PURPOSE: The mechanisms underlying febrile convulsions, which have multiple etiological factors, are not yet clear. The aim of the present study was to determine whether there were any changes and correlations in serum and cerebro-spinal fluid(CSF) zinc(zn) levels and the levels of tumor necrosis factor-alpha(TNF-alpha), Interleukin-1beta(IL-1beta) and Interleukin-6(IL-6) in children with febrile convulsions. METHODS: Serum and CSF zinc levels and the levels of TNF-alpha, IL-1beta and IL-6 were measured in 20 children with febrile convulsions : 14 with simple febrile convulsions, 6 with complex convulsions and 20 as health controls. Zinc levels were measured by automic absorption spectrophotometry(Thermo Jarrell Ash/Smith-Hieftje 1000). The TNF-alpha, IL-1beta and IL-6 were measured by sandwich-type ELISA kit(Genzyme co.). RESULTS: The CSF and serum zn levels of the febrile convulsion group were found to have a mean of a 58.92+/-64.85micro gram/dl, 106.5+/-64.9micro gram/dl, respectively. In the controls, the CSF and serum zn levels were a mean of a 68.66+/-43.0micro gram/dl, 109.6+/-36.9micro gram/dl, respectively. We found that the TNF-alpha were undetectable in serum and CSF of all children with febrile convulsions and control subjects. CONCLUSION: No significant relationship was found between zinc levels of the serum and CSF and the levels of TNF-alpha, IL-1beta and IL-6 in children with febrile convulsions or controls. These results do not support the hypothesis that febrile convulsions are related to reduced serum and CSF zn levels and also elevated levels of TNF-alpha, IL-1beta and IL-6.
Absorption ; Cerebrospinal Fluid* ; Child ; Enzyme-Linked Immunosorbent Assay ; Humans ; Interleukin-6 ; Necrosis ; Seizures ; Seizures, Febrile* ; Tumor Necrosis Factor-alpha ; Zinc*

BACKGROUNDAlthough traumatic brain injury can lead to opening the blood-brain barrier and leaking of blood substances (including water) into brain tissue, few studies of brain antigens leaking into the blood and the pathways have been reported. Brain antigens result in damage to brain tissues by stimulating the immune system to produce anti-brain antibodies, but no treatment has been reported to reduce the production of anti-brain antibodies and protect the brain tissue. The aim of the study is to confirm the relationship between immune injury and arachnoid granulations following traumatic brain injury, and provide some new methods to inhibit the immune injury.

METHODSIn part one, methylene blue was injected into the rabbits' cisterna magna after traumatic brain injury, and concentrations of methylene blue and tumor necrosis factor (TNF)-α in blood were detected to determine the permeability of arachnoid granulations. In part two, umbilical cord mesenchymal stem cells and immature dendritic cells were injected into veins, and concentrations of interleukin 1 (IL-1), IL-10, interferon (IFN)-γ, transforming growth factor (TGF)-β, anti-brain antibodies (ABAb), and IL-12 were measured by ELISA on days 1, 3, 7, 14 and 21 after injury, and the numbers of leukocytes in the blood were counted. Twenty-one days after injury, expression of glutamate in brain tissue was determined by immunohistochemical staining, and neuronal degeneration was detected by H&E staining.

RESULTSIn part one, blood concentrations of methylene blue and TNF-α in the traumatic brain injury group were higher than in the control group (P < 0.05). Concentrations of methylene blue and TNF-α in the trauma cerebrospinal fluid (CSF) injected group were higher than in the control cerebrospinal fluid injected group (P < 0.05). In part two, concentrations of IL-1, IFN-γ, ABAb, IL-12, expression of glutamate (Glu), neuronal degeneration and number of peripheral blood leukocytes were lower in the group with cell treatment compared to the control group. IL-10 and TGF-β were elevated compared to the control group.

CONCLUSIONSTraumatic brain injury can lead to stronger arachnoid granulations (AGs) permeability; umbilical cord mesenchymal stem cells and immature dendritic cells can induce immune tolerance and reduce inflammation and anti-brain antibodies to protect the brain tissue.

Adipocytes ; cytology ; Animals ; Antigens ; blood ; metabolism ; Brain Injuries ; blood ; cerebrospinal fluid ; metabolism ; Cell Differentiation ; physiology ; Cells, Cultured ; Dendritic Cells ; metabolism ; Enzyme-Linked Immunosorbent Assay ; Interleukin-1 ; blood ; cerebrospinal fluid ; Interleukin-10 ; blood ; cerebrospinal fluid ; Interleukin-12 ; blood ; cerebrospinal fluid ; Mesenchymal Stromal Cells ; cytology ; Methylene Blue ; metabolism ; Osteoblasts ; cytology ; Rabbits ; Transforming Growth Factor beta ; blood ; cerebrospinal fluid ; Tumor Necrosis Factor-alpha ; blood ; cerebrospinal fluid

Subarachnoid hemorrhage (SAH) induces an inflammatory reaction and may lead to ischemic brain damage. The pathogenesis of brain dysfunction and delayed ischemic symptoms remain difficult to understand despite extensive surveys of such reactions. Cytokine production in the central nervous system following SAH and its relation with clinical outcome have hardly been studied. This study was aimed to determine whether the levels of IL-1 beta, IL-6 and TNF-alpha in the initial cerebrospinal fluid would increase following aneurysmal SAH, and be related with development of delayed ischemic deficit and clinical outcome. Nineteen patients suffering from aneurysmal SAH and 12 control volunteers were the subjects in this study. Cerebrospinal fluid samples were obtained on admission and the levels of each cytokine were determined with enzyme-linked immunosorbent assay. Patients with aneurysmal subarachnoid hemorrhage showed elevated levels of IL-1 beta, and TNF-alpha on admission. The patients with poor neurological status showed high levels of IL-1 beta, and IL-6. The patients who developed delayed ischemic deficit had high level of IL-6. We suggest that elevated level of IL-6 in cerebrospinal fluid of patients with aneurysmal SAH on admission can predict the high risk of delayed ischemic deficit.
Adult ; Aged ; Brain Ischemia/*cerebrospinal fluid/*diagnosis/immunology ; Cytokines/*cerebrospinal fluid ; Female ; Glasgow Outcome Scale ; Human ; Interleukin-1/cerebrospinal fluid ; Interleukin-6/cerebrospinal fluid ; Male ; Middle Age ; Predictive Value of Tests ; Subarachnoid Hemorrhage/*cerebrospinal fluid/*diagnosis/immunology ; Tumor Necrosis Factor/cerebrospinal fluid

No abstract available.
Animals ; Bacteremia* ; Cerebrospinal Fluid* ; Haemophilus influenzae* ; Haemophilus* ; Interleukin-6* ; Kinetics* ; Meningitis* ; Models, Animal* ; Rats* ; Tumor Necrosis Factor-alpha*

OBJECTIVETo investigate the association among serous and cerebrospinal fluid (CSF) TNF-alpha level, gene polymorphisms of TNF-alpha and multiple sclerosis (MS) in Han nationality of southern China.

METHODSMS diagnosis was base on Poser (1983) criteria. Fifty-five patients with nonimmulogical diseases and 68 patients with MS from southern China were enrolled in the study, and their TNF-alpha level of serum and CSF were measured by double antibody sandwich ABC-ELISA. TNF-alpha -308G/A in 106 normal healthy subjects and 68 MS patients was genotyped with polymerase chain reaction-restriction fragment length polymorphism.

RESULTSThere was significant difference in the serous TNF-alpha level between nonimmune patients and active MS patients (234+/- 76 pg/mL vs 276+/- 71 pg/mL, P< 0.05), but not in the CSF (245+/- 83 pg/mL vs 265+/- 78 pg/mL, P> 0.05). The gene frequency distribution of TNF-alpha -308G/A was corresponding with Hardy-Weinberg equilibrium. The positive rate of genotype AA and the gene frequency of allele A of TNF-alpha were 4.4% and 14.0% in MS group, and 0 and 8.50% in healthy subjects, there was no statistical significance (P> 0.05).

CONCLUSIONThe TNF-alpha level in serum is associated with active MS, but not in the CSF. The gene polymorphisms of TNF-alpha -308G/A is not associated with MS in Han nationality of southern China.

Adolescent ; Adult ; Aged ; Asian Continental Ancestry Group ; genetics ; China ; Enzyme-Linked Immunosorbent Assay ; Female ; Gene Frequency ; Genotype ; Humans ; Male ; Middle Aged ; Multiple Sclerosis ; blood ; cerebrospinal fluid ; genetics ; Polymorphism, Genetic ; Tumor Necrosis Factor-alpha ; blood ; cerebrospinal fluid ; genetics

This study was conducted to determine the level of inflammatory cytokines in the cerebrospinal fluid (CSF) of patients with meningitis. All the CSF of the patients were examined by Gram and acid-fast stain, culture, and PCR for Mycobacterium tuberculosis and Mycoplasrma spp..The levels of sugar, protein and leukocytes count were also evaluated in the CSFs. Concentrations of Interleukin (IL)-1B, IL-6, IL-8, tumor necrosis factor (TNF)-a in the CSF were evaluated by the ELISA kit (Genzyme, USA). General bacteria, tubercle bacilli, and Mycoplasma spp. were not detected with stain and culture methods, but, Mycoplasma spp. was detected by PCR method from four (6.3%) patients with meningitis. The mean CSF concentration of IL-1B, IL-6, IL-8, and TNF-cx in the control group were 0.6+/-0.2, 896.8+/-107.6, 50.1+/-5.1, and 4.8+/-1.4 pg/ml, respectively. The mean CSF concentration of IL-1B, IL-6, IL-8, and TNF-a in the patients with aseptic meningitis were 3.8+/-0.6, 1261.6+/-144.3, 466.7+/-42.3, and 10.8+/-2.0 pg/ml, respectively. The mean CSF concentration of IL-1B, IL-6, IL-8, and TNF-a in the patients with mycoplasmal meningitis were 10.2+/-8.1, 1979.5+/-133.8, 459.7+/-96.4, and 17.5+/-5.1 pg/ml, respectively. There were significantly differences in the levels of IL-1B, IL-6, IL-8, and TNF-a between control and patients with aseptic meningitis or Mycoplasmal meningitis (each p<0.001). These results suggest that increased levels of IL-1B, IL-8, and TNF-a could be higly suggestive of meningitis.
Bacteria ; Cerebrospinal Fluid* ; Cytokines ; Enzyme-Linked Immunosorbent Assay ; Humans ; Interleukin-6* ; Interleukin-8* ; Interleukins ; Leukocytes ; Meningitis* ; Meningitis, Aseptic ; Mycobacterium tuberculosis ; Mycoplasma ; Polymerase Chain Reaction ; Tumor Necrosis Factor-alpha

Marchiafava-Bignami disease (MBD) is a rare disorder of demyelination or necrosis of the corpus callosum. Mainly, MBD is associated with alcohol and malnutrition. We report a 60-year-old woman with no history of alcohol consumption or malnutrition who had MBD as a possible complication of normal pressure hydrocephalus (NPH). The patient presented with a 2-month history of progressive gait unsteadiness, urinary incontinence, and forgetfulness, for which the patient underwent ventriculoperitoneal shunt surgery with remarkable improvement. Magnetic resonance imaging (MRI) demonstrated hyperintensity in the body and splenium of corpus callosum when she was brought to the hospital again with rapid deterioration of her mental ststus. It might be postulated that cerebrospinal fluid (CSF) tumor necrosis factor-alpha (TNF-alpha) might have contributed to the development of MBD although not measured in this patient, given that TNF-alpha, as a proinflammatory cytokine mediating demyelinating process have been found in be increased in the CSF of NPH.
Alcohol Drinking ; Cerebrospinal Fluid ; Corpus Callosum ; Demyelinating Diseases ; Female ; Gait ; Humans ; Hydrocephalus, Normal Pressure* ; Magnetic Resonance Imaging ; Malnutrition ; Marchiafava-Bignami Disease* ; Middle Aged ; Necrosis ; Negotiating ; Tumor Necrosis Factor-alpha ; Urinary Incontinence ; Ventriculoperitoneal Shunt

We evaluated the efficacy of non-competitive N-methyl-D-aspartate receptor antagonist MK-801 (dizocilpine) as an adjuvant therapy in experimental neonal bacterial meningitis. Meningitis was induced by injecting 10(6) colony forming units of Escherichia coli into the cisterna magna. MK-801 3 mg/kg was given as a bolus intravenous injection, 30 min before the induction of meningitis. MK-801 did not down-modulate the inflammatory parameters, such as increased intracranial pressure, cerebrospinal fluid (CSF) leukocytosis, increased lactate and TNF-alpha levels in the CSF, and hypoglycorrhachia observed in the meningitis group. MK-801 did not significantly attenuate the elevated glutamate concentration in the CSF. However, MK-801 showed some neuroprotective effects as evidenced by significant attenuation of cerebral lipid peroxidation products (conjugated dienes) and increase of brain high-energy phosphate compounds (ATP and PCr). Improvement in cerebral cortical cell membrane Na+, K+ -ATPase activity did not reach a statistical significance. These results suggest that MK-801 was effective in ameliorating brain injury in neonatal bacterial meningitis, although it failed to attenuate the inflammatory responses.
Animals ; Animals, Newborn ; Blood Glucose/metabolism ; Brain/cytology ; Brain/drug effects* ; Brain/metabolism ; Cell Membrane/drug effects* ; Cell Membrane/metabolism ; Cerebral Cortex/metabolism ; Dizocilpine Maleate/pharmacology* ; Energy Metabolism* ; Excitatory Amino Acid Antagonists/pharmacology ; Glutamic Acid/cerebrospinal fluid ; Lactic Acid/blood ; Leukocytes/metabolism ; Meningitis, Escherichia coli/drug therapy ; Meningitis, Escherichia coli/metabolism* ; Neurons/drug effects* ; Neurons/metabolism ; Neuroprotective Agents/pharmacology* ; Random Allocation ; Swine ; Tumor Necrosis Factor/cerebrospinal fluid