OBJECTIVE: To explore the distribution of inflammatory cells and positive expression of P-se- lectin glycoprotein ligand-1 (PSGL-1) in infant brainstem tissue from hand-foot-mouth disease related fatal brainstem encephalitis. METHODS: Twenty brainstem samples from infants suffered from brainstem en- cephalitis were collected as the experimental group. Ten brainstem samples from infants died of non- brain diseases and injuries were collected as the control group. The distribution of inflammatory cells and the expression of PSGL-1 in the two groups were examined by immunohistochemical method. The characteristics of the positive cells were observed. RESULTS: In brainstem tissue of the experimental group, there were sleeve infiltrations of inflammatory cells around the vessels and in the glial nodule. Microglia was the most and following was neutrophils around the vessels and in the glial nodule. There was a significant statistical difference among microglias, neutrophils and lymphocytes (P < 0.05). There was no sleeve infiltration in the control group. PSGL-1 protein was expressed widely in inflammatory cells in the experimental group, especially in the inflammatory cells around the vessels and in the glial nodule. But PSGL-1 positive staining could be observed significantly less in the control group comparing with the experimental group (P < 0.05). CONCLUSION Microglia is the main type of inflammatory cells involved in the progress of the fatal disease. Moreover, PSGL-1 could participate in the pathogenesis of hand-foot-mouth disease related fatal brainstem encephalitis.
Brain Stem/pathology* ; Encephalitis/pathology* ; Hand, Foot and Mouth Disease/pathology* ; Humans ; Infant ; Membrane Glycoproteins/metabolism* ; Microglia/pathology* ; Neutrophils/pathology*

Glioma is the most common and lethal intrinsic primary tumor of the brain. Its controversial origins may contribute to its heterogeneity, creating challenges and difficulties in the development of therapies. Among the components constituting tumors, glioma stem cells are highly plastic subpopulations that are thought to be the site of tumor initiation. Neural stem cells/progenitor cells and oligodendrocyte progenitor cells are possible lineage groups populating the bulk of the tumor, in which gene mutations related to cell-cycle or metabolic enzymes dramatically affect this transformation. Novel approaches have revealed the tumor-promoting properties of distinct tumor cell states, glial, neural, and immune cell populations in the tumor microenvironment. Communication between tumor cells and other normal cells manipulate tumor progression and influence sensitivity to therapy. Here, we discuss the heterogeneity and relevant functions of tumor cell state, microglia, monocyte-derived macrophages, and neurons in glioma, highlighting their bilateral effects on tumors. Finally, we describe potential therapeutic approaches and targets beyond standard treatments.
Humans ; Glioma/metabolism* ; Neuroglia/metabolism* ; Carcinogenesis/pathology* ; Neural Stem Cells/metabolism* ; Microglia/metabolism* ; Brain Neoplasms/metabolism* ; Tumor Microenvironment

Detailed characterizations of genomic alterations have not identified subtype-specific vulnerabilities in adult gliomas. Mapping gliomas into developmental programs may uncover new vulnerabilities that are not strictly related to genomic alterations. After identifying conserved gene modules co-expressed with EGFR or PDGFRA (EM or PM), we recently proposed an EM/PM classification scheme for adult gliomas in a histological subtype- and grade-independent manner. By using cohorts of bulk samples, paired primary and recurrent samples, multi-region samples from the same glioma, single-cell RNA-seq samples, and clinical samples, we here demonstrate the temporal and spatial stability of the EM and PM subtypes. The EM and PM subtypes, which progress in a subtype-specific mode, are robustly maintained in paired longitudinal samples. Elevated activities of cell proliferation, genomic instability and microenvironment, rather than subtype switching, mark recurrent gliomas. Within individual gliomas, the EM/PM subtype was preserved across regions and single cells. Malignant cells in the EM and PM gliomas were correlated to neural stem cell and oligodendrocyte progenitor cell compartment, respectively. Thus, while genetic makeup may change during progression and/or within different tumor areas, adult gliomas evolve within a neurodevelopmental framework of the EM and PM molecular subtypes. The dysregulated developmental pathways embedded in these molecular subtypes may contain subtype-specific vulnerabilities.
Humans ; Brain Neoplasms/pathology* ; Neoplasm Recurrence, Local/metabolism* ; Glioma/pathology* ; Neural Stem Cells/pathology* ; Oligodendrocyte Precursor Cells/pathology* ; Tumor Microenvironment

In healthy individuals, energy intake is in balance with energy expenditure, which helps to maintain a normal body weight. The brain's inability to control energy homeostasis underlies the pathology of hyperphagia and obesity. The brain detects body energy excess and deficit by sensing the levels of circulating metabolic hormones and nutrients and by receiving metabolic information from the periphery via the autonomic nervous system. A specialized neuronal network coordinates energy intake behavior and the metabolic processes affecting energy expenditure. Here, we briefly review neuronal mechanisms by which our body maintains energy balance.
Autonomic Nervous System ; Brain Stem ; Brain* ; Energy Intake ; Energy Metabolism* ; Homeostasis ; Hyperphagia ; Hypothalamus ; Ideal Body Weight ; Metabolism ; Neurons ; Obesity ; Pathology

Animals ; Brain Neoplasms ; etiology ; metabolism ; pathology ; Glioma ; etiology ; metabolism ; pathology ; Humans ; Neoplastic Stem Cells ; pathology ; physiology ; Signal Transduction ; Stem Cell Research

OBJECTIVE: To observe e-jun protein expression after rat brain concussion and explore the forensic pathologic markers following brain concussion. METHODS: Fifty-five rats were randomly divided into brain concussion group and control group. The expression of c-jun protein was observed by immunohistochemistry. RESULTS: There were weak positive expression of c-jun protein in control group. In brain concussion group, however, some neutrons showed positive expression of c-jun protein at 15 min after brain concussion, and reach to the peak at 3 h after brain concussion. CONCLUSION The research results suggest that detection of c-jun protein could be a marker to determine brain concussion and estimate injury time after brain concussion.
Animals ; Brain/pathology* ; Brain Concussion/pathology* ; Brain Stem/metabolism* ; Cerebral Cortex/metabolism* ; Disease Models, Animal ; Female ; Forensic Pathology ; Immunohistochemistry ; Male ; Neurons/metabolism* ; Proto-Oncogene Proteins c-jun/metabolism* ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Time Factors

OBJECTIVE: To evaluate the expression of Bcl-2 protein after brain concussion. METHODS: Expression levels of Bel-2 protein in cortex, pontine and cerebellum of rats were investigated using immunohistochemistry. RESULTS: There was no expression of Bcl-2 protein in control group seen. The expression of Bcl-2 protein in brain concussion groups was detected at l hour, and the expression level reached its peak 4 days after the concussion and then declined gradually. CONCLUSION Our findings suggest that the detection of Bel-2 protein could be an indicator for diagnosis of brain concussion and for estimation of the post injury time interval.
Animals ; Brain/pathology* ; Brain Concussion/metabolism* ; Brain Stem/pathology* ; Cerebral Cortex/pathology* ; Contusions/pathology* ; Disease Models, Animal ; Female ; Immunohistochemistry ; Male ; Neurons/pathology* ; Proto-Oncogene Proteins c-bcl-2/metabolism* ; Rats ; Rats, Sprague-Dawley ; Time Factors

Neurocytoma, a rare brain tumor, is characterized by a mass located mainly in cerebral ventricles. It is prone to be misdiagnosed as oligodendroglioma or ependymoma due to their similar histopathological features in clinical practice. This study aimed to examine the clinicopathological features and differential diagnosis of central and extraventricular neurocytoma. The clinical and histopathological data of 17 patients (male: female=7:10; age: 4-41 years; mean age: 27.4 years) with central or extraventricular neurocytoma were retrospectively analyzed. These patients showed typical radiological, histopathological and immunohistochemical features of neurocytoma. The tumor tissue was found to be composed of small uniform cells with round nuclei and clear cytoplasm resembling that of oligodendroglioma and ependymoma. Immunohistochemistry revealed the tumor tissues were positive for neuronal markers such as synaptophysin (SYN) and neuronal nuclear antigen (NeuN). It was concluded histopathological features of neurocytoma overlaps with some tumors in the central neural system. Immunopositivity for SYN and NeuN can help differentially diagnose neurocytoma.
Adolescent ; Adult ; Antigens, Nuclear ; metabolism ; Biomarkers, Tumor ; metabolism ; Brain Neoplasms ; pathology ; Brain Stem ; pathology ; Cerebral Ventricle Neoplasms ; pathology ; Child ; Child, Preschool ; Female ; Humans ; Male ; Nerve Tissue Proteins ; metabolism ; Neurocytoma ; pathology ; Retrospective Studies ; Synaptophysin ; metabolism ; Young Adult

OBJECTIVE: To study the changes of expression of c-myc protein on rats' brains after brain concussion. METHODS: sixty rats were randomly divided into brain concussion groups and control group. The expression of c-myc protein was microscopically observed by immunohistochemical method. RESULTS: No expression of c-myc protein in control group were observed. However, positive expression of c-myc protein in some neurons was seen at 20 min after brain concussion, and reach to the peak at 8h after brain concussion and then decreased gradually. CONCLUSION These findings suggest that the detection of c-myc protein could be an index of diagnosis of brain concussion.
Animals ; Brain/pathology* ; Brain Concussion/pathology* ; Brain Stem/pathology* ; Cerebral Cortex/pathology* ; Disease Models, Animal ; Female ; Immunohistochemistry ; Male ; Neurons/pathology* ; Proto-Oncogene Proteins c-myc/metabolism* ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Time Factors

OBJECTIVECD133(+) tumor cells are regarded as cancer stem cells (CSCs), responsible for tumor initiation, development, and relevant with chemo- and radio-resistance of tumors. However, how the destiny of CD133(+) cells is regulated by their niche remains largely unknown. In this study the interpretation of the relationship between CD133(+) cells and their niche were performed through investigating the distribution characteristics of CD133(+) cells in transplanted human glioma xenograft.

METHODSCD133(+) tumor cell spheres or tumor cells transfected with red fluorescent protein (RFP) gene were implanted in situ, subcutaneously or intraperitonealy in nude mice, then the xenografts were dissected and embedded in paraffin, stained with hematoxylin-eosin (HE), tumor tissues were further stained against CD133 with immunohistochemical and immunofluorescent techniques. The pathological structures of tumors and distribution characteristics of CD133(+) tumor cells were observed under microscope and confocal fluorescence microscope.

RESULTSUnder microscope, distribution of CD133(+) glioma cells showed certain regularity and can be classified morphologically into three types: cell clusters, in pairs and single cells. Distribution of CD133(+) cells can also be classified according to their distribution location: accumulating around tumor vasculature areas, among the vascular endothelial cells, or in the normal brain tissue and ventricles. Under fluorescence microscope and laser confocal microscope, some of vascular endothelial cells inside the tumor region and some cells around tumor vessels co-express CD133 and RFP.

CONCLUSIONCD133(+) tumor cell clusters in nude mice are actually similar to those in CSCs spheres cultured in vitro. The single CD133(+) cells and CD133(+) cells in pairs represent asymmetric and symmetric division of CSCs within the CSCs niche, respectively. CD133(+) cells residing along tumor vessels are CSCs depending on CSC niche, and those locating far away from tumor blood vessels or tumor tissues, residing in normal brain tissues are the disseminated CSCs or neural stem cells which are not controlled or regulated by CSCs niche.

AC133 Antigen ; Animals ; Antigens, CD ; metabolism ; Brain Neoplasms ; metabolism ; pathology ; Cell Differentiation ; Cell Line, Tumor ; Glioma ; metabolism ; pathology ; Glycoproteins ; metabolism ; Humans ; Luminescent Proteins ; metabolism ; Mice ; Mice, Nude ; Neoplasm Transplantation ; Neoplastic Stem Cells ; metabolism ; pathology ; Peptides ; metabolism ; Phenotype