Diagnosing growth in low-grade gliomas with and without longitudinal volume measurements: A retrospective observational study.

BACKGROUND: Low-grade gliomas cause significant neurological morbidity by brain invasion. There is no universally accepted objective technique available for detection of enlargement of low-grade gliomas in the clinical setting; subjective evaluation by clinicians using visual comparison of longitudinal radiological studies is the gold standard. The aim of this study is to determine whether a computer-assisted diagnosis (CAD) method helps physicians detect earlier growth of low-grade gliomas. METHODS AND FINDINGS: We reviewed 165 patients diagnosed with grade 2 gliomas, seen at the University of Alabama at Birmingham clinics from 1 July 2017 to 14 May 2018. MRI scans were collected during the spring and summer of 2018. Fifty-six gliomas met the inclusion criteria, including 19 oligodendrogliomas, 26 astrocytomas, and 11 mixed gliomas in 30 males and 26 females with a mean age of 48 years and a range of follow-up of 150.2 months (difference between highest and lowest values). None received radiation therapy. We also studied 7 patients with an imaging abnormality without pathological diagnosis, who were clinically stable at the time of retrospective review (14 May 2018). This study compared growth detection by 7 physicians aided by the CAD method with retrospective clinical reports. The tumors of 63 patients (56 + 7) in 627 MRI scans were digitized, including 34 grade 2 gliomas with radiological progression and 22 radiologically stable grade 2 gliomas. The CAD method consisted of tumor segmentation, computing volumes, and pointing to growth by the online abrupt change-of-point method, which considers only past measurements. Independent scientists have evaluated the segmentation method. In 29 of the 34 patients with progression, the median time to growth detection was only 14 months for CAD compared to 44 months for current standard of care radiological evaluation (p \u3c 0.001). Using CAD, accurate detection of tumor enlargement was possible with a median of only 57% change in the tumor volume as compared to a median of 174% change of volume necessary to diagnose tumor growth using standard of care clinical methods (p \u3c 0.001). In the radiologically stable group, CAD facilitated growth detection in 13 out of 22 patients. CAD did not detect growth in the imaging abnormality group. The main limitation of this study was its retrospective design; nevertheless, the results depict the current state of a gold standard in clinical practice that allowed a significant increase in tumor volumes from baseline before detection. Such large increases in tumor volume would not be permitted in a prospective design. The number of glioma patients (n = 56) is a limitation; however, it is equivalent to the number of patients in phase II clinical trials. CONCLUSIONS: The current practice of visual comparison of longitudinal MRI scans is associated with significant delays in detecting growth of low-grade gliomas. Our findings support the idea that physicians aided by CAD detect growth at significantly smaller volumes than physicians using visual comparison alone. This study does not answer the questions whether to treat or not and which treatment modality is optimal. Nonetheless, early growth detection sets the stage for future clinical studies that address these questions and whether early therapeutic interventions prolong survival and improve quality of life

Effects of Anti-Angiogenesis on Glioblastoma Growth and Migration: Model to Clinical Predictions

International audienceGlioblastoma multiforme (GBM) causes significant neurological morbidity and short survival times. Brain invasion by GBM is associated with poor prognosis. Recent clinical trials of bevacizumab in newly-diagnosed GBM found no beneficial effects on overall survival times; however, the baseline health-related quality of life and performance status were maintained longer in the bevacizumab group and the glucocorticoid requirement was lower. Here, we construct a clinical-scale model of GBM whose predictions uncover a new pattern of recurrence in 11/70 bevacizumab-treated patients. The findings support an exception to the Folkman hypothesis: GBM grows in the absence of angiogenesis by a cycle of proliferation and brain invasion that expands necrosis. Furthermore, necrosis is positively correlated with brain invasion in 26 newly-diagnosed GBM. The unintuitive results explain the unusual clinical effects of bevacizumab and suggest new hypotheses on the dynamic clinical effects of migration by active transport, a mechanism of hypoxia-driven brain invasion

Characteristics of patients with GBM at first recurrence.

<p>Necrosis (+) and (-) indicate that the tumor showed, respectively, the presence or absence of expanding area of necrosis (see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0115018#pone-0115018-g002" target="_blank">Fig. 2</a>). M =  Male. F =  Female. Age  =  age at initial diagnosis in years. Initial Therapy  =  therapy given prior to first recurrence. Surgery  =  initial surgical procedure at the time of diagnosis. Chemo + Bev  =  chemotherapy given with bevacizumab. XRT  =  radiation therapy. Tem  =  Temozolomide. XRT/Tem  =  radiation therapy with concurrent Temozolomide. XRT, Tem  =  radiation therapy followed by Temozolomide. CCNU  =  Lomustine. CPT-11 =  Irinotecan. STR  =  subtotal resection. ICT-107 =  ICT-107 vaccine. Gliadel  =  Gliadel wafers. GTR  =  gross total resection. R =  craniotomy surgical details unknown. ** =  This patient had a diagnosis of gliosarcoma. The mean age of patients 1–11 is 48.4 years. The mean age of patients 12–23 is 54.7 years.</p><p>Characteristics of patients with GBM at first recurrence.</p

Summary of Tumor Response under AT only verses PD only in the Full and Treatments models.

<p>Summary of Tumor Response under AT only verses PD only in the Full and Treatments models.</p

Sensitivity Analysis.

<p>Percent Proliferation (), Percent Necrosis ( brain death), and Percent Invasion () for different parameter choices at time  = 3000. , transition rate from to <i>I</i>. , transition rate from to . , active transport of cells. , diffusion coefficient of cells. , mitotic rate of cells. , death rate of living cells. , angiogenic rate. , initial hypoxic threshold. .</p

Hidroginástica na terceira idade

O processo de envelhecimento no indivíduo saudável está relacionado com inúmeras alterações psicológicas e físicas que interferem na área motora, concorrendo para a inatividade e contribuindo para o aparecimento e agravamento de determinadas doenças, além de influenciar negativamente a realização das atividades de vida diária. Portanto, a prática de atividade física é fundamental para o idoso, não só na prevenção de doenças como na reabilitação de suas habilidades motoras, promovendo um estilo de vida saudável que é fator preponderante para a melhoria da qualidade de vida. Contudo, algumas precauções devem ser adotadas na prescrição da atividade direcionada para o idoso, a fim de que esta seja segura e prazerosa. Dentre os exercícios mais adequados aos idosos estão a caminhada, o ciclismo, a natação e a hidroginástica. Devido a sua grande procura, a hidroginástica vem aumentando o número de adeptos na terceira idade. Ela propicia ao idoso o aumento de sua capacidade aeróbia, força muscular, flexibilidade articular e o treinamento de habilidades específicas como equilíbrio e coordenação motora. Soma-se ainda o fato de esta atividade oferecer ambiente de relaxamento e incentivo ao contato social, atuando no combate ao estresse, depressão, na melhoria da autopercepção corporal e da auto-estima. Devemos, então, estar atentos às particularidades da hidroginástica, a fim de aproveitar todas as vantagens que esta oferece para o programa de exercícios direcionado para a terceira idade

Effects of Anti-Angiogenesis on Glioblastoma Growth and Migration: Model to Clinical Predictions

Glioblastoma multiforme (GBM) causes significant neurological morbidity and short survival times. Brain invasion by GBM is associated with poor prognosis. Recent clinical trials of bevacizumab in newly-diagnosed GBM found no beneficial effects on overall survival times; however, the baseline health-related quality of life and performance status were maintained longer in the bevacizumab group and the glucocorticoid requirement was lower. Here, we construct a clinical-scale model of GBM whose predictions uncover a new pattern of recurrence in 11/70 bevacizumab-treated patients. The findings support an exception to the Folkman hypothesis: GBM grows in the absence of angiogenesis by a cycle of proliferation and brain invasion that expands necrosis. Furthermore, necrosis is positively correlated with brain invasion in 26 newly-diagnosed GBM. The unintuitive results explain the unusual clinical effects of bevacizumab and suggest new hypotheses on the dynamic clinical effects of migration by active transport, a mechanism of hypoxia-driven brain invasion