Proliferation Of Brain Cells Research Articles

Prompt Multi-level Segmentation with Denoising Model with Fragile Correlated Feature Subset for Brain Tumor Classification.

Background Classifying brain tumors with extraordinary precision using images is critical for prognosis and treatment planning. The aberrant proliferation of brain cells characterizes brain tumors. Variations in neuronal development may occur among individuals. The classification of tumors as benign or malignant is contingent upon their rate of growth. A benign tumor remains localized at its site of origin; one that has spread to distant sites is malignant. Brain tumor identification may be difficult due to the unique characteristics of brain tumor cells. Objective This study presents a method that methodically improves the identification of brain tumor cells and the analysis of functional structures through the utilization of sample training that incorporates features extracted from Magnetic Resonance Imaging (MRI) images. In the image enhancement phase, the color information of the MRI image is converted to greyscale, and its margins are sharpened to facilitate the detection of finer details. For specialists or general practitioners to accurately diagnose life-threatening conditions, such as brain tumors, medical images are required. Picture denoising has been identified in recent research as a potentially fruitful area of study. It is critical to perform image cleanup while preserving the sharpness of the boundaries. Methods In this research, a Prompt Multi Level Segmentation Denoising model with a Fragile Correlated Feature Subset (PMLSD-FCFS) model is proposed for accurate denoising of MRI images and to extract the most relevant features set by applying a feature dimensionality reduction model for better brain tumor predictions. Results The proposed model achieves 98.2% accuracy in Multi-Level Image Segmentation and 98.4% accuracy in Fragile Correlated Feature Subset Generation. Conclusion The experimental findings indicated that the model proposed exhibits superior performance compared to the traditional algorithms. Furthermore, it successfully eliminates the noise from the MRI images, and most relevant features are only considered for brain tumor detection, thereby enhancing the accuracy of classification.

Designing efficient brain tumor classifier using hybrid EfficientNet-faster R-CNN deep learning model

Purpose. Brain tumors have historically posed a significant risk to individuals, potentially leading to fatality. However, in contemporary times, they have emerged as one of the most dangerous health issues affecting both children and adults. The effects of this phenomenon result in the unregulated proliferation of brain cells. Therefore, early detection and precise classification of brain tumor is very necessary and important for saving lives and avoid future complications. Within the field of biological image processing, the utilisation of deep learning algorithms offers a distinct and unparalleled experience. The Convolutional Neural Network (CNN) is a pivotal component in brain tumor categorization applications. However, a notable limitation of CNNs is their extensive execution time, primarily attributed to the substantial number of trainable parameters involved. Also, the automatic detection and classification of brain tumor is still a challenging task due to its variability in shape, size and location. Methods. This study proposes a hybrid model for brain tumor classification that combines faster R-CNN and EfficientNet. The objective is to minimise the time required for classification without compromising accuracy. The data collection from Figshare was employed during the model’s development. Results and Conclusion. The hybrid model proposed in this study demonstrates a notable accuracy of 98.96% during the training phase and 99.2% during the testing phase, surpassing the performance of both the EfficientNet model and the Faster R-CNN model when employed individually. The aforementioned findings were derived through a comparative analysis of the Hybrid model, the EfficientNet model, and the Faster R-CNN model.

Organotypic hippocampal culture model reveals differential responses to highly similar Zika virus isolates

IntroductionZika virus (ZIKV) caused an outbreak in Brazil, in 2015, being associated to microcephaly. ZIKV has a strong neurotropism leading to death of infected cells in different brain regions, including the hippocampus, a major site for neurogenesis. The neuronal populations of the brain are affected differently by ZIKV from Asian and African ancestral lineages. However, it remains to be investigated whether subtle variations in the ZIKV genome can impact hippocampus infection dynamics and host response.ObjectiveThis study evaluated how two Brazilian ZIKV isolates, PE243 and SPH2015, that differ in two specific missense amino acid substitutions, one in the NS1 protein and the other in the NS4A protein, affect the hippocampal phenotype and transcriptome.MethodsOrganotypic hippocampal cultures (OHC) from infant Wistar rats were infected with PE243 or SPH2015 and analyzed in time series using immunofluorescence, confocal microscopy, RNA-Seq and RT-qPCR.ResultsUnique patterns of infection and changes in neuronal density in the OHC were observed for PE243 and SPH2015 between 8 and 48 h post infection (p.i.). Phenotypic analysis of microglia indicated that SPH2015 has a greater capacity for immune evasion. Transcriptome analysis of OHC at 16 h p.i. disclosed 32 and 113 differentially expressed genes (DEGs) in response to infection with PE243 and SPH2015, respectively. Functional enrichment analysis suggested that infection with SPH2015 activates mostly astrocytes rather than microglia. PE243 downregulated biological process of proliferation of brain cells and upregulated those associated with neuron death, while SPH2015 downregulated processes related to neuronal development. Both isolates downregulated cognitive and behavioral development processes. Ten genes were similarly regulated by both isolates. They are putative biomarkers of early hippocampus response to ZIKV infection. At 5, 7, and 10 days p.i., neuronal density of infected OHC remained below controls, and mature neurons of infected OHC showed an increase in the epigenetic mark H3K4me3, which is associated to a transcriptionally active state. This feature is more prominent in response to SPH2015.ConclusionSubtle genetic diversity of the ZIKV affects the dynamics of viral dissemination in the hippocampus and host response in the early stages of infection, which may lead to different long-term effects in neuronal population.

A Novel Approach for Brain Tumor Classification Using an Ensemble of Deep and Hand-Crafted Features.

One of the most severe types of cancer caused by the uncontrollable proliferation of brain cells inside the skull is brain tumors. Hence, a fast and accurate tumor detection method is critical for the patient's health. Many automated artificial intelligence (AI) methods have recently been developed to diagnose tumors. These approaches, however, result in poor performance; hence, there is a need for an efficient technique to perform precise diagnoses. This paper suggests a novel approach for brain tumor detection via an ensemble of deep and hand-crafted feature vectors (FV). The novel FV is an ensemble of hand-crafted features based on the GLCM (gray level co-occurrence matrix) and in-depth features based on VGG16. The novel FV contains robust features compared to independent vectors, which improve the suggested method's discriminating capabilities. The proposed FV is then classified using SVM or support vector machines and the k-nearest neighbor classifier (KNN). The framework achieved the highest accuracy of 99% on the ensemble FV. The results indicate the reliability and efficacy of the proposed methodology; hence, radiologists can use it to detect brain tumors through MRI (magnetic resonance imaging). The results show the robustness of the proposed method and can be deployed in the real environment to detect brain tumors from MRI images accurately. In addition, the performance of our model was validated via cross-tabulated data.

Selective Deeply Supervised Multi-Scale Attention Network for Brain Tumor Segmentation.

Brain tumors are among the deadliest forms of cancer, characterized by abnormal proliferation of brain cells. While early identification of brain tumors can greatly aid in their therapy, the process of manual segmentation performed by expert doctors, which is often time-consuming, tedious, and prone to human error, can act as a bottleneck in the diagnostic process. This motivates the development of automated algorithms for brain tumor segmentation. However, accurately segmenting the enhanced and core tumor regions is complicated due to high levels of inter- and intra-tumor heterogeneity in terms of texture, morphology, and shape. This study proposes a fully automatic method called the selective deeply supervised multi-scale attention network (SDS-MSA-Net) for segmenting brain tumor regions using a multi-scale attention network with novel selective deep supervision (SDS) mechanisms for training. The method utilizes a 3D input composed of five consecutive slices, in addition to a 2D slice, to maintain sequential information. The proposed multi-scale architecture includes two encoding units to extract meaningful global and local features from the 3D and 2D inputs, respectively. These coarse features are then passed through attention units to filter out redundant information by assigning lower weights. The refined features are fed into a decoder block, which upscales the features at various levels while learning patterns relevant to all tumor regions. The SDS block is introduced to immediately upscale features from intermediate layers of the decoder, with the aim of producing segmentations of the whole, enhanced, and core tumor regions. The proposed framework was evaluated on the BraTS2020 dataset and showed improved performance in brain tumor region segmentation, particularly in the segmentation of the core and enhancing tumor regions, demonstrating the effectiveness of the proposed approach. Our code is publicly available.

Precise Multi-Class Classification of Brain Tumor via Optimization Based Relevance Vector Machine

The objective of this research is to examine the use of feature selection and classification methods for distinguishing different types of brain tumors. The brain tumor is characterized by an anomalous proliferation of brain cells that can either be benign or malignant. Most tumors are misdiagnosed due to the variability and complexity of lesions, which reduces the survival rate in patients. Diagnosis of brain tumors via computer vision algorithms is a challenging task. Segmentation and classification of brain tumors are currently one of the most essential surgical and pharmaceutical procedures. Traditional brain tumor identification techniques require manual segmentation or handcrafted feature extraction that is error-prone and time-consuming. Hence the proposed research work is mainly focused on medical image processing, which takes Magnetic Resonance Imaging (MRI) images as input and performs preprocessing, segmentation, feature extraction, feature selection, similarity measurement, and classification steps for identifying brain tumors. Initially, the median filter is practically applied to the input image to reduce the noise. The graph-cut segmentation technique is used to segment the tumor region. The texture feature is extracted from the output of the segmented image. The extracted feature is selected by using the Ant Colony Optimization (ACO) algorithm to improve the performance of the classifier. This probabilistic approach is used to solve computing issues. The Euclidean distance is used to calculate the degree of similarity for each extracted feature. The selected feature value is given to the Relevance Vector Machine (RVM) which is a multi-class classification technique. Finally, the tumor is classified as abnormal or normal. The experimental result reveals that the proposed RVM technique gives a better accuracy range of 98.87% when compared to the traditional Support Vector Machine (SVM) technique.

Apis Mellifera Propolis Extract As A Stimulator Of Brain Cell Development (Study On Experimental Animals)

Apis mellifera could have potential as cell growth stimulator ability of the propolis. It also expected to increase the growth and proliferation of brain cells. This study aimed to analyze Apis mellifera Propolis Extract as a Stimulator of Brain Cell Development in Experimental Animals. This research is an experimental study using a completely randomized design (CRD) with 6 treatments and 4 replications. The research consisted of making Propolis Extract, Making Media (DMEM Stock Media, Washing Media, Culture and Treatment Media), Brain Cell Isolation and Culture, Observation of Culture Results (Cell Viability, Population Doubling Time, The results found that all treatments with propolis extract showed higher average viability than the control, which had average viability of 86.3%. Based on PDT (Population Doubling Time value), propolis extract has a good effect on brain cell growth, hence increasing cell proliferation. In addition, the confluent brain cells of rats given propolis extract had higher average confluency than those not given propolis extract. Propolis extract can protect neurons from damage by increasing the brain-derivatedneurotrophic factor (BDNF) gene expression in cell line neuron cultures. 

A fractional diffusion model of CD8+T cells response to parasitic infection in the brain

Toxoplasma gondii(T. gondii) is a parasitic pathogen that causes serious brain diseases in fetuses and patients with immunodeficiency, particularly AIDS patients. In the field of immunology, a large number of studies have shown that effector CD8+T cells can respond toT. gondiiinfection in the brain tissue through controlling the proliferation of intracellular parasites and killing infected brain cells. These protective mechanisms do not occur without T cell movement and searching for infected cells, as a fundamental feature of the immune system. Following infection with a pathogen in a tissue, in their search for infected cells, CD8+T cells can perform different stochastic searches, including Lévy and Brownian random walks. Statistical analysis of CD8+T cell movement in the brain ofT. gondii-infected mouse has determined that the search strategy of CD8+T cells in response to infected brain cells could be described by a Lévy random walk. In this work, by considering a Lévy distribution for the displacements, we propose a space fractional-order diffusion equation for the T cell density in the infected brain tissue. Furthermore, we derive a mathematical model representing CD8+T cell response to infected brain cells. By solving the model equations numerically, we perform a comparison between Lévy and Brownian search strategies. we demonstrate that the Lévy search pattern enables CD8+T cells to spread over the whole brain tissue and hence they can rapidly destroy infected cells distributed throughout the brain tissue. However, with the Brownian motion assumption, CD8+T cells travel through the brain tissue more slowly, leading to a slower decline of the infected cells faraway from the source of T cells. Our results show that a Lévy search pattern aids CD8+T cells in accelerating the elimination of infected cells distributed broadly within the brain tissue. We suggest that a Lévy search strategy could be the result of natural evolution, as CD8+T cells learn to enhance the immune system efficiency against pathogens.

Ketamine exerts neurotoxic effects on the offspring of pregnant rats via the Wnt/β-catenin pathway.

Ketamine is an anesthetic and analgesic drug widely used in clinical anesthesia. To ensure the safety of anesthesia, it is necessary to study its side effects. Pregnancy is a key period for the development and growth of offspring. During this period, the proliferation and differentiation of brain cells and the synaptic formation are easily affected by external stimuli. Therefore, the aim of this study was to evaluate the effect of ketamine. Ketamine anesthesia was administered to rats in the second trimester of pregnancy, and two behavioral tests were performed, including contextual and cued fear conditioning test (CFC) and Morris water maze (MWM). At the end of the behavioral test, Nissl and Golgi staining were used to detect the dendrite density of hippocampal neurons to reveal the effect of maternal ketamine anesthesia on the hippocampus of offspring. Key proteins and their downstream transcription factors in Wnt/β-catenin signaling pathway from the embryonic development to the adulthood were studied. Our results showed that rats receiving maternal ketamine suffered from nerve injury. The density of hippocampal nerves and dendritic spine changed. Some genes related to Wnt/β-catenin pathway and Tcf/Lef were downregulated. In conclusion, maternal anesthesia with ketamine in the second trimester of pregnancy can lead to cognitive memory impairment and neurotoxicity in the hippocampus of offspring through Wnt/ β-catenin signaling pathway.

The Relationships Between Vitamin K and Cognition: A Review of Current Evidence.

Vitamin K is a fat-soluble nutrient discovered in 1935 and its role in blood coagulation has been thoroughly explored. In recent years, studies conducted in vitro and on animals highlighted vitamin K involvement in brain cells development and survival. In particular, vitamin K seems to have an antiapoptotic and anti-inflammatory effect mediated by the activation of Growth Arrest Specific Gene 6 and Protein S. Moreover, this vitamin is involved in sphingolipids metabolism, a class of lipids that participate in the proliferation, differentiation, and survival of brain cells. An altered expression in sphingolipids profile has been related to neuroinflammation and neurodegeneration. This review stems from a growing interest in the role of vitamin K in brain functions, especially in cognition, also in view of an expected increase of prevalence of Alzheimer's disease and other forms of dementia. It collects recent researches that show interesting, even though not definitive, evidence of a direct correlation between vitamin K levels and cognitive performance. Moreover, vitamin K antagonists, used worldwide as oral anticoagulants, according to recent studies may have a negative influence on cognitive domains such as visual memory, verbal fluency and brain volume. The aim of this review is to analyze the evidence of clinical studies carried out up to date on the relationship between vitamin K intake and cognitive performances. The involvement of vitamin K antagonists (VKAs) in declining cognitive performances is also addressed separately.

Effect of endocannabinoid signalling on cell fate: life, death, differentiation and proliferation of brain cells.

Cell fate events are regulated by different endogenous developmental factors such as the cell micro-environment, external or remote signals and epigenetic factors. Among the many regulatory factors, endocannabinoid-associated signalling pathways are known to conduct several of these events in the developing nervous system and in the adult brain. Interestingly, endocannabinoids exert modulatory actions in both physiological and pathological conditions. Endocannabinoid signalling can promote cell survival by acting on non-transformed brain cells (neurons, astrocytes or oligodendrocytes) and can have either a protumoural or antitumoural effect on transformed cells. Moreover, endocannabinoids are able to attenuate the detrimental effects on neurogenesis and neuroinflammation associated with ageing. Thus, the endocannabinoid system emerges as an important regulator of cell fate, controlling cell survival/cell death decisions depending on the cell type and its environment. LINKED ARTICLES: This article is part of a themed section on 8th European Workshop on Cannabinoid Research. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v176.10/issuetoc.

In vitro Antioxidant and Antiproliferative Activities of Various Solvent Fractions from Clerodendrum viscosum Leaves.

Background:Free radicals such as reactive oxygen and nitrogen species, generated in the body, play an important role in the fulfillment of various physiological functions but their imbalance in the body lead to cellular injury and various clinical disorders such as cancer, neurodegenaration, and inflammation.Objective:The objective of this study is to fight this problem, natural antioxidant from plants can be considered as possible protective agents against various diseases such as cancer which might also modify the redox microenvironment to reduce the genetic instability. This study was designed to evaluate the antioxidant and antiproliferative potential of Clerodendrum viscosum fractions against various carcinomas.Materials and Methods:In this present study, 70% methanolic extract of C. viscosum leaves have been fractionated to obtain hexane, chloroform, ethyl acetate, butanol, and water fractions, which were tested for their antioxidant and anticancer properties.Results:It was observed that chloroform and ethyl acetate fractions showed good free radical scavenging properties as well as inhibited the proliferation of human lung cancer (A459), breast (MCF-7), and brain (U87) cells. Moreover, they arrested the cell cycle at G2/M phase of breast and brain cancer. These inhibitory effects were further confirmed by bromodeoxyuridine uptake imaging. Phytochemical investigations further indicate the presence of tannic acid, quercetin, ellagic caid, gallic acid, reserpine, and methyl gallate which might be the reason for these fractions’ antioxidant and antiproliferative activities.Conclusion:Clerodendrum viscosum leaf chloroform and Clerodendrum viscosum leaf ethyl acetate fractions from C. viscosum showed good reactive oxygen species and reactive nitrogen species scavenging potential. Both the fractions arrested cell cycle at G2/M phase in MCF-7 and U87 cells which lead to induce apoptosis.SUMMARY Crude extract of Clerodendrum viscosum leaves was fractionated using different solventsAmong them, chloroform and ethyl acetate fractions exhibited excellent free radical scavenging propertiesThe same fractions inhibited the proliferation of human lung cancer (A459), breast (MCF-7), and brain (U87) cellsChloroform and ethyl acetate fractions arrested the cell cycle at G2/M phase of breast and brain cancerPhytochemical investigations further indicate the presence of several bioactive principles present in them. Abbreviations used: CVLME: Clerodendrum viscosum leaf methanolic extract; CVLH: Clerodendrum viscosum leaf hexane; CVLC: Clerodendrum viscosum leaf chloroform; CVLE: Clerodendrum viscosum leaf ethyl acetate; CVLB: Clerodendrum viscosum leaf butanol; CVLW: Clerodendrum viscosum leaf water; BrdU: Bromodeoxyuridine; WST-1: Water soluble tetrazolium salt.

EGFR promoter exhibits dynamic histone modifications and binding of ASH2L and P300 in human germinal matrix and gliomas

Several signaling pathways important for the proliferation and growth of brain cells are pathologically dysregulated in gliomas, including the epidermal growth factor receptor (EGFR). Expression of EGFR is high in neural progenitors during development and in gliomas but decreases significantly in most adult brain regions. Here we show that EGFR expression is maintained in the astrocyte ribbon of the adult human subventricular zone. The transcriptional regulation of EGFR expression is poorly understood. To investigate the role of epigenetics on EGFR regulation in the contexts of neural development and gliomagenesis, we measured levels of DNA methylation and histone H3 modifications at the EGFR promoter in human brain tissues, glioma specimens, and EGFR-expressing neural cells, acutely isolated from their native niche. While DNA was constitutively hypomethylated in non-neoplastic and glioma samples, regardless of their EGFR-expression status, the activating histone modifications H3K27ac and H3K4me3 were enriched only when EGFR is highly expressed (developing germinal matrix and gliomas). Conversely, repressive H3K27me3 marks predominated in adult white matter where EGFR is repressed. Furthermore, the histone methyltransferase core enzyme ASH2L was bound at EGFR in the germinal matrix and in gliomas where levels of H3K4me3 are high, and the histone acetyltransferase P300 was bound in samples with H3K27ac enrichment. Our studies use human cells and tissues undisturbed by cell-culture artifact, and point to an important, locus-specific role for chromatin remodeling in EGFR expression in human neural development that may be dysregulated during gliomagenesis, unraveling potential novel targets for future drug therapy.

Vesicular stomatitis virus infects primary murine microglia and astocytes and induces replication-dependent inflammatory cytokine production (133.47)

Abstract Vesicular stomatitis virus (VSV) is a rhabdovirus that closely resembles its deadly cousin, rabies virus. Intranasal inoculation of mice with VSV leads to infection of the central nervous system (CNS) and an acute encephalitis that results in a high rate of mortality similar to that observed during human rabies infections. Importantly, this encephalitis is accompanied by the rapid activation and proliferation of resident brain cells including microglia and astrocytes, suggesting a role for such cells in the initiation and/or progression of CNS inflammation. Our recent study showed that these glial cells express RIG-I and MDA5, cytosolic receptors for replicating RNA virus motifs. However, it is presently unclear whether microglia and astrocytes can harbor replicating VSV, or if such replication is required for the inflammatory immune responses of these resident CNS cells. In this study we demonstrate that primary murine microglia and astrocytes are permissive for VSV infection and replication. Importantly, active replication appears to be required for robust inflammatory mediator production as such responses were markedly lower in cells exposed to either inactivated or replication defective viral particles. Interestingly, this effect is not limited to neurotropic Mononegaviruses as the paramyxovirus, Sendai virus, can similarly infect glial cells and elicit inflammatory immune responses. Finally, we have confirmed that in vivo intranasal VSV administration results in viral infection and replication within mouse glial cells in situ. This study suggests that viral replication within resident glial cells could play a key role in the development of lethal CNS inflammation following neurotropic Mononegavirus infection.

ECT May Stimulate Brain Cell Growth: An Animal Study

Electroconvulsive shock (ECS), an animal model of ECT, enhances proliferation of brain cells (Journal Watch Psychiatry Nov 27 2006 and Feb 8 2006). In a recent rat study, researchers examined the effects of ECS on cell growth in the infralimbic prefrontal cortex (ILPFC), which has a major role in processing emotion. In the analogous region in …

Nitric oxide and gamma-aminobutyric acid as regulators of neurogenesis in the brain of adult mammals: Models of seizure activity

New neurons are known to be generated in the brain of adult mammals throughout their entire life in the area of the lateral ventricles and the subgranular zone of the dentate gyrus. The regulatory mechanisms of neurogenesis are complex and poorly understood. Numerous studies performed during the last decade have shown that the intensity of generation of new cells in the germinative regions of the brain is significantly influenced by various environmental factors. Pronounced changes in neurogenesis were also found in the models of various pathologies of the central nervous system (such as neurodegeneration, brain ischemia, and epilepsy). This review is focused on the regulation of neurogenesis in the brain of adult mammals in the course of experimental epilepsy. The involvement of nitric oxide and gamma-aminobutyric acid in the regulation of the proliferation and differentiation of brain cells during seizure activity is discussed.

Constitutive and inflammatory induction of α and β chemokines in human first trimester forebrain astrocytes and neurons

Chemokine effects on leukocyte infiltration into the central nervous system (CNS) are key events in the inflammatory processes of neuroimmunologic and neuroinfectious diseases. Because, chemokines may play important roles in proliferation and differentiation of brain cells and in the initiation and progression of CNS inflammatory disorders, we analyzed constitutive and inflammatory-induced expression of α and β chemokines in human first trimester forebrain cells. Constitutive induction of IL-8, MIP-1α, MIP-1β, MCP-1 and regulated on activation, normal T-cell expressed, and secreted (Rantes) was detected in cryostat sections of embryonic forebrains in an age-dependant manner. Dissociated cell cultures were studied for spontaneous chemokine induction and after stimulation with the trypanosome lymphocyte triggering factor (TLTF), a novel trypanokine secreted by African trypanosomes that triggers a complex of immune responses. LPS and variant surface glycoprotein (VSG) were used as controls. In cultures, unstimulated cells expressed minimal chemokine levels except for Rantes. In response to TLTF and LPS, but not VSG, all chemokines were highly induced at the mRNA and protein levels in a dose- and age-dependent manner. Combined assays (in situ hybridization and immunohistochemistry) revealed that astrocytes and neurons are major sources for chemokines. These results illustrate the ability of resident brain cells to constitutively express chemokine genes, which may suggest an important role for chemokines during brain development. Furthermore, TLTF-induced chemokine expression in astrocytes and neurons indicate the capacity of TLTF to provoke neuroinflammation in the brain, which may have important therapeutic implications for the neurological manifestations of African trypanosomiasis.

Does the taurine transporter gene play a role in 3p-syndrome?

Taurine has been shown to be essential for the development and survival of mammalian cells, especially cells of the cerebellum and retina18. Notably, taurine concentration reaches the mM range in the CNS20. The highest intracellular concentration of taurine is found in neonatal and early postnatal brain, suggesting a developmental role. Sturman's group found that the surviving F1 offspring of taurine-deficient female cats have a large number of neurologic defects, including degeneration of retinal pigmented epithelium and ocular tapetum, delayed cerebellar granule cell division and migration, and abnormal cerebral cortical development. Taurine also appears to optimize the proliferation and differentiation of human fetal cerebral brain cells in culture. Addition of taurine to the medium improves neuron growth, neurite expansion, and neuronal survival2. Taurine is considered a conditionally essential amino acid in man, as the enzymatic activity of cysteine sulfonic acid decarboxylase (CSAD), which catalyzes the formation of taurine from cysteine, is low in humans, and even lower or absent in term and preterm infant liver28. This ontogeny of catalytic enzyme activity is also true in other primates21. In children with short gut syndrome, taurine is an essential component of total parenteral nutrition (TPN) solutions to prevent a defined retinopathy, which is reversed only by taurine administration. Human milk also contains high concentrations of taurine11. We have shown previously that taurine is a semi-conditionally essential amino acid in very low birth weight premature infants, especially those who cannot ingest food and are obliged to be fed by TPN28. Plasma taurine values in preterm infants fall to almost non-detectable values,

Effects of estrogen and neurotransmitters on the primary cultures of tilapia brain from different ages

The effects of estrogen and neurotransmitters on the proliferation of brain cells were investigated in the primary cultures of tilapia brain from different ages. Treatment of brain cells that were cultured on day 1, 3, 5, 7, 10, 30, and 180 posthatching with serotonin (5-HT), resulted in a significant increase of the Brdu +-cell number. By contrast, norepinephrine (NE) resulted in a significant decrease and γ-aminobutyric acid (GABA) had no effect. 17β-Estradiol (E 2) significantly increased the Brdu +-cell number when the brain cells were cultured after 5 days of age, but had no effect when cultured on day 1 or 3 of age. These results indicate that the proliferation of brain cell is enhanced by 5-HT at each stage. This effect is mimicked by E 2 when given after 5 days of age. Conversely, NE has an effect to depress the proliferation of brain cells. Whereas, GABA has no effect.

Effects of altered cyclophilin A expression on growth and differentiation of human and mouse neuronal cells.

1. Cyclophilin A (CyP-A), a soluble cytoplasmic immunophilin, is known for its involvement in T cell differentiation and proliferation. Although CyP-A has a pivotal role in the immune response, it is most highly concentrated in brain, where its functions are largely unknown. 2. We reported previously that a murine neuroblastoma (NB-P2) cell line can partially differentiate into neurons when treated with cyclosporin A (CyS-A), implicating a role for CyP-A in neuronal differentiation (Hovland et al. [1999]. Neurochem. Int. 3:229-235). 3. The role of CyP-A in regulating neuronal growth and differentiation is not well defined. To investigate this, we first tested the utility of retroviral-mediated gene transfer and expression in human embryonic brain (HEB) and NB-P2 cells. Second, we examined the effects of retroviral-mediated overexpression or antisense-mediated reduction of CyP-A in HEB and NB-P2 cells. 4. Our data show that retroviral vectors are efficient for stable gene transfer and expression in both cell lines. Moreover, neither overexpression nor reduction of CyP-A expression in NB-P2 cells altered the growth rate or induced differentiation. More importantly, the up-or down-regulation of CyP-A expression did not affect the magnitude of cAMP-induced NB-P2 differentiation. However, overexpression of CyP-A increased the growth rate of HEB cells. 5. In summary, the utility of retroviral vectors for stable gene expression in human embryonic brain and murine neuroblastoma cells was shown. Furthermore, a novel role for CyP-A in augmenting the proliferation of human embryonic brain cells was demonstrated in vitro.