Neuroplasticity Can Improve Quality Of Life For Seniors

Barron’s Medical Journal Reporting from Texas Medical Center M.D. Anderson Research Center Houston, Texas USA B. Bobby Graham Reporting

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Neuroplasticity Can Improve Quality Of Life For Seniors

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Houston ( AP ) Neuroplasticity explains why people who knew me as a elementary student and my ability to learn is so much different as in today, where in many circles when people meet me it is clear to them they are speaking to one of superior abilities.

Neuroplasticity demonstrate that the adult brain can continue to form novel neural connections and grow new neurons in response to learning or training even into old age. Brought To You By Dream So Big Book

Neuroplasticity, also known as brain plasticity, is an umbrella term that encompasses both synaptic plasticity and non-synaptic plasticity—it refers to changes in neural pathways and synapses due to changes in behavior, environment, neural processes, thinking, emotions, as well as changes resulting from bodily injury.

The human brain is a complex, self-organizing, biological system, consisting of trillions of interconnected nerve cells called neurons. The operation of neurons results in two distinct forms of information processing: signaling and integration. Each neuron propagates signals Brought To You By JulieBeth HandBags via action potentials, electrochemical currents that travel the length of its axon. This current leads to the release of neurotransmitters which traverse synapses, the gaps between neurons. These chemical messages are received via specialized receptor cells at the ends of numerous, tree-like branches of the receiving neuron, called dendrites. The stimulation of dendritic receptors by neurotransmitters leads to integration, whereby large amounts of information from many neurons is summed up before reaching a threshold to fire the action potential JulieBeth HandBags down the next axon. In this manner, perceptual information from the external environment and the internal milieu of the body is transmitted and processed in the brain, leading to cognition, emotion, and behavior, the essence of human experience.

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The notion that social experience can lead to changes in gene expression was voiced most prominently by Nobel laureate, Eric Kandel, who regarded this observation as the core component of a new paradigm for psychiatry (1998). Kandel summarized the current state of biological thinking with regard to the relation between social experiences and neurobiology, observing that:

The regulation of gene expression by social factors makes all bodily functions, including all functions of the brain, susceptible to social influences. These social influences will be biologically incorporated in the altered expressions of specific genes in specific nerve cells of specific regions of the brain. These socially influenced alterations are transmitted culturally

The brains of infants and children are known to be plastic, undergoing spurts of neuronal development in response to stimulus exposure during critical periods. This development consists of the genesis of neurons, increased connectivity between extant neurons, and the routing of new synaptic connections between previously unrelated neurons. For instance, violinists evidence neural growth in the portion of their somatosensory cortex devoted to their fingering hand through hours of musical practice.

Persons suffering from what was once thought to be permanent brain injury can heal through rehabilitation designed to stimulate the damaged area, such as in the case of stroke However, although largely speculative, it is possible that neuroplasticity may undergird not only rehabilitation of physical illness but that of select psychological disorders as well, mediating natural recovery from mental illness in some cases as well as improvements related to psychosocial interventions. At present, it has been demonstrated that psychotherapy can induce functional changes in brain activation.

The DNA code of the human genome does not determine protein synthesis in a one-toone fashion; instead, genes are subject to epigenetic processes (i.e. modifications that do not occur due to changes in the basic genetic sequence of amino acids but that instead result from biological and environmental influences on the expression of genes as proteins During gene expression, the genetic code serves as a “blueprint” that guides the construction of proteins from amino acids. However, this construction process is modulated by signals from the internal and external environments, which steer and modify the manner in which basic organic molecules are organized into anatomy and physiology. 1. In neuroscience, synaptic plasticity is the ability of synapses to strengthen or weaken over time, in response to increases or decreases in their activity. Plastic change also results from the alteration of the number of neurotransmitter receptors located on asynapse.

Nerve cells communicate by using chemical messengers, which are released from neurons after a “priming” step. It seems that priming may be the key to controlling the strength of chemical transmission. The roots of cognition, behavior, learning and memory are embedded in the brain’s intricate network of nerve cells and their specialized points of contact, the synapses. Synapses can convert electrical impulses into chemical signals and back again, as well as modulate the strength of the transmitted signals. This ability to modify the strength of transmission—known as synaptic plasticity—is thought to be the cellular basis of the brains ability to compute, learn and remember. A goal of many neurobiologists is to understand the molecular basis of synaptic plasticity

Neuroinformatics stands at the intersection of neuroscience and information science. Other fields, like genomics, have demonstrated the effectiveness of freely-distributed databases and the application of theoretical and computational models for solving complex problems. In Neuroinformatics, such facilities allow researchers to more easily quantitatively confirm their working theories by computational modeling. Additionally, neuroinformatics fosters collaborative research—an important fact that facilitates the field's interest in studying the multi-level complexity of the brain.

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There are three main directions where neuroinformatics has to be applied:[2] 1. the development of tools and databases for management and sharing of neuroscience data at all levels of analysis,

2. the development of tools for analyzing and modeling neuroscience data,

3. the development of computational models of the nervous system and neural processes.

Fashion Week Houston Makes Downtown Feel like New York City Without The Stress

Fashion Week Houston makes Downtown feel like New York City without the stress

Barron's Medical Journal Style Reporting from Houston Fashion Week Houston, TX USA -- Contributing Editor: Trenette Allen

Bobby Graham Reporting From Downtown Houston --- Houston, Texas USA GlobeNewswire>< PRWire> < PRNewswire>

Houston --- ( AP ) In one of the greatest weeks in my life where my son had his first child, who is now living in Virginia, and my daughter received a major award at her work place and is relocating to Atlanta GA , -- I said to myself the Houston, TX they were born in, is not the Houston of today. If you take this week alone, Mayor Parker is bring businesses back in to downtown Houston. No better example of this greatness is the Houston Fashion week shows put on every year by Jared Lang and Audi of North America. This year’s show was anchored by one of the fashion geniuses of the designer world, Mr. David Peck. David is ready for the global fashion world. Neiman Marcus, Saks Fifth Ave you need to find space for David Peck’s designs. Models ignited the sold -out crowd to standing ovations.

The Marriot Corporation opened one of its grandiose locations to date. The Downtown Houston JW Marriot Opening Party showed off again their new uniform collection for hotel associates (aka employees).The seriously stylish collection was actually inspired by the 104-year-old Samuel F. Carter Building, which was Houston's first skyscraper and which now houses the luxury hotel brand. A custom blouse print even features a photograph of the building taken in 1910.

David Peck USA designed the men's and women's line which features classic silhouettes for the ladies in the form of pencil skirts, structured jackets, sheath dresses and blouses with neckties and chiffon panels and for the men, neutral tones with splashes of bright blue and peridot and some dandy accessories like bow ties and suspenders. Both the women's and mens lines feature custom, hand-woven and fair trade tweed in several pieces.

Also opening in its new location, was the Esperson Gallery in the Houston Pavilion . While there Barron’s Medical Journal found the Christmas find of the year. My heart just dropped when JulieBeth showed her handbag line. Yes, Mayor Parker Downtown Houston has a super star. Beth Younger Purpich is the CEO and designer. Beth uses her Auburn University degree and MBA from the Weatherhead School of Management (Case Western Reserve University) on a daily basis. She loves using both the left and right side of her brain to design and also manage. Beth's love of leather goods can most likely be attributed to her time spent on her family's century-old cattle ranch in Middle Tennessee. Beth has spent most of her life as a basketball player (Auburn University) and even did a year stint in Australia upon graduation, where she was paid to play...in beer. True story. Just don't ask her about the uniforms...yikes! See For Yourself The Ideal Bag For Christmas says Fashion Writer B.Bobby Graham

Judith team includes Phillip Purpich who is the Chief Operating Officer and manages the operations and supply chain for JulieBeth. Phillip has a degree in Chemical Engineering from Texas A&M University. Phil serves on the board of directors of the Education Foundation of Harris County and lives with his wife, Beth, in Houston, Texas. JulieBeth prides herself on superior quality and most importantly, superior customer service. “We are in business because we love making our customers supremely happy! Should you choose to make a return, you may do so up to 14 days from the delivery of your bags. “

All bags are hand-cut and stitched by artisans using top-grain leather and superior hardware. JulieBeth selects only the best and believes streamlined designs with clean lines make the best accessories. All JulieBeth Handbags interiors come with luxurious cerise lining, sturdy metal zippers and detailed leather trim. The creative process begins with a design idea and finishes with a handcrafted luxury bag. Ideas come from anywhere. In fact, the Cocktail Napkin was designed at a speakeasy in Kansas City by simply folding a paper napkin onto itself. JulieBeth believes the best designs are simple and functional and all bags are handmade to order, one at a time. Yes , Houston is looking and feeling like Manhattan in New York City USA. Again, Houston Fashion Week starts the Christmas season with style and awe.

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How Did That Lump Get On Your Breast

Barron's Medical Journal Reporting From John Hopkins University Baltimore Md USA

Governors of Texas Greg Abbott And Maryland‘s Larry Hogan Mandate: How Did That Lump Get On Your Breast

Houston ( AP ) --- Barron’s Medical Journal ask the question: How did that lump get on to your breast. B.Bobby Graham Interviewed Rose Conrad Ph.D. Conrad responded with a smile on her face and said let’s open up the breast cancer playbook. Two Companies are leading the way in the personalized medicine space. Genomic Health and Base Health has mastered the science says Barron’s Medical Journal. What is needed is for the newly elected Governors of Texas Greg Abbott And Maryland‘s Larry Hogan to collaborate using Rice University Rice University Institute of Biosciences and Bioengineering and Texas A&M Health Science Center Institute of Biosciences & Technology in Houston. The FDA and a World of Biotech Companies plus National Institute of Health is located in Maryland. Universities like John Hopkins collaborating together can put a end to breast cancer.

Genomic Health, Inc. (NASDAQ: GHDX) is a global cancer company focused on the development and commercialization of genomic-based clinical laboratory services that analyze the underlying biology of cancer allowing physicians and patients to make individualized treatment decisions.

Over the past decade, we have redefined personalized medicine through the innovation of Oncotype DX, making genomics an indispensable part of breast, colon and prostate cancer diagnosis and treatment. BaseHealth™ makes an integrated health management platform that combines genomic data with clinical and behavioral analysis to engage patients with their physicians in a highly-collaborative way. Our evidence-based assessments help physicians intervene early and often with tailored action plans that span each patient’s unique activity, diet, environmental and lifestyle needs. Personalized medicine starts with a comprehensive understanding of the individual, around whom today’s most successful physicians orient care. This is the first time that a patient can responsibly explore genomic data and non-genomic data in one place, in collaboration with their physician.

Oncogene are genes that take your genes and DNA and convert the your genes to breast cancer genes. The most known gene associated with breast cancer is the KCNK9 Gene. KCNK9 encodes a potassium channel that allows the breast cancer tumor to grow on your breast. This process is aided by Hypoxia. Hypoxia refers to an inadequate oxygen supply to the cells and tissues of the Breast. The Main Gene that stops the growth of KCNK9 Genes is gene is p53. p53 is a fundamental determinant of cancer susceptibility, p53 integrates stress signals and elicits apoplectic responses that maintain genomic stability.

In 2006 and 2007, promising to take customers’ DNA and create personalized health reports to help us understand the medical risks lurking in our genomes, the pressures facing genomic health services seemed clear. Sequencing a human genome was prohibitively expensive, coming in at well over a million dollars — would they be able to narrow down their DNA targets enough to come in at an attractive price point, while still collecting useful information? Would the FDA and other regulators smile on these products, or regard them as unproven medical tests? Was there even a market for DNA data?

Fast forward to today, and the whole business of genomic health looks very different indeed. The genome is a commodity within reach of the middle class, coming in at the price of a cheap used car. Genetic health reports are decidedly “medical devices,” and the FDA is vocally worried that consumers could be dangerously misinformed if providers don’t go through a careful regulatory process.

When cells sense a decrease in oxygen availability (hypoxia), they develop adaptive responses in order to sustain this condition and survive. If hypoxia lasts too long or is too severe, the cells eventually die. Hypoxia is also known to modulate the p53 pathway, in a manner dependent or not of HIF-1 (hypoxia-inducible factor-1), the main transcription factor activated by hypoxia. The p53 protein is a transcription factor, which is rapidly stabilized by cellular stresses and which has a major role in the cell responses to these stresses. This process is why it is important Conrad says for people that are first degree relatives of breast cancer patients, must take a genomic test to see if they are the carrier of gene KCNK9. By identifying this gene we can direct patients with the correct advise as to deal with the fact that they have a lunp on the breast to they are going to get a lump on their breast. Often what happens is that a breast cancer patients dose not go to the doctor or take important test to see if there is a lump on the breast. what happens is the spread of breast cancer is responsible for more than 90 percent of breast cancer deaths. The process by which breast cancer spreads — or metastasizes is where Metastasis was long thought as a late event in breast cancer progression, With Genomics we now shown metastasis to be an early event that is dependent on Hypoxia HIF-1. HIF-1 protein controls genes that enable cells to survive in low oxygen, like cells in solid breast tumors. In order for breast cancer cells to spread to lungs, they must leave the breast,enter blood vessels that lead to the lungs, and exit those same vessels. “

Blood vessels are pretty tight; a cell has to work pretty hard to get through the vessel wall. How this process works is breast cancer cells turn on genes called ANGPTL4, ANGPTL4, helps breast cancer to travel through blood vessel walls. Research is now being performed with Genomics. The Gennxeix Biotech Team found by injecting these cells either with normal or “knocked-down” levels of ANGPTL4 into mice and examining their lungs. Cells lacking HIF-1 and containing extra ANGPTL4 were better able to invade the lungs than cells without extra ANGPTL4. There are other genes that are involved in the creation of a breast cancer tumor on the breast. Her-2, p63, 73. Conrad goes on to say that in their genomic test uses 21 different genes to project ,stop the growth and the spread of a patients breast cancer Lump. HIF-1 as a therapeutic target can extend the life of many stage four breast Cancer patients.
Gennxeix discovered The tumor suppressors VHL (von Hippel-Lindau protein) and p53 target HIF-1α for ubiquitination to inactivation breast cancer tumors cells increases the of HIF-1. This process Increased phosphatidylinositol 3-kinase (PI3K) and AKT.

In breast cancer, increased activity of the HER2 (also known as neu) receptor tyrosine kinase is associated with increased tumor grade, chemotherapy resistance, and decreased patient survival. HER2 has also been implicated as an inducer of VEGF expression. GenNXeix demonstrate that HER2 signaling induced by over expression in mouse 3T3 cells or human MCF-7 breast cancer cells results in increased HIF-1α protein and VEGF mRNA expression that is dependent upon activity of PI3K, AKT (also known as protein kinase B), and the downstream kinase FRAP (KBPS-rapamycin-associated protein)
Gennxeix concern with patients with diabetes and breast cancer may not receive full Benefit of HIF-1. All women having access to a physician can have access to HIF-1 treatments

Houston Science Community Solves The Ebola Puzzle

Houston Science Community Solves The Ebola Puzzle Barron's Medical Medical Journal Reporting From Rice University Houston, Texas USA

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Houston ( AP) Houston Science Community has the goods to solve the Ebola puzzle. Barron’s Medical Journal has discovered the research conducted by Houston Methodist Research Institute. Dr. James Musser is using genomic science and mice models to find a cure for embola. It turns out not all Americans will react to exposure to the embola virus the same way. This is a amazing find. To discover the Gene TIE1 has moved the ball down the field for a complete cure.

----TIE1 is a cell surface protein expressed exclusively in endothelial cells, however it has also been shown to be expressed in immature hematopoietic cells[2] and platelets.[3] TIE1 upregulates the cell adhesion molecules (CAMs)VCAM-1, E-selectin, and ICAM-1 through a p38-dependent mechanism. Attachment of monocyte derived immune cells to endothelial cells is also enhanced by TIE1 expression. TIE1 has a proinflammatory effect and may play a role in the endothelial inflammatory diseases such as atherosclerosi.

Dr. James Musser, director of the Center for Molecular and Translational Human Infectious Diseases Research at Houston Methodist Research Institute. Using mice in experiments, he said, can change the nature of Ebola research. Until now, investigators have mostly used macaques, guinea pigs, and Syrian hamsters because the mouse strain they usually study does not get an Ebola infection that mimics how human patients react.

“This provides a tremendous opportunity to drive toward answers to questions that heretofore were intractable,” Dr. Musser said, mentioning in particular the question of how much genetics determines susceptibility or resistance to Ebola. He added that the mice could be invaluable in initial tests of vaccines and potential drugs. Dr. Matthew Waldor, an infectious disease researcher at Brigham and Women’s Hospital who also was not involved with the study, had the same opinion, calling it “a cool study.” The work, by Angela L. Rasmussen and Michael G. Katze of the University of Washington and their colleagues, began three years ago, long before the current Ebola epidemic. They were inspired by their studies with the 1918 influenza virus that caused a worldwide lethal pandemic. Using a variety of mouse strains, they found that genetics determined whether a mouse got sick or died from the flu, or never got sick at all. People, too, seem to have different responses to the same influenza virus. Dr. Katze, who has studied Ebola for the past decade, and Dr. Rasmussen, who chose to study infectious diseases because when she was in college she read “The Hot Zone,” a book that told a terrifying tale of Ebola in Africa, wanted to find out if genes determine responses to Ebola.

The better News is that Genomics is on the Clock. Genomics provide a faster cheaper more effective way to detect the TIE1 gene by using Semiconductor Sequencing. A example of this technique is Hybrid Pharmaceuticals. Gennxeix Semiconductor Sequencing. “Quantum Theory” In Action for Ebola Patients. A polymerase is an enzyme whose central function is associated with polymers of nucleic acids such as RNA and DNA. The primary function of a polymerase is the polymerization of new DNA or RNA against an existing DNA or RNA template in the processes of replication and transcription. In association with a Hybrid Pharma , Gennxeix also uses a Visualize Real-Time Ebola Data using Signal Stochastic Resonance Units Neurons Detection and Analysis for Ebola model after McCulloch-Pitts.

Hybrid Pharmaceuticals computer-assisted diagnosing of Ebola. Hybrid Pharmaceuticals works is a genetic network simulation trained with tumor incidence data from knockout experiments. Gennxeix Biotech uses Semiconductor Sequencing Chips that create a direct connection between Biochemical and digital information, bringing these two languages together. Hybrid’s chips are designed like any other semiconductor chips. Pairing proprietary semiconductor technology with sequencing chemistry a nucleotide is incorporated into a strand of DNA by a polymerase, a hydrogen ion is released. Gennxeix Biotech used a high-density array of micro-machined wells for bioctechnology process in a massive way. Each well holds a different DNA template. Beneath the wells is an ion-sensitive layer and beneath that a proprietary Ion sensor. TIE1 in many patients respond differently. Genomics can be the GPS to Extend life in Ebola Patients. formalin fixed, paraffin embedded techniques and TIE1 Approximately Where do you really come from? And how can this information Solve Breast Cancer? Approximately 30% of malignant breast cancers demonstrate overamplification of the human epidermal receptor type 2 (HER2) gene. TIE1 can be resistant to low-doses of anthracycline-based Hybrid Pharma have demonstrated that they can be used to map DNase (deoxyribonuclease) DNA origins of replication. Hybrid Pharma Recent progress in microarray technology has been related to the development of high resolution microarrays which can map genomic alterations and constitutional variants in DNA copy number at an extremely high resolution for Ebola chemotherapy. formalin fixed, paraffin embedded techniques.

The Good News is that science has advanced. Sections of microarray provide targets for parallel in situ detection of DNA, RNA and protein targets in each specimen on the array. The better News is that Genomics is on the Clock. Genomics provide a faster cheaper more effective way to detect the TIE1 gene by using Semiconductor Sequencing. A example of this technique is Hybrid Pharma Semiconductor Sequencing. “Quantum Theory”, In Action for Ebola Patients. A polymerase is an enzyme whose central function is associated with polymers of nucleic acids such as RNA and DNA. The primary function of a polymerase is the polymerization of new DNA or RNA against an existing DNA RNA template in the processes of replication and transcription. In association with a Hybrid Pharma also uses a Visualize Real-Time Ebola Data using Signal Stochastic Resonance Units Neurons Detection and Analysis for Ebola model after McCulloch-Pitts. Hybrid Pharma computer-assisted diagnosing of Ebola from mammograms. Hybrid Pharma Gennxeix works is a genetic network simulation trained with tumor incidence data from knockout experiments. Gennxeix Biotech uses Semiconductor Sequencing Chips that create a direct connection between Biochemical and digital information, bringing these two languages together. Hybrid’s chips are designed like any other semiconductor chips. Pairing proprietary semiconductor technology with sequencing chemistry a nucleotide is incorporated into a strand of DNA by a polymerase, a hydrogen ion is released.

Gennxeix Biotech used a high-density array of micro-machined wells for bioctechnology process in a massive way. Each well holds a different DNA template. Beneath the wells is an ion-sensitive layer and beneath that a proprietary Ion sensor. The TIE1 genes in many patients response differently. Genomics is the GPS to Extend life in Ebola Patients

Houston Grand Opera launches Its 60th Anniversary Season:

Trenette Allen and B.Bobby Graham News Reporting From Houston Grand Opera Houston, Texas USA GlobeNewswire>< PRWire> < PRNewswire> < HR>

Houston ( AP -- Ailyn Pérez’s operatic soprano voice made Houston's Grand Opera opening season feel like Milan, Italy’s famous opera house, Teatro Alla Scala.

Teatro Alla Scala reopened in December 2004 after an extensive renovation. It has a bookshop, bar, and a history museum. The original opera house, designed by neoclassical architect, Giuseppe Piermarini, opened in 1778 and many famous operas were first performed there. Brought To You By 2014 Cadillac ELR

La Scala was badly bombed during World War II but reopened in 1946 and quickly regained its reputation as a top Italian opera house.

Houston Grand Opera (HGO) launches its 60th anniversary season on October 24 with a production of Verdi’s late masterpiece, Otello. The opera, which HGO last staged in 1989, stars New Zealand–born tenor Simon O’Neill, “the most complete Otello since Domingo” (BBC Music magazine), who is also HGO’s 2014–15 Lynn Wyatt’s Great Artist. Singing opposite of Mr. O’Neill will be recent Tucker and Domingo Award-winner, Ailyn Pérez—fast emerging as “a major soprano” (New York Times)—in her house and in her debut as Desdemona. Italian baritone, Marco Vratogna, revisits Iago, a role in which he shone at the San Francisco Opera. HGO Studio alumnus Norman Reinhardt, a frequent HGO guest artist, returns to play Cassio, with Grammy-nominated, mezzo Victoria Livengood as Emilia, and bass Morris Robinson, who impressed Houston audiences in 2013 as Joe in HGO’s Show Boat and the Commendatore in Don Giovanni, singing the part of Lodovico. HGO Artistic and Music Director, Patrick Summers conducted the performance. The production is directed by John Cox, of Glyndebourne and Covent Garden fame, who directed HGO’s Ariadne Auf Naxos in the 2010–11 season and the 2012 Studio Showcase. According to the Orange County Register, Cox’s “production carries weight and force. It compels admiration.”

Operatic tenor

Simon O'Neill is a New Zealand-born operatic tenor and Ailyn Pérez is an American operatic soprano and the winner of the 2012 Richard Tucker Award. The HGO interpretation of Shakespeare’s Otello accurately portrayed the themes of racism, love, jealousy, betrayal, and revenge with such culture and confidence that made this Houstonian’s experience " The Greatest Replication Of Otello In The Last One Hundred Years " says Barron's Medical Journal

On October 31, HGO revives Harry Silverstein’s much-loved staging of Mozart’s Così Fan Tutte. The staging was originally created as a tribute to the late Swedish director, Göran Järvefelt’s 1988 production. According to the Houston Press, “under the deft direction of Harry Silverstein,” the production “fully realized the potential of Järvefelt’s inventive, multiple-use staging.” Now HGO remounts this treatment with a stellar sextet of singers. Taking time out from his signature Romantic fare, Tucker Award–winner, Stephen Costello, HGO’s Duke in last season’s Rigoletto, makes his professional role debut as Ferrando. South African baritone, Jacques Imbrailo, hailed by The Times of London as “the hottest young baritone on the block,” returns as Guglielmo after his success in HGO’s Rape of Lucretia during the 2011–12 season. HGO Studio alumna and first-prize winner of the 2014 Operalia competition, soprano Rachel Willis-Sørensen, reprises her “radiant Fiordiligi” (Opera Today) alongside the Dorabella of soprano Melody Moore; an audience Brought To You By Theresa Roemer True and Real collection and critical favorite in HGO’s Show Boat, Moore was also seen as Marta in the company’s American premiere of The Passenger in HGO’s 2013–14 season, as well as in its performances at the Lincoln Center Festival. Italian bass-baritone Alessandro Corbelli revisits his “authoritative Alfonso” (Opera News), with Italian soprano Nuccia Focile, Seattle Opera’s 2012–13 Artist of the Year, as Despina.

Shakespeare himself would be proud of the 100% perfect interpretation of Otello.

Notables at the opera were Houston fashion designer David Peck and the Museum of Fine Arts ,C.E.O Gary Tinterow.

President Obama legacy: Helping Millions Live 23% Longer

President Obama legacy: Helping Millions Live 23% Longer

Barron's Medical Journal reporting from National Institution Of Health ( NIH ) Bethesda, Maryland USA Reporting B.Bobby Graham .

Bethesda ( AP ) --- President Obama legacy is helping millions of people live 23% longer. An example of The American People living longer is happening in Genomics and Alzheimer's

While scientists know Alzheimer's disease involves progressive brain cell failure, the science world has discovered two important genes. APOE-e4 and TREM2 are game changers. Like other chronic conditions, experts believe that Alzheimer's develops as a complex result of multiple factors rather than any one overriding cause. Both age and genetics have been identified as risk factors, The discovery of additional risk factors has deepen our understanding of why Alzheimer's develops in some people and not others.

Apolipoprotein E-e4 (APOE4), discovered in 1993, is the first gene variation found to increase risk of Alzheimer's and remains the risk gene with the greatest known impact. Having this mutation, however, does not mean that a person will develop the disease. APOE-e4 is the first risk gene identified, and remains the gene with strongest impact on risk. APOE-e4 is one of three common forms of the APOE gene; the others are APOE-e2 and APOE-e3.

“It is a giant step forward for the field,” said Dr. P. Murali Doraiswamy, an Alzheimer’s researcher at Duke University. “It could dramatically accelerate testing of new drug candidates.”

Of course, a petri dish is not a brain, and the petri dish system lacks certain crucial components, like immune system cells, that appear to contribute to the devastation once Alzheimer’s gets started. But it allows researchers to quickly, cheaply and easily test drugs that might stop the process in the first place. The crucial step, of course, will be to see if drugs that work in this system stop Alzheimer’s in patients.

Science in the next four years. Ms Conrad says a great example of the power of genomics was publicized in the New England Journal Of Medicine on November 14, 2012. The Gene TREM2. The TREM2 gene provides instructions for making a protein called triggering receptor expressed on myeloid cells 2. As its name suggests, this protein is made in myeloid cells, which are cells produced in bone marrow. The TREM2 protein is found on the cell surface, where it interacts with the protein produced from the TYROBP gene. The TREM2 and TYROBP proteins form a complex that transmits chemical signals to activate the cell. When the gene is not mutated, white blood cells in the brain spring into action, gobbling up and eliminating the plaque-forming toxic protein, beta amyloid. As a result, Alzheimer’s can be staved off or averted. But when the gene is mutated, the

brain’s white blood cells are hobbled, making them less effective in their attack on beta amyloid. People with the mutated gene have a threefold to five fold increase in the likelihood of developing Alzheimer’s disease in old age. Conrad says If The Mom And The Dad Has Gene Trem2 ....The Child has a 89% Chance Of Getting Alzheimer's

Alzheimer’s disease (AD) is the most common form of dementia in the elderly. The genetic basis of lateonset AD (LOAD) is not well known. However, since 1993 the relationship with APOE gene is known, recently it has established a new relationship with the TREM2 gene. This review aims to show the implications of mutations in TREM2 gene in AD. Background: Mutations in TREM2 have been involved in Nasu-Hakola disease that causes frontotemporal dementia like (FTD-like) phenotype. Recently it has been involved in AD with an odds ratio as strong as previously reported with APOEε4. Methods and results: We review relevant papers concerning to TREM2 gene, not only its implication in neurodegenerative disease, but also those focused on Alzheimer´s Disease. Conclusion: There is an increased frequency of rare heterozygous TREM2 variations in AD and FTD, and TREM2 variants may play a role in neurodegenerative diseases in general. However, the relationship between TREM2 gene and neurodegenerative diseases is complex and ambiguous results. Surely the TREM2 variants have great interest in future research of neurodegenerative diseases.

President Obama Genomics is leading the way in a new discovery TREM2 Triggering receptor expressed on myeloid cells 2 is a protein that in humans is encoded by the TREM2 gene. The New Leading Technology To Cure Breast Cancer is also here according to Rose Conrad Ph.D. CEO GenNxeix Inc Nanoparticles and Semi Conductors GenNxeix Biotech Conrad explains: Quantum dots (QDs), also known as semiconducting nanoparticles, are promising zero‐dimensional advanced materials because of their nanoscale size and because they can be engineered to suit particular applications such as nonlinear optical devices (NLO), electro‐optical devices, and computing applications. QDs can be joined to polymers in order to produce nanocomposites which can be considered a scientific revolution of the 21st century. One of the fastest moving and most exciting interfaces of nanotechnology is the use of QDs in medicine, cell and molecular biology.

Recent advances in nanomaterials have produced a new class of markers and probes by conjugating semiconductor QDs with biomolecules that have affinities for binding with selected biological structures. The nanoscale of QDs ensures that they do not scatter light at visible or longer wavelengths, which is important in order to minimize optical losses in practical applications. Moreover, at this scale, quantum confinement and surface effects become very important and therefore manipulation of the dot diameter or modification of its surface allows the properties of the dot to be controlled. Quantum confinement affects the absorption and emission of photons from the dot. Thus, the absorption edge of a material can be tuned by control of the particle size. Nanocomposite systems for nanomedicine and bioengineering applications Nanoparticles has the potential to enable breast cancer research and improve molecular imaging, early detection, prevention, and treatment of breast cancer. GenNxeix scientist say photoluminescent nanoparticles will allow oncologists to discriminate between cancerous cells and healthy cells.

Proteomics and bioinformatics will enable researchers to identify markers of Breast cancer susceptibility and precancerous lesions Numerous investigations have shown that both tissue and cell distribution profiles of anticancer drugs can be controlled by their entrapment in submicronic colloidal systems (nanoparticles). The rationale behind this approach is to increase antitumor efficacy, while reducing systemic side-effects. This review provides an update of tumor targeting with conventional or long-circulating nanoparticles. The in vivo f

The discovery, said Dr. Sam Gandy of the Icahn School of Medicine at Mount Sinai in New York, is “a real game changer” and “a paradigm shifter.” He added, “I’m really enthusiastic to take a crack at this in my lab.”

Karen Duff, an Alzheimer’s researcher at Columbia University, while praising the work as “a tour de force,” cautioned that once Alzheimer’s starts, tangles can take off on their own and may need to be attacked by drugs that strike them specifically in order to stop devastation in the brain.

Dr. Tanzi is now starting an ambitious project to test 1,200 drugs on the market and 5,000 experimental ones that have finished the first phase of clinical testing — a project that is impossible with mice, for which each drug test takes a year. With their petri dish system, Dr. Tanzi said, “we can test hundreds of thousands of drugs in a matter of months.”

He already has used his system to look at drugs designed to prevent the formation of amyloid, the protein that clumps into plaques. The drugs, he reports, prevented both plaques and tangles in the petri dishes. Some are in clinical trials, and it is not known if they work in people. One was tested in patients and failed because it was too toxic. One hope is to find drugs for other diseases that are known to be safe and work on Alzheimer’s in the petri dish.

He also found an enzyme needed to make tangles after plaques are present. When he blocked that enzyme, plaques formed but not tangles. The enzyme is another potential drug target, he said.

Dr. Gandy wants to use the system to study the effects of genes that predispose someone to have Alzheimer’s, especially the most powerful one, ApoE4, which contributes to about half of all Alzheimer’s cases. No one really knows how or why it is linked to the disease, Dr. Gandy said. “I think I would go after that to begin with,” he said.

Dr. Tanzi said that once his group had gotten the idea of growing neurons in a gel, setting up Alzheimer’s in a dish system had been straightforward. Group members used human embryonic stem cells — those cells that can become any cell of the body — and grew them with a mixture of chemicals that made them turn into neurons. They gave those neurons Alzheimer’s genes and grew them in wells in petri dishes that were lined with a commercially available gel.

Again genomics science is amazing.