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.