Who Purchased The Washington Post And How Can Breast Cancer Patients Benefit

Barron’s Medical Journal Robert Graham Ph.D. Reporting from Rice University Houston, Texas USA (Global Newswire ) ( PRNewswire )

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Who Purchased The Washington Post And How Can Breast Cancer Patients Benefit

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Brought To You By Skyline Deli/Cafe- Houston Medical Center:

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Houston ( AP )

Who is this person that has purchased one of the most prestigious News Papers in The United States and around the World, The Washington Post? How can breast cancer patients benefit from this transaction? Jeff Bezos. Yes Jeff Bezos, founder and chief executive officer of Amazon.com. The Washington Post along with another one of the Bezos Transactions ,Bezos Center for Neural Circuit Dynamics. Before Barron’s Medical Journal get in to the benefits of this transaction for breast cancer, here is some background on the Bezos Center for Neural Circuit Dynamics.

Jeff and his wife MacKenzie Bezos, both graduates of Princeton University, donated $15

million to the school’s neuroscience institute. By purchasing the Washington Post, Bezos now has reporters in Washington DC that will have firsthand knowledge of President Obama New Brain Activity Mapping program which in turn, will be great for when the Washington Post Incorporate Amazon digital cloud computing, that will send information out to the science communities around the world. To accomplish this The Washing Post is going to have to upgrade their science reporting. One way to accomplish this is to partner with News Organizations like Barron’s Medical Journal and The Nature Magazine.

The gift will establish the Bezos Center for Neural Circuit Dynamics. Reason for this epic quest is to unravel one of humankind’s greatest challenges — understanding the brain. “New tools and techniques are making possible discoveries that would have been unthinkable just

two decades ago. We can hope for advancements that lead to understanding deep behaviors, more effective learning methods for young children, and cures for neurological diseases. MacKenzie and I are delighted and excited to support Princeton in their focus on fundamental neuroscience.”

Breast Cancer Patients often struggle with Neurogenesis. Neurogenesis is prolonged chemotherapy decreases the development of new brain cells, a process known as neurogenesis. Neurogenesis disrupts ongoing brain rhythms in the part of the brain responsible for making new memories. That affected by learning and in some cases are necessary for learning to occur.

"One of the things that these brain rhythms do is to connect information across brain

regions "Scientist are starting to have a better understanding of how these natural rhythms are used in the process of communication and how they change with experience."

A substantial proportion of breast cancer survivors report significant, long-lasting impairments in cognitive function, often referred to as "chemobrain." Advances in detection and treatment mean that many more patients are surviving long-term following diagnosis of invasive breast cancer. Thus, it is important to define the types, extent, and persistence of cognitive impairments following treatment with cytotoxic cancer drugs. Sam Houston Biotech examined the effects of chronic treatment with two agents commonly used in patients with breast cancer, cyclophosphamide and doxorubicin (Adriamycin). Athymic nude rats were given 50 mg/kg cyclophosphamide, 2 mg/kg doxorubicin, or saline injections once per week for 4 weeks. A novel place recognition task and contextual and cued fear conditioning were used to characterize learning and memory ability. Immunofluorescence staining for immature and mature neurons and activated microglia was used to assess changes in neurogenesis and neuroinflammation.

Cyclophosphamide- and doxorubicin-treated rats showed significantly impaired performance on the novel place recognition task and the contextual fear conditioning task compared with untreated controls, suggesting disrupted hippocampal-based memory function. Chemotherapy-treated animals showed a significant decline in neurogenesis [80%-90% drop in bromodeoxyuridine (BrdUrd)-labeled cells expressing NeuN]. Activated microglia (ED1-

positive) were found after cyclophosphamide but not doxorubicin treatment. Our results show that chronic treatment with either of two commonly used chemotherapeutic agents impairs cognitive ability and suggest that strategies to prevent or repair disrupted hippocampal neurogenesis may be effective in ameliorating this serious side effect in cancer survivors.

The human olfactory bulb displays high morphologic dynamics changing its volume with olfactory function, which has been explained by active neurogenetic processes. Discussion continues whether the human olfactory bulb hosts a continuous turnover of neurons. Sam Houston Biotech analyzed the transcriptome via RNA quantification of adult human olfactory bulbs and intersected the set of expressed transcriptomic genes with independently available proteomic expression data. To obtain a functional genomic perspective, this intersection was analyzed for higher-level organization of gene products into biological pathways established in the gene ontology database.Sam Houston Biotech reports that a fifth of genes expressed in adult human olfactory bulbs serve functions of nervous system or neuron development, half of them functionally converging to axonogenesis but no other non-neurogenetic biological processes. Other genes were expectedly involved in signal transmission and response to chemical stimuli. This provides a novel, functional genomics perspective supporting the existence of neurogenesis in the adult human olfactory bulb.

Neurogenesis and Epidermal Growth Factor Receptor genes can partner with , Genomics and President Obama Brain Acivity Mapping all working hand in hand will look for tumors identified recurrent genomic aberrations in each molecular subtype. The classical subtype was characterised by frequent EGFR amplification and EGFRvIII mutations, CDKN2A deletion, and a lack of TP53mutations, whereas the mesenchymal subtype was characterised by NF1, TP53, and PTEN mutations. Consensus neuropathological review of a subset of TCGA cases has shown that the proneural, classical, and mesenchymal subtypes are enriched for GBM with oligodendroglial features, small-cell GBM, and gliosarcoma (a morphological variant of GBM with mesenchymal differentiation (Miller and Perry, 2007)), respectively (Cameron Brennan, personal communication). Moreover, pseudopalisading necrosis and to a lesser extent florid microvascular proliferation are frequent in mesenchymal GBM, but the proneural subtype typically lacks necrosis. These findings suggest that mesenchymal GBM may be uniquely susceptible to angiogenesis inhibitors, a hypothesis currently being tested in the RTOG 0825 trial discussed below. The proneural subtype, which like previous studies (Phillips et al, 2006; Lee et al, 2008) was found in younger patients, harboured frequent PDGFRAamplification and mutations in IDH1, TP53, andPIK3CA/PIK3R1, suggesting susceptibility to PDGFRA- and PI3K-targeted therapies. A recent proteomic analysis confirmed protein- and phosphorylation-level signalling abnormalities in the EGFR, PDGFR, and NF1 pathways in classical, proneural, and mesenchymal subtypes of GBM, respectively, further suggesting that these GBM subtypes may be uniquely susceptible to targeted agents (Brennan et al, 2009).

It is a great day for Science and News organization around The World