glycogen and Brain-Neoplasms

Most meningiomas are benign and correspond to World Health Organization grade I, whereas chordoid meningioma is a rare subtype, which is regarded as grade II. This report presents 1 case of intraparenchymal chordoid meningioma. The intraparenchymal chordoid meningioma consisted predominantly of tissue that was histologically similar to chordoma, featuring cords or trabeculae of eosinophilic and often vacuolated cells in an abundant mucoid matrix background. Tumor cells were diffusing positive for epithelial membrane antigen and vimentin, and focusing positively for progesterone receptor, but showed lack of immunoreactivity with cytokeratin, S-100, and glial fibrillary acidic protein. Follow-up at 8 months showed no recurrence. Reports about chordoid meningioma are not uncommon, but reports on intraparenchymal lesion are rare. Besides, the result of magnetic resonance imaging in the present case suggested that intraparenchymal chordoid meningioma was a metastasis tumor. This report reminds of the importance of differential diagnosis in the case of intraparenchymal lesion.

Topics: Aged; Biomarkers, Tumor; Brain Neoplasms; Choroid Plexus; Diagnosis, Differential; Female; Glycogen; Humans; Magnetic Resonance Imaging; Meningeal Neoplasms; Meningioma; Mucin-1; Parietal Lobe; S100 Proteins; Treatment Outcome

Topics: Adenosine Diphosphate; Adenosine Monophosphate; Adenosine Triphosphate; Aerobiosis; Anaerobiosis; Animals; Brain; Brain Neoplasms; Creatine; Ependymoma; Glioma; Glucose; Glycogen; Glycolysis; Humans; Hypoxia; Ischemia; Lactates; Meningioma; Mice; Neoplasms, Experimental; Neurilemmoma; Oxygen Consumption; Periodic Acid; Phosphofructokinase-1; Phosphorus; RNA; Vestibulocochlear Nerve

Hypoxia is a common feature of solid tumours and is associated with poor prognosis, resistance to radio- and chemotherapy, and tumour aggressiveness. For predictive purposes as well as for improved therapeutic intervention, it is increasingly needed to have direct and specific diagnostic tools in order to measure the extent of, and changes in, tumour hypoxia. In this article, we have investigated the potential of Fourier Transform Infrared (FTIR) microspectroscopy, at cellular and subcellular resolution, for detecting hypoxia-induced metabolic changes in brain tumour (glioblastoma) cell lines and in short term primary cultures derived from patient samples. The most prominent and common changes observed were the increase in glycogen (specifically in the U87MG cell line) and lipids (all cell lines studied). Additionally, each cell line presented specific individual metabolic fingerprints. The metabolic changes did not evolve markedly with time (from 1 to 5 days hypoxic incubation), and yet were harder to detect under chronic hypoxic conditions, which is consistent with cellular adaptation occurring upon long term changes in the microenvironment. The metabolic signature was similar regardless of the severity of the hypoxic insult and was replicated by the hypoxia mimetic drug dimethyloxalylglycine (DMOG). To investigate any specific changes at subcellular levels and to improve the sensitivity of the detection method, spectra were recorded separately in the cytoplasm and in the nucleus of D566 glioblastoma cells, thanks to the use of a synchrotron source. We show that this method provides improved detection in both cell compartments. Whilst there was a high spectral variability between cell lines, we show that FTIR microspectroscopy allowed the detection of the common metabolic changes triggered by hypoxia regardless of cell type, providing a potential new approach for the detection of hypoxic tumours.

Topics: Biomarkers, Tumor; Brain Neoplasms; Cell Hypoxia; Cell Nucleus; Cytoplasm; Fatty Acids, Unsaturated; Glioblastoma; Glycogen; HeLa Cells; Humans; Hypoxia-Inducible Factor 1, alpha Subunit; Microspectrophotometry; Phospholipids; Spectroscopy, Fourier Transform Infrared

Given the involvement of telomerase activation and dysregulated metabolism in glioma progression, the connection between these two critical players was investigated. Pharmacological inhibition of human Telomerase reverse transcriptase (hTERT) by Costunolide induced glioma cell apoptosis in a reactive oxygen species (ROS)-dependent manner. Costunolide induced an ROS-dependent increase in p53 abrogated telomerase activity. Costunolide decreased Nrf2 level; and ectopic Nrf2 expression decreased Costunolide-induced ROS generation. While TERT knock-down abrogated Nrf2 levels, overexpression of Nrf2 increased TERT expression. Inhibition of hTERT either by Costunolide, or by siRNA or dominant-negative hTERT (DN-hTERT) abrogated (i) expression of Glucose-6-phosphate dehydrogenase (G6PD) and Transketolase (TKT) - two major nodes in the pentose phosphate (PPP) pathway; and (ii) phosphorylation of glycogen synthase (GS). hTERT knock-down decreased TKT activity and increased glycogen accumulation. Interestingly, siRNA-mediated knock-down of TKT elevated glycogen accumulation. Coherent with the in vitro findings, Costunolide reduced tumor burden in heterotypic xenograft glioma mouse model. Costunolide-treated tumors exhibited diminished TKT activity, heightened glycogen accumulation, and increased senescence. Importantly, glioblastoma multiforme (GBM) patient tumors bearing TERT promoter mutations (C228T and C250T) known to be associated with increased telomerase activity; exhibited elevated Nrf2 and TKT expression and decreased glycogen accumulation. Taken together, our findings highlight the previously unknown (i) role of telomerase in the regulation of PPP and glycogen accumulation and (ii) the involvement of Nrf2-TERT loop in maintaining oxidative defense responses in glioma cells.

Topics: Animals; Antineoplastic Agents, Phytogenic; Brain Neoplasms; Cell Line, Tumor; Cellular Senescence; Gene Expression Regulation, Neoplastic; Glioblastoma; Glucosephosphate Dehydrogenase; Glycogen; Glycogen Synthase; Humans; Mice; Mice, Nude; NF-E2-Related Factor 2; Pentose Phosphate Pathway; Phosphorylation; Reactive Oxygen Species; RNA, Small Interfering; Sesquiterpenes; Signal Transduction; Telomerase; Transketolase; Tumor Suppressor Protein p53; Xenograft Model Antitumor Assays

Breast cancer brain metastasis is resistant to therapy and a particularly poor prognostic feature in patient survival. Altered metabolism is a common feature of cancer cells, but little is known as to what metabolic changes benefit breast cancer brain metastases. We found that brain metastatic breast cancer cells evolved the ability to survive and proliferate independent of glucose due to enhanced gluconeogenesis and oxidations of glutamine and branched chain amino acids, which together sustain the nonoxidative pentose pathway for purine synthesis. Silencing expression of fructose-1,6-bisphosphatases (FBP) in brain metastatic cells reduced their viability and improved the survival of metastasis-bearing immunocompetent hosts. Clinically, we showed that brain metastases from human breast cancer patients expressed higher levels of FBP and glycogen than the corresponding primary tumors. Together, our findings identify a critical metabolic condition required to sustain brain metastasis and suggest that targeting gluconeogenesis may help eradicate this deadly feature in advanced breast cancer patients.

Topics: Amino Acids; Animals; Brain; Brain Neoplasms; Breast Neoplasms; Cell Line, Tumor; Cell Proliferation; Cell Survival; Female; Fructose-Bisphosphatase; Gene Silencing; Glucose; Glycogen; Glycolysis; Humans; Mass Spectrometry; Mice; Mice, Inbred BALB C; Oxygen; RNA, Small Interfering

Glioblastoma (GBM) remains the most aggressive primary brain cancer in adults. Similar to other cancers, GBM cells undergo metabolic reprogramming to promote proliferation and survival. Glycolytic inhibition is widely used to target such reprogramming. However, the stability of glycolytic inhibition in GBM remains unclear especially in a hypoxic tumor microenvironment. In this study, it was determined that glucose-6-phosphatase (G6PC/G6Pase) expression is elevated in GBM when compared with normal brain. Human-derived brain tumor-initiating cells (BTIC) use this enzyme to counteract glycolytic inhibition induced by 2-deoxy-d-glucose (2DG) and sustain malignant progression. Downregulation of G6PC renders the majority of these cells unable to survive glycolytic inhibition, and promotes glycogen accumulation through the activation of glycogen synthase (GYS1) and inhibition of glycogen phosphorylase (PYGL). Moreover, BTICs that survive G6PC knockdown are less aggressive (reduced migration, invasion, proliferation, and increased astrocytic differentiation). Collectively, these findings establish G6PC as a key enzyme with promalignant functional consequences that has not been previously reported in GBM and identify it as a potential therapeutic target.. This study is the first to demonstrate a functional relationship between the critical gluconeogenic and glycogenolytic enzyme G6PC with the metabolic adaptations during GBM invasion.

Topics: Animals; Astrocytes; Brain Neoplasms; Cell Differentiation; Cell Line, Tumor; Cell Movement; Cell Survival; Gene Knockdown Techniques; Glioblastoma; Glucose-6-Phosphatase; Glycogen; Glycogen Phosphorylase; Glycogen Synthase; Glycolysis; Humans; Male; Mice, Nude; Neoplasm Invasiveness; Neoplastic Stem Cells; Phenotype; RNA, Small Interfering; Up-Regulation

Glioblastoma Multiforme (GBM) is an aggressive form of brain Tumor that has few cures. In this study, we analyze the anti-proliferative effects of a new molecule JQ1 against GBMs induced in Wistar Rats. JQ1 is essentially a Myc inhibitor. c-Myc is also known for altering the biochemistry of a tumor cell. Therefore, the study is intended to analyze certain other oncogenes associated with c-Myc and also the change in cellular biochemistry upon c-Myc inhibition. The quantitative analysis of gene expression gave a co-expressive pattern for all the three genes involved namely; c-Myc, Bcl-2, and Akt. The cellular biochemistry analysis by transmission electron microscopy revealed high glycogen and lipid aggregation in Myc inhibited cells and excessive autophagy. The study demonstrates the role of c-Myc as a central metabolic regulator and Bcl-2 and Akt assisting in extending c-Myc half-life as well as in regulation of autophagy, so as to regulate cell survival on the whole. The study also demonstrates that transient treatment by JQ1 leads to aggressive development of tumor and therefore, accelerating death, emphasizing the importance of dosage fixation, and duration for clinical use in future.

Topics: Animals; Azepines; Brain Neoplasms; Cell Line, Tumor; Down-Regulation; Gene Expression Regulation, Neoplastic; Gene Silencing; Glioblastoma; Glycogen; Immunohistochemistry; Lipid Metabolism; Male; Proto-Oncogene Proteins c-myc; Rats, Wistar; Survival Analysis; Triazoles

DU145 human prostate carcinoma cells are typically poorly differentiated and contain only scantily distributed organelles. However, among numerous tumor cells randomly examined by electron microscopy out of in vitro cultivation, a peculiar, rare oncocyte-like cell type has been observed whose nucleus appears to be of small dimension and with a cytoplasm almost entirely filled with often distorted mitochondria. A few small, dispersed lysosomal bodies, small cisterns of the endoplasmic reticulum and a few glycogen patches can be found among highly osmiophilic contrasted, cytosolic spaces filled by innumerable ribonucleoproteins. The excessive population of mitochondria may have arisen from a more populated tumor cell type wherein the altered mitochondria are found to appear burgeoning into a spherical-like size progeny crowding the tumor cells. Literature cited between 1950 and the present suggests that this rare, oncocytic, benign prostatic tumor cell type is likely appear epigenetically, stemming from an original secretory cell, which is confirmed by the origin of the cell line originally maintained as cell line out of a brain metastatic, adenocarcinoma niche.

Topics: Adenocarcinoma; Brain Neoplasms; Cell Line, Tumor; Cell Nucleus Shape; Cell Size; Glycogen; Humans; Male; Microscopy, Electron, Transmission; Mitochondria; Oxyphil Cells; Prostatic Neoplasms; Ribonucleoproteins

Central nervous system space-occupying lesions with clear-cell features encompass a nosologically heterogeneous array, ranging from reactive histiocytic proliferations to neuroepithelial or meningothelial neoplasms of various grades and to metastases. In the face of such differential diagnostic breadth, recognizing cytoplasmic lucency as part of the morphological spectrum of some low grade gliomas will directly have an impact on patient care. We describe a prevailing clear-cell change in an epileptogenic left temporal pleomorphic xanthoastrocytoma surgically resected from a 36-year-old man. Mostly subarachnoid and focally calcified, the tumor was composed of fascicles of moderately atypical spindle cells with optically lucent cytoplasm that tended to intermingle with a desmoplastic mesh of reticulin fibers. Immunohistochemically, coexpression of S100 protein, vimentin, GFAP, and CD34 was noted. Conversely, neither punctate staining for EMA nor positivity for CD68 was seen. Mitotic activity was absent, and the MIB1 labeling index was 2-3% on average. Diastase-sensitive PAS-positive granula indicated clear-cell change to proceed from glycogen storage. Electron microscopy showed tumor cell cytoplasm to be largely obliterated by non-lysosomal-bound pools of glycogen, while hardly any fat vacuole was encountered. Neither ependymal-derived organelles nor annular lamellae suggesting oligodendroglial differentiation were detected. The latter differential diagnosis was further invalidated by lack of codeletion of chromosomal regions 1p36 and 19q13 on molecular genetic testing. By significantly interfering with pattern recognition as an implicit approach in histopathology, clear-cell change in pleomorphic xanthoastrocytoma is likely to suspend its status as a "classic", and to prompt more deductive differential diagnostic strategies to exclude look-alikes, especially clear-cell ependymoma and oligodendroglioma.

Topics: Adult; Antigens, CD34; Astrocytoma; Biomarkers, Tumor; Brain Neoplasms; Diagnosis, Differential; Ependymoma; Glial Fibrillary Acidic Protein; Glycogen; Humans; Immunohistochemistry; Magnetic Resonance Imaging; Male; Microscopy, Electron; Oligodendroglioma; S100 Proteins; Seizures; Vimentin

Abnormal regulation of brain glycogen metabolism is believed to underlie insulin-induced hypoglycaemia, which may be serious or fatal in diabetic patients on insulin therapy. A key regulator of glycogen levels is glycogen targeted protein phosphatase 1 (PP1), which dephosphorylates and activates glycogen synthase (GS) leading to an increase in glycogen synthesis. In this study, we show that the gene PPP1R3F expresses a glycogen-binding protein (R3F) of 82.8 kDa, present at the high levels in rodent brain. R3F binds to PP1 through a classical 'RVxF' binding motif and substitution of Phe39 for Ala in this motif abrogates PP1 binding. A hydrophobic domain at the carboxy-terminus of R3F has similarities to the putative membrane binding domain near the carboxy-terminus of striated muscle glycogen targeting subunit G(M)/R(GL), and R3F is shown to bind not only to glycogen but also to membranes. GS interacts with PP1-R3F and is hyperphosphorylated at glycogen synthase kinase-3 sites (Ser640 and Ser644) when bound to R3F(Phe39Ala). Deprivation of glucose or stimulation with adenosine or noradrenaline leads to an increased phosphorylation of PP1-R3F bound GS at Ser640 and Ser644 curtailing glycogen synthesis and facilitating glycogen degradation to provide glucose in astrocytoma cells. Adenosine stimulation also modulates phosphorylation of R3F at Ser14/Ser18.

Topics: Adenosine; Adrenergic alpha-Agonists; Amino Acid Sequence; Animals; Astrocytoma; Brain; Brain Neoplasms; Carrier Proteins; Cell Line, Tumor; DNA; Extracellular Space; Glucose; Glycogen; Glycogen Synthase; Humans; Immunohistochemistry; Male; Mice; Mice, Inbred C57BL; Molecular Sequence Data; Mutagenesis; Norepinephrine; Phosphoprotein Phosphatases; Phosphorylation; Protein Phosphatase 1; RNA; Signal Transduction; Subcellular Fractions

The anaerobic mobilization of astrocyte glycogen in anoxic-ischemic regions of the oedematous human cerebral cortex is analysed.. Seventeen cortical biopsies of patients with brain trauma, brain tumours and congenital malformations were examined by conventional transmission electron microscopy.. Glycogen-rich and glycogen-depleted, clear or dense astrocytes cell bodies were observed in anoxic ischaemic regions of different brain cortical areas in perineuronal, neuropilar and perivascular localization. Glycogen-rich astrocytes showed clear or moderately dense cytoplasm and accumulation of both beta-type or monogranular glycogen granules and alpha-type or multigranular glycogen particles. Focal regions of translucent cytoplasm were observed in areas of glycogen degradation. Glycogen-depleted astrocytes exhibited a clear cytoplasm and scarce amount or absence of beta-type glycogen granules. Coexisting glycogen-rich and glycogen-depleted neuropilar astrocytic processes were observed in the vicinity of degenerated myelinated axons and degenerated axodendritic contacts. Glycogen-rich and glycogen-depleted perivascular astrocytic processes were also found surrounding injured and collapsed cerebral capillaries.. The findings suggest astrocytic glycogen mobilization during anoxic and ischaemic conditions, revealing the important contribution of astrocytes on neuronal survival under conditions of energy substrate limitations.

Topics: Adolescent; Adult; Astrocytes; Biopsy; Brain; Brain Edema; Brain Injuries; Brain Neoplasms; Cerebral Cortex; Child; Female; Glycogen; Humans; Infant; Infant, Newborn; Male; Microscopy, Electron; Middle Aged

In this study we report that substance P stimulated [3H]glycogen breakdown and elevation of intracellular Ca2+ concentration in the human astrocytoma cell line UC-11MG. Both effects were dose dependent, and completely blocked by CP-96,345 suggesting the involvement of an NK1 receptor. Our previous studies indicated that norepinephrine and histamine stimulate glycogenolysis via cAMP and Ca2+ respectively. Combined stimulation with substance P and norepinephrine or histamine resulted in additive effects suggesting that there is no interaction between these neurotransmitters in regulating glycogenolysis in these cells. These results confirm that UC-11MG cells are a useful model system to investigate the functional role of neurotransmitter receptors in astroglial cells.

Topics: Astrocytoma; Biphenyl Compounds; Brain Neoplasms; Dose-Response Relationship, Drug; Drug Combinations; Glycogen; Histamine; Humans; Norepinephrine; Receptors, Neurokinin-1; Substance P; Tumor Cells, Cultured

Biopsies from 15 human gliomas, five meningiomas, four Schwannomas, one medulloblastoma, and four normal brain areas were analyzed for 12 enzymes of energy metabolism and 12 related metabolites and cofactors. Samples, 0.01-0.25 microgram dry weight, were dissected from freeze-dried microtome sections to permit all the assays on a given specimen to be made, as far as possible, on nonnecrotic pure tumor tissue from the same region. Great diversity was found with regard to both enzyme activities and metabolite levels among individual tumors, but the following generalities can be made. Activities of hexokinase, phosphorylase, phosphofructokinase, glycerophosphate dehydrogenase, citrate synthase, and malate dehydrogenase levels were usually lower than in brain; glycogen synthase and glucose-6-phosphate dehydrogenase were usually higher; and the averages for pyruvate kinase, lactate dehydrogenase, 6-phosphogluconate dehydrogenase, and beta-hydroxyacyl coenzyme A dehydrogenase were not greatly different from brain. Levels of eight of the 12 enzymes were distinctly lower among the Schwannomas than in the other two groups. Average levels of glucose-6-phosphate, lactate, pyruvate, and uridine diphosphoglucose were more than twice those of brain; 6-phosphogluconate and citrate were about 70% higher than in brain; glucose, glycogen, glycerol-1-phosphate, and malate averages ranged from 104% to 127% of brain; and fructose-1,6-bisphosphate and glucose-1,6-bisphosphate levels were on the average 50% and 70% those of brain, respectively.

Topics: Adolescent; Adult; Aged; Brain; Brain Neoplasms; Child; Child, Preschool; Energy Metabolism; Female; Glioma; Glycogen; Glycolysis; Humans; Male; Medulloblastoma; Meningioma; Middle Aged; Mitochondria; Neurilemmoma; Oxidative Phosphorylation

Topics: Adenosine Diphosphate; Adenosine Monophosphate; Adenosine Triphosphate; Adolescent; Adult; Aged; Brain Neoplasms; Child; Creatine Kinase; Energy Metabolism; Female; Glioma; Glycogen; Humans; Lipids; Male; Meningioma; Middle Aged; Neurilemmoma; Phosphates; Phosphocreatine; Uridine Triphosphate

The commonest pineal gland tumor, the germinoma, is more apparently related to germ cells than to pineal cells. Although ultrastructural studies of this tumor have confirmed this similarity, comparable characterization of a pineocytoma has not been reported, due to its rarity. Here we define the electron microscopic features of a rapidly growing human pineocytoma and compare the tumor cells in the present study with normal mammalian pinealocytes, as well as with cells described in the literature of pineal body pathology. Two cell types populate the tumor: one resembles the neuron, while the second, less frequently encountered, is often indistinguishable from the fibrous astrocyte. Synaptic complexes and dense-cored vesicles were not conspicuous fine-structural elements. Whereas emphatic morphological differences exist between the germinoma and pineocytoma, the similarities in ultrastructure between the pineocytoma cells and adult mammalian pinealocytes are even more striking.

Topics: Adult; Animals; Basement Membrane; Biopsy; Brain Neoplasms; Cell Nucleus; Endoplasmic Reticulum; Female; Glycogen; Golgi Apparatus; Haplorhini; Humans; Microscopy, Electron; Mitochondria; Papio; Pineal Gland; Pinealoma; Ribosomes

Electron microscopy was performed on two CNS lymphomas, one primary and the second a skull metastasis from a brain primary lymphoma. The former revealed a tumor perivascularly arranged, which was composed of rounded cells having no specialized organellae. Biopsies from the primary and metastasis of the second case revealed a predominance of rounded cells with scanty cytoplasm, another population of cells with phagocytic activity and a third group with elongated ctyoplasmic processes which stain positively for microglia. By electron microscopy some of these processes resembled neurites or oligondendroglia, while others suggested an astrocytic appearance.

Topics: Adult; Blood Vessels; Brain Neoplasms; Cell Differentiation; Glycogen; Hodgkin Disease; Humans; Male; Microtubules; Middle Aged; Neoplasm Metastasis; Neuroglia; Organoids; Phagocytes; Skull Neoplasms

Topics: Animals; Brain; Brain Edema; Brain Neoplasms; Central Nervous System; Dogs; Glycogen; Guinea Pigs; Haplorhini; Hibernation; Humans; Hypoglycemia; Hypoxia; Ischemia; Mice; Microscopy, Electron; Neuroglia; Neurons; Physical Exertion; Rabbits; Radiation Effects; Rats; Seizures; Shock; Starvation

Topics: Adult; Brain Neoplasms; Carcinoma, Adenoid Cystic; Female; Glycogen; Histocytochemistry; Humans; Inclusion Bodies; Microscopy, Electron; Trigeminal Nerve

Topics: Animals; Axons; Biopsy; Brain Neoplasms; Cerebral Cortex; Cytoplasm; Dendrites; Glycogen; Histocytochemistry; Humans; Meningioma; Microscopy, Electron; Mitochondria; Neuroglia; Rabbits; Synapses; Synaptic Membranes; Synaptic Vesicles

Topics: Brain Neoplasms; Bromodeoxyuridine; Dactinomycin; DNA; Fluorouracil; Glycogen; Humans; Neoplasms; Oxygen; Radiation-Sensitizing Agents; RNA; Vitamin K

Topics: Astrocytoma; Brain Neoplasms; Caudate Nucleus; Cell Nucleus; Child; Endoplasmic Reticulum; Female; Glycogen; Golgi Apparatus; Humans; Inclusion Bodies; Microscopy, Electron; Ribosomes; Tuberous Sclerosis

Topics: Acid Phosphatase; Adenosine Triphosphate; Adult; Alkaline Phosphatase; Brain; Brain Neoplasms; Esterases; Female; Fructose-Bisphosphate Aldolase; Glucosephosphate Dehydrogenase; Glucuronidase; Glutamates; Glycerophosphates; Glycogen; Histocytochemistry; Humans; Lactates; Lipid Metabolism; Malates; Neoplasm Metastasis; Neuroectodermal Tumors, Primitive, Peripheral; Succinate Dehydrogenase

Topics: Adenosine Triphosphate; Animals; Brain Neoplasms; Disease Models, Animal; Fluorometry; Freezing; Glioblastoma; Glucose; Glycogen; Histocytochemistry; Lactates; Mice; NAD; NADP; Neoplasm Transplantation; Neoplasms, Experimental; Neuroglia; Oxygen Consumption; Pentoses; Phosphates; Phosphocreatine; Transplantation, Homologous

Topics: Animals; Brain Neoplasms; Cerebral Cortex; Glioblastoma; Glycogen; Humans; Meningioma; Microscopy, Electron; Neuroglia; Neurons; Rabbits

Topics: Basement Membrane; Blood-Brain Barrier; Brain Neoplasms; Capillaries; Cell Membrane Permeability; Collagen; Cytoplasm; Densitometry; Extracellular Space; Glycogen; Humans; Hyperplasia; Mitochondria; Neoplasm Proteins; Neuroglia

Topics: Animals; Brain; Brain Damage, Chronic; Brain Neoplasms; Carbohydrate Metabolism; Glucosephosphate Dehydrogenase; Glycogen; Hippocampus; Histocytochemistry; Humans; Hypothalamus; Hypoxia; Ischemia; Neurons; Nucleic Acids; Rats; Succinate Dehydrogenase; Transferases

Topics: Astrocytoma; Brain Neoplasms; Ependymoma; Ganglioneuroma; Glioblastoma; Glycogen; Histocytochemistry; Humans; Medulloblastoma; Neurilemmoma; Oligodendroglioma; Papilloma; Tuberous Sclerosis

Topics: Adult; Brain; Brain Neoplasms; Capillaries; Cell Nucleus; Cerebellar Neoplasms; Cerebellum; Cytoplasm; Endoplasmic Reticulum; Female; Glycogen; Hemangiosarcoma; Histocytochemistry; Humans; Male; Mast Cells; Medulla Oblongata; Microscopy, Electron; Middle Aged; Organoids

Topics: Adenine Nucleotides; Adenosine Triphosphate; Brain; Brain Neoplasms; Fluorometry; Frontal Lobe; Glioma; Glucose; Glycogen; Glycolysis; Hexoses; Humans; In Vitro Techniques; Ischemia; Lactates; Phosphocreatine; Spectrophotometry; Tissue Extracts

Topics: Adenosine Triphosphate; Adult; Aged; Animals; Astrocytoma; Brain; Brain Neoplasms; Cerebral Cortex; Craniopharyngioma; Fluorometry; Frontal Lobe; Glucose; Glycogen; Glycolysis; Humans; In Vitro Techniques; Ischemic Attack, Transient; Mice; Middle Aged; Oxygen Consumption; Parietal Lobe; Phosphocreatine; Spectrophotometry

Topics: Adenosine Triphosphate; Animals; Brain Neoplasms; Glucose; Glycogen; Ischemia; Lactates; Mice; Phosphorus

Topics: Adenosine Triphosphate; Animals; Brain Neoplasms; Creatine Kinase; Glioblastoma; Glucose; Glucosephosphate Dehydrogenase; Glucosyltransferases; Glutamate Dehydrogenase; Glycogen; Glycolysis; Hexokinase; Histocytochemistry; Ischemia; Lactates; Mice; NAD; NADP; Neoplasms, Experimental; Phosphates; Phosphocreatine; Phosphoglucomutase; Phosphogluconate Dehydrogenase

Topics: Adenosine Triphosphate; Brain Neoplasms; Coenzymes; Glucose; Glycogen; Glycolysis; Hexosephosphates; Ischemia; Lactates; Phosphates; Phosphocreatine; Research

Topics: Brain Neoplasms; Carbohydrate Metabolism; Glycogen; Glycosides; Humans; Uracil Nucleotides

Topics: Astrocytoma; Brain Neoplasms; Carbohydrate Metabolism; Cerebellar Neoplasms; Ependymoma; Glioma; Glycogen; Glycosaminoglycans; Histocytochemistry; Humans; Lipid Metabolism; Lipids; Medulloblastoma; Meningeal Neoplasms; Meningioma