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At least 217 records · Page 12Linked to original sources

Therapeutic dose and timing of administration of RNA synthesis inhibitors for preventing cerebral vasospasm after subarachnoid hemorrhage.

A RNA synthesis inhibitor, dactinomycin, intended to suppress induction of vasoconstrictor peptide endothelin, prevented cerebral vasospasm almost completely in the dog subarachnoid hemorrhage (SAM) model [8]. Since endothelin receptor antagonists have not shown so potent effect as dactinomycin in animal SAH models, we aimed clinical use of dactinomycin for improvement of final outcomes of severe SAH patients now suffering vasospasm. Before clinical application, we examined therapeutic dose and timing of administration of dactinomycin in animal models. In the dog two-hemorrhage model, dactinomycin treatment (0.01 mg/kg i.v. for 5 days) started at 6 hours after the second blood injection on Day 2 prevented vasospasm, but that started on Day 3 did not. Low dose of dactinomycin (0.003 mg/kg i.v. for 5 days) rather aggravated vasospasm even though the treatment started on Day 0. In the rat vasospasm model, high dose of dactinomycin (0.03 mg/kg i.p. for 3 days) or relatively low dose of doxorubicin (0.6 mg/kg i.p. once) prevented vasospasm even though the treatment started on Day 4. The present study suggests that RNA synthesis inhibitors, such as dactinomycin and doxorubicin, may aufficiently prevent or ameliorate cerebral vasospasm in severe SAH patients.

Animals↗

Effect of recombinant human lipocortin I on brain oedema in a rat glioma model.

Glucocorticoids have been extensively used to treat brain oedema, but little is known on the mechanisms of steroids in the prevention and resolution of tumour-induced brain oedema. Recently, the mechanism of steroid action is thought to involve synthesis of proteins with antiphospholipase activity called lipocortins. In a previous study, we have demonstrated the efficacy of dexamethasone (DEX) in resolving peritumoural oedema in a rat glioma model. Using the same model, we studied the effect of recombinant human lipocortin I on the resolution of peritumoural oedema. Intracerebral tumours were produced in 6-week-old Wistar rats by implantation of rat glioma C6 cells. In comparison with sham-operated controls, the tumour-implanted animals showed significant increase in the cortical water content, which was reduced by DEX administration to the level in the sham-operated controls. The water content within the tumour was also significantly decreased by DEX treatment. On the other hand, there was no difference in water content between lipocortin-treated and non-treated animals. These findings suggest that tumour-induced brain oedema can be reduced by DEX treatment but not by lipocortin. In conclusion, it is doubtful whether glucocorticoids exert their action in resolving brain oedema by inducing PLA2 inhibitory proteins named lipocortins.

Animals↗

Somatosensory evoked potentials following proprioceptive stimulation of finger in man.

Brisk passive flexion of the proximal interphalangeal joint of the middle finger, produced by using a newly devised instrument, elicited evoked potentials on the scalp. The present study carefully excluded the possible contribution of sensory modalities other than proprioception. The initial part of cortical response was a positive deflexion at the contralateral central area (P1 at 34.6 ms after the stimulus). This was followed by a midfrontal negative wave (N1 at 44.8 ms) and a clear positivity at the contralateral centroparietal area (P2 at 48.0 ms). The evoked responses persisted in spite of the abolition of cutaneous and joint afferents of the finger caused by ischemic anesthesia, but they were lost by ischemic anesthesia of the forearm. Thus, the cortical evoked responses obtained in this study most probably reflect muscle afferent inputs. The scalp distribution of P1 suggested that its cortical generator source was different from that of the N20-P20 components of evoked potentials to electrical median nerve stimulation. Brodmann areas 2 and 3a of human brain, which are known to receive deep receptor inputs, are the most plausible generator sites for the early components of the proprioception-related evoked responses. The amplitude of P2 was related to the velocity but not to the magnitude of movement. In conclusion, the present study established a method for recording the evoked responses to the brisk passive movement of the finger joint, which mainly reflect the dynamic aspects of proprioception mediated through muscle afferent.

Adult↗

Assessment of the teratogenicity of di(2-ethylhexyl)phthalate and mono(2-ethylhexyl)phthalate in mice.

Di(2-ethylhexyl)phthalate (DEHP) and mono-(2-ethylhexyl)phthalate (MEHP) were administered PO or IP to pregnant ICR mice at varying doses on days 7, 8, and 9 of gestation. In groups given DEHP orally, resorptions and malformed fetuses increased significantly at 1,000 mg/kg. Fetal weights were also significantly suppressed. Anterior neural tube defects (anencephaly and exencephaly) were the malformations most commonly produced. No teratogenic effects were revealed by IP doses of DEHP and PO or IP doses of MEHP, although high doses were abortifacient and lethal to pregnant females. Thus DEHP is highly embryotoxic and teratogenic in mice when given PO but not IP. The difference in metabolism, disposition, or excretion by the route of administration may be responsible for the difference in DEHP teratogenicity. Although MEHP is a principal metabolite of DEHP and is several times more toxic than DEHP to adult mice, it seems that MEHP and its metabolites are not teratogenic in ICR mice.

Abnormalities, Drug-Induced↗

Reactive hyperaemic flow characteristics of the right coronary artery compared to the left anterior descending coronary artery in the open-chest dog.

Reactive hyperaemia, the cardiovascular response to transient occlusion of a vessel, was examined and compared in the right coronary artery (RCA) and the left anterior descending coronary artery (LAD) in the same heart of an open-chest dog. First, to study the relationship between reactive hyperaemia and occlusion time in the RCA and LAD, respective flows were measured and reactive hyperaemia was induced with different occlusion times. Occlusion time required for half the maximum peak percentage reactive hyperaemic flow (%PRH), t 1/2, for the RCA was approximately twice that of the LAD: 11.4 +/- 2.3 s versus 5.9 +/- 1.4 s. Maximum %PRH of the RCA was significantly greater than that of the LAD while the percentage repayment of the RCA was lower than that of the LAD. Augmentation of right ventricular oxygen consumption shortened t 1/2 and increased percentage repayment significantly. Second, to determine "critical pressure", which was defined as the perfusion pressure below which reactive hyperaemia was abolished completely, the RCA and LAD were perfused through a shunt from the carotid artery, perfusion pressure was varied in the range of 100 to 20 mmHg and reactive hyperaemia was induced. Critical pressure in the RCA was significantly lower than in the LAD: 32.2 +/- 5.7 mmHg versus 41.5 +/- 5.0 mmHg. These results suggest that the RCA has a greater flow reserve than the LAD. These results were consistent with the difference of oxygen metabolism between the right and left ventricles. The difference of oxygen metabolism between the two ventricles would, at least partly, account for these results.

Animals↗

Variations of hepatitis B virus precore/core gene sequence in acute and fulminant hepatitis B.

Variations of the hepatitis B virus (HBV) precore/core sequence has been shown to play a role in the development of active liver disease in chronic hepatitis B. Whether this is also an important viral factor in the pathogenesis of acute and fulminant hepatitis B is unknown. To determine the precore/core gene sequence in patients with acute and fulminant hepatitis B, 11 patients with fulminant hepatitis B and seven patients with acute hepatitis B were studied. The sequences of precore/core gene were determined by direct sequencing of the polymerase chain reaction amplicons generated from the HBV isolated from patients' serum. For the 11 patients with fulminant hepatitis B, the precore/core regions were successfully amplified in 10 patients. Eight patients exhibited precore stop codon mutations. In addition, nine of the 10 fulminant hepatitis B patients had frequent nucleotide substitutions with corresponding changes in the predicted amino acid sequences in the mid-core and the 5' terminus region of the core gene. In contrast, precore stop codon mutants were not detected, and variations of the HBV core gene were minimal in patients with acute hepatitis B. The association of HBV precore mutants and HBV core gene variations with fulminant hepatitis B and not acute hepatitis B suggested that these variations may be important in modulating the clinical course of HBV infection.

Acute Disease↗

Histone deacetylase inhibitors such as sodium butyrate and trichostatin A inhibit vascular endothelial growth factor (VEGF) secretion from human glioblastoma cells.

We investigated the effects of histone deacetylase (HDAC) inhibitors such as sodium butyrate (SB) and trichostatin A (TSA) on the expression of vascular endothelial growth factor (VEGF) by human glioblastoma T98G, U251MG, and U87MG cells. The glioblastoma cells secreted three VEGF isoforms, VEGF (189), (165), and (121), although the expression levels of VEGF differed between the cell types. Treatment with either 5mM SB or 100 ng/ml TSA reduced VEGF secretion in conditioned media and reduced VEGF mRNA expression. We also studied the expression of VEGF-B, -C, and -D mRNA in human glioblastoma cells and their modulation by HDAC inhibitors. The PCR products of VEGF-B (357bp), VEGF-C (501bp), and VEGF-D (484bp) were amplified in all glioblastoma cells examined. Treatment with SB reduced the expression of VEGF-D mRNA in U251MG cells and the expression of VEGF-B mRNA in U87MG cells. TSA treatment reduced the expression of VEGF-D in U251MG cells. These results suggest that HDAC inhibitors reduce VEGF secretion and modulate the expression of the other VEGF family members, and therefore may inhibit angiogenesis in glioblastoma tissues.

Blotting, Western↗

Carbon dioxide reactivity during prostaglandin E1 induced hypotension for cerebral aneurysm surgery.

The cerebral vasomotor reactivity to carbon dioxide was studied, using a thermal gradient blood flow meter in 43 patients with intracranial cerebral aneurysm under deliberate hypotension induced by prostaglandin E1 (PGE1) infusion. The patients were divided into three groups according to the neurological status. Patients in Groups A and B had subarachnoid haemorrhage due to ruptured cerebral aneurysms. Group A consisted of 23 patients with a neurological grade of I-II and Group B consisted of 11 patients with a grade of III-V. Nine patients with non-ruptured cerebral aneurysm served as controls (Group C). After the dura was opened, local cerebral blood flow (LCBF) was measured. The PGE1 was started with an initial dose of 0.1 microgram.-kg-1.min-1 and the dose was adjusted to maintain MAP at about 70 mmHg. The LCBF and carbon dioxide (CO2) reactivity were estimated during and after PGE1 administration. The LCBF did not change among groups throughout the study period. Carbon dioxide reactivity was estimated as follows: absolute; delta LCBF/delta PaCO2, and relative; % delta LCBF/delta PaCO2 after changing PaCO2 by increasing minute ventilation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Oxygen embolism due to hydrogen peroxide irrigation during cervical spinal surgery.

Hydrogen peroxide is used to cleanse and irrigate wounds. As it decomposes immediately into water and oxygen on contact with organic tissue, it is usually regarded as a safe agent. We report a case of oxygen embolism associated with hydrogen peroxide irrigation of the surgical field during anterior fusion of the cervical vertebrae. It was accompanied by precipitous hypotension and decrease in pulse oximetry oxygen saturation and end-tidal CO2 tension. Semi-closed spaces formed under the apatite dowel and between the apatite dowel and vertebral bodies may have precipitated the absorption of oxygen bubbles into the vasculature. Although this case was associated with a rapid recovery and uneventful sequelae, it discourages the use of hydrogen peroxide in this procedure because of the potential hazards including cardiovascular collapse.

Carbon Dioxide↗

Opioid potentiation of N-type Ca2+ channel currents via pertussis-toxin-sensitive G proteins in NG108-15 cells.

Opioids have both inhibitory and stimulatory effects on neurotransmitter release. While the inhibitory effect has been ascribed to presynaptic inhibition of Ca2+ channels, the cellular mechanism underlying the stimulatory effect is not clear. In order to address this issue, we analyzed the effects of [d-Ala2, d-Leu5]-enkephalin (DADLE) on whole-cell Ba2+ currents (IBa) through voltage-gated Ca2+ channels in NG108-15 neuroblastoma x glioma hybrid cells. Application of DADLE inhibited and washout of DADLE transiently potentiated IBa. Furthermore, potentiation of IBa was elicited even in the presence of DADLE, when inhibition was relieved by a large depolarizing prepulse. DADLE-induced potentiation, as well as inhibition, had both voltage-sensitive and -insensitive components and was abolished by treatment with ICI174864, a delta-opioid antagonist, pertussis toxin (PTX) and omega-conotoxin GVIA. Potentiation developed over @3 min and took 5-20 min to recover, whereas inhibition was complete within 30 s and recovered within 1 min. Although this potentiation should contribute to DADLE-induced desensitization of Ca2+ channel inhibition, it was not the sole mechanism for desensitization. We conclude that the delta-opioid receptor exerts a dual action on N-type Ca2+ channels via PTX-sensitive G proteins, i.e., rapid inhibition followed by slowly developing potentiation.

Barium↗

Human presupplementary motor area is active before voluntary movement: subdural recording of Bereitschaftspotential from medial frontal cortex.

Bereitschaftspotential (BP) was recorded directly from the right supplementary motor area proper (SMA-proper) and its rostral part by chronically implanted subdural electrodes in three patients with intractable focal motor seizure. Cortical electrical stimulation of the SMA-proper revealed the somatotopy as previously reported, and the supplementary negative motor area (SNMA) was identified just anterior to the SMA-proper in two of three cases. In patient 1, eight kinds of simple movements, i.e., left and right middle finger extension, left arm abduction, left and right foot dorsiflexion, left knee extension, tongue protrusion and saccadic eye movement, were studied to record BP. In patient 2, three kinds of movements, i.e., left and right middle finger extension and left foot dorsiflexion, were adopted as movement tasks. In patient 3, four kinds of movements, i.e., left and right middle finger extension and left and right foot dorsiflexion, were adopted. In the SMA-proper, somatotopically distributed BP preceding movements were observed in all three patients. In the SNMA and its rostrally adjacent areas, "SNMA-plus" BPs were generated invariably regardless of the sites of movement. There was no significant difference in the onset time of BPs between the SMA-proper and the SNMA-plus. The present findings suggest that the SNMA-plus is more consistently involved in the preparation for various simple movements than the SMA-proper. This functionally independent region (SNMA-plus) just rostral to the SMA-proper most likely corresponds to a part of the presupplementary motor area which was originally defined in nonhuman primates. Since a part of this area elicited the inhibition of various movements by cortical stimulation, and since it generated BPs regardless of the sites of movement, it may play a higher role in the movement preparatory process than the SMA-proper.

Adult↗

Systems for the detection and analysis of protein-protein interactions.

The analysis of protein-protein interactions is important for developing a better understanding of the functional annotations of proteins that are involved in various biochemical reactions in vivo. The discovery that a protein with an unknown function binds to a protein with a known function could provide a significant clue to the cellular pathway concerning the unknown protein. Therefore, information on protein-protein interactions obtained by the comprehensive analysis of all gene products is available for the construction of interactive networks consisting of individual protein-protein interactions, which, in turn, permit elaborate biological phenomena to be understood. Systems for detecting protein-protein interactions in vitro and in vivo have been developed, and have been modified to compensate for limitations. Using these novel approaches, comprehensive and reliable information on protein-protein interactions can be determined. Systems that permit this to be achieved are described in this review.

Chromatography, Affinity↗

To what extent has the pathophysiology of normal-pressure hydrocephalus been clarified?

The causes and pathophysiology of idiopathic normal-pressure hydrocephalus (NPH) still remain poorly understood. We reviewed the recent pertinent literature on NPH from the past 3 years (1994- 1996) in this journal [Crit Rev Neurosurg (1997) 7:263-275] and here review further manuscripts that appeared mainly in 1997. Recent investigations suggest that idiopathic NPH may be a primary cerebral parenchymal disease rather than a disorder of cerebrospinal fluid (CSF) absorption. The pathophysiology of idiopathic NPH has a wide spectrum ranging from purely hydrodynamic problems owing to a CSF absorption defect to parenchymal changes caused by hemodynamic problems owing to ischemic vascular risk factors. Magnetic resonance imaging (MRI) of NPH frequently shows ischemic vas-cular encephalopathy. NPH may coexist with subcortical white matter vascular encephalopathy, because Binswanger's encephalopathy and idiopathic NPH share common clinical symptoms. Most patients with suspected NPH may suffer from both problems. Because of MRI findings of suspected NPH, ischemic parenchymal changes caused by vasculopathy have been receiving attention. Brain biopsy findings of suspected NPH suggest the presence of parenchymal changes caused by vasculopathy such as arteriosclerosis. Patients with brain biopsy findings of Alzheimer's disease may benefit from shunting. Pathological changes seen by brain biopsy are not specific for NPH. The information accumulated so far about NPH shows a wide clinical spectrum and multifactorial etiology. Therefore, patients with NPH are inhomogeneous, and this makes it difficult to diagnose and select patients for shunting.

Journal Article↗

Aberrant expression of neurotrophic factors in the ventricular progenitor cells of infant congenitally hydrocephalic rats.

OBJECTS: This study was conducted to investigate the roles of neurotrophic factors in the development of hydrocephalus in HTX rats. METHODS: Expressions of brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), and fibroblast growth factor (FGF)-1 were examined immunohistochemically in the cerebral cortex and ventricular zone of 6-day-old rats with congenital hydrocephalus (HTX rats). In the ventricular zone of hydrocephalic rats, potent BDNF-like immunoreactivity (-LI) and weak but significant signals for NT-3- and FGF-1-LIs were observed. However, no significant signals were detected in non-HTX rats. A small subpopulation of ventricular cells was positive for microtubule-associated protein 2 in HTX and non-HTX rats. The positive cells in the HTX rats had neurites much longer than those in the non-HTX animals, suggesting that some ventricular cells of the hydrocephalics had ectopically differentiated into mature neurons. CONCLUSIONS: This abnormal differentiation may have been responsible for the aberrant expressions of neurotrophic factors. In contrast, the cerebral neuronal layers did not show such prominent alterations in neurotrophic factor expression.

Animals↗

Demyelination in severe combined immunodeficient mice by intracisternal injection of cerebrospinal fluid cells from patients with multiple sclerosis: neuropathological investigation.

Demyelinating lesions have been observed in severe combined immunodeficient (SCID) mice after intracisternal administration of cerebrospinal fluid cells (CSFC) from patients with multiple sclerosis (MS). Further investigation in our laboratory revealed that CSFC from 6 to 15 patients at exacerbation of MS caused demyelination. The factor leading to demyelination appears to be the high frequency of relapses during a short period, but not to the severity of the disease. Neuropathological and immunohistochemical studies revealed that a lack of inflammatory mononuclear cell infiltration within and around the demyelinating lesions or in leptomeninges was a common characteristic in all SCID mice with CSFC-induced demyelination. In affected mice killed 2-3 weeks after intracisternal administration of CSFC, foamy/vacuolar lesions with a small or moderate number of lipid-laden macrophages were seen in the white matter. Ultrastructurally, relative preservation of axons, in contrast to myelinoclastic features, as well as some remyelinated axons were observed. In affected SCID mice killed 4-6 weeks after intracisternal administration, more widespread foamy macrophages and necrotic foci with poor remyelination were seen. The findings were similar to those seen in experimental allergic encephalomyelitis, though without lymphocytic infiltration, but were quite different from the lesions observed in Theiler's murine encephalitis virus infection. The absence of an immunohistochemical reaction to the human leukocyte common antigen in the infiltrating mononuclear cells suggested that the graft-versus-host reaction was unlikely cause of the demyelinating lesions.

Adolescent↗

Tyrosine kinase inhibitors suppress N-type and T-type Ca2+ channel currents in NG108-15 cells.

Modulation of Ca2+ channel activity by protein kinases constitutes one of the major mechanisms regulating neuronal functions. Here, we explored the possible modulation of neuronal Ca2+ channels by protein tyrosine kinases (PTKs). To this end, the effects of PTK inhibitors on whole-cell Ba2+ currents (IBa) through voltage-gated Ca2+ channels were analysed in differentiated NG108-15 neuroblastoma x glioma hybrid cells. Genistein suppressed IBa in a concentration-dependent fashion (IC50 = 22 microM). Although daidzein, an analogue of genistein that is devoid of PTK inhibitory activity, also suppressed IBa, we estimated that specific PTK inhibition by genistein reduced IBa amplitude by 30%. In addition, lavendustin A (20 microM) and herbimycin A (20 microM), two other distinct PTK inhibitors, depressed IBa by 22% and 20%, respectively. Genistein suppressed N-type and T-type currents, sparing L-type current, and its effect was independent of G protein activation. The results suggest that the activity of neuronal Ca2+ channels can be modulated by PTKs, opening the possibility that some of the functions of PTKs in the nervous system are mediated by Ca2+ channel modulation.

Animals↗