摘要:
A system for conducting wireless site surveys of a wireless environment is provided. A wireless interface controller controls a wireless interface during a scan of a wireless frequency band. A user interface module receives a set of wireless network design criteria, and a measurement module obtains a set of wireless signal information based on a set of wireless signals received during the scan of the wireless frequency band. An analysis module compares the set of wireless signal information to the set of wireless network design criteria and automatically determines whether the set of wireless network design criteria is, at least in part, satisfied. The user interface module provides an indicator that indicates whether the set of wireless network design criteria is, at least in part, satisfied.
摘要:
The present invention relates to a method for assessing a hypoxia phenotype of a tumour of a subject in which the gene expression of between 3 and 50 hypoxia-related genes of a sample obtained from said tumour of the subject is determined, thereby obtaining a sample expression profile of said hypoxia-related genes. The sample gene expression profile is then compared with a reference expression profile of said hypoxia-related genes. The hypoxia-related genes comprise at least SLC2A1, VEGFA and PGAM1. Probes, arrays and kits for use in the method are also disclosed.
摘要:
The MN/CA IX protein is identified herein as a hypoxia marker. The MN/CA9 gene promoter is characterized, and the location of the HIF-1 binding site within the MN/CA9 promoter is identified. Further, the hypoxia inducibility of the MN/CA9 gene and the uses of such inducibility are disclosed. In one aspect, the invention provides diagnostic/prognostic tools for determining the presence of hypoxia in a tissue in a vertebrate, preferably a human, and for measuring the relative degree of hypoxia in said vertebrate. In another aspect, the invention provides methods using tumor biopsies to predict the radioresistance of a preneoplastic/neoplastic tissue in a vertebrate subject, preferably a human patient, for diseases in which MN/CA IX levels can be used to indicate radiobiologically relevant tumor hypoxia. Such predictive methods can be used as an aid in patient therapy selection.
摘要翻译:本文将MN / CA IX蛋白质鉴定为缺氧标记。 表征MN / CA9基因启动子,鉴定MN / CA9启动子内HIF-1结合位点的位置。 此外,公开了MN / CA9基因的缺氧诱导能力和这种诱导性的用途。 一方面,本发明提供用于确定脊椎动物,优选人类的组织中缺氧的存在并用于测量所述脊椎动物中的相对缺氧程度的诊断/预后工具。 在另一方面,本发明提供了使用肿瘤活组织检查来预测脊椎动物受试者,优选人类患者中对于其中可以使用MN / CA IX水平来表示放射生物学相关的肿瘤缺氧的疾病的肿瘤前/肿瘤组织的放射抗性的方法。 这种预测方法可用作患者治疗选择的辅助。
摘要:
The disclosure provides methods of treating cancer, tumors, and neoplasias by administering ionizing radiation and an anti-DLL4 antibody or a DLL4-binding fragment.
摘要:
The disclosure provides methods of treating cancer, tumors, and neoplasias by administering ionizing radiation and an anti-DLL4 antibody or a DLL4-binding fragment.
摘要:
Identified herein is the location of the MN protein binding site, and MN proteins/polypeptides that compete for attachment to vertebrate cells with immobilized MN protein. Such MN proteins/polypeptides prevent cell-cell adhesion and the formation of intercellular contacts. The MN protein binding site is a therapeutic target that can be blocked by organic or inorganic molecules, preferably organic molecules, more preferably proteins/polypeptides that specifically bind to that site. Therapeutic methods for inhibiting the growth of preneoplastic/neoplastic vertebrate cells that abnormally express MN protein are disclosed. Vectors are provided that encode the variable domains of MN-specific antibodies and a flexible linker polypeptide separating those domains. Further vectors are disclosed that encode a cytotoxic protein/polypeptide operatively linked to the MN gene promoter or a MN gene promoter fragment comprising the HIF-1 consensus binding sequence, and which vectors preferably further encode a cytokine. The MN gene promoter is characterized, and the binding site for a repressor of MN transcription is disclosed. Further, the hypoxia inducibility of the MN gene and the uses of such induciblity inducibility are disclosed.