RESUMO
BACKGROUND: Taxanes are routinely used for the treatment of prostate cancer, however the majority of patients eventually develop resistance. We investigated the potential efficacy of EL102, a novel toluidine sulphonamide, in pre-clinical models of prostate cancer. METHODS: The effect of EL102 and/or docetaxel on PC-3, DU145, 22Rv1 and CWR22 prostate cancer cells was assessed using cell viability, cell cycle analysis and PARP cleavage assays. Tubulin polymerisation and immunofluorescence assays were used to assess tubulin dynamics. CWR22 xenograft murine model was used to assess effects on tumour proliferation. Multidrug-resistant lung cancer DLKPA was used to assess EL102 in a MDR1-mediated drug resistance background. RESULTS: EL102 has in vitro activity against prostate cancer, characterised by accumulation in G2/M, induction of apoptosis, inhibition of Hif1α, and inhibition of tubulin polymerisation and decreased microtubule stability. In vivo, a combination of EL102 and docetaxel exhibits superior tumour inhibition. The DLKP cell line and multidrug-resistant DLKPA variant (which exhibits 205 to 691-fold greater resistance to docetaxel, paclitaxel, vincristine and doxorubicin) are equally sensitive to EL102. CONCLUSION: EL102 shows potential as both a single agent and within combination regimens for the treatment of prostate cancer, particularly in the chemoresistance setting.
Assuntos
Membro 1 da Subfamília B de Cassetes de Ligação de ATP/metabolismo , Antineoplásicos/farmacologia , Protocolos de Quimioterapia Combinada Antineoplásica/farmacologia , Neoplasias da Próstata/tratamento farmacológico , Sulfonamidas/farmacologia , Toluidinas/farmacologia , Subfamília B de Transportador de Cassetes de Ligação de ATP , Animais , Apoptose/efeitos dos fármacos , Ciclo Celular/efeitos dos fármacos , Linhagem Celular Tumoral , Sobrevivência Celular/efeitos dos fármacos , Docetaxel , Relação Dose-Resposta a Droga , Resistencia a Medicamentos Antineoplásicos , Ensaios de Seleção de Medicamentos Antitumorais , Sinergismo Farmacológico , Humanos , Masculino , Camundongos , Microtúbulos/efeitos dos fármacos , Microtúbulos/metabolismo , Neoplasias da Próstata/metabolismo , Neoplasias da Próstata/patologia , Distribuição Aleatória , Sulfonamidas/administração & dosagem , Taxoides/administração & dosagem , Toluidinas/administração & dosagem , Tubulina (Proteína)/metabolismo , Ensaios Antitumorais Modelo de XenoenxertoRESUMO
BACKGROUND AND PURPOSE: Patients who have benign enlargement of the subarachnoid spaces (BESS) have long been suspected of having an increased propensity for subdural hematomas either spontaneously or as a result of accidental injury. Subdural hematomas in infants are often equated with nonaccidental trauma (NAT). A better understanding of the clinical and imaging characteristics of subdural hematomas that occur either spontaneously or as a result of accidental trauma may help distinguish this group of patients from those who suffer subdural hematomas as a result of NAT. The purpose of this study is to describe the clinical and imaging characteristics of subdural hematomas that occur either spontaneously or as a result of accidental injury in infants with BESS. METHODS: We conducted a retrospective review of all patients with BESS complicated by subdural hematomas evaluated at a single institution from 1998 to 2004. Data concerning the patient's clinical presentation, physical findings, imaging, and management are described. RESULTS: During the study period, 7 patients with BESS complicated by subdural hematoma were identified. Their mean age at identification of the subdural hematoma was 7.4 months of age. In 5 cases, there was no recognized trauma before identification of the subdural hematoma. In 3 cases, baseline CT or MR imaging was available, showing prominent subarachnoid spaces without any evidence of subdural hemorrhage. CONCLUSION: Although suspicious for NAT, subdural hematomas can occur in children either spontaneously or as a result of accidental trauma. Caution must be exercised when investigating for NAT based on the sole presence of subdural hematomas, especially in children who are otherwise well and who have BESS.
Assuntos
Síndrome da Criança Espancada/diagnóstico , Hematoma Subdural/diagnóstico , Processamento de Imagem Assistida por Computador , Imageamento por Ressonância Magnética , Espaço Subaracnóideo/patologia , Tomografia Computadorizada por Raios X , Acidentes de Trânsito , Diagnóstico Diferencial , Dilatação Patológica , Dominância Cerebral/fisiologia , Feminino , Traumatismos Cranianos Fechados/diagnóstico , Humanos , Lactente , Masculino , Estudos Retrospectivos , Espaço Subdural/patologiaRESUMO
Development of the nervous system is a complex process, involving coordinated regulation of diverse cellular processes including proliferation, differentiation and synaptogenesis. Disturbances to brain development such as pre- and perinatal hypoxia have been linked to behavioural and late onset of neurological disorders. This study examines the effect of hypoxia on neurite outgrowth in PC12 cells. Hypoxia not only caused a rapid induction of neurite outgrowth, but also synergistically enhanced nerve growth factor (NGF)-induced neurite outgrowth up to 24 h. Transactivation of TrkA receptors was ruled out since the TrkA inhibitor K252a did not block hypoxia-induced neurite outgrowth. Adenosine deaminase prevented hypoxia-induced neurite outgrowth indicating that the effect is mediated by adenosine. Use of the specific adenosine A2A receptor agonist CGS21680 and antagonist 8-3(chlorostyryl)caffeine demonstrated that activation of this receptor is critical for hypoxia-induced neurite outgrowth. Hypoxia-induced neurite outgrowth was blocked by the adenylate cyclase inhibitor, MDL-12,330A, indicating a role for activation of this enzyme in the pathway. Hypoxia was further shown to cause a decrease in growth-associated protein (GAP)-43 levels and a lack of induction of betaIII tubulin, in contrast to NGF treatment which resulted in increased cellular levels of both of these proteins. These findings suggest that hypoxia induces neurite outgrowth in PC12 cells via a pathway distinct from that activated by NGF. Thus, exposure to hypoxia at critical stages of development may contribute to aberrant neurite outgrowth and could be a factor in the pathogenesis of certain delayed developmental neurological disorders.
Assuntos
Adenosina/análogos & derivados , Neuritos/fisiologia , Receptor A2A de Adenosina/fisiologia , Adenosina/farmacologia , Animais , Hipóxia Celular/efeitos dos fármacos , Hipóxia Celular/fisiologia , Relação Dose-Resposta a Droga , Fator de Crescimento Neural/farmacologia , Neuritos/efeitos dos fármacos , Células PC12 , Fenetilaminas/farmacologia , RatosRESUMO
The formation of the unique fusion gene, bcr-abl, and the resultant increase in abl tyrosine kinase activity, is seen as the major driving force in the initiation of chronic myelogenous leukaemia (CML). The deregulation of abl tyrosine kinase activity, brought about by the binding of a portion of the Scr molecule to the SH2 regulatory domain of abl, appears to play a role in promoting resistance to drug-induced apoptosis. Thus the large increase In mature myeloid cells seen in CML could be the direct result of the suppression of apoptosis by the bcr-abl fusion protein. The role and contribution of apoptosis in the progression of CML and the possible role of antisense oligonucleotides to the bcr-abl gene as therapeutic agents is discussed.
Assuntos
Apoptose/genética , Proteínas de Fusão bcr-abl/fisiologia , Leucemia Mielogênica Crônica BCR-ABL Positiva/fisiopatologia , Oligonucleotídeos Antissenso/uso terapêutico , Humanos , Leucemia Mielogênica Crônica BCR-ABL Positiva/genética , Leucemia Mielogênica Crônica BCR-ABL Positiva/metabolismo , Leucemia Mielogênica Crônica BCR-ABL Positiva/patologia , Leucemia Mielogênica Crônica BCR-ABL Positiva/terapiaRESUMO
HL-60 acute myeloblastic and U937 monoblastoid leukaemic cell lines both cleave poly(ADP-ribose)polymerase (PARP), at the onset of apoptosis, in response to a wide range of cytotoxic agents. This appears to be a common feature of leukaemic cell apoptosis. However, in the chronic myelogenous leukaemic (CML) derived cell line, K562, no such cleavage was detectable. This correlated with previous findings that this cell line is particularly resistant to apoptosis induced by cytotoxic agents. Proteolytic cleavage of PARP and the subsequent progression to apoptosis was inhibited by two protease inhibitors NEM and IOD. As both PARP cleavage and DNA fragmentation appeared closely linked in these cell lines, anti-oxidants (previously shown to be effective inhibitors of DNA fragmentation and apoptosis) were also demonstrated to prevent PARP cleavage. These results combine to suggest that ROI may mediate PARP cleavage, DNA fragmentation and the eventual apoptosis of these cells following cytotoxic insult.
Assuntos
Apoptose/fisiologia , Leucemia/metabolismo , Poli(ADP-Ribose) Polimerases/metabolismo , Espécies Reativas de Oxigênio/metabolismo , Antioxidantes/farmacologia , Cisteína Endopeptidases/metabolismo , Inibidores de Cisteína Proteinase/farmacologia , DNA/metabolismo , Humanos , Leucemia/tratamento farmacológico , Leucemia/patologia , Inibidores de Poli(ADP-Ribose) Polimerases , Células Tumorais CultivadasRESUMO
We examined the hypothesis that reactive oxygen species (ROS) contribute to the induction of heat shock proteins (hsps) during stress response. Exposure of HL-60 human myelocytic cells to 42 degrees C induced both hsp72 and hsp27. In the presence of the antioxidant molecules pyrrolidine dithiocarbamate or 1,10-phenanthroline induction of hsp72 and 27 was significantly decreased, while N-acetyl-L-cysteine caused a slight reduction. Prevention of hsp induction was associated with heat sensitization and increased caspase activity, indicating that the cells were undergoing apoptosis. These data suggest that ROS contribute to the induction of hsps and furthermore, that hsp induction and apoptosis are mutually exclusive events within the same cell.
Assuntos
Antioxidantes/farmacologia , Apoptose/efeitos dos fármacos , Resposta ao Choque Térmico/efeitos dos fármacos , Sobrevivência Celular , Indução Enzimática , Células HL-60 , Proteínas de Choque Térmico HSP72 , Proteínas de Choque Térmico/metabolismo , Humanos , Peptídeos e Proteínas de Sinalização Intracelular , Proteínas Serina-Treonina Quinases/metabolismoRESUMO
The authors describe three children with septo-optic dysplasia (SOD)-plus: SOD and an associated malformation of cortical development. All three children had developmental delay, and two of the children had significant associated motor deficits. The associated cortical malformations with SOD include a spectrum of disorders of neuronal organization, not limited, as previously described, to schizencephaly. SOD-plus should be suspected in children with SOD and developmental delay.
Assuntos
Anormalidades Múltiplas/diagnóstico , Encefalopatias/diagnóstico , Córtex Cerebral/anormalidades , Doenças do Nervo Óptico/diagnóstico , Septo Pelúcido/anormalidades , Encefalopatias/complicações , Córtex Cerebral/crescimento & desenvolvimento , Córtex Cerebral/patologia , Criança , Pré-Escolar , Cóclea/anormalidades , Cóclea/patologia , Deficiências do Desenvolvimento/diagnóstico , Deficiências do Desenvolvimento/etiologia , Eletroencefalografia , Feminino , Humanos , Imageamento por Ressonância Magnética , Masculino , Quiasma Óptico/anormalidades , Quiasma Óptico/patologia , Doenças do Nervo Óptico/complicações , Paresia/etiologia , Septo Pelúcido/diagnóstico por imagem , Septo Pelúcido/patologia , Tomografia Computadorizada por Raios XRESUMO
To date, in vivo apoptosis within the thymus has been assessed using morphological criteria and/or detection of a DNA ladder indicative of oligonucleosomal fragmentation of the DNA. Here, we have used a fluorometric method to investigate activation of the caspase protease family in the thymus following in vivo induction of apoptosis by injection of the synthetic glucocorticoid hydrocortisone. Cleavage of DEVD-MCA by caspase-3 and other group II caspases releases free MCA which can be detected fluorimetrically. We demonstrate a time-dependent increase in DEVD-MCA cleavage activity within this tissue indicating the activation of caspase-3 like enzymes. This activity was inhibited by the specific group II caspase inhibitor DEVD-CHO. The interpretation of increased caspase activity was confirmed by immunoblot analysis to reveal cleavage of the caspase-3 substrate, fodrin. In addition, agarose gel electrophoresis of the DNA yielded a ladder pattern, confirming the occurrence of apoptosis. This study demonstrates that DEVD-MCA cleavage activity may be a useful quantitative method for the analysis of apoptosis in thymus tissue. It is a relatively rapid procedure not requiring thymocyte isolation or gel electrophoresis and detects fairly early biochemical changes occurring during apoptosis. In the present study we have used this method to demonstrate the involvement of caspases in thymocyte apoptotic death induced in vivo by glucocorticoids. Thus, measurement of caspase activity in thymus tissue may have applications for studying the in vivo effects of immunotoxicants.
Assuntos
Apoptose , Caspases/metabolismo , Fluorometria/métodos , Timo/enzimologia , Animais , Fragmentação do DNA , Masculino , Ratos , Ratos Sprague-Dawley , Timo/citologiaRESUMO
Glucocorticoids are known to influence the ability of cells to undergo apoptosis, directly inducing apoptosis in thymocytes while inhibiting it in hepatoma and carcinoma cells. Dexamethasone, a synthetic glucocorticoid, is reported to induce partial resistance to certain anticancer drugs in glioma cell lines. In the present study, the effect of dexamethasone on apoptosis of glioma and astrocytoma cell lines was investigated. Exposure of D384 human astrocytoma and C6 rat glioma cells to staurosporine induced apoptosis as judged by the formation of condensed nuclei and caspase activation. Pre-treatment of cells with dexamethasone caused a reduction in staurosporine-induced apoptosis. In addition, dexamethasone also conferred protection against the induction of apoptosis by anticancer agents including camptothecin and etoposide. The protective effect of dexamethasone was dose and time dependent, with maximal protection obtained with concentrations equal to or greater than 100 nM and a pre-incubation period of at least 24h. The earliest significant inhibition was seen with a pre-incubation period of 8h. Co-treatment with the glucocorticoid receptor antagonist RU38486 abolished the effect of dexamethasone, indicating that the protection due to dexamethasone is mediated via this receptor. Dexamethasone was found to induce a time-dependent up-regulation of Bcl-x(L) protein expression. However, the ability of cytochrome c/dATP to activate the caspase cascade in cytosolic extracts of D384 cells was unaffected by prior exposure of the cells to dexamethasone (1 microM) for 48 h. In conclusion, dexamethasone inhibits the induction of apoptosis in astrocytoma cells, probably via an up-regulation of Bcl-x(L), which could prevent cytochrome c release from mitochondria and subsequent caspase activation. Since glucocorticoids are often used in the treatment of gliomas to relieve cerebral oedema, the inhibition of apoptosis by these compounds could potentially interfere with the efficacy of chemotherapeutic drugs.
Assuntos
Antineoplásicos Hormonais/farmacologia , Apoptose/efeitos dos fármacos , Apoptose/fisiologia , Astrocitoma , Neoplasias Encefálicas , Dexametasona/farmacologia , Animais , Inibidores Enzimáticos/farmacologia , Humanos , Metabolismo/efeitos dos fármacos , Ratos , Estaurosporina/farmacologia , Células Tumorais Cultivadas/citologia , Células Tumorais Cultivadas/efeitos dos fármacos , Células Tumorais Cultivadas/metabolismoRESUMO
We report on a 4-year-old boy with Knobloch syndrome. He has vitreoretinal degeneration, high myopia, cataract, telecanthus, hypertelorism, and a high-arched palate. He also has a defect of the anterior midline scalp with involvement of the frontal bone as documented by a computed tomography (CT) scan. The brain was normal on CT scan and magnetic resonance imaging. We present a review of the 23 published cases with this syndrome. Our patient illustrates the importance of investigating for underlying ocular and central nervous system pathology whenever midline scalp defects are present.
Assuntos
Anormalidades Múltiplas , Anormalidades Craniofaciais , Pré-Escolar , Humanos , Masculino , Couro Cabeludo , SíndromeRESUMO
Apoptosis is a controlled form of cell death involving cascades of degradative events. Proteolysis during apoptosis is largely due to the activity of a family of cysteine proteases called caspases. In recent years different roles for members of this family have been revealed. In the central nervous system caspase-2 is highly expressed in the brain during development although many caspases are expressed at low levels in the adult. However, an involvement of caspases in apoptosis of mature neurons has been demonstrated in vivo, where specific inhibitors of caspases are found to protect against ischemic injury. We have reviewed the evidence for the existence of caspases in the central nervous system and their activation during neuronal cell death.
Assuntos
Apoptose/fisiologia , Encéfalo/fisiologia , Cisteína Endopeptidases/fisiologia , Neurônios/fisiologia , Animais , Encéfalo/citologia , Encéfalo/enzimologia , Cisteína Endopeptidases/biossíntese , Humanos , Neurônios/enzimologiaRESUMO
To establish inherent potential for the induction of neural tube defects the ability of selected anticonvulsant agents to interfere with cell division has been established in vitro using an antiproliferative assay in clonal cell lines and a cytotoxicity assay using primary cultures of cerebral cortex neurons at different stages of development. In order to evaluate the relative toxicities of these agents their in vitro effects were determined at 2-3 times the plasma therapeutic level. By these procedures valproate and the benzodiazepines, diazepam and clonazepam, exerted a potent antiproliferative action which could not be attributed to increased cytotoxicity. In contrast phenytoin was markedly cytotoxic but was without an antiproliferative action. This cytotoxicity was most pronounced during the periods of extensive fibre outgrowth. When compared to epidemiological and animal study data, agents which inhibited cell proliferation within twice therapeutic concentration were consistently associated with major neural tube malformations. However phenytoin, found to be positive in the cell cytotoxicity assay, is not associated with neural tube malformations but rather is primarily associated with mental retardation. Thus assessment of antiproliferative activity of anticonvulsant drugs may be one criterion for identification of teratogenic potential during neurulation.
Assuntos
Anticonvulsivantes/farmacologia , Benzodiazepinas/farmacologia , Córtex Cerebral/citologia , Fenitoína/toxicidade , Teratogênicos/farmacologia , Ácido Valproico/farmacologia , Animais , Anticonvulsivantes/toxicidade , Benzodiazepinas/toxicidade , Divisão Celular/efeitos dos fármacos , Linhagem Celular , Células Cultivadas , Córtex Cerebral/efeitos dos fármacos , Camundongos , Ácido Valproico/toxicidadeRESUMO
An elevated, sustained expression of c-fos mRNA was found in primary cultures of mouse cerebellar granule cells following exposure to toxic concentrations of the excitatory amino acids, L-glutamate, L-homocysteate, S-sulpho-L-cysteine and N-methyl-D-aspartate (NMDA), using leakage of lactate dehydrogenase (LDH) as an indicator of cytotoxicity. In contrast, when used at non-toxic concentrations these compounds induced a rapid and transient increase in c-fos mRNA levels. Both LDH release and elevated, sustained c-fos mRNA induction were blocked (in the case of L-homocysteate) or reduced (in the case of L-glutamate and S-sulpho-L-cysteine) by the selective NMDA receptor antagonist (DL(+/-)-2-amino- 5-phosphonopentanoic acid) whereas 6-cyano-7-nitroquinoxaline-2,3-dione (a selective antagonist at non-NMDA ionotropic receptors) had no effect. These data suggest a role for altered c-fos mRNA expression in excitotoxic mechanisms.
Assuntos
Cerebelo/citologia , Aminoácidos Excitatórios/toxicidade , Expressão Gênica/efeitos dos fármacos , Genes fos/efeitos dos fármacos , Neurônios/efeitos dos fármacos , Animais , Sobrevivência Celular/efeitos dos fármacos , Células Cultivadas , Cerebelo/efeitos dos fármacos , Antagonistas de Aminoácidos Excitatórios/farmacologia , L-Lactato Desidrogenase/metabolismo , Camundongos , RNA Mensageiro/biossíntese , Receptores de N-Metil-D-Aspartato/antagonistas & inibidoresRESUMO
Thirteen patients with pathologically proven gangliogliomas were studied radiographically. The computed tomographic (CT) features of these 13 lesions and the other 35 cases in the literature were analyzed. Although the CT appearance of gangliogliomas was varied, certain characteristics were noted. The most common location was in the cerebral hemispheres, most often the temporal lobe. At least part of the tumor was low density in 71% of the unenhanced CT examinations. There were focal calcifications in 35% and enhancement with contrast material in 50%.
Assuntos
Neoplasias Encefálicas/diagnóstico por imagem , Neuroblastoma/diagnóstico por imagem , Tomografia Computadorizada por Raios X , Adolescente , Adulto , Idoso , Criança , Feminino , Humanos , Masculino , Pessoa de Meia-IdadeRESUMO
We describe a duplication of the odontoid process in a 6-year-old patient that included a partially fused midline ossicle on the anterior arch of C-1, fusion of the anterior lip of the foramen magnum and the arch of C-1, and an incomplete bony posterior arch of C-1.
Assuntos
Vértebras Cervicais/anormalidades , Processo Odontoide/anormalidades , Tomografia Computadorizada por Raios X , Vértebras Cervicais/diagnóstico por imagem , Criança , Feminino , Movimentos da Cabeça/fisiologia , Humanos , Processo Odontoide/diagnóstico por imagemRESUMO
The pathogenesis of neurodegenerative diseases such as Parkinson's diseases, amyotrophic lateral sclerosis and Alzheimer's disease is unknown. These diseases are characterized by a slow, progressive loss of particular subsets of neurons. Much evidence has accumulated which supports the hypothesis that oxidative stress and damage by free radicals may play an important part in these diseases. In particular recent studies with the inherited form of amyotrophic lateral sclerosis have revealed mutations in the superoxide dismutase gene, which is one of the cell's main defence mechanisms against oxidative stress. These findings suggest a direct link between oxidative stress and the development of a neurodegenerative disease.
Assuntos
Apoptose/fisiologia , Degeneração Neural/fisiologia , Doenças do Sistema Nervoso/metabolismo , Estresse Oxidativo/fisiologia , Humanos , Doenças do Sistema Nervoso/patologiaRESUMO
OBJECTIVE AND IMPORTANCE: We present a 6-week-old infant who developed a traumatic aneurysm from clearly documented shaken baby syndrome. Despite the theoretical similarity in the mechanism of such injuries, this is the first aneurysm reported that resulted from such a cause. The infant is also the youngest reported patient to have suffered from a traumatic aneurysm. CLINICAL PRESENTATION: Police records documented shaking of the child as well as direct impact on the child's head. Three weeks later, the patient developed an intracerebral hemorrhage, which was revealed by angiography to have resulted from a pericallosal artery aneurysm. TECHNIQUE: The aneurysm was totally resected through a porencephalic cyst, which had developed secondary to ischemic injury to the brain. CONCLUSION: The temporal course, as well as the location of this traumatic aneurysm, is similar to that in older patients.
Assuntos
Maus-Tratos Infantis , Aneurisma Intracraniano/etiologia , Angiografia Cerebral , Artérias Cerebrais/patologia , Hemorragia Cerebral/diagnóstico por imagem , Hemorragia Cerebral/etiologia , Hemorragia Cerebral/cirurgia , Cistos/etiologia , Cistos/cirurgia , Hematoma/diagnóstico por imagem , Hematoma/etiologia , Hematoma/cirurgia , Humanos , Lactente , Aneurisma Intracraniano/diagnóstico por imagem , Tomografia Computadorizada por Raios XRESUMO
Forty-six neonates with intracranial hemorrhage were classified into three groups on the basis of the major computerized tomography (CT) scan findings: Group I consisted of 24 cases of subarachnoid hemorrhage, Group II 20 cases of intracerebral and/or intraventricular hemorrhage, and Group III two cases of subdural hemorrhage. The initial scans in Group I showed blood in the interhemispheric fissure and the supratentorial recess. Sixty percent had an associated hypodensity in the frontal and/or parietal areas, thought to be an indication of ischemia. Changes in the configuration of the ventricular system were infrequent. Initial scans in Group II showed hematomas as follows: one in the brain stem, five in the basal ganglia, 10 in the temporal lobes, and 11 in the ventricles. In 70% of these cases, changes in the configuration of the ventricular system were seen, including compression of a lateral ventricle by mass effect, ventricular dilatation with blood, and obstructive hydrocephalus. Subarachnoid blood was an associated finding in 55% of cases, and focal and diffuse cerebral edema in 40%. Scans in both Group III patients initially showed a mass effect from a subdural clot. In all, 30 patients had one or more follow-up CT scans, and 13 of these were scanned at regular intervals. None of the Group I patients developed hydrocephalus, but 85% of Group II patients with intraventricular blood extending from an intracerebral hemorrhage had this complication. A seizure disorder occurred in 31% of Group I patients and 20% of Group II patients, where it was seen exclusively in those with an intralobar hematoma. A major motor disturbance occurred in 16% of patients; their Ct scans showed evidence of brain destruction involving enlargement of a lateral ventricle, porencephaly, or focal atrophy. Computerized tomography is a useful adjunct to the diagnosis, management, and follow-up study of neonatal intracranial hemorrhage, and correlates well with the clinical findings.
Assuntos
Hemorragia Cerebral/diagnóstico , Doenças do Recém-Nascido/diagnóstico , Peso ao Nascer , Encéfalo/diagnóstico por imagem , Hemorragia Cerebral/complicações , Hemorragia Cerebral/diagnóstico por imagem , Parto Obstétrico , Feminino , Idade Gestacional , Humanos , Recém-Nascido , Doenças do Recém-Nascido/diagnóstico por imagem , Masculino , Tomografia Computadorizada por Raios XRESUMO
The authors present the case of a 10-year-old boy admitted for evaluation of a generalized seizure and a history of headaches. Computerized tomography (CT) and gadolinium-enhanced magnetic resonance (MR) imaging demonstrated a large nonhomogeneous contrast-enhancing mass of the left frontal lobe, with a large cystic component. Cerebral angiography revealed the lesion to be highly vascular and fed entirely by the internal carotid artery system. The patient underwent craniotomy and the lesion was completely removed. Neuropathological study revealed that the tumor was a ganglioglioma. On review of the literature, it was found that gangliogliomas often present in the second and third decade, are known to have cystic components, and are contrast-enhancing on CT and MR imaging; however, they are classically known to be avascular on angiography. This case of a markedly vascular ganglioglioma emphasizes that these tumors should be included in the differential diagnosis of vascular supratentorial lesions.
Assuntos
Neoplasias Encefálicas/diagnóstico , Transtornos Cerebrovasculares/diagnóstico , Lobo Frontal , Ganglioglioma/diagnóstico , Neoplasias Encefálicas/cirurgia , Angiografia Cerebral , Criança , Diagnóstico Diferencial , Ganglioglioma/cirurgia , Humanos , Imageamento por Ressonância Magnética , Masculino , Tomografia Computadorizada por Raios XRESUMO
Crystallographic symmetry plays an important role in structure determination from diffraction or scattering data, in spectroscopy and in simulations. It is convenient and insightful to integrate the display and use of such symmetry data with data analysis and modeling methods. We outline the integration of a suite of crystallographic algorithms, closely coupled with interactive graphical displays. These include techniques for identifying the unit cell of a solid, for automatically determining space and point group symmetries, for generalized displays of symmetry elements overlaid on structural models, and for construction, editing, and transformation of models subject to symmetry constraints. In addition, electron densities derived from periodic density functional calculations can be symmetrized and displayed with the corresponding symmetry elements. Applications of these various capabilities in crystallographic research are illustrated by topical examples.