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PubMed2001

Evidence for telomerase involvement in the angiogenesis of astrocytic tumors: expression of human telomerase reverse transcriptase messenger RNA by vascular endothelial cells.

OBJECT: Evidence from recent in vitro studies indicates that reactivation of telomerase, the enzyme that synthesizes the telomere ends of chromosomes, is a crucial event in the unlimited clonal expansion of endothelial cells that precedes the neoplastic conversion of these cells. It is known that high-grade gliomas express telomerase and that, in these neoplasms, proliferating endothelial cells may undergo transformational changes with development of sarcomatous components within the primitive tumor. To assess whether telomerase is involved in the endothelial cell proliferation that characterizes brain tumor angiogenesis, the authors investigated at the single-cell level the expression of messenger (m)RNA for the human telomerase catalytic subunit human telomerase reverse transcriptase (hTERT) by vascular cells of astrocytic tumors. METHODS: The in situ hybridization (ISH) method was performed by processing histological sections with specific riboprobes for hTERT and for c-myc, an oncogene that is known to upregulate hTERT. Results of the ISH studies were compared with proliferative activity, as estimated by Ki-67 immunostaining. The expression of hTERT mRNA by vascular endothelial cells was related to the histological grade of the tumor because it was detected in five (29%) of 17 low-grade astrocytomas, nine (56%) of 16 anaplastic astrocytomas, and 19 (100%) of 19 glioblastomas multiforme (GBMs). Expression of c-myc mRNA was strictly correlated with that of hTERT mRNA. In low-grade astrocytomas and anaplastic astrocytomas, a dissociation was noted between hTERT mRNA expression and the proliferation rate of endothelial cells. Conversely, GBMs displayed a significant correlation between the level of hTERT mRNA expression and endothelial cell proliferation. Data from an in vitro assay in which human umbilical vein endothelial cells were stimulated to proliferate by adding vascular endothelial growth factor and an ISH study of newly formed vessels surrounding brain infarcts confirmed that expression of hTERT mRNA does not merely reflect the proliferative status of endothelial cells but represents a specific feature of brain tumor neovascularization. CONCLUSIONS: The results of this study are consistent with a role of telomerase in the angiogenesis of astrocytic tumors. Expression of hTERT mRNA by tumor vascular cells is an early event during the progression of astrocytic tumors, which precedes endothelial cell proliferation and may represent a first sign of dedifferentiation. Other than elucidating the mechanisms of tumor angiogenesis, these results encourage research on antitelomerase drugs for the treatment of malignant gliomas.

Adult↗
PubMed2001

[Hyperglycemia: a predictor of poor prognosis in acute stroke].

Hyperglycemia is common and involves up to 50% of the acute stroke patients. Several clinical studies have revealed that hyperglycemia is associated with a poor outcome in terms of mortality and neurological recovery. The results obtained from experimental studies have shown that hyperglycemia exacerbates the ischemic lesions and is associated with an increase of the edema and size of the infarct, as well as a decrease in the cerebral blood flow. In contradiction with animal models no increase in hemorrhagic transformation of the brain infarct after reperfusion is observed among patients with hyperglycemia, unless they are treated with rt-PA. Elevated plasma glucose levels (glycemia > 8 mmol/L) predict poor prognosis, irrespective of age, severity, or stroke sub-type. The benefit to treat a glycemia >=11 mmol/l has been established in terms of mortality for patients with myocardial infarction. Although the clinical benefit of plasma glucose lowering therapy remains unknown regarding acute stroke, based on current evidence, we recommend to treat moderate to mild hyperglycemia with glucose potassium insulin infusions.

Cerebrovascular Circulation↗
PubMed1998

Synthetic combined superoxide dismutase/catalase mimetics are protective as a delayed treatment in a rat stroke model: a key role for reactive oxygen species in ischemic brain injury.

Stroke is a severe and prevalent syndrome for which there is a great need for treatment, including agents to block the cascade of brain injury that occurs in the hours after the onset of ischemia. Reactive oxygen species (ROS) have been implicated in this destructive process, but antioxidant enzymes such as superoxide dismutase (SOD) have been unsatisfactory in experimental stroke models. This study is an evaluation of the effectiveness of salen-manganese complexes, a class of synthetic SOD/catalase mimetics, in a rat focal ischemia model involving middle cerebral artery occlusion. We focus on EUK-134, a newly reported salen-manganese complex demonstrated here to have greater catalase and cytoprotective activities and equivalent SOD activity compared with the previously described prototype EUK-8. The administration of EUK-134 at 3 hr after middle cerebral artery occlusion significantly reduced brain infarct size, with the highest dose apparently preventing further infarct growth. EUK-8 was also protective but substantially less effective. These findings support a key role for ROS in the cascade of brain injury after stroke, even well after the onset of ischemia. The enhanced activity of EUK-134 suggests that, in particular, hydrogen peroxide contributes significantly to this injury. Overall, this study suggests that synthetic SOD/catalase mimetics might serve as novel, multifunctional therapeutic agents for stroke.

Animals↗
PubMed1996

[Value of glucose, glycosylated hemoglobin and fructosamine in blood of patients with ischemic cerebral infarction without diabetes during the early stage of the disease].

Fasting blood glucose level, glycosylated haemoglobin (HBA1) and fructosamine (FA) were measured in 37 non-diabetic patients with a recent (48 h) brain infarction of the carotid territory. The severity of hemiparesis was assessed on admission, and in the 2nd week and 1st month. The functional outcome and fatality rate was estimated after 1 month. On the basis of elevated the HBA1 concentration the group of 54% patients was diagnosed to have prestroke hyperglycemia. Hyperglycemia predating cerebral infarction did not influence fasting glycemia during the few days after stroke. Fasting blood glucose concentration but not the preceding 2-3 months and 2-3 weeks glycemia correlated strongly with the severity of hemiparesis and predicted stroke outcome. Measurement of HBA1 seems to be useful as a screening test for mild, clinically silent diabetes in patients without other risk factors for cerebral stroke.

Aged↗
PubMed1994

[The use of protocols in a neurological department].

OBJECTIVE: To assess the use of protocols in a neurological department. DESIGN: Prospective study. SETTING: Academic Medical Centre, Amsterdam. METHOD: Protocols were drafted by residents and staff members, criticised in protocol meetings and amended if necessary. During 6 months it was ascertained in each newly admitted patient (n = 317), whether a protocol was available, whether it was used and if not, why not. RESULTS: During the period before the introduction of the protocol for brain infarction and TIA (the largest category), protocols were available for 20% of the patients and used in 61% of those patients. After introduction of the brain infarction/TIA protocol, these percentages rose to 46 and 82, respectively. Protocols were not used if doctors were not aware of them or forgot to use them or if they were not applicable to individual patients. CONCLUSION: Writing and implementing protocols are feasible in neurological departments.

Algorithms↗
PubMed1998

Pathophysiology of the ischemic penumbra--revision of a concept.

1. The original concept of the ischemic penumbra surrounding a focus of dense cerebral ischemia is based on electrophysiological observations. In the cortex of baboons following middle cerebral artery occlusion, complete failure of the cortical evoked potential was observed at a cerebral blood flow (CBF) threshold level of approx. 0.15 ml/g/min--a level at which extracellular potassium ion activity was only mildly elevated. With a greater CBF decrement to the range of 0.06-0.10 ml/g/min, massive increases in extracellular potassium occurred and were associated with complete tissue infarction. Thus, the ischemic penumbra has been conceptualized as a region in which CBF reduction has exceeded the threshold for failure of electrical function but not that for membrane failure. 2. Recent studies demonstrate that the penumbra as defined classically by the flow thresholds does not survive prolonged periods of ischemia. The correlation of CBF autoradiograms with diffusion-weighted MR images and the regional distribution of cerebral metabolites reveals that the ischemic core region enlarges when adjacent, formerly penumbral, areas undergo irreversible deterioration during the initial hours of vascular occlusion. At the same time, the residual penumbra becomes restricted to the periphery of the ischemic territory, and its fate may depend critically upon early therapeutic intervention. 3. In the border zone of brain infarcts, marked uncoupling of local CBF and glucose utilization is consistently observed. The correlation with electrophysiological measurements shows that metabolism-flow uncoupling is associated with sustained deflections of the direct current (DC) potential resembling transient depolarizations. Such penumbral cell depolarizations, which are associated with an increased metabolic workload, induce episodes of tissue hypoxia due to the constrained collateral flow, stimulate anaerobic glycolysis leading to lactacidosis, suppress protein synthesis, and, finally, compromise energy metabolism. The frequency of their occurrence correlates with the final volume of ischemic injury. Therefore, penumbral depolarizations are regarded as a key event in the pathogenesis of ischemic brain injury. Periinfarct DC deflections can be suppressed by NMDA and non-NMDA antagonists, resulting in a significant reduction of infarct size. 4. The histopathological sequelae within the penumbra consist of various degrees of scattered neuronal injury, also termed "incomplete infarction." The reduction of neuronal density at the infarct border is a flow- and time-dependent event which is accompanied by an early response of glial cells. As early as 3 hr after vascular occlusion a generalized microglial activation can be detected throughout the ipsilateral cortex. Astrocytic activation is observed in the intact parts of the ischemic hemisphere from 6 hr postocclusion onward. Thus, the penumbra is a spatially dynamic brain region of limited viability which is characterized by complex pathophysiological changes involving neuronal function as well as well as glial activation in response to local ischemic injury.

Animals↗
PubMed1990

[Cerebral infarction in pernicious malaria. Diagnostic value of computed tomography].

Case report of a severe form of neuropaludism, contracted in a territory with Plasmodium falciparum completely insensitive to chloroquine. CAT Scan views displayed a small brain infarction. Complete recovery was obtained with a treatment including quinine, tracheal intubation and ventilatory support, sedation with barbiturates. CAT Scan views demonstrated a complete regression of cerebral lesions.

Adult↗
PubMed1994

Baseline silent cerebral infarction in the Asymptomatic Carotid Atherosclerosis Study.

BACKGROUND AND PURPOSE: In a group of patients with high-grade asymptomatic carotid artery stenosis, we prospectively determined the prevalence and radiological characteristics of clinically asymptomatic brain infarction evident on computed tomography. Risk factors and extent of carotid disease were also determined. METHODS: Patients randomized into the Asymptomatic Carotid Atherosclerosis Study (ACAS) underwent a neurological history, a detailed stroke/transient ischemic attack questionnaire, and a detailed neurological examination. Computed tomography scans were examined by standardized criteria developed as part of a quality-control program supervised by a neuroradiologist. The presence, location, and size of all cerebral infarctions evident by computed tomography were determined. RESULTS: Among 1132 patients, 848 had no history of stroke or transient ischemic attack. One hundred twenty-six patients (15%) had a silent infarct; 95 (11%) had one, 24 (3%) had two, and 7 (1%) had three or more infarcts. The infarct size was small and deep for 117 patients (72%), less than one-half lobe for 45 (28%), and one-half to less than one lobe for 1 (0.5%). The silent infarcts were evenly distributed ipsilaterally and contralaterally to the study artery but were significantly more frequent in the right hemisphere (P < .05). Factors associated with silent infarction were abnormal gait (P < .001), abnormal deep tendon reflexes or plantar responses (P = .038), but not degree of carotid stenosis. Silent infarction was less frequent among this totally asymptomatic cohort (15%) compared with those with transient ischemic attacks (34/139, 25%; P < .001). CONCLUSIONS: Silent infarction in the setting of asymptomatic carotid stenosis is not uncommon, but silent infarctions are rarely sizable. The clinical significance of silent cerebral infarction in patients with asymptomatic carotid artery stenosis has yet to be established.

Adult↗
PubMed1991

Restricted and anisotropic displacement of water in healthy cat brain and in stroke studied by NMR diffusion imaging.

The occlusion of the middle cerebral artery in cat brain was used as an experimental stroke model to investigate the physical basis of the recently reported lowered diffusion constant of water in acute infarcted brain tissue (Moseley et al., Magn. Reson. Med. 14, 330, 1990). The original findings were confirmed in this study of 12 animals investigated with the diffusion-sensitized stimulated echo sequence. The following additional results were obtained: First, the onset of significant lowering of the diffusion constant in the stroke area varied significantly (up to 2.5 h depending on the animal). Second, the affected area is much more clearly outlined in diffusion-weighted images than in T2-weighted images, even in the period between 3 to 12 h following occlusion. Third, for diffusion times between 50 and 2000 ms. the diffusion constant of water is independent of diffusion time in healthy tissue, as well as in the stroke area. Fourth, the diffusion anisotropy is similar in healthy and in stroke area and remains similar regardless of the diffusion time used.

Animals↗
PubMed1996

Expression of tumor necrosis factor alpha after focal cerebral ischaemia in the rat.

Induction of tumor necrosis factor alpha was studied in the brain of rats after focal cerebral ischaemia by occlusion of the left middle cerebral artery. Using a specific antisense riboprobe for in situ hybridization histochemistry, cells positive for tumor necrosis factor alpha messenger RNA were detected within 30 min in the brain regions known to be necrotic within one to two days after onset of ischaemia. Their number increased over a time period of 1-8 h and then declined. Only a few tumor necrosis factor alpha messenger RNA positive cells could be detected four days after the onset of ischaemia. Reverse-transcription polymerase chain reaction experiments showed that maximal increase of tumor necrosis factor alpha messenger RNA level in the ischaemic brain hemisphere occurred 3 h after occlusion of the middle cerebral artery. Immunocytochemical experiments using an anti-tumor necrosis factor alpha antibody showed the presence of tumor necrosis factor alpha immunopositive cells as early as 30 min after occlusion of the middle cerebral artery in the same brain regions where tumor necrosis factor alpha messenger RNA positive cells were detected. Tumor necrosis factor alpha positive cells were highly abundant in the infarcted brain 8-24 h, but only few of them were detectable four days after the onset of ischaemia. Specificity of the anti-tumor necrosis factor alpha antibody and of the induction of tumor necrosis factor alpha protein was confirmed by western blot analysis. Tumor necrosis factor alpha messenger RNA- and protein-positive cells were also detected in the watershed zone and in some structures of the contralateral brain hemisphere. According to their morphology, tumor necrosis factor alpha-positive cells could be identified as microglial cells and macrophages at different states of activation. This assumption was further confirmed by double-labeling studies using the isolectin B4 from Griffonia simplicifolia, a specific microglial/macrophage cell marker. These results demonstrate that expression of tumor necrosis factor alpha is part of an intrinsic inflammatory reaction of the brain after ischaemia.

Animals↗
PubMed1983

Barbiturate-enhanced detection of brain lesions by carbon-14-labeled 2-deoxyglucose autoradiography.

Cerebral glucose metabolism in rats was examined 1 week after the production by ibotenic acid of unilateral striatal lesions. The incorporation of carbon-14-labeled deoxyglucose decreased within the lesion but much less than that of carbon-14-labeled glucose. Barbiturate anesthesia caused a reversal of the asymmetric striatal deoxyglucose labeling, such that the lesioned striatum retained more tracer than the contralateral side. The combined use of barbiturates and radiolabeled deoxyglucose may enhance the identification of recent brain infarction in experimental animals and in man.

Animals↗
PubMed1983

Cerebral infarction due to carotid occlusion and carbon monoxide exposure. II. Influence of preganglionic cervical sympathectomy.

Unilateral cerebral infarcts were produced in the rat by ligation of one common carotid artery and subsequent exposure to carbon monoxide. The incidence and extension of brain infarcts was increased in animals with additional ipsilateral cervical preganglionic sympathectomy. Sympathectomy did not affect markedly the respiration and systemic circulation. The effect of sympathectomy was attributed to a cutaneous vasodilation, leading to an extracranial steal phenomenon.

Animals↗
PubMed2001

Hyperdense sylvian fissure MCA "dot" sign: A CT marker of acute ischemia.

BACKGROUND AND PURPOSE: The hyperdense appearance of the main middle cerebral artery (HMCA) is now a familiar early warning of large cerebral infarction, brain edema, and poor prognosis. This article describes the hyperdensity associated with embolic occlusion of branches of the middle cerebral artery in the sylvian fissure (MCA "dot" sign). We define it and determine its incidence, diagnostic value, and reliability. METHODS: CT scans performed on patients with acute ischemic stroke within 3 hours of symptom onset were analyzed for signs of thromboembolic stroke and evidence of early CT ischemia. Two neuroradiologists and 2 stroke neurologists initially blinded to all clinical information and then with knowledge of the affected hemisphere evaluated scans for the presence of the MCA dot sign, the HMCA sign, and early MCA territory ischemic changes. RESULTS: Of 100 consecutive patients who presented within 3 hours of symptom onset, 91 were considered at symptom onset to have anterior circulation stroke syndromes. Early CT ischemia was seen in 74% of these baseline CT scans. The HMCA sign was seen in 5% of CT scans, whereas the MCA dot sign was seen in 16%. All patients then received intravenous tissue plasminogen activator. All 5 patients with an HMCA sign, including 2 with an associated MCA dot sign, were either dead or dependent at 3 months. The 14 patients with an MCA dot sign alone were independent at 3 months in 64% of cases, compared with 50% without the sign (Fisher's exact test P:=0.79). Balanced kappa statistics for both the HMCA and the MCA dot sign were in the moderate to good range when the stroke symptom side was given. CONCLUSIONS: The MCA dot sign is an early marker of thromboembolic occlusion of the distal MCA branches seen in the sylvian fissure and is associated with better outcome than the HMCA sign.

Acute Disease↗
PubMed2005

Results of a phase II trial of gemcitabine in patients with non-small-cell lung cancer and a performance status of 2.

This trial was designed to determine the 1-year survival rate, efficacy, progression-free survival (PFS), and toxicity with gemcitabine in patients with stage IIIB (with pleural effusion) or stage IV non-small-cell lung cancer (NSCLC) with Eastern Cooperative Oncology Group (ECOG) performance status (PS) of 2. Gemcitabine 1250 mg/m2 was administered intravenously on days 1 and 8 of each 21-day cycle. Treatment consisted of 6 cycles; patients who responded with complete response or partial response received < or = 2 additional cycles. Forty-two patients were enrolled at 31 community-based centers between March and November 2002. Most patients had stage IV disease (74%). The median age was 73 years (range, 58-84 years), and 19% had received prior palliative radiation therapy. Patients received a median of 3 cycles (range, 1-8 cycles). The median survival was 4.8 months (range, < 1 to 19.2 months), and the estimated 1-year survival was 20%. Median PFS was 2.5 months (range, < 1 to 19.2 months), and PFS at 1 year was 11.1%. Thirty-one patients died of disease progression, and 1 each died of myocardial infarction, brain herniation, pneumonia, and respiratory failure. Seven patients were not evaluable for response; 4 refused or received no treatment, treatment in 2 failed (myocardial infarction and pneumonia), and 1 was lost to follow-up. Among 35 evaluable patients, there were 5 partial responses (14%), 10 with stable disease (29%), and 20 with disease progression (57%). Drug-related grade > or = 3 toxicities included neutropenia (18%), anemia (8%), and dyspnea (2.6%). These results suggest that patients with NSCLC with an ECOG PS of 2 may benefit from single-agent chemotherapy gemcitabine. General toxicity, including myelotoxicity, was relatively low. Further studies comparing single-agent chemotherapy with combination chemotherapy for patients with a PS of 2 are warranted.

Aged↗
PubMed2004

[Study on changes of neuron apoptosis after focal cerebral ischemia/reperfusion in the aged rats].

OBJECTIVE: To study ultrastructured change and neuron apoptosis after focal cerebral ischemia/reperfusion (I/R) in the aged rats. METHODS: The aged SD rats (20-21 months) and the young (4-5 months) were subjected to 3 hours of middle cerebral artery occulsion with the intraluminal filament technique, followed by reperfusion for 3 hours, 6 hours, 12 hours, 24 hours, 72 hours. The ultrastructure of brain, infarct zone and neuron apoptosis were observed. RESULTS: The cerebral infarct zone increased in the aged rats with ischemia for 3 hours and I/R for 12 hours compared with those in the young. The brain injury was obviously deteriorated with I/R time longer, which was serious in the aged than that in the young. The neuron apoptosis increase with I/R time longer, and showed earlier and lasted longer in the aged. CONCLUSION: The cerebral injury is serious and neuron apoptosis increase shows early and lasts longer.

Age Factors↗
PubMed1978

[Cerebral infarct risk factors].

The possible risk factors were evaluated in 249 patients with cerebral infarction and in the control group consisting of 190 subjects of the same age and sex distribution. The following factors were significantly associated with brain infarction: elevated blood pressure, cardiac abnormalities, elevated blood glucose content, abnormal glucose tolerance, elevated blood cholesterol and beta-lipoproteid content and hemoglobin level. It was concluded that at present the key to stroke prevention is the early detection and control of hypertension and cardiac activity impairment.

Adult↗
PubMed1992

Assessment of craniocerebral asymmetries in children by computed tomography.

Computed tomographic (CT) scans of 32 children (mean age 2.8 +/- 2.5 years) with a wide range of craniocerebral asymmetry (CCA) were analyzed. Hemiparesis and epilepsy were the main clinical presentations. Two-thirds of the patients had brain infarcts. The degree of cerebral and ventricular asymmetry was evaluated by ratios obtained by linear measurements. The patients were divided into two groups according to the index of maximal asymmetry. The incidence of hemiparesis and the width of the cerebral ventricles did not differ in the two groups. This may be due to the fact that most of our patients suffered from perinatal insult to the brain, allowing time for remodeling and plastic changes to occur. The use of measurable structural parameters in craniocerebral asymmetry offers a basis for comparable radiological assessment.

Asphyxia Neonatorum↗
PubMed1997

Postischemic brain injury is affected stereospecifically by pentazocine in rats.

We tested whether rats treated with the sigma1-receptor ligand, (+)-pentazocine, during transient focal ischemia would have a smaller volume of postischemic brain infarction than rats treated with the nonspecific opioid-receptor ligand (-)-pentazocine. Rats underwent focal cerebral ischemia using the filament occlusion technique for 2 h, followed by 22 h of reperfusion. Rats received (+) or (-)-pentazocine (n = 9 each group) at a dose of 2 mg x kg(-1) x h(-1) by continuous intravenous infusion from 1 h of ischemia to 22 h of reperfusion. Triphenyltetrazolium-determined infarction volume of ipsilateral striatum ([+]-pentazocine, 19 +/- 4 mm3, mean +/- SEM; [-]-pentazocine, 44 +/- 5 mm3) and cerebral cortex ([+]-pentazocine, 26 +/- 12 mm3; [-]-pentazocine, 134 +/- 29 mm3) was smaller in rats treated with (+) compared with (-)-pentazocine. Infarction volume in rats treated with (-)-pentazocine was also very similar to the infarction volume in saline-treated control rats from our previous study (striatum 44 +/- 4 mm3; hemisphere 136 +/- 27 mm3). These data indicate that sigma1-receptors may play an important role in the mechanism of injury both in cortex and striatum after 2 h of transient focal ischemia in rat.

Analgesics, Opioid↗