1,251 research outputs found
Venous congestive myelopathy: a mimic of neoplasia
No full textVenous congestive myelopathy is a progressive disorder frequently associated with arteriovenous fistulas, usually dural. By causing diffuse spinal cord enlargement and enhancement on imaging, it may simulate a neoplasm and prompt a biopsy. We evaluated the biopsy findings in seven such patients ( M = 5, F = 2, mean age 59711 years) who presented variably with progressive lower extremity weakness (86%), bowel and bladder dysfunction ( 86%), sensory changes ( 86%) or pain (29%). Preoperative magnetic resonance imaging showed spinal cord enlargement with T2-hyperintensity ( 86%) and contrast enhancement (57%) at the cervical (14%), thoracolumbar ( 57%), and/or conus medullaris ( 57%) level. Prebiopsy spinal angiogram, performed in two patients, was negative. Spinal cord biopsy showed architecturally distorted parenchyma with gliosis and thick hyalinized vessels (100%), variable myelin loss (71%), mild glial atypia ( 57%), hemosiderin deposition ( 71%), Rosenthal fibers (43%), vascular thrombosis ( 29%), and necrosis ( 29%), features highly suggestive of venous congestive myelopathy. Postbiopsy spinal angiograms were performed in five patients. A dural arteriovenous fistula was identified by selective angiography in three patients, including the two with a negative preoperative angiogram. Additional postbiopsy angiographic studies in two patients were negative, and two patients were followed up without angiography. Mean follow-up after biopsy was 13.6 months. Histologic changes characteristic of venous congestive myelopathy may be seen in spinal cord biopsies with or without an associated fistula. Recognition of this entity by surgical pathologists is important, leading to the correct identification of a non-neoplastic lesion as well as of a surgically treatable disease
p53 gene mutations in medulloblastoma. Immunohistochemistry, gel shift analysis, and sequencing.
No full textImmunohistochemical detection of EGFRvIII in high malignancy grade astrocytomas and evaluation of prognostic significance
No full textThe purpose of this study was to establish an accurate and accessible immunohistochemical (IHC) method for detecting vIII Egf receptor and to assess the prognostic significance of the method as applied to the detection of vIII in malignant astrocytomas. The accuracy of the method was determined by comparing vIII immunoreactivity in formalin-fixed and paraffin-embedded tumor sections versus RT-PCR results from the analysis of RNA extracted from corresponding frozen specimens. RT-PCR revealed vIII transcript in 18 of 44 cases in this series, and IHC analysis of matched formalin-fixed and paraffin-embedded sections showed EGFRvIII reactivity in each of these 18 tumors, as well as 1 additional tumor that was negative for vIII transcript. EGFR amplification was evident in all tumors expressing vIII; none of the 15 tumors lacking amplified EGFR were positive for vIII transcript or vIII protein. IHC analysis for vIII expression was next applied to a large series of anaplastic astrocytomas (AAs) and glioblastoma multiforme (GBMs) from clinical trial patients with complete follow-up and that had been previously examined by FISH for amplified EGFR. Among the GBMs, vIII detection by IHC was determined in 19 of 46 cases (41.3%) with EGFR amplification, and in only 3 of 59 tumors lacking amplified EGFR (5.1%). Among the AAs, vIII expression was observed in 3 of 14 cases with amplified EGFR (21.4%) and in 6 of 49 cases without EGFR amplification (12.2%). GBM and AA patient survival analysis as a function of vIII expression showed contrasting results, with vIII positivity having no association with survival among GBM patients (p = 0.84), but being highly associated with reduced survival among AA patients (p = 0.0016). This latter finding, though quite possibly a result of vIII's association with increasing AA patient age, suggests that vIII IHC will be useful for identifying and/or confirming the identity of malignant astrocytomas whose clinical behavior is consistent with that of GBM
Elevated Intracranial Pressure Associated with a Cervical Meningioma
No full textHeadache; TinnitusA 39-year old male with intracranial pressure, headache and Dx cervical meningioma.Diplopia; Transient visual obscurationCT; MRIMelanocytic tumorCarbonic anhydrase inhibitors1. Cai DX, Banerjee R, Scheithauer BW, Lohse CM, Kleinschmidt-DeMasters BK and Perry A: Chromosome 1p and 14q FISH analysis in clinicopathologic subsets of meningioma: Diagnostic and prognostic implications. J Neuropathol Exp Neurol 60:628-36, 2001. 2. Perry A, Giannini C, Raghavan R, Scheithauer BW, Banerjee R, Margraf L, Bowers DC, Lytle RA, Newsham IF and Gutmann DH: Aggressive phenotypic and genotypic features in pediatric and NF2-associated meningioma: A clinicopathologic study of 53 cases. J Neuropathol Exp Neurol 60:994-1001, 2001. 3. Brat DJ, Giannini C, Scheithauer BW and Burger PC: Primary melanocytic neoplasms of the central nervous system. Am J Surg path 23(7): 745-754, 1999
Trisomy 19 ependymoma, a newly recognized genetico-histological association, including clear cell ependymoma
No full textEpendymal tumors constitute a clinicopathologically heterogeneous group of brain tumors. They vary in regard to their age at first symptom, localization, morphology and prognosis. Genetic data also suggests heterogeneity. We define a newly recognized subset of ependymal tumors, the trisomy 19 ependymoma. Histologically, they are compact lesions characterized by a rich branched capillary network amongst which tumoral cells are regularly distributed. When containing clear cells they are called clear cell ependymoma. Most trisomy 19 ependymomas are supratentorial WHO grade III tumors of the young. Genetically, they are associated with trisomy 19, and frequently with a deletion of 13q21.31-31.2, three copies of 11q13.3-13.4, and/or deletions on chromosome 9. These altered chromosomal regions are indicative of genes and pathways involved in trisomy 19 ependymoma tumorigenesis. Recognition of this genetico-histological entity allows better understanding and dissection of ependymal tumors
19.1 A 300MHz-BW, 27-to-38dBm In-Band OIP3 sub-7GHz Receiver for 5G Local Area Base Station Applications
No full textRecently, the so-called sub-6GHz band of the 5G new radio (NR) has been extended to 7.125GHz to address the relentless customer demand for higher data-rate communication. This demands a new design approach for the local area base-station (LA-BS) receivers (RXs) to cover a wide operating frequency range of 0.41 to 7.125GHz. Moreover, for NR bands above 3GHz, the maximum RF bandwidth (BW) is as high as 400MHz, in which a -35dBm modulated in-band (IB) blocker can be present. These impose stringent BW and IB linearity requirements for the baseband amplifiers in the LA-BS receivers. In addition to IB interferences, a -15dBm continuous-wave (CW) out-of-band (OOB) close-in blocker can also be present at 60MHz offset frequency from the passband edges, thus demanding a highly selective RX. Finally, the blocker 1dB compression point (B1textdB) becomes a key parameter for local area co-location applications in which the power of the far-out OOB blocker can be as large as -4dBm.Green Open Access added to TU Delft Institutional Repository ‘You share, we take care!’ – Taverne project https://www.openaccess.nl/en/you-share-we-take-care Otherwise as indicated in the copyright section: the publisher is the copyright holder of this work and the author uses the Dutch legislation to make this work public.Electronic
A 4 GHz Continuous-Time ΔΣ ADC With 70dB DR and -74dBFS THD in 125MHz BW
No full textA 4 GHz third-order continuous-time ΔΣ ADC is presented with a loop filter topology that absorbs the pole caused by the input capacitance of its 4-bit quantizer and also compensates for the excess delay caused by the quantizer's latency. The ADC was implemented in 45 nm-LP CMOS and achieves 70 dB DR and -74 dBFS THD in a 125 MHz BW, while dissipating 260 mW from 1.1/1.8 V supply. The ADC occupies 0.9 mm 2 including the modulator, clock circuitry and decimation filter.Accepted Author ManuscriptElectronic Instrumentatio
Using bacterial biomarkers to identify early indicators of cystic fibrosis pulmonary exacerbation onset
No full textAcute periods of pulmonary exacerbation are the single most important cause of morbidity in cystic fibrosis patients, and may be associated with a loss of lung function. Intervening prior to the onset of a substantially increased inflammatory response may limit the associated damage to the airways. While a number of biomarker assays based on inflammatory markers have been developed, providing useful and important measures of disease during these periods, such factors are typically only elevated once the process of exacerbation has been initiated. Identifying biomarkers that can predict the onset of pulmonary exacerbation at an early stage would provide an opportunity to intervene before the establishment of a substantial immune response, with major implications for the advancement of cystic fibrosis care. The precise triggers of pulmonary exacerbation remain to be determined; however, the majority of models relate to the activity of microbes present in the patient's lower airways of cystic fibrosis. Advances in diagnostic microbiology now allow for the examination of these complex systems at a level likely to identify factors on which biomarker assays can be based. In this article, we discuss key considerations in the design and testing of assays that could predict pulmonary exacerbations
p53 in nonneoplastic central nervous system lesions: An immunohistochemical and genetic sequencing study
No full textOBJECTIVE: Immunostaining for p53 commonly is considered a marker of neoplasia. Previous studies of nonneoplastic processes have yielded conflicting results. METHODS: To test the assumption that p53 irnmunoreactivity indicates neoplasia; we examined 60 formal in-fixed,, paraffin-embedded biopsies of nonneoplastic central nervous system lesions, including gliosis (n = 12), infarction (n = 9), demyelinating disease (n = 23), progressive multifocal leukoencephalopathy (n = 11), and herpes simplex virus encephalitis (n = 5). Diffuse astrocytomas (n = 50) of World Health Organization Grades 2 to 4 also were studied, as were six control autopsy brains. The avidin-biotin-peroxidase complex method was used with commercially available monoclonal antisera to both p53 (clone DO7; Dako, Carpinteria, CA) and mdm2 (Dako), a protein known to stabilize p53. Two-samples of each nonneoplastic lesion also were subjected to deoxyribonucleic acid isolation, amplification, and sequencing of exons 5 to 8 of TP53. RESULTS: Although it was low level in most instances, p53 immunoreactivity was noted in all but normal control samples. In reactive lesions, staining was largely observed in astrocytes and histiocytes. Scant oligodendroglia also were labeled in demyelinating disease. The progressive multifocal leukoencephalopathy samples revealed exceptionally strong staining in astrocytes and infected oligodendrocytes. Staining also was noted in occasional endothelial cells and neurons, and in rare lymphocytes. Immunoreactivity for mdm2, studied only in nonneoplastic lesions, was moderate to strong in all cases and limited to reactive astrocytes and histiocytes. No TP53 mutations were noted in the nonneoplastic lesions studied. To some extent, all astrocytomas exhibited p53 immunopositivity, particularly high-grade lesions. CONCLUSION: p53 immunoreactivity is not limited to astrocytomas, but it can be observed in lesions that often are mistaken for glioma. No TP53 mutations accompany p53 expression in nonneoplastic lesions, and mdm2 may be responsible for persistence of p53 expression in these processes
- …
