PubMed Health⌕ Search

Biomedical subjects

J J Olson

Publications and source records attributed to J J Olson.

At least 19 recordsLinked to original sources
PubMed2001

Effectiveness of oral or nebulized dexamethasone for children with mild croup.

OBJECTIVE: To assess the efficacy of oral dexamethasone or nebulized dexamethasone sodium phosphate in children with mild croup. METHODS: Double-blind, placebo-controlled study of 264 children between 6 months and 6 years of age with symptoms of croup for fewer than 48 hours. Patients were excluded if they received racemic epinephrine or corticosteroid treatment. Other exclusion criteria included corticosteroid treatment during the 14 days prior to enrollment or complicating medical condition. Subjects randomly received oral dexamethasone (0.6 mg/kg), nebulized dexamethasone sodium phosphate (160 microg), or placebo. Telephone follow-up was obtained on days 1, 2, 3, 4, and 7. MAIN OUTCOME MEASURES: The primary outcome measure was treatment failure, defined as receiving corticosteroid or racemic epinephrine treatment during the 7 days after enrollment in the study. Secondary outcome measures included seeking additional care and the parental assessments of the patients' condition obtained during follow-up (worse, same, better, or gone). RESULTS: Eighty-five patients received oral dexamethasone, 91 received nebulized dexamethasone, and 88 received placebo. There were 3 treatment failures in the oral dexamethasone-treated group, 12 in the nebulized dexamethasone-treated group, and 10 in the placebo-treated group (P =.05). Ten children in the oral dexamethasone-treated group sought additional care compared with 27 and 29 in the nebulized dexamethasone-treated and placebo-treated groups, respectively (P =.002). Parents of children in the oral dexamethasone-treated group reported greater improvement on day 1 (P<.001) compared with the nebulized dexamethasone-treated and placebo-treated groups. CONCLUSIONS: Children with mild croup who receive oral dexamethasone treatment are less likely to seek subsequent medical care and demonstrate more rapid symptom resolution compared with children who receive nebulized dexamethasone or placebo treatment.

Administration, Inhalation↗
PubMed2000

Extraneural metastatic glioblastoma after interstitial brachytherapy.

PURPOSE: This is a report of 3 cases of extraneural metastasis of glioblastoma after interstitial radiation and assessment of pertinent literature addressing concern over an increased risk of these events with this therapy. METHODS AND MATERIALS: In a series of 82 patients treated with (125)I brachytherapy for primary malignant brain tumors over a 7-year interval, 3 cases of extraneural glioblastoma were identified. The multicatheter technique for delivery of (125)I sources was utilized in all. Extraneural metastases were documented by imaging studies or biopsy. Over the same period, 310 patients with primary malignant brain tumors were treated without brachytherapy. RESULTS: Biopsy-proven scalp and skull metastases occurred in 2 patients, at 3 and 8 months following brachytherapy. Each developed radiographic evidence of systemic metastases at 7 and 14 months postbrachytherapy, respectively. The third patient developed biopsy-proven cervical node involvement 4 months after brachytherapy. No patients with malignant gliomas undergoing craniotomy or stereotactic biopsy, but not brachytherapy, during the same time period developed extraneural metastases. Incidence in previously reported series commenting on this otherwise rare process range from 0% to 4.3%. The incidence of extraneural metastases in this series is 3.7% (3/82) and is comparable to those reports. CONCLUSIONS: Percutaneous catheter-delivered brachytherapy may be associated with an increased incidence of extraneural metastatic glioma.

Adult↗
PubMed2000

Cloning of neuronal mtDNA variants in cultured cells by synaptosome fusion with mtDNA-less cells.

Synaptosome cybrids were used to confirm the presence of heteroplasmic mtDNA sequence variants in the human brain. Synaptosomes contain one to several mitochondria, and when fused to mtDNA-deficient (rho degrees ) mouse or human cell lines result in viable cybrid cell lines. The brain origin of mouse synaptosome cybrid mtDNAs was confirmed using sequence polymorphisms in the mtDNA COIII, ND3 and tRNA(Arg)genes. The brain origin of the human synaptosome cybrids was confirmed using a rare mtDNA Mbo I polymorphism. Fusion of synaptosomes from the brain of a 35-year-old woman resulted in 71 synaptosome cybrids. Sequencing the mtDNA control region of these cybrid clones revealed differences in the number of Cs in a poly C track between nucleotide pairs (nps) 301 and 309. Three percent of the cybrid clones had mtDNAs with 10 Cs, 76% had nine, 18% had eight and 3% had seven Cs. Comparable results were obtained by PCR amplification, cloning and sequencing of mtDNA control regions directly from the patient's brain tissue, but not when the control region was amplified and cloned from a synaptosome cybrid homoplasmic for a mtDNA with nine Cs. Thus, we have clonally recovered mtDNA control region length variants from an adult human brain without recourse to PCR, and established the variant mtDNAs within living cultured cells. This confirms that some mtDNA heteroplasmy can exist in human neurons, and provides the opportunity to study its functional significance.

Adult↗
PubMed2000

Neurosurgical advances in the treatment of brain tumors.

Surgery remains an important part of the treatment of primary malignant brain tumors. When surgery is utilized, care must be taken to maximize the safety of the procedures. This article emphasizes advances in lesion localization within the brain and technology used to identify the function of normal tissue around the tumor. Many of the new treatment paradigms involve a surgical procedure. For example, surgery is necessary for biodegradable treatment delivery systems, and for some focal radiation therapy. Neurosurgeons are familiar with implantable catheter systems for other types of disease such as hydrocephalus; however, there is now an opportunity to take advantage of such technology to assist in the delivery of treatment agents locally within a tumor. Although no specific surgical advance has offered cure of malignant tumors, surgery remains necessary for utilization of the treatment advances now becoming available.

Brachytherapy↗
PubMed2000

Intracranial extraskeletal mesenchymal chondrosarcoma: case report.

OBJECTIVE AND IMPORTANCE: We present a patient with a dural-based intracranial extraskeletal mesenchymal chondrosarcoma, which was initially thought to be an atypical meningioma. This rare tumor should be considered in the differential diagnosis of young adults with an aggressive-appearing dural-based lesion. CLINICAL PRESENTATION: A 21-year-old woman reported a 3-week history of severe headaches and intermittent nausea and vomiting. Neurological examination revealed right optic nerve swelling. Magnetic resonance imaging demonstrated a large, intensely enhancing extra-axial mass, which appeared to originate from the right side of the falx cerebri with significant mass effect. A presumptive diagnosis of meningioma was made. INTERVENTION: The patient underwent preoperative embolization of the lesion and then underwent a bicoronal craniotomy, gross total resection of the tumor, removal of invaded calvarial bone, and cranioplasty. Pathological examination revealed an extraskeletal mesenchymal chondrosarcoma. Because of the potential for recurrence, the patient received subsequent radiotherapy. She remains free of recurrence 18 months after surgery. CONCLUSION: Intracranial mesenchymal chondrosarcoma is a rare neoplasm that can mimic a meningioma radiographically. We present the first patient in whom this lesion has been documented with computed tomography, cardiography, magnetic resonance imaging, and pathological findings. We emphasize the importance of gross total resection and close follow-up for this potentially aggressive tumor, and we present a review of the literature.

Adult↗
PubMed1999

Analysis of cyclin dependent kinase inhibitors in malignant astrocytomas.

The cyclin-dependent kinase inhibitors p16, p21, and p27 in human brain, and brain tumors were examined to explore clinicopathologic correlations. Western analysis and immunohistochemistry was performed and correlated retrospectively with the patients clinical characteristics. A trend was found between increased progression-free survival and p27 expression. There was no correlation between p27 expression and age or gender. The expression of p27 in malignant gliomas may have prognostic value. In addition, an investigation of the therapeutic benefit of overexpression of this cyclin-dependent kinase inhibitor is warranted given reports of diminished malignant potential of tumors expressing p27.

Adolescent↗
PubMed1999

Tumor suppressor gene alterations in malignant gliomas: histopathological associations and prognostic evaluation.

We have examined a series of 135 gliomas for alterations of the p53, CDKN2A (p16) and PTEN tumor suppressor genes (TSGs) in order to evaluate the incidence of their inactivation as a function of tumor malignancy and cellular differentiation, and to examine potential associations with patient outcome. The composition of this series, classified using WHO criteria, is as follows: 27 grade 2 tumors (11 astrocytomas, 12 oligoastrocytomas, 4 oligodendrogliomas), 42 grade 3 tumors (22 astrocytomas, 16 oligoastrocytomas, 4 oligodendrogliomas), and 66 grade 4 tumors (63 astrocytomas and 3 oligoastrocytomas). Similar frequencies of p53 mutation were observed among grade 2 (37.0%), and grade 3 tumors (38.1%), as well as between astrocytomas and mixed tumors. CDKN2A and PTEN mutations were clearly associated with increasing tumor malignancy (occurring in 0% of grade 2 tumors, 14.3% and 4.8% respectively of grade 3 tumors, and 27.3% and 30.3% respectively of grade 4 tumors) and were observed at substantially higher rates among astrocytomas. For the tumor suppressor genes examined, there was no relationship between the occurrence of any two TSG inactivation events. With regard to outcome, the p53 genetic status showed no significant relationship with patient survival. The CDKN2 and PTEN alterations were negative prognostic indicators of survival when evaluated in all 135 gliomas, but failed to predict outcome when evaluated in either of the high grade (3 or 4) tumor groups.

Adolescent↗
PubMed1998

Lipomatous glioneurocytoma of the posterior fossa with divergent differentiation: case report.

OBJECTIVE AND IMPORTANCE: We report a case of a posterior fossa neuroepithelial tumor with unusual clinical presentation, magnetic resonance imaging appearance, and morphological features. CLINICAL PRESENTATION: This 66-year-old man presented with a history of gait ataxia, dizziness, and tinnitus and was found to have a large tumor in the posterior fossa and cerebellopontine angle. INTERVENTION: Gross total excision of the tumor was accomplished. Histologically, the most unique features were macrovesicular accumulations of lipid, giving the tumor (at least focally) an appearance virtually identical to that of mature adipose tissue. Evidence of biphasic neuronal and glial differentiation was noted by immunohistochemistry and electron microscopy. CONCLUSION: A literature review is presented. Diagnostically, this neoplasm seems to fit in a unique group of rarely described, lipomatous neuroectodermal tumors that show divergent neuronal and glial differentiation.

Aged↗
PubMed1998

Gene amplification as a prognostic factor in primary brain tumors.

The most reliable prognostic factors for patients with primary malignant brain tumors remain histology, age, and functional status. Management of these individuals might be improved by quantifying pertinent molecular markers. We have measured the gene dosage of the epidermal growth factor receptor (EGFR), mouse double minute 2 (MDM2), and cyclin-dependent kinase 4 (CDK4) genes in a series of brain tumor specimens and correlated their amplification status with standard prognostic factors and survival. Individual tumor DNA was successively hybridized with probes for EGFR, MDM2, and CDK4. The signal was quantified by densitometry, and amplification was defined as gene signal > or = 2 times normal. Survival, age, Karnofsky performance status, and histology were correlated with gene amplification. Nineteen astrocytomas, 20 anaplastic astrocytomas, and 70 glioblastomas had complete data available. Median survival with and without any form of gene amplification was 70.7 and 88.6 weeks, respectively (P = 0.0369). For the EGFR gene alone, those with and without amplification had a median survival of 58.9 and 88.6 weeks, respectively (P = 0.0104). By Cox analysis, only tumor histology (P = 0.04) and Karnofsky performance status (P = 0.0157) were significant independent predictors of survival. Gene amplification by itself was not predictive of survival, even for glioblastomas (P = 0.8249). The lack of correlation between gene amplification and survival for patients with primary malignant brain tumors may be because EGFR, MDM2, and CDK4 are only portions of larger signaling systems. Therefore, the lack of a direct correlation between a single gene and outcome is not entirely unexpected.

Adult↗
PubMed1997

Stereotactic radiosurgery of malignant and benign intracranial lesions utilizing a patient rotator.

This study examines the characteristics of the patient groups, treatment parameters, and results of therapy for 126 intracranial lesions treated with stereotactic radiosurgery utilizing a "patient rotator" and a linear accelerator. A retrospective review was conducted and data on 122 patients (21 patients with arteriovenous malformations-AVMs, 40 patients with 41 metastatic tumors, 24 patients with malignant gliomas and 37 patients with other benign lesions) were analyzed. Clinical and radiographic response was obtained from chart review and/or telephone follow-up. The average follow-up was 12.1, 13.0, 5.7, and 23.1 months in patients with AVMs, malignant gliomas, metastases, and other lesions, respectively. Median survival times (MST) of the metastatic and glioma group were 9 and 38 months, respectively. Complete or partial radiographic response at follow-up was seen in 62.5% of AVM patients, 33.3% of patients with metastases, 11.8% of patients with malignant gliomas, and 19.3% of patients with other lesions. (1) Local control of brain metastases and benign intracranial lesions can be obtained with single dose stereotactic radiosurgery. (2) The MST and local control rate for metastatic disease obtained are comparable with those in the literature. (3) The patient rotator method for stereotactic radiosurgery is an effective tool for treating selected intracranial lesions.

Adult↗
PubMed1996

Intra-arterial cisplatin in malignant brain tumors: incidence and severity of otic toxicity.

Intra-arterial (IA) cisplatin is used to treat gliomas with the goal of maximizing drug concentration in the brain while minimizing systemic toxicity. The present study is based on the author's experience with IA cisplatin administration in 12 patients. The primary goal of the study was to document the extent of otic toxicity in these individuals. Hearing was tested clinically and with audiograms, before each IA cisplatin injection. Eight women and four men with a mean age of 39 1/2 years (range 22-61) were treated. Diagnoses included 7 glioblastoma multiformes, 4 anaplastic astrocytomas, and 1 gliosarcoma. Diagnosis was obtained by stereotactic biopsy in four and craniotomy for resection and debulking in eight. The mean number of IA injections per patient was 4.58 (range 3-6). The cisplatin dose was 60 mg/m2 with the average dose of cisplatin per cycle being 116 mg (range 96-130 mg). Eleven patients had the agent administered via the internal carotid and one received it by way of a vertebral artery. Nine of the twelve patients (75%) demonstrated pure tone loss, as measured by audiography, of greater than 15 dB in the higher frequencies range (> or = 3 kHz) bilaterally. One patient became deaf and two others had clinically significant hearing loss. The severity of the auditory damage increased after each administration in each of the cases with clinical abnormality. IA cisplatin may have a role in the treatment of patients with primary malignant brain tumors, but further developments to limit otic toxicity would be of value.

Adult↗
PubMed1996

Molecular genetics and molecular biology advances in brain tumors.

As the genes that regulate cell growth and proliferation are being identified and their encoded proteins characterized, our understanding of the molecular basis of tumor development is expanding rapidly. This review focuses on recent studies examining alterations of growth-regulatory genes in brain tumors, including those involving the inactivation of gene products that normally suppress cell growth (tumor-suppressor genes) or those involving the activation of gene products that promote cell growth (oncogenes) and presents information concerning the molecular biology associated with these changes.

Brain Neoplasms↗
PubMed1996

Transfection of IFNalpha in human glioblastoma cells and tumorigenicity in association with induction of PKR and OAS gene expression.

Previously these authors and others demonstrated frequent homozygous deletions of the chromosome 9p-localized class I interferon (IFN) gene cluster in glioblastoma tumors and cell lines. To investigate the biological effects of class I IFN gene transfer and constitutive expression in glioblastoma cells devoid of this gene cluster, the authors have developed a stable IFNalpha "transfectant" of the cell line U118. The expression of IFNalpha protein in the U118 transfectant clone is associated with decreased levels of DNA synthesis exhibited by cultures of transfected cells, reduced colony-forming ability in soft agar, and loss of tumorigenicity in athymic nude mice. To address the molecular consequences of constitutive IFNalpha synthesis, they examined the expression of four genes whose transcription has been shown to be responsive to IFN-mediated signal transduction and could be important to the observed antiproliferative and antitumor effects. Northern blot analysis revealed that changes in the levels of messenger (m)RNA for two of these genes, c-myc and mhc class I, are minor. However, mRNAs for oligoadenylate synthetase (OAS) as well as double-stranded RNA-activated protein kinase (PKR), which are not expressed in parental U118 cells, were constitutively expressed in IFNalpha transfectants. These results indicate a differential responsiveness among these four genes to constitutive IFNalpha expression, and suggest that the suppression of U118-transformed phenotypes by IFNalpha transfection may be mediated by the induction of specific IFN response genes thought to have a negative growth-regulatory function.

2',5'-Oligoadenylate Synthetase↗
PubMed1995

Lack of p16INK4 or retinoblastoma protein (pRb), or amplification-associated overexpression of cdk4 is observed in distinct subsets of malignant glial tumors and cell lines.

In this study the expression of p16INK4, retinoblastoma protein (pRb), and cdk4 proteins have been examined in 18 malignant glioma cell lines and in 45 malignant glial tumors. Loss of p16INK4 expression associated with p16INK4 gene homozygous deletion was evident in 12 cell lines and in 10 primary tumors. Lack of p16INK4 expression was also evident in five tumors for which there was no evidence of p16INK4 gene homozygous deletion. Two of the cell lines and six of the primary tumors in which p16INK4 was present were determined to overexpress cdk4 in association with CDK4 gene amplification. Absence of pRb was determined in two of the cell lines and in ten of the tumors. In total, 16 of 18 cell lines and 25 of 45 tumors showed either a lack of p16INK4 or pRb or amplification-associated overexpression of cdk4. Two additional tumors showed an absence of pRb and p16INK4, and one tumor showed a lack of pRb combined with amplification-associated overexpression of cdk4. These results suggest a common growth-regulatory mechanism that is disrupted in gliomas by either suppressing the expression of p16INK4 or pRb or by increasing the expression of cdk4.

Blotting, Western↗
PubMed1995

Loss of vertical palpebral fissure height on downgaze in acquired blepharoptosis.

OBJECTIVE: To determine criteria to diagnose and document functional visual impairment from upper eyelid ptosis in the downgaze position of reading. DESIGN: Prospective clinical study. PATIENTS: From September 1991 to June 1992, 47 consecutive patients with adult-onset acquired ptosis were enrolled in the study. Downgaze eyelid and relative brow position were evaluated in 88 eyelids of these patients. INTERVENTIONS: Surgical repair of blepharoptosis by the Müller muscle conjunctival resection ptosis procedure, levator aponeurosis advancement and/or resection, or levator muscle resection. MAIN OUTCOME MEASURE: Postoperative change in the eyelid and brow position in downgaze. RESULTS: Of all ptotic eyelids, 43% had zero vertical palpebral fissure height in downgaze when the brows were relaxed and therefore were functionally blind in the downgaze position. After ptosis repair, there was a significant widening of the vertical palpebral fissure height in downgaze (P < .001), a significant decrease in frontalis muscle use (P < .001), and return of the patients' ability to sustain downgaze function. CONCLUSIONS: Measurement of palpebral fissure height in downgaze and frontalis muscle use in patients with acquired ptosis identifies patients with a functional visual deficit in the downgaze reading position. These measurements can be easily performed in the office and may be added to criteria for documenting functional impairment from blepharoptosis.

Adult↗
PubMed1995

Low-grade astrocytomas arising from the pineal gland.

Two cases of low-grade astrocytoma arising from the pineal gland are described in this report. These rare lesions have only been reported on two previous occasions to arise distinctly from the pineal gland. Histologically, one tumor was consistent with a juvenile pilocytic astrocytoma, while the other was consistent with a fibrillary astrocytoma. The pathological features, clinical implications, and treatment of low-grade astrocytomas in the pineal region are discussed.

Adult↗
PubMed1995

Metastatic follicular thyroid carcinoma masquerading as a chordoma.

A 61-year-old Caucasian man presented with otalgia, dysarthria, and weight loss. Neurological examination revealed palatal hypomotility, and weakness of the facial and tongue muscles. Magnetic resonance imaging of the head demonstrated the presence of a soft tissue mass in the clivus. Histologic examination of resected tumor disclosed well-differentiated thyroid follicles that invaded the local osseous tissues. Physical examination and radioiodine images of the thyroid gland were normal. The serum thyroglobulin concentration was markedly elevated (1011 ng/mL). A 0.9-cm well-differentiated benign-appearing left thyroid lobe follicular neoplasm with a thick fibrous capsule was found following diagnostic thyroidectomy. This report illustrates that clinically significant distant metastases can arise from occult follicular thyroid neoplasms that, according to standard histologic criteria, are benign. The presence of a thick fibrous capsule, even in the absence of vascular or capsular invasion, may identify follicular neoplasms that have metastatic potential.

Adenocarcinoma, Follicular↗