Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085437 (bacterial meningitis)
 4,038 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous studies of neuronal degeneration induced by the neurotoxin, kainic acid, employed silver stain techniques that are non-quantitative or ELISA measurement of the non-neuronal protein, glial fibrillary acidic protein. As previous studies employed biomarkers that were either non-quantitative or non-neuronal, the present study employed a new neuronally localized biomaker of neuronal damage, cleaved microtubule-associated protein (MAP)-tau (C-tau). The time course of kainate neurotoxicity was quantitatively determined in several brain regions in the present study employing a C-tau specific ELISA. Differences in ELISA determined regional brain levels of C-tau were compared with the density of somatodendritic C-tau labeling qualitatively determined in immunohistochemical anatomical mapping studies of kainic acid-treated animals. Immunoblot studies revealed that the C-tau antibodies employed in the present study were highly specific for proteolytic cleaved C-tau. Immunolabeling of 45 kD-50 kD C-tau proteins was observed only in brain samples from kainic acid-treated but not vehicle-treated rats. Time course studies revealed that C-tau levels determined by ELISA were maximal 3 days after kainic acid with C-tau levels increasing 26-fold in hippocampus, 16-fold in cortex and four-fold in both striatum and hypothalamus. These statistical differences in maximal C-tau levels observed in the ELISA studies were similar to differences qualitatively observed in C-tau immunohistochemical studies. C-tau immunohistochemistry revealed extensive damage in hippocampal regions CA1 and 3, moderate damage in several cortical regions and mild damage in striatum and hypothalamus. Similar cleavage of rat MAP-tau to C-tau has been reported after neuronal degeneration induced by neurotoxic doses of methamphetamine and neuronal degeneration resulting from bacterial meningitis. In humans, C-tau proteolysis has been demonstrated to be a reliable biomarker of neuronal damage in traumatic brain injury and stroke where cerebrospinal C-tau levels are correlated with patient clinical outcome. These data suggest that C-tau proteolysis may prove a reliable species independent biomarker of neuronal degeneration regardless of source of injury.
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PMID:Quantification and localization of kainic acid-induced neurotoxicity employing a new biomarker of cell death: cleaved microtubule-associated protein-tau (C-tau). 1452 98

The frequency of fatalities due to acute bacterial meningitis has decreased significantly due to vaccinations, early diagnoses, and treatments. We studied brain tissues of patients with fatal neutrophilic meningitis referred to the Centers for Disease Control for etiologic diagnosis from 2000-2009 to highlight aspects of the disease that may be preventable or treatable. Demographic, clinical, and laboratory data were extracted from records. Of 117 cases in the database with a diagnosis of meningitis or meningoencephalitis, 39 had neutrophilic inflammation in the meninges. Inflammatory cells infiltrated the superficial cortex in 16 of 39 (41%) cases. Bacteria were found using Gram and bacterial silver stains in 72% of cases, immunohistochemistry in 69% (including two cases where the meningococcus was found outside the meninges), and PCR in 74%. Streptococcus pneumoniae was the cause of the meningitis in 14 patients and Neisseria meningitidis in 9. In addition, Streptococcus spp. were found to be the cause in six cases, while Staphylococcus aureus, Staphylococcus spp., Enterococcus spp., and Fusobacterium were the cause of one case each. There were six cases in which no specific etiological agent could be determined. The mean age of the patients with S. pneumoniae was 39 years (range 0-65), with N. meningitidis was 19 years (range 7-51), whereas that for all others was 31 years (range 0-68). In summary, our study shows that S. pneumoniae continues to be the most frequent cause of fatal neutrophilic bacterial meningitis followed by N. meningitidis, both vaccine preventable diseases.
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PMID:Neutrophilic bacterial meningitis: pathology and etiologic diagnosis of fatal cases. 2355 77