suitable and convenient choice for the animal model of cochlea implant (CI), in the present study, normal-hearing guinea pigs were implanted with CIs. Four-hour electrical stimulation with the intensity of 6 dB above electrically evoked compound action potential (ECAP) threshold (which can decrease the quantity of IHC synapses and the excitability of the auditory nerve) resulted in the upregulation of Bdnf (p < 0.0001) and downregulation of Nt-3 (p < 0.05). Intracochlear perfusion of exogenous NT-3 or TrkC/Fc (which blocks NT-3) can, respectively, resist or aggravate the synaptic loss induced by electrical stimulation. In contrast, local delivery of exogenous BDNF or TrkB/Fc (which blocks BDNF) to the cochlea, respectively, exacerbated or protected against the synaptic loss caused by electrical stimulation. Notably, the synaptic changes were only observed in the basal and middle halves of the cochlea. All the findings above suggested that NT-3 and BDNF may play opposite roles in the remodeling of IHC synapses induced by intracochlear electrical stimulation, i.e. NT-3 and BDNF promoted the regeneration and degeneration of IHC synapses, respectively.
      PubDate: 2021-11-01
       
  • Blood–Brain Barrier Dysfunction in the Pathogenesis of Major
           Depressive Disorder

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      Abstract: Major depression represents a complex and prevalent psychological disease that is characterized by persistent depressed mood, impaired cognitive function and complicated pathophysiological and neuroendocrine alterations. Despite the multifactorial etiology of depression, one of the most recent factors to be identified as playing a critical role in the development of depression is blood–brain barrier (BBB) disruption. The occurrence of BBB integrity disruption contributes to the disturbance of brain homeostasis and leads to complications of neurological diseases, such as stroke, chronic neurodegenerative disorders, neuroinflammatory disorders. Recently, BBB associated tight junction disruption has been shown to implicate in the pathophysiology of depression and contribute to increased susceptibility to depression. However, the underlying mechanisms and importance of BBB damage in depression remains largely unknown. This review highlights how BBB disruption regulates the depression process and the possible molecular mechanisms involved in development of depression-induced BBB dysfunction. Moreover, insight on promising therapeutic targets for treatment of depression with associated BBB dysfunctions are also discussed.
      PubDate: 2021-10-12
       
  • L-type Ca2+ Channels at Low External Calcium Differentially Regulate
           Neurotransmitter Release in Proximal–Distal Compartments of the Frog
           Neuromuscular Junction

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      Abstract: L-type Ca2+ channels (LTCCs) are key elements in electromechanical coupling in striated muscles and formation of neuromuscular junctions (NMJs). However, the significance of LTCCs in regulation of neurotransmitter release is still far from understanding. Here, we found that LTCCs can increase evoked neurotransmitter release (especially asynchronous component) and spontaneous exocytosis in two functionally different compartment of the frog NMJ, namely distal and proximal parts. The effects of LTCC blockage on evoked and spontaneous release as well as timing of exocytotic events were prevented by inhibition of either protein kinase C (PKC) or P2Y receptors (P2Y-Rs). Hence, endogenous signaling via P2Y-R/PKC axis can sustain LTCC activity. Application of ATP, a co-neurotransmitter able to activate P2Y-Rs, suppressed both evoked and spontaneous exocytosis in distal and proximal parts. Surprisingly, inhibition of LTCCs (but not PKC) decreased the negative action of exogenous ATP on evoked (only in distal part) and spontaneous exocytosis. Lipid raft disruption suppressed (1) action of LTCC antagonist on neurotransmitter release selectively in distal region and (2) contribution of LTCCs in depressant effect of ATP on evoked and spontaneous release. Thus, LTCCs can enhance and desynchronize neurotransmitter release at basal conditions (without ATP addition), but contribute to ATP-mediated decrease in the exocytosis. The former action of LTCCs relies on P2Y-R/PKC axis, whereas the latter is triggered by exogenous ATP and PKC-independent. Furthermore, relevance of lipid rafts for LTCC function as well as LTCCs for ATP effects is different in distal and proximal part of the NMJ. Graphic
      PubDate: 2021-10-04
       
  • Correction to: Involvement of Nuclear Receptor REV-ERBβ in Formation of
           Neurites and Proliferation of Cultured Adult Neural Stem Cells

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      Abstract: A correction to this paper has been published: https://doi.org/10.1007/s10571-021-01076-5
      PubDate: 2021-10-01
       
  • Microglial TLR9: Plausible Novel Target for Therapeutic Regime Against
           Glioblastoma Multiforme

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      Abstract: An understanding of pattern recognition receptors (PRRs) and immunomodulatory approach based on activation of these receptors has provided insights critical for the management of neurological health disorders. Toll-like receptors (TLRs) are one of the most widely explored PRRs and have been exploited in the recent past for development of novel immunomodulatory therapeutic agents. Glioblastoma multiforme is characterized by significant infiltration of resident microglia and expresses all the members of the TLR family. The present report is focused on exciting findings pertaining to probable implications of TLR9 activation by unmethylated CG sequences for novel therapeutic intervention against glioblastoma multiforme, which could be a discrete step toward the effective management of neurological health issues.
      PubDate: 2021-10-01
       
 
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