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At least 1,207 records · Page 67Linked to original sources
PubMed1985

Synthesis of arachidonoyl coenzyme A and docosahexaenoyl coenzyme A in synaptic plasma membranes of cerebrum and microsomes of cerebrum, cerebellum, and brain stem of rat brain.

Synthesis of arachidonoyl CoA and docosahexaenoyl CoA in homogenates and microsomes from cerebrum, cerebellum, and brain stem and in synaptic plasma membranes from cerebrum of control rats and rats undergoing bicuculline-induced status epilepticus were studied. Arachidonoyl CoA synthesis was 3-5 times higher than docosahexaenoyl CoA in homogenates and microsomes. The synaptic plasma membranes showed only 1.5- to 2.5-fold higher activity. The presence of Triton X-100 (0.1%) in the incubation medium did not alter the activity of arachidonoyl CoA synthesis but did increase the synthesis of docosahexaenoyl CoA in homogenates, microsomes, and especially in synaptic plasma membranes. The synthesis of these polyenoic fatty acyl CoAs were 4-6 times higher in microsomes than in homogenates. Synaptic plasma membranes exhibited about the same amount of activity as homogenates in the synthesis of docosahexaenoyl CoA, but only half the activity of the latter in arachidonoyl CoA synthesis. The synthesis of arachidonyl CoA and docosahexaenoyl CoA in cerebral homogenates and microsomes was higher than that of cerebellum and brain stem. The apparent Km values for labeled arachidonic acid (17 microM) and docosahexaenoic acid (12 microM) in synaptic plasma membranes were lower than the values for microsomes isolated from different brain regions. The Vmax values were also 4-10 times lower. Microsomes from different regions did not differ in their apparent Km values, but did show variations in apparent Vmax values. Cerebellar microsomes showed lower Vmax values than the other two regions. The presence of Triton X-100 caused a significant decrease in the apparent Km values with little change in the Vmax values. Bicuculline-induced seizures did not alter the kinetic properties of arachidonoyl CoA and docosahexaenoyl CoA synthesis, except there was a significant decrease in the apparent Km and Vmax values for cerebellar microsomal docosahexaenoyl CoA synthesis. In conclusion, there were marked differences in the activation of polyenoic fatty acids in different parts of the brain and in subcellular fractions. Although bicuculline-induced convulsions accumulate free polyenoic fatty acids in the brain, no changes were detected when the fatty activation was assayed with exogenous cofactors, except in cerebellum.

Acyl Coenzyme A↗
PubMed1994

Nicotine downregulates alpha 2 isoform of Na,K-ATPase at the blood-brain barrier and brain in rats.

Effects of chronic nicotine treatment on the relative levels of expression of Na,K-ATPase alpha and beta subunit isoforms were determined in rat cerebral microvessels and capillary-depleted brain homogenates by Western blot analysis. Nicotine, 4.5 mg/kg/day, was administered s.c. by osmotic mini-pumps for 14 days. Expression of alpha 2 isoform in microvessels and brains of nicotine-treated rats was reduced to 0.26 and 0.58 of control levels, respectively. Expression of alpha 1, alpha 3, beta 1 or beta 2 was unchanged. Nicotine decreased cerebromicrovascular and brain Na,ATPase enzymatic activities by 22% and 17%, respectively. It is suggested that chronic exposure to nicotine reduces expression of functional Na,K-ATPase at the blood-brain barrier and brain by downregulating the alpha 2 isoform.

Animals↗
PubMed2002

A space for measuring mind and brain: interdisciplinarity and digital tools in the development of brain mapping and functional imaging, 1980-1990.

Brain mapping is said to have opened up the possibility of a new collaboration between the sciences of mind and the sciences of the brain, potentially leading to a new kind of scientist, sometimes called "cognitive neuroscientist." This article traces the recent history of brain mapping and analyzes the processes that have led to a new "close working relationship" between the sciences of mind and brain. A key part of the working relationship is shown to be constituted through the development of the Talairach system, a digital space in which to measure structure and function. The development of meaningful brain mapping data involves the creation of measurement spaces that allow interdisciplinary collaboration and is not the result solely of theoretical developments or of the application of a technology.

Brain↗
PubMed2000

Does (99m)Tc-Sestamibi in high-grade malignant brain tumors reflect blood-brain barrier damage only?

(99m)Tc-Sestamibi (MIBI) has been successfully applied in recurrent glioblastoma. The aim of this study was to evaluate the incremental diagnostic information of MIBI as a tumor-avid radiopharmaceutical compared with (99m)Tc-pertechnetate ((99m)Tc) as sole indicator of the integrity of the blood-brain barrier. Twenty-five patients with confirmed recurrent brain tumors were included. MIBI SPET was performed 10 min after injection of 555 MBq MIBI intravenously with a triple-headed gamma camera equipped with LE-UHR-PAR collimators over 360 degrees (3 degrees /step) and stored in a 128(2) matrix. Identical acquisition parameters were used for (99m)Tc SPET, which was acquired 3 h after injection of 740 MBq (99m)Tc. Normalized tumor uptake (NU) was calculated from attenuation-corrected transaxial slices. In addition, tumor/plexus, tumor/nasopharynx, and tumor/parotid gland ratios were assessed in both studies. No statistically significant differences were detected for the mean NU of tumor tissue with MIBI (0.26 +/- 0.10) and (99m)Tc (0.39 +/- 0. 33) and for the tumor/nasopharynx and tumor/parotid gland ratios; only the tumor/plexus ratio was significantly higher for (99m)Tc than for MIBI (p < 0.05). In conclusion, our data indicate that MIBI scintigraphy in brain tumors at 10 min postinjection reveals no additional visual information over that provided by the conventional (99m)Tc-pertechnetate brain scan, and in addition, tracer retention reflects primarily blood-brain barrier damage.

Adult↗
PubMed2002

Brain regions involved in fatigue sensation: reduced acetylcarnitine uptake into the brain.

Fatigue is an indispensable sense for ordering rest. However, the neuronal and molecular mechanisms of fatigue remain unclear. Chronic fatigue syndrome (CFS) with long-lasting fatigue sensation seems to be a good model for studying these mechanisms underlying fatigue sensation. Recently, we found that most patients with CFS showed a low level of serum acetylcarnitine, which well correlated with the rating score of fatigue, and that a considerable amount of acetyl moiety of serum acetylcarnitine is taken up into the brain. Here we show by metabolite analysis of the mouse brain that an acetyl moiety taken up into the brain through acetylcarnitine is mainly utilized for the biosynthesis of glutamate. When we studied the cerebral uptake of acetylcarnitine by using [2-(11)C]acetyl-L-carnitine in 8 patients with CFS and in 8 normal age- and sex-matched controls, a significant decrease was found in several regions of the brains of the patient group, namely, in the prefrontal (Brodmann's area 9/46d) and temporal (BA21 and 41) cortices, anterior cingulate (BA24 and 33), and cerebellum. These findings suggest that the levels of biosynthesis of neurotransmitters through acetylcarnitine might be reduced in some brain regions of chronic fatigue patients and that this abnormality might be one of the keys to unveiling the mechanisms of the chronic fatigue sensation.

Acetylcarnitine↗
PubMed1992

In vivo CT measurement of blood-brain transfer constant of iopamidol in human brain tumors.

We have developed an in vivo method of measuring the blood-brain transfer constant (K) of iopamidol and the cerebral plasma volume (Vp) in brain tumors using a clinical X-ray CT scanner. In patient studies, Isovue 300 (iopamidol) was injected at a dosage of 1 ml/kg patient body weight. Serial CT scans of the tumor site and arterial blood samples from a radial artery were taken up to 48 min after injection. The leakage of iopamidol into the brain through the blood-brain barrier was modelled as an exchange process between two compartments, the intravascular plasma space and the tissue interstitial space. Using this model and the concentration measurements in blood plasma and tissue, quantitative estimates of K and Vp in brain tumors were obtained. In addition, distribution of the estimated values of K and Vp in tumors were displayed as false colour functional images overlaid on the conventional CT scan. In a study of twelve patients with anaplastic astrocytoma (n = 3), glioblastoma multiforme (n = 4) or metastases (n = 5) the mean K and Vp values in tumor were found to be 0.0273 +/- 0.0060 ml/min/g and 0.068 +/- 0.11 ml/g respectively. These values were significantly higher than those in grey or white matter in the contralateral 'normal' hemisphere (p less than 0.05). The functional images showed variations in K and Vp within the tumor which were difficult to perceive in the original contrast enhanced CT scans.

Astrocytoma↗
PubMed1989

Susceptibility of brain cells to murine cytomegalovirus infection in the developing mouse brain.

Mouse embryos were infected with murine cytomegalovirus (MCMV) by injecting the virus into the cerebral ventricles in the late stage of gestation; the brains of the offspring were than analyzed using the histological and immunohistochemical methods. Brains of the offspring, which were injected with relatively high titers of MCMV [1 X 10(4) plaque-forming units (pfu)] on day 13 of gestation exo utero or on day 15 of gestation in utero, showed massiv necrosis of the cerebral cortex with gliomesodermal proliferation around 9 to 10 days after birth. In these brains, viral antigen-positive cells were observed in zonal arrangement in the lesion-free cortex and in the hippocampus. Immunohistochemical double staining showed that some of the viral antigen-positive cells had also reacted with antibody to neuron-specific enolase at the same time, but had hardly reacted with antibodies to brain-type creatine kinase or glial fibrillary acidic protein. Brains of the offspring, which were injected with relatively low titers of virus (1 x 10(3) pfu) on day 15 of gestation, showed zonal arrangement of viral antigen-positive cells mainly in the cerebral cortex and in the hippocampus 7 days after birth, although the numbers of the positive cells were low. Fourteen days after birth, some of these offspring showed atrophy of the cerebral cortex and the hippocampus. These results suggest that some of the neuronal cells in the cerebral cortex and the hippocampus have special susceptibility to MCMV infection.

Animals↗
PubMed1987

Correlation of morphologic brain lesions with physiologic alterations and blood-brain barrier impairment in 3-nitropropionic acid toxicity in rats.

3-Nitropropionic acid (NPA), a toxin which irreversibly inhibits the Krebs cycle enzyme succinate dehydrogenase, causes severe neurologic disease and a specific pattern of morphologic brain damage when given subcutaneously to rats. To determine whether hypotension or hypoxemia were necessary for development of morphologic brain lesions in NPA neurotoxicity, systemic blood pressure and arterial blood gases were measured in NPA-intoxicated rats. The extent and distribution of albumin extravasation was examined by immunohistochemistry, and was compared to the extent and severity of morphological injury in the caudate-putamen. Neither hypotension nor hypoxemia were necessary for the development of morphologic injury in the brains of NPA-intoxicated rats. In fact, intoxicated rats had significantly higher systolic blood pressure and arterial blood oxygen than did controls. Arterial bicarbonate and pH were significantly lower in intoxicated rats than controls, however, suggesting that acidosis may be involved in the pathogenesis of NPA toxicity. When morphologic injury was severe, albumin extravasation was extensive occupying approximately 30%-80% of the lesion area in the caudate-putamen of NPA-intoxicated rats. When morphologic injury was mild, albumin extravasation was absent, or limited to small cuffs around individual capillaries (less than 1% of the lesion area). There was no leakage of albumin in the cerebral cortex, which was resistant to morphologic injury. It was concluded that leakage of protein-rich fluid into cerebral parenchyma from blood-brain barrier impairment is not responsible for the initiation of morphologic injury in NPA toxicity, but may contribute to the severity of injury later in the evolution of brain lesions.

Albumins↗
PubMed1994

Effect of steroids on iopamidol blood-brain transfer constant and plasma volume in brain tumors measured with X-ray computed tomography.

Tumor blood-brain transfer constant of iopamidol (K) and plasma volume (Vp) were measured in 10 patients with primary brain tumors before and after 7 days of dexamethasone treatment (4 x 4 mg per oral per day) using X-ray computed tomography. Both K and Vp decreased significantly after dexamethasone treatment with p < 0.01 and 0.09 respectively according to one-tail paired t-test. The mean percentage decrease in K and Vp was 32% and 10% respectively. Functional images of the two parameters before and after treatment were generated and showed clearly the effect of steroids on the reduction of K in brain tumors. In contrast, when before and after treatment contrast enhanced CT scans were compared, no difference was observed in the enhancement in 8 out of 10 cases. The result obtained support the conclusion that: (1) corticosteroids reduce the blood-brain permeability to small hydrophilic molecules; (2) the X-ray computed tomography method we have developed can be used to measure the K and Vp response of brain tumors to steroid therapy; and, (3) ordinary contrast enhanced CT scans at one fixed time or multiple times after contrast injection are not sensitive in detecting the reduction of K due to steroids.

Blood-Brain Barrier↗
PubMed1983

Acute dimethyl sulphoxide therapy in experimental brain oedema, effect of dose and concentration on brain water and electrolyte content.

Albino rabbits with experimental brain oedema produced by a combined left hemisphere cryogenic injury and a metabolic insult by a 6-aminonicotinamide (6-ANA) were administered intravenous dimethyl sulphoxide (DMSO) in varying concentrations and doses in the following manner: Subgroup A (concentration response) received 1.0 g/kg bolus of a 10, 20, 30, or 40% solution. Subgroup B (dose response) received as a 20% solution a 1.0 g/kg bolus, 1.5 g/kg bolus, or 2.0 g/kg infusion. One hour following administration of the agent, the animals were killed, their brains rapidly removed by craniectomy and brain water, sodium and potassium measured. Significant decreases in brain sodium and water content in the right hemisphere were noted in both subgroups A (p less than 0.05) and B (p less than 0.005) and in the left hemisphere in subgroup B only (p less than 0.005). There is an apparent effect on brain oedema by a DMSO mediated sodium dependent water mobilization.

Animals↗
PubMed1995

Significance of electrical brain activity in brain-stem death.

A 46-year-old man was diagnosed clinically brain dead after sustaining head trauma. The patient was in deep coma, brain nerves were unresponsive and spontaneous breathing was absent. However, EEG showed well preserved activity, but no reactivity to external stimuli. EEG activity disappeared within 40 h. BAEP were highly abnormal, flash-VEP as recorded 3 h after the diagnosis of brain stem death was of high amplitude but of simplified form. The neurophysiological findings revealed that the main reason for deep coma was brain stem damage while cortical activity was still present. This condition raises ethical questions when brain death is diagnosed clinically prior to removal of organs for transplantation.

Accidental Falls↗
PubMed1993

Reassessment of quantitative thallium-201 brain SPECT for miscellaneous brain tumors.

In order to reassess the value of quantitative thallium-201 brain SPECT in the differentiation of miscellaneous brain tumors, we studied a total of 89 patients--35 pre-operative patients suspected of having a brain tumor and 54 post-operative patients with a brain tumor. We came to the conclusion that quantitative Tl-201 brain SPECT was very useful in discriminating cerebral radiation necrosis from recurrent tumor, estimating residual tumor burden, and detecting tumor regrowth earlier in postoperative patients. In preoperative patients, however, Tl-201 SPECT cannot be used effectively to differentiate glioma from other intracranial tumors, although intense uptake of Tl-201 may provide evidence of glioblastoma or a hypervascular lesion.

Adolescent↗
PubMed2005

Phase I/II trial of simultaneous whole-brain irradiation and dose-escalating topotecan for brain metastases.

BACKGROUND AND PURPOSE: Topotecan penetrates the blood-brain barrier and sensitizes tumor cells against radiation. A phase I/II dose-escalating trial of repetitive daily i. v. topotecan application simultaneously with whole-brain irradiation (WBRT) was conducted to estimate toxicity, maximum tolerated dose and survival in patients with inoperable brain metastases. PATIENTS AND METHODS: In 47 patients suffering from previously untreated brain metastases, topotecan was applied on a daily i. v. schedule simultaneously with WBRT (36 Gy/3-Gy fractions). The infusion schedule started at the beginning of WBRT and was discontinued during weekends. Each infusion was completed within 1-2 h before irradiation. In a dose-finding study, topotecan was escalated from 5 x 0.5 mg/m(2), 8 x 0.5 mg/m(2), 12 x 0.5 mg/m(2) to 12 x 0.6 mg/m(2). RESULTS: Altogether, 38/47 patients (81%) completed the prescribed schedule. Leukopenia and thrombocytopenia were dose-limiting. Grade 3/4 hematologic toxicity occurred in 5/32 chemonaïve patients (16%) and 7/15 patients (47%) with previous chemotherapy. At 12 x 0.6 mg/m(2), 2/4 patients experienced grade 4 leukopenia/thrombopenia. Nonhematologic toxicities were generally mild to moderate and unrelated to topotecan. Response evaluation was possible in 26/47 patients, overall response rate was 58% (CR [complete remission] 5/26, PR [partial remission] 10/26, NC [no change] 8/26). Median survival amounted to 5.1 months. In 15/42 patients (36%), brain metastases were the dominant cause of death. CONCLUSION: For a daily topotecan schedule simultaneous to WBRT, the maximum tolerated dose is 12 x 0.5 mg/m(2) in chemonaïve patients. For chemo-pretreated patients, daily doses should be reduced to 0.4 mg/m(2). A phase III trial has now been started to find out whether WBRT + topotecan increases survival compared to WBRT alone.

Adult↗
PubMed2006

[The undetected brain lesion in sports. Minor traumatic brain injury and its sequelae].

The minor traumatic brain injury (mTBI) in sports is often looked at as a bagatelle. The treating physician underestimates the severity of the injury suspecting that a mTBI is a nonstructural lesion with an overall excellent prognosis in the majority of the cases. This paper shows that the minor traumatic brain injury may be a structural brain lesion with potentially life-threatening dangers. The therapy should follow exactly defined guidelines, e.g., stepwise protocol of the Concussion in Sports (CIS-) Group. Return to sports activities should happen only when all physical but also cognitive symptoms have subsided. All mTBIs that have been sustained prior to the actual injury have to be recorded properly because repeated mTBIs may cause chronic degenerative brain damage. Neuropsychological testing will aid in the correct diagnosis of a mTBI and is a useful parameter in the course of the injury. In the future biochemical markers may serve as indicators of the severity of the brain injury and may also aid in predicting the outcome after TBI. Today biochemical markers do not serve as a substitute for neuroimaging.

Adolescent↗
PubMed2001

[New insights into brain function by combination of transcranial magnetic stimulation and functional brain mapping].

The present paper aims to summarize potential applications of transcranial magnetic stimulation (TMS) combined with functional brain imaging. Transcranial magnetic stimulation is a well-established noninvasive tool for stimulating circumscribed areas of the human cortex. Functional imaging techniques such as positron emission tomography, functional magnetic resonance imaging, and electroencephalographic mapping enable assessment of TMS-related functional brain activation. A combination of TMS and functional imaging can be useful in three principal ways. (1) Brain imaging before TMS is helpful in defining the accurate coil position over a distinct cortical area which is targeted by TMS. Since TMS can be used to interfere with regional cortical function during a given task, the effects of focal TMS on task performance can help to clarify the task-specific functional contribution of a given cortical area which has previously shown task-related activation in a functional imaging study. (2) Imaging the brain during TMS is a promising approach for assessing cortical excitability and intracerebral functional connectivity. (3) By evaluating lasting effects of TMS, brain imaging after TMS can be employed to study the plasticity of the human cortex. Moreover, this approach will help to advance our understanding of therapeutical effects related to TMS.

Brain↗
PubMed2001

Chronic lithium treatment increases the expression of brain-derived neurotrophic factor in the rat brain.

RATIONALE: Lithium is the most widely prescribed mood stabilizer, but the precise mechanism of lithium is unresolved. OBJECTIVE: We examine the effects of the administration of therapeutically relevant concentrations of lithium on the expression of brain-derived neurotrophic factor (BDNF) and its receptor, Trk B, as well as glia-derived neurotrophic factor (GDNF) and its receptors, RET and GDNFR-alpha, in the rat brain. In addition, we also examined the effect of another well-prescribed mood stabilizer, valproate, on the expression of BDNF and GDNF. METHODS: Rats were kept on a 0.2% lithium carbonate-containing diet for 1, 7, 14, or 28 days or treated with valproate (400 mg/kg per day i.p.) for 1 or 14 days. After the brains were rapidly removed, the levels of BDNF, GDNF, and their receptors were measured by ELISA or western blot analysis. RESULTS: Chronic lithium treatment for 14 and 28 days significantly increased the expression of BDNF in the hippocampus and temporal cortex. In addition, chronic lithium treatment for 14 days significantly increased the expression of BDNF in the frontal cortex. In contrast, acute or chronic dietary lithium treatment did not alter GDNF expression in these brain regions. In addition, acute or chronic lithium treatments did not change the levels of Trk B, RET, or GDNFR-alpha immunoreactivity. As well as lithium, repeated administration of valproate also increased the expression of BDNF in the frontal cortex and hippocampus. CONCLUSIONS: Our results suggest that the chronic administration of mood stabilizers may produce a neurotrophic effect mediated by the upregulation of BDNF in the rat brain.

Administration, Oral↗
PubMed2003

Correlation of emmprin expression in vascular endothelial cells with blood-brain-barrier function: a study using magnetic resonance imaging enhanced by Gd-DTPA and immunohistochemistry in brain tumors.

In a previous study, we demonstrated that the expression levels in tumor cells of emmprin (CD147) correlated with the grade of astrocytic tumors. Also, we found that emmprin was expressed in vascular endothelial cells of the non-neoplastic brain and hypothesized that emmprin expression could be associated with normal blood-brain-barrier (BBB) function of vascular endothelial cells. In this study, this possibility was examined in non-neoplastic brain, glioma and metastatic carcinoma tissues by comparing emmprin immunohistochemistry with gadolinium diethylenetriaminepentaacetic acid (Gd-DTPA) enhancement of magnetic resonance imaging (MRI), which is a clinical indicator of the BBB function. This study included 10 cases of non-neoplastic brain tissues, 7 of metastatic carcinoma, 7 of diffuse astrocytoma, 4 of anaplastic astrocytoma and 13 of glioblastoma multiforme. In all the cases, MRI with administration of Gd-DTPA was performed. The lesions were resected using the microdissection method with the help of ultrasonography and a neuronavigator. The tissues from Gd-DTPA-enhanced or non-enhanced areas were processed into frozen sections and subjected to immunohistochemistry with anti-emmprin antibody. The expression of emmprin in brain vascular endothelial cells inversely correlated with Gd-DTPA-enhancement of MRI: emmprin was positive in tissues not enhanced by Gd-DTPA and was negative in DTPA-enhanced tissues. Since BBB function presumably remains unimpaired in regions in which MR images are not Gd-DTPA-enhanced, emmprin expression appears to be associated with unimpaired BBB function. This is the first report to demonstrate a possible correlation between emmprin expression and BBB function in humans.

Adult↗
PubMed2004

Nocardia brain abscess mimicking brain tumour in immunocompetent patients: report of two cases and review of the literature.

Nocardia brain abscess is a rare intracranial lesion and has been reported in immunocompromised patients. An optimal treatment approach has not been established. However, early diagnosis and appropriate antimicrobial therapy are very important factors for a good outcome. We report two unusual cases of Nocardia brain abscess simulating brain tumour in immunocompetent patients. One of the cases was presumed to be a primary brain tumour and the other a metastatic brain tumour. They underwent surgical gross total resection. After Nocardia asteroides was seen on Gram's stain and subsequently identified by culture, appropriate antibiotic therapy was initiated.

Adolescent↗