scholarly journals DeadEasy neurons: Automatic counting of HB9 neuronal nuclei in Drosophila

2010 ◽  
Vol 77A (4) ◽  
pp. 371-378 ◽  
Author(s):  
Manuel G. Forero ◽  
Jenny A. Pennack ◽  
Alicia Hidalgo
Keyword(s):  
Neuronal Nuclei ◽  
Automatic Counting

Analysis of the Clinical Diagnostic Value of GMFB in Cerebral Infarction

2020 ◽  
Vol 21 (10) ◽  
pp. 955-963
Author(s):  
Zhaohu Yuan ◽  
Zhiwu Yu ◽  
Yiyu Zhang ◽  
Huikuan Yang
Keyword(s):  
Myocardial Infarct ◽  
Diagnostic Value ◽  
Artery Occlusion ◽  
Response Dynamics ◽  
Stroke Patients ◽  
Ischaemic Injury ◽  
Neuronal Nuclei ◽  
Diagnosis And Prognosis ◽  
Maturation Factor ◽  
Injury And Repair

Background: Glial Maturation Factor Beta (GMFB) is a highly conserved brain-enriched protein implicated in immunoregulation, neuroplasticity and apoptosis, processes central to neural injury and repair following cerebral ischaemia. Therefore, we examined if changes in neurocellular GMFB expression and release can be used to assess brain injury following ischaemia. Methods and Results: Immunofluorescence staining, Western blotting, immunohistochemistry and ELISA were used to measure GMFB in cultured neurons and astrocytes, rat brain tissues and plasma samples from stroke model rats and stroke patients, while cell viability assays, TTC staining and micro- PET were used to assess neural cell death and infarct severity. Immunofluorescence and immunohistochemistry revealed GMFB expression mainly in astrocyte and neuronal nuclei but also in neuronal axons and dendrites. Free GMFB concentration increased progressively in the culture medium during hypoxia-hypoglycaemia treatment. Plasma GMFB concentration increased in rats subjected to middle cerebral artery occlusion (MCAO, a model of stroke-reperfusion) and in stroke patients. Plasma GMFB in MCAO model rats was strongly correlated with infarct size (R2=0.9582). Plasma GMFB concentration was also markedly elevated in stroke patients within 24 h of onset and remained elevated for more than one week. Conversely, plasma GMFB elevations were not significant in myocardial infarct patients and stroke patients without infarction. Conclusion: GMFB has the prerequisite stability, expression specificity and response dynamics to serve as a reliable indicator of ischaemic injury in animal models and stroke patients. Plasma GMFB may be a convenient non-invasive adjunct to neuroimaging for stroke diagnosis and prognosis.

scholarly journals Assessing the treatment of cannabidiolic acid methyl ester: a stable synthetic analogue of cannabidiolic acid on c-Fos and NeuN expression in the hypothalamus of rats

2021 ◽  
Vol 3 (1) ◽  
Author(s):  
Eric Murillo-Rodríguez ◽  
Diana Millán-Aldaco ◽  
Gloria Arankowsky-Sandoval ◽  
Tetsuya Yamamoto ◽  
Roger G. Pertwee ◽  
...  
Keyword(s):  
Methyl Ester ◽  
Cannabis Sativa ◽  
Brain Area ◽  
Acid Methyl Ester ◽  
Hypothalamic Nucleus ◽  
Synthetic Analogue ◽  
Neuronal Nuclei ◽  
Cannabidiolic Acid ◽  
Dorsomedial Hypothalamic Nucleus ◽  
Psychotropic Compound

Abstract Background Cannabidiol (CBD), the non-psychotropic compound from Cannabis sativa, shows positive results on controlling several health disturbances; however, comparable data regarding additional chemical from C. sativa, such as cannabidiolic acid (CBDA), is scarce due to its instability. To address this limitation, a stable CBDA analogue, CBDA methyl ester (HU-580), was synthetized and showed CBDA-like effects. Recently, we described that HU-580 increased wakefulness and wake-related neurochemicals. Objective To extend the comprehension of HU-580´s properties on waking, the c-Fos and NeuN expression in a wake-linked brain area, the hypothalamus was evaluated. Methods c-Fos and NeuN expression in hypothalamic sections were analyzed after the injections of HU-580 (0.1 or 100 μg/kg, i.p.). Results Systemic administrations of HU-580 increased c-Fos and neuronal nuclei (NeuN) expression in hypothalamic nuclei, including the dorsomedial hypothalamic nucleus dorsal part, dorsomedial hypothalamic nucleus compact part, and dorsomedial hypothalamic nucleus ventral part. Conclusion HU-580 increased c-Fos and NeuN immunoreactivity in hypothalamus nuclei suggesting that this drug might modulate the sleep–wake cycle by engaging the hypothalamus.

scholarly journals The ESCRT-III protein VPS4, but not CHMP4B or CHMP2B, is pathologically increased in familial and sporadic ALS neuronal nuclei

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Alyssa N. Coyne ◽  
Jeffrey D. Rothstein
Keyword(s):  
Nuclear Pore Complex ◽  
Mammalian Cells ◽  
Nuclear Accumulation ◽  
Nuclear Pore ◽  
Dependent Manner ◽  
Structured Illumination Microscopy ◽  
Neuronal Nuclei ◽  
Complex Injury ◽  
Sporadic Als ◽  
Human Neurons

AbstractNuclear pore complex injury has recently emerged as an early and significant contributor to familial and sporadic ALS disease pathogenesis. However, the molecular events leading to this pathological phenomenon characterized by the reduction of specific nucleoporins from neuronal nuclear pore complexes remain largely unknown. This is due in part to a lack of knowledge regarding the biological pathways and proteins underlying nuclear pore complex homeostasis specifically in human neurons. We have recently uncovered that aberrant nuclear accumulation of the ESCRT-III protein CHMP7 initiates nuclear pore complex in familial and sporadic ALS neurons. In yeast and non-neuronal mammalian cells, nuclear relocalization of CHMP7 has been shown to recruit the ESCRT-III proteins CHMP4B, CHMP2B, and VPS4 to facilitate nuclear pore complex and nuclear envelope repair and homeostasis. Here, using super resolution structured illumination microscopy, we find that neither CHMP4B nor CHMP2B are increased in ALS neuronal nuclei. In contrast, VPS4 expression is significantly increased in ALS neuronal nuclei prior to the emergence of nuclear pore injury in a CHMP7 dependent manner. However, unlike our prior CHMP7 knockdown studies, impaired VPS4 function does not mitigate alterations to the NPC and the integral transmembrane nucleoporin POM121. Collectively our data suggest that while alterations in VPS4 subcellular localization appear to be coincident with nuclear pore complex injury, therapeutic efforts to mitigate this pathogenic cascade should be targeted towards upstream events such as the nuclear accumulation of CHMP7 as we have previously described.

Identification and quantification of microplastics in table sea salts using micro-NIR imaging methods

2018 ◽  
Vol 10 (24) ◽  
pp. 2881-2887 ◽  
Author(s):  
Jixiong Zhang ◽  
Kuangda Tian ◽  
Chunli Lei ◽  
Shungeng Min
Keyword(s):  
Sea Salts ◽  
Imaging Methods ◽  
Nir Imaging ◽  
Automatic Counting ◽  
Identification And Quantification

A method for the identification and quantification of microplastics in table sea salts. The method meets the need for detecting and automatic counting microplastics simultaneously.

Vision Based Real-time High-accuracy Automatic Counting with Applications for Smart Pharmacy

2021 ◽  
Author(s):  
Haotian Wu ◽  
YuRan Wang ◽  
Hongbin Ma ◽  
Baokui Li ◽  
Ying Jin
Keyword(s):  
Real Time ◽  
High Accuracy ◽  
Automatic Counting

scholarly journals The Immunopathogenesis of Neuroinvasive Lesions of SARS-CoV-2 Infection in COVID-19 Patients

2021 ◽  
Vol 12 ◽  
Author(s):  
Shamila D. Alipoor ◽  
Esmaeil Mortaz ◽  
Mohammad Varahram ◽  
Johan Garssen ◽  
Ian M. Adcock
Keyword(s):  
Transport Mechanism ◽  
Respiratory Rhythm ◽  
Olfactory Nerve ◽  
Severe Respiratory Distress ◽  
Neuronal Nuclei ◽  
The World ◽  
Neurological Effects ◽  
The Brain ◽  
Trigger Cell Death

The new coronavirus disease COVID-19 was identified in December 2019. It subsequently spread across the world with over 125 M reported cases and 2.75 M deaths in 190 countries. COVID-19 causes severe respiratory distress; however, recent studies have reported neurological consequences of infection by the COVID-19 virus SARS-CoV-2 even in subjects with mild infection and no initial neurological effects. It is likely that the virus uses the olfactory nerve to reach the CNS and that this transport mechanism enables virus access to areas of the brain stem that regulates respiratory rhythm and may even trigger cell death by alteration of these neuronal nuclei. In addition, the long-term neuronal effects of COVID-19 suggest a role for SARS-CoV-2 in the development or progression of neurodegerative disease as a result of inflammation and/or hypercoagulation. In this review recent findings on the mechanism(s) by which SARS-CoV-2 accesses the CNS and induces neurological dysregulation are summarized.

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