934 resultados para Neoplasms, Multiple Primary
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In this paper, we propose a multiuser cognitive relay network, where multiple secondary sources communicate with a secondary destination through the assistance of a secondary relay in the presence of secondary direct links and multiple primary receivers. We consider the two relaying protocols of amplify-and-forward (AF) and decode-and-forward (DF), and take into account the availability of direct links from the secondary sources to the secondary destination. With this in mind, we propose an optimal solution for cognitive multiuser scheduling by selecting the optimal secondary source, which maximizes the received signal-to-noise ratio (SNR) at the secondary destination using maximal ratio combining. This is done by taking into account both the direct link and the relay link in the multiuser selection criterion. For both AF and DF relaying protocols, we first derive closed-form expressions for the outage probability and then provide the asymptotic outage probability, which determines the diversity behavior of the multiuser cognitive relay network. Finally, this paper is corroborated by representative numerical examples.
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In this paper, we propose physical layer security for cooperative cognitive radio networks (CCRNs) with relay selection in the presence of multiple primary users and multiple eavesdroppers. To be specific, we propose three relay selection schemes, namely, opportunistic relay selection (ORS), suboptimal relay selection (SoRS), and partial relay selection (PRS) for secured CCRNs, which are based on the availability of channel state information (CSI) at the receivers. For each approach, we derive exact and asymptotic expressions for the secrecy outage probability. Results show that under the assumption of perfect CSI, ORS outperforms both SoRS and PRS.
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Malignant initiation, leukaemic transformation, and disease progression in haematological malignancies involves a series of mutational events in genes involved in normal housekeeping functions of the cell. These acquired genetic changes can lead to either increased proliferation or a decreased rate of apoptosis, thus allowing expansion of the malignant clone. Although leukaemia can arise as a de novo disease, it has become increasingly clear that therapies, including the use of irradiation and/or chemotherapy, can give rise to malignancy. Therapy-associated myelodysplasia (t-MDS) and therapy-associated acute myeloid leukaemia (t-AML) account for 10-20% of new cases of these diseases. Although these secondary malignancies have been recognised as a clinical entity for nearly 30 years, molecular studies are now pinpointing various regions of the genome that are susceptible to DNA damage by these chemotherapeutic/radiotherapeutic strategies. The detection of new malignancies (both solid tumours and haematological tumours) following allogeneic bone marrow transplantation (BMT) is also providing us with some clues to the nature of leukaemogenesis, particularly with the observation that leukaemia can occur in donor cells postallogeneic BMT.
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Os estuários são ambientes complexos, biologicamente diversos e muito importantes no que respeita à produtividade primária. As zonas intertidais destes ecossistemas são ocupadas por organismos que possuem uma elevada capacidade de sobrevivência e adaptação face às variadas e rápidas alterações nos factores ambientais (tais como temperatura, salinidade, conteúdo hídrico, etc.). As cadeias tróficas com origem no ecossistema estuarino bentónico são essencialmente herbívoras, regulando o fluxo de energia desde o fundo sedimentar e através do ecossistema. Nas áreas estuarinas intertidais a produção primária é essencialmente suportada pelo microfitobentos (MPB). Estas comunidades de microalgas bênticas constituem uma importante fonte de matéria orgânica e são por si só a principal fonte alimentar para as populações de Hydrobia. Neste contexto, a interacção MPB - Hydrobia é um modelo-chave na investigação da cadeia trófica estuarina de origem bentónica, actuando como um importante canal de transporte de energia para os níveis tróficos superiores, especialmente se considerarmos que Hydrobia é uma importante presa para peixes, aves e caranguejos. O presente estudo tem por objectivos gerais: i) a investigação do controlo ambiental (particularmente da luz e do teor em água do sedimento) e endógeno na migração vertical do MPB e ii) a identificação e potencial utilização de marcadores tróficos (pigmentos e ácidos gordos) úteis à investigação da interacção MPB – Hydrobia em laboratório e em condições naturais, considerando a existência de uma elevada plasticidade trófica por parte da Hydrobia e a elevada densidade populacional que estes organismos podem apresentar. A primeira fase de investigação resultou na comparação do papel dos estímulos ambientais e do controlo endógeno nos padrões de comportamento migratório vertical do microfitobentos, demonstrando a existência de um controlo essencialmente endógeno na formação e desintegração do biofilme superficial. A regulação e manutenção da biomassa à superfície do sedimento são claramente controladas pela variação dos factores ambientais, em especial da luz, cuja presença é essencial à formação total do biofilme microalgal à superfície do sedimento intertidal. Foi proposta uma nova abordagem metodológica com vista à estimativa nãodestrutiva do teor de água de sedimentos intertidais vasosos , possibilitando o estudo da influência da acção do vento no conteúdo hídrico dos sedimentos e o consequente impacto da dessecação na comunidade microfitobêntica. Observou-se que a dessecação provoca efeitos limitantes não só na biomassa superficial mas também na actividade fotossintética dos biofilmes microfitobênticos, conduzindo à diminuição da produtividade primária. No que respeita à dinâmica trófica da interacção MPB - Hydrobia foi estabelecido o uso do pigmento feoforbide a, quantificado nas partículas fecais da fauna, como marcador trófico que permite estimar a quantidade de biomassa de microalgas (clorofila a) incorporada pelos organismos animais.Para tal foi investigada e comprovada a existência de uma relação significativa entre a concentração de feopigmentos excretados e a concentração de clorofila a ingerida. Estes estudos foram desenvolvidos numa primeira fase à escala diária, considerando os efeitos dos ciclos sazonais, dia-noite e maré, e depois com a validação em condições naturais, numa escala mensal. A taxa de ingestão média de indivíduos de H. ulvae varia ao longo do dia, com o máximo em torno dos períodos diurnos de maré baixa, o que pode estar relacionado com a disponibilidade de MPB. As taxas de ingestão (TI) de H. ulvae variam ainda em função da estação do ano (TI verão > TI primavera) e em função da densidade de indivíduos (> densidade, < ingestão). Verificou-se um efeito negativo na concentração de clorofila disponível após herbívoria independentemente da densidade de indivíduos. Finalmente, a comparação dos perfis de ácidos gordos de H. ulvae provenientes de diferentes habitats com os perfis de potenciais fontes alimentares permitiu demonstrar que os ácidos gordos são ferramentas úteis na identificação do habitat ocupado por estes organismos. No entanto, apesar da ocupação de diferentes habitats e da integração de múltiplas fontes de produção primária na sua dieta foram sempre observados significativos níveis de ácidos gordos específicos de microalgas (em particular diatomáceas), reforçando o papel importante das comunidades de microalgas bênticas na dieta das populações de H. ulvae.
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To make a comprehensive evaluation of organ-specific out-of-field doses using Monte Carlo (MC) simulations for different breast cancer irradiation techniques and to compare results with a commercial treatment planning system (TPS). Three breast radiotherapy techniques using 6MV tangential photon beams were compared: (a) 2DRT (open rectangular fields), (b) 3DCRT (conformal wedged fields), and (c) hybrid IMRT (open conformal+modulated fields). Over 35 organs were contoured in a whole-body CT scan and organ-specific dose distributions were determined with MC and the TPS. Large differences in out-of-field doses were observed between MC and TPS calculations, even for organs close to the target volume such as the heart, the lungs and the contralateral breast (up to 70% difference). MC simulations showed that a large fraction of the out-of-field dose comes from the out-of-field head scatter fluence (>40%) which is not adequately modeled by the TPS. Based on MC simulations, the 3DCRT technique using external wedges yielded significantly higher doses (up to a factor 4-5 in the pelvis) than the 2DRT and the hybrid IMRT techniques which yielded similar out-of-field doses. In sharp contrast to popular belief, the IMRT technique investigated here does not increase the out-of-field dose compared to conventional techniques and may offer the most optimal plan. The 3DCRT technique with external wedges yields the largest out-of-field doses. For accurate out-of-field dose assessment, a commercial TPS should not be used, even for organs near the target volume (contralateral breast, lungs, heart).
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OBJECTIVE: To investigate the usefulness of assessing the immunoreactivity of cytokeratins 7 (CK7) and 20 (CK20) as well as several cytomorphologic parameters in effusions with metastatic adenocarcinomas in the search for the primary site of the tumor. STUDY DESIGN: From the files of the Pathology Department, A. C. Camargo Hospital, we studied cytologic smears from 73 metastatic adenocarcinomas originally from the breast, 63 from the ovary, 40 from the lung and 32 from the stomach, looking for morphologic parameters that could have discriminant potential in suggesting the primary site in a routine situation, including intranuclear inclusions, prominent nucleoli, mitosis, signet-ring cells, psammoma bodies, nuclear crease, binucleation and multinucleation, papillary features, acinar profile (including ball cells) and single cells. Immunoreactions were performed with monoclonal antibodies to CK7 (OV-TL 12/30 and CK20 (Ks 20.8) and included morphologic analysis. Both analyses were studied in a blind fashion regarding the primary site of the tumors. RESULTS: Positivity ratios for breast, ovary, stomach and lung cases were 67.6%, 63.5%, 29.7% and 45.5%, respectively, for CK7 and 17.2%, 15.8%, 13.5% and 32.2%, respectively, for CK20. Discriminant analysis of morphologic and immunocytochemical parameters had an error rate of 42.9% in recognizing the primary site and a Wilk's lambda of .7290. CONCLUSION: The more efficient parameter with discriminant function was the papillary appearance showed by CK7, which should be used in further studies with a similar scope. The set of parameters used in this study were insufficient to discriminate the primary site of female adenocarcinomas in effusions with significant accuracy.
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We briefly review the characteristics of pituitary tumors associated with multiple endocrine neoplasia type 1. Multiple endocrine neoplasia type 1 is an autosomal-dominant disorder most commonly characterized by tumors of the pituitary, parathyroid, endocrine-gastrointestinal tract, and pancreas. A MEDLINE search for all available publications regarding multiple endocrine neoplasia type 1 and pituitary adenomas was undertaken. The prevalence of pituitary tumors in multiple endocrine neoplasia type 1 may vary from 10% to 60% depending on the studied series, and such tumors may occur as the first clinical manifestation of multiple endocrine neoplasia type 1 in 25% of sporadic and 10% of familial cases. Patients were younger and the time between initial and subsequent multiple endocrine neoplasia type 1 endocrine lesions was significantly longer when pituitary disease was the initial manifestation of multiple endocrine neoplasia type 1. Tumors were larger and more invasive and clinical manifestations related to the size of the pituitary adenoma were significantly more frequent in patients with multiple endocrine neoplasia type 1 than in subjects with non-multiple endocrine neoplasia type 1. Normalization of pituitary hypersecretion was much less frequent in patients with multiple endocrine neoplasia type 1 than in subjects with non-multiple endocrine neoplasia type 1. Pituitary tumors in patients with multiple endocrine neoplasia type 1 syndrome tend to be larger, invasive and more symptomatic, and they tend to occur in younger patients when they are the initial presentation of multiple endocrine neoplasia type 1.
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BACKGROUND: Autofluorescence imaging is used widely for diagnostic evaluation of various epithelial malignancies. Cancerous lesions display loss of autofluorescence due to malignant changes in epithelium and subepithelial stroma. Carcinoma of unknown primary site presents with lymph node or distant metastasis, for which the site of primary tumour is not detectable. We describe here the use of autofluorescence imaging for detecting a clinically innocuous appearing occult malignancy of the palate which upon pathological examination was consistent with a metastatic squamous cell carcinoma. CASE DESCRIPTION: A submucosal nodule was noted on the right posterior hard palate of a 59-year-old white female during clinical examination. Examination of this lesion using a multispectral oral cancer screening device revealed loss of autofluorescence at 405 nm illumination. An excisional biopsy of this nodule, confirmed the presence of a metastatic squamous cell carcinoma. Four years ago, this patient was diagnosed with metastatic squamous cell carcinoma of the right mid-jugular lymph node of unknown primary. She was treated with external beam irradiation and remained disease free until current presentation. CONCLUSION: This case illustrates the important role played by autofluorescence tissue imaging in diagnosing a metastatic palatal tumour that appeared clinically innocuous and otherwise would not have been biopsied.
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Pedigree analysis of certain families with a high incidence of tumors suggests a genetic predisposition to cancer. Li and Fraumeni described a familial cancer syndrome that is characterized by multiple primary tumors, early age of onset, and marked variation in tumor type. Williams and Strong (1) demonstrated that at least 7% of childhood soft tissue sarcoma patients had family histories that is readily explained by a highly penetrant autosomal dominant gene. To characterize the mechanism for genetic predisposition to many tumor types in these families, we have studied genetic alterations in fibroblasts, a target tissue from patients with the Li-Fraumeni Syndrome (LFS).^ We have observed spontaneous changes in initially normal dermal fibroblasts from LFS patients as they are cultured in vitro. The cells acquire an altered morphology, chromosomal anomalies, and anchorage-independent growth. This aberrant behavior of fibroblasts from LFS patients had never been observed in fibroblasts from normal donors. In addition to these phenotypic alterations, patient fibroblasts spontaneously immortalize by 50 population doublings (pd) in culture; unlike controls that remain normal and senesce by 30-35 (2). At 50 pd, immortal fibroblasts from two patients were found to be susceptible to tumorigenic transformation by an activated T24 H-ras oncogene (3). Approximately 80% of the oncogene expressing transfectants were capable of forming tumors in nude mice within 2-3 weeks. p53 has been previously associated with immortalization of cells in culture and cooperation with ras in transfection assays. Therefore, patients' fibroblast and lymphocyte derived DNA was tested for point mutations in p53. It was shown that LFS patients inherited certain point mutations in one of the two p53 alleles (4). Further studies on the above LFS immortal fibroblasts have demonstrated loss of the remaining p53 allele concomitant with escape from senescence. While the loss of the second allele correlates with immortalization it is not sufficient to transformation by an activated H-ras or N-ras oncogene. These immortal fibroblasts are resistant to tumorigenic transformation by v-abl, v-src, c-neu or v-mos oncogene; implying that additional steps are required in the tumorigenic progression of LFS patients' fibroblasts.^ References. (1) Williams et al., J. Natl. Cancer Inst. 79:1213, 1987. (2) Bischoff et al., Cancer Res. 50:7979, 1990. (3) Bischoff et al., Oncogene 6:183, 1991. (4) Malkin et al., Science 250:1233, 1990. ^
One-stage laparoscopic procedure for a patient with bilateral colorectal tumours and renal carcinoma
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We describe a case of a patient with synchronous bilateral colorectal tumours and renal carcinoma who underwent one-stage laparoscopic surgery procedure with right transperitoneal nefrectomy, right hemicolectomy and sigmoidectomy. One-stage laparoscopic procedure can be used safely and successfully for a patient with multiple primary tumours.
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Background Cancer survivors face an increased likelihood of being subsequently diagnosed with another cancer. The aim of this study was to quantify the relative risk of survivors developing a second primary cancer in Queensland, Australia. Methods Standardised incidence rates stratified by type of first primary cancer, type of second primary cancer, sex, age at first diagnosis, period of first diagnosis and follow-up interval were calculated for residents of Queensland, Australia, who were diagnosed with a first primary invasive cancer between 1982 and 2001 and survived for a minimum of 2 months. Results A total of 23,580 second invasive primary cancers were observed over 1,370,247 years of follow-up among 204,962 cancer patients. Both males (SIR = 1.22; 95% CI = 1.20-1.24) and females (SIR = 1.36; 95% CI = 1.33-1.39) within the study cohort were found to have a significant excess risk of developing a second cancer relative to the incidence of cancer in the general population. The observed number of second primary cancers was also higher than expected within each age group, across all time periods and during each follow-up interval. Conclusions The excess risk of developing a second malignancy among cancer survivors can likely be attributed to factors including similar aetiologies, genetics and the effects of treatment, underlining the need for ongoing monitoring of cancer patients to detect subsequent tumours at an early stage. Education campaigns developed specifically for survivors may be required to lessen the prevalence of known cancer risk factors.
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Extrapulmonary small cell and small cell neuroendocrine tumors of unknown primary site are, in general, aggressive neoplasms with a short median survival. Like small cell lung cancer (SCLC), they often are responsive to chemotherapy and radiotherapy. Small cell lung cancer and well differentiated neuroendocrine carcinomas of the gastrointestinal tract and pancreas tend to express somatostatin receptors. These tumors may be localized in patients by scintigraphic imaging using radiolabeled somatostatin analogues. A patient with an anaplastic neuroendocrine small cell tumor arising on a background of multiple endocrine neoplasia type 1 syndrome is reported. The patient had a known large pancreatic gastrinoma and previously treated parathyroid adenopathy. At presentation, there was small cell cancer throughout the liver and skeleton. Imaging with a radiolabeled somatostatin analogue, 111In- pentetreotide (Mallinckrodt Medical B. V., Petten, Holland), revealed all sites of disease detected by routine biochemical and radiologic methods. After six cycles of chemotherapy with doxorubicin, cyclophosphamide, and etoposide, there was almost complete clearance of the metastatic disease. 111In-pentetreotide scintigraphy revealed uptake consistent with small areas of residual disease in the liver, the abdomen (in mesenteric lymph nodes), and posterior thorax (in a rib). The primary gastrinoma present before the onset of the anaplastic small cell cancer showed no evidence of response to the treatment. The patient remained well for 1 year and then relapsed with brain, lung, liver, and skeletal metastases. Despite an initial response to salvage radiotherapy and chemotherapy with carboplatin and dacarbazine, the patient died 6 months later.
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To minimise the number of load sheddings in a microgrid (MG) during autonomous operation, islanded neighbour MGs can be interconnected if they are on a self-healing network and an extra generation capacity is available in the distributed energy resources (DER) of one of the MGs. In this way, the total load in the system of interconnected MGs can be shared by all the DERs within those MGs. However, for this purpose, carefully designed self-healing and supply restoration control algorithm, protection systems and communication infrastructure are required at the network and MG levels. In this study, first, a hierarchical control structure is discussed for interconnecting the neighbour autonomous MGs where the introduced primary control level is the main focus of this study. Through the developed primary control level, this study demonstrates how the parallel DERs in the system of multiple interconnected autonomous MGs can properly share the load of the system. This controller is designed such that the converter-interfaced DERs operate in a voltage-controlled mode following a decentralised power sharing algorithm based on droop control. DER converters are controlled based on a per-phase technique instead of a conventional direct-quadratic transformation technique. In addition, linear quadratic regulator-based state feedback controllers, which are more stable than conventional proportional integrator controllers, are utilised to prevent instability and weak dynamic performances of the DERs when autonomous MGs are interconnected. The efficacy of the primary control level of the DERs in the system of multiple interconnected autonomous MGs is validated through the PSCAD/EMTDC simulations considering detailed dynamic models of DERs and converters.
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Multiple sclerosis is a common disease of the central nervous system in which the interplay between inflammatory and neurodegenerative processes typically results in intermittent neurological disturbance followed by progressive accumulation of disability. Epidemiological studies have shown that genetic factors are primarily responsible for the substantially increased frequency of the disease seen in the relatives of affected individuals, and systematic attempts to identify linkage in multiplex families have confirmed that variation within the major histocompatibility complex (MHC) exerts the greatest individual effect on risk. Modestly powered genome-wide association studies (GWAS) have enabled more than 20 additional risk loci to be identified and have shown that multiple variants exerting modest individual effects have a key role in disease susceptibility. Most of the genetic architecture underlying susceptibility to the disease remains to be defined and is anticipated to require the analysis of sample sizes that are beyond the numbers currently available to individual research groups. In a collaborative GWAS involving 9,772 cases of European descent collected by 23 research groups working in 15 different countries, we have replicated almost all of the previously suggested associations and identified at least a further 29 novel susceptibility loci. Within the MHC we have refined the identity of the HLA-DRB1 risk alleles and confirmed that variation in the HLA-A gene underlies the independent protective effect attributable to the class I region. Immunologically relevant genes are significantly overrepresented among those mapping close to the identified loci and particularly implicate T-helper-cell differentiation in the pathogenesis of multiple sclerosis. © 2011 Macmillan Publishers Limited. All rights reserved.