Affordable Care Act Is A Win: Ninety Four Percent Of People With Pancreatic Cancer Will Have Insurance

Barron’s Medical Journal Robert Graham Ph.D. Reporting from GeorgeTown University Washington, DC USA.

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Affordable Care Act Is A Win: Ninety Four Percent Of People With Pancreatic Cancer Will Have Insurance

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Washington DC ( AP ) Barron’s Medical Journal has discovered that In Houston Texas we have one of the best Researchers in the World to work with pancreatic cancer. Yes The Baylor College of Medicine Kim Worley, Ph.D.

Number of New Cases and Deaths per 100,000: The number of new cases of pancreas cancer was 12.2 per 100,000 men and women per year. The number of deaths was 10.9 per 100,000 men and women per year. These rates are age-adjusted and based on 2006-2010 cases and deaths.

For several decades, the incidence of pancreatic cancer has been 50% to 90% higher among blacks than among whites in the United States

Lifetime Risk: Lifetime risk is the probability of developing or dying from a disease in the course of one's lifespan. Based on the most recent data, approximately 1.5 percent of men and women will be diagnosed with pancreas cancer at some point during their lifetime.

Prevalence of this cancer: There are an estimated 41,609 people currently living with pancreas cancer in the United States

Kim’s Work with Sea urchin genome is showing advances in the medical and science communities. President Obama now enrolling millions of patients and sixteen percent of Black Men is going to experience pancreatic cancer. We want to put a light on where treatment options can produce the best success. Kim and BCM-HGSC uses genomic and mouse models to work with Sea urchin genome and their research has sequenced chromosomes 6 and 10 of the laboratory mouse (Mus musculus).

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The genome sequence of the mouse was produced by the Mouse Genome Sequencing Consortium. BCM-HGSC finished 178Mb of redundant sequence or ~120 Mb of unique sequence for the mouse project that was completed in December 2005. Barron’s Medical Journal Also wants to high light Dr. Rose Conrad Ph.D. of Sam Houston Biotech. Conrads researchers can compare normal and tumor DNA has shown that the gene for a subunit of the multi-subunit SWI/SNF protein complex was either deleted, mutated or rearranged in about a third of the 70 human pancreatic cancers from the region that the Sam Houston team examined. Sam Houston researchers found that restoring the expression of one of the missing genes slowed the growth of pancreatic cancer cells. The pancreatic cancer enter a state called senescence. "This is really strong genetic evidence that this complex plays a role in pancreatic cancer, and it suggests the influence of the SWI/SNF complex is on par with that of other well-known tumor suppressors, such as p53. The tumor-suppressing role of the SWI/SNF complex We should not that, one person's pancreatic cancer might have a mutation or deletion in one protein subunit, while another's could have a change in a different subunit. Sam Houston used a array comparative genomic hybridization, or CGH, to pinpoint places in the genome that differed among normal and cancerous pancreatic epithelial cells. The procedure relies on the ability of single-stranded DNA to seek out and bind to its mirror image. By comparing the relative amounts of tumor and normal DNA that bind to a panel of reference sequences, the researchers can tell whether the cancer cell contains amplifications or deletions of genetic material in specific regions throughout the genome. These copy-number variations often occur in genes or regions important in regulating uncontrolled cell growth. The researchers examined about 35 different pancreatic cancers, . 24 of the cancers were primary samples from human patients that had been asked to grow in immune-deficient mice; 11 had been maintained as laboratory-grown cancer cell lines. Sam Houston used high-density arrays of reference DNA sequences for the CGH, which allowed the identifi mplified or deleted regions at a much higher resolution than previously possible -- narrowing the areas of interest to just a few

Thousand nucleotides rather than larger stretches of DNA. Sam Houston looked at the results of the array CGH analysis, and observed that genes known to be involved in pancreatic cancer, and also some new candidates. In particular, they noticed that the genes for individual subunits of the SWI/SNF complex were altered in about 5 to 10 percent of the cancer samples -- an interesting finding, but not prevalent enough to spark further immediate investigation under normal circumstances. realized that more than a third of the cancer samples contained a deletion, mutation or rearrangement in the genes.

There are still things to be fixed, for an example many people that earn between $5 and $15 an hour, do not own or use computers and are more comfortable speaking Spanish than English. Sixty-five percent of East Palo Alto’s population is Latino, a group seen as crucial to the success of the health law. Many lack health insurance and pose a lower financial risk because they are typically younger and healthier than others. Yet California, with the greatest number of Latinos in the country, is far behind in reaching this population. And across the nation, the picture appears even worse.

Those who primarily speak Spanish are largely being left out of the first wave of coverage under Obamacare. Many missed this week’s deadline for enrollment in plans beginning Jan. 1. People who want to be covered for any part of 2014 must sign up by March 31.

The Obama administration said Tuesday that it would provide more time for people to complete their applications for health insurance if they could show that they missed the deadline because of problems with the federal health care website.

The deadline has been extended by a day for those who want to receive health insurance coverage through the federal exchange beginning Jan. 1, 2014.

Families with relatives with pancreatic cancer can rest and be assured that help is on the way.

The Dallas Cowboys Tony Dorsett Is losing His Memory Because Tony Has Neuroblastoma And Gene TDP-43

Barron’s Medical Journal Reporting From Baylor College Of Medicine In The Texas Medical Center Houston, Texas USA

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The Dallas Cowboys Tony Dorsett Is losing His Memory Because Tony Has Neuroblastoma And Gene TDP-43

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Houston, Texas ( AP ) Barron’s Medical Journal Sports was concerned after seeing Tony Dorsett the famous running back for The Dallas Cowboys announced that he was losing his memory. Barron’s

decided to ask the question, can some football players have a gene that would cause football players to lose their memory while playing Football?

The Gene TDP-43 In Adults And Gene MYCN or CD44 In Kids has shown some amazing results. Neuroblastoma is a malignant (cancerous) tumor that develops from nerve tissue. It usually occurs in infants and children.

Barrons Medical Journal ask Sam Houston Biotech CEO for answers. To our surprise Rose Conrad Sam Houston CEO says that it has been known for years that some football players have a gene called TDP- 43. TAR DNA-binding protein of 43kDa (TDP-43). Genomics is again the key to equalize a patient’s risk. Conrads says new Genomics genetic risk factor for amyotrophic lateral sclerosis, commonly known as ALS or Lou Gehrig's disease.

There is no cure for ALS and the current treatment only slows disease progression. The identification of pathological interactions between ataxin 2 and TDP-43, another ALS-associated disease protein, together with the strong genetic association of ataxin 2 intermediate-length polyQ expansions and ALS, should aid in the development of biomarkers and empower the development of new therapies for this disease.

Barron’s Medical Journal Researched Joshua M. Shulman, M.D., Ph.D. of Laboratory for Integrative Functional Genomics Departments of Neurology and Molecular & Human Genetics Baylor College of Medicine. Their mission is to offer clinical manifestation of neurodegenerative disease is the culmination of a multi-tiered pathogenic cascade that evolves over decades—understanding how genetic variants impact this causal chain is essential. Although 2% of the population over age 65 are clinically diagnosed with Parkinson's disease, the defining pathology of disease (alpha-synuclein Lewy bodies) is discovered in 20% of brains from population-based autopsy studies. We are therefore investigating the impact of genomic variation on directly measured Lewy pathology, neuronal loss in the midbrain substantia nigra, and progressive motor impairment, leveraging human subject cohorts with detailed clinical and pathological data. We also participate in collaborative studies for the functional genetic dissection of Alzheimer's disease, focusing on the responsible neuropathology, amyloid neuritic plaques and Tau neurofibrillary tangles.

Despite the promise of current human genetic methods, such as genome-wide association studies, they often fail to identify disease susceptibility genes with certainty, instead highlighting broad genomic regions. We are taking advantage of the rapid and powerful genetics available in the fruit fly Drosophila melanogaster in order to accelerate the validation of responsible genes and an understanding of their functions in disease pathogenesis. Expression of human amyloid-beta, Tau, or alpha-synuclein proteins in the fly nervous system recapitulates many core features of Alzheimer's disease and Parkinson's disease pathogenesis. We are testing candidate human susceptibility genes for functional genetic interactions in these fly models of neurodegeneration. Implicated molecular pathways are probed in greater depth, using both Drosophila and human genetic approaches. Our strategy has recently identified cell adhesion converging on the cytoskeleton as likely important for Tau-mediated neurodegeneration and Alzheimer's disease susceptibility, and we are now following up these insights to elucidate the detailed mechanisms.

Chronic traumatic encephalopathy (CTE) is the term coined for the neurodegenerative disease often suspected in athletes with histories of repeated concussion and progressive dementia. Histologically, CTE is defined as a tauopathy with a distribution of tau-positive neurofibrillary tangles (NFTs) that is distinct from other tauopathies, and usually shows an absence of beta-amyloid deposits, in contrast to Alzheimer's disease (AD). Although the connection between repeated concussions and CTE-type neurodegeneration has been recently proposed, this causal relationship has not yet been firmly established. Also, the prevalence of CTE among athletes with multiple concussions is unknown.

All participants had progressive neurocognitive decline prior to death; however, only 3 cases had post-mortem neuropathological findings consistent with CTE. The other 3 participants had pathological diagnoses

of AD, amyotrophic lateral sclerosis (ALS), and Parkinson's disease (PD). Moreover, the CTE cases showed co-morbid pathology of cancer, vascular disease, and AD

Parents can look for in their kids disease called Neuroblastoma. 8% of 30 Million Uninsured has Familial Cancer 1% of the 8% Kids has the ALK Gene on Chromosome2 that results in Neuroblastoma Cancer. Sam Houston Biotech Analytics Business Intelligence CIO Reports - 50% of the Moms with the Gene MYCN or CD44 Kids will have Neuroblastoma Cancer. The way Moms can recognized Neuroblastoma is a Abdominal Mass. The symptoms in high-risk patients are due to this tumor mass or bone pain from the cancer metastases. Extensive bone marrow metastasis may result in pancytopenia. Abdominal distention with respiratory compromise due to massive liver metastases may occur in infants. Because they originate in paraspinal ganglia, neuroblastomas may invade through neural foramina and compress the spinal cord extradurally, causing paralysis. The survival rate is twice as high if diagnosed in infants less that one years old. Genes that encode RNA-binding proteins (RBPs) such as PTB, hnRNP L, and SRSF1 are auto regulated to maintain a constant level of mRNA (Buratti and Baralle 2011). This autoregulatory process may be achieved in part by selective alternative splicing events that trigger nonsense-mediated decay (NMD)-mediated RNA degradation (Lejeune and Maquat 2005). The general term RUST (regulated unproductive splicing and translation) has been proposed to describe this category of gene regulation (Lareau et al. 2007a). Conrad also says that science labs use Genomics to generated multiple antibodies specific to phosphorylated TDP-43 by immunizing phosphopeptides of TDP-43, and analyzed

FTLD-U and ALS brains by immunohistochemistry, immunoelectron microscopy, and immunoblots. In addition, we performed investigations aimed at identifying the responsible kinases, and we assessed the effects of phosphorylation on TDP-43 oligomerization and fibrillization.

As we see in the above picture of A Future National Football League (NFL ) Quarter Back Greyson Dean Secades Of Pope John XXIII High School In Houston, Texas playing is his State Championship Game and planning on being a "Pre-Med-Major" will have the benefit of having a Genomic Science Test to ensure that player thirty years from now will remain healthy after their Football playing days are over.

http://www.hudl.com/athlete/o/520388/highlights/31158406