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NF-kappaB, inflammation, and metabolic disease, Article at Research Gate,( requires membership to see), R. G. Baker, M. S. Hayden, S. Ghosh, Cell Metab 01/2011
ABSTRACT:
" Metabolic disorders including obesity, type 2 diabetes, and atherosclerosis have been viewed historically as lipid storage disorders brought about by overnutrition. It is now widely appreciated that chronic low-grade inflammation plays a key role in the initiation, propagation, and development of metabolic diseases. Consistent with its central role in coordinating inflammatory responses, numerous recent studies have implicated the transcription factor NF-kappaB in the development of such diseases, thereby further establishing inflammation as a critical factor in their etiology and offering hope for the development of new therapeutic approaches for their treatment."
Paper at:
http://www.researchgate.net/publication/215835485_NF-kappaB_inflammation_and_metabolic_disease
Call for papers: NF-kappaB signalling pathway in Neurological diseases at Frontiers in Molecular NeuroScience
Topic Editors:
Jun Yan, University of Queensland, Centre for for Clinical Research, The University ofQueensland., Australia
Deadline for abstract submission: 22 Feb 2014
Deadline for full article submission: 14 May 2014
Extended deadline for full article submission: 19 Jun 2014
Excerpt:
"[b]The reports of the involvement of NF-kappa B in chronic inflammatory diseases have dramatically increased in recent years. Diseases such as, Multiple Sclerosis, Rheumatoid Arthritis, Atherosclerosis, Chronic-inflammatory Demyelinating Polyradiculoneuritis, Asthma, Inflammatory Bowel Disease, Helicobacter pylori -associated gastritis and Systemic Inflammatory Response Syndrome (SIRS).
This research topic aims to explore the effects of the NF-kappa B signalling pathway in the pathogenesis of neurological diseases, and investigate NF-kappa B regulation in context of disease and genetic factors influencing the NF-kappa B pathway. Most importantly it is aimed to foster discussion on NF-kappa B related therapeutic design in neurological diseases. Research work and review articles are all encouraged for submission."
Announcement at:
http://www.frontiersin.org/molecular_neuroscience/researchtopics/nf-kappab_signalling_pathway_i/2354
NF-?B and its relevance to arthritis and inflammation in UK ePubs,
Rachel E. Simmonds and Brian M. Foxwell
Kennedy Institute of Rheumatology Division, Faculty of Medicine, Imperial College London, no date
Abstract:
"In the synovial cells of patients with rheumatoid arthritis (RA), activation of the NF-?B pathway results in the
transactivation of a multitude of responsive genes that contribute to the inflammatory phenotype, including
TNFa from macrophages, matrix metalloproteinases from synovial fibroblasts and chemokines that recruit
immune cells to the inflamed pannus. This is largely a consequence of activation of the ‘canonical’ NF-?B
pathway that involves heterodimers of p50/p65. Whilst much information on the role of NF-?B in inflammation
has been gleaned from genetic deficiency of the respective genes in mice, important differences exist in the
signalling networks between human and murine immune cells and immortalised cell lines. Despite these
differences at the molecular level, the importance of NF-?B in inflammation is undisputed and inhibition of the
pathway is widely believed to have great potential as a therapeutic target in RA. Commercial effort has gone
into developing inhibitors of NF-?B activation. However, inhibition of the NF-?B activation can result in an
exacerbation of inflammation if TNFa production by macrophages is not controlled. It will be important that
such inhibitors are carefully monitored before their long term use in chronic inflammatory conditions such as
RA. "
Article at:
http://epubs.surrey.ac.uk/129804/3/Simmonds_and_Foxwell.pdf
Celebrating 25 years of NF-?B in Nature Immunology, Editorial, August 2011
Excerpt:
"Few proteins have had as profound an influence on immunity and biology as the transcription factor NF-?B.
Systems analyses and bioinformatics metadata mining are commonly used today as state-of-the-art approaches for identifying nodal components, whether proteins, genes or regulatory pathways, that intersect to affect biological processes or influence phenotypes. This approach allows connections to be made where none are readily apparent. Twenty-five years ago, using a simple gel-electrophoresis mobility-shift assay, Ranjan Sen and David Baltimore identified a DNA-binding factor that has since been found to be ancient and evolutionarily conserved and to be linked to many biological pathways. It influences cellular development, innate and adaptive immune responses, the induction of inflammatory mediators and wound repair, and, when dysregulated, can lead to various forms of cancer, autoimmunity and chronic inflammatory syndromes. This factor is NF-?B.
Article at:
http://www.nature.com/ni/journal/v12/n8/full/ni0811-681.html
The complexity of NF-?B signaling in inflammation and cancer in Molecular Cancer, Bastian Hoesel and Johannes A Schmid*, Department of Vascular Biology and Thrombosis Research, Center for Physiology and Pharmacology, Medical University Vienna, Schwarzspanierstraße 17, 1090 Vienna, Austria, 12-2013
Abstract:
The NF-?B family of transcription factors has an essential role in inflammation and innate immunity. Furthermore, NF-?B is increasingly recognized as a crucial player in many steps of cancer initiation and progression. During these latter processes NF-?B cooperates with multiple other signaling molecules and pathways. Prominent nodes of crosstalk are mediated by other transcription factors such as STAT3 and p53 or the ETS related gene ERG. These transcription factors either directly interact with NF-?B subunits or affect NF-?B target genes. Crosstalk can also occur through different kinases, such as GSK3-ß, p38, or PI3K, which modulate NF-?B transcriptional activity or affect upstream signaling pathways. Other classes of molecules that act as nodes of crosstalk are reactive oxygen species and miRNAs. In this review, we provide an overview of the most relevant modes of crosstalk and cooperativity between NF-?B and other signaling molecules during inflammation and cancer.
Article at:
http://www.molecular-cancer.com/content/12/1/86#
Nonsteroidal Anti-inflammatory Agent Toxicity
Author: Timothy J Wiegand, MD; Chief Editor: Asim Tarabar, MD, March 3, 2014 in Medscape
Excerpt:
"Nonsteroidal anti-inflammatory drugs (NSAIDs) have been prescribed extensively throughout the world. More than 70 million prescriptions for NSAIDs are written each year in the United States. With over-the-counter use included, more than 30 billion doses of NSAIDs are consumed annually in the United States alone"
"Both acute and chronic poisoning with NSAIDs results in significant morbidity and mortality. The Arthritis, Rheumatism, and Aging Medical Information System (ARAMIS) system has estimated that more than 100,000 hospitalizations and more than 16,000 deaths in the United States each year are due to NSAID-related complications with costs greater than $2 billion. Gastrointestinal (GI), renal, central nervous system (CNS), hematologic, and dermatologic symptoms may ensue (see Complications)."
Article at:
http://emedicine.medscape.com/article/816117-overview
Anti-inflammatory drugs in the 21st century in PubMed., Rainsford KD. Biomedical Research Centre, Faculty of Health & Wellbeing, Sheffield Hallam University, UK., 2007
Abstract:
Historically, anti-inflammatory drugs had their origins in the serendipitous discovery of certain plants and their extracts being applied for the relief of pain, fever and inflammation. When salicylates were discovered in the mid-19th century to be the active components of Willow Spp., this enabled these compounds to be synthesized and from this, acetyl-salicylic acid or Aspirin was developed. Likewise, the chemical advances of the 19th-20th centuries lead to development of the non-steroidal anti-inflammatory drugs (NSAIDs), most of which were initially organic acids, but later non-acidic compounds were discovered. There were two periods of NSAID drug discovery post-World War 2, the period up to the 1970's which was the pre-prostaglandin period and thereafter up to the latter part of the last century in which their effects on prostaglandin production formed part of the screening in the drug-discovery process. Those drugs developed up to the 1980-late 90's were largely discovered empirically following screening for anti-inflammatory, analgesic and antipyretic activities in laboratory animal models. Some were successfully developed that showed low incidence of gastro-intestinal (GI) side effects (the principal adverse reaction seen with NSAIDs) than seen with their predecessors (e.g. aspirin, indomethacin, phenylbutazone); the GI reactions being detected and screened out in animal assays. In the 1990's an important discovery was made from elegant molecular and cellular biological studies that there are two cyclo-oxygenase (COX) enzyme systems controlling the production of prostanoids [prostaglandins (PGs) and thromboxane (TxA2)]; COX-1 that produces PGs and TxA2 that regulate gastrointestinal, renal, vascular and other physiological functions, and COX-2 that regulates production of PGs involved in inflammation, pain and fever. The stage was set in the 1990's for the discovery and development of drugs to selectively control COX-2 and spare the COX-1 that is central to physiological processes whose inhibition was considered a major factor in development of adverse reactions, including those in the GI tract. At the turn of this century, there was enormous commercial development following the introduction of two new highly selective COX-2 inhibitors, known as coxibs (celecoxib and rofecoxib) which were claimed to have low GI side effects. While found to have fulfilled these aims in part, an alarming turn of events took place in the late 2004 period when rofecoxib was withdrawn worldwide because of serious cardiovascular events and other coxibs were subsequently suspected to have this adverse reaction, although to a varying degree. Major efforts are currently underway to discover why cardiovascular reactions took place with coxibs, identify safer coxibs, as well as elucidate the roles of COX-2 and COX-1 in cardiovascular diseases and stroke in the hope that there may be some basis for developing newer agents (e.g. nitric oxide-donating NSAIDs) to control these conditions. The discovery of the COX isoforms led to establishing their importance in many non-arthritic or non-pain states where there is an inflammatory component to pathogenesis, including cancer, Alzheimer's and other neurodegenerative diseases. The applications of NSAIDs and the coxibs in the prevention and treatment of these conditions as well as aspirin and other analogues in the prevention of thrombo-embolic diseases now constitute one of the major therapeutic developments of the this century. Moreover, new anti-inflammatory drugs are being discovered and developed based on their effects on signal transduction and as anti-cytokine agents and these drugs are now being heralded as the new therapies to control those diseases where cytokines and other nonprostaglandin components of chronic inflammatory and neurodegenerative diseases are manifest. To a lesser extent safer application of corticosteroids and the applications of novel drug delivery systems for use with these drugs as well as with NSAIDs also represent newer technological developments of the 21st century. What started out as drugs to control inflammation, pain and fever in the last two centuries now has exploded to reveal an enormous range and type of anti-inflammatory agents and discovery of new therapeutic targets to treat a whole range of conditions that were never hitherto envisaged
Article at:
http://www.ncbi.nlm.nih.gov/pubmed/17612044
Chronic inflammatory diseases are stimulated by current lifestyle: how diet, stress levels and medication prevent our body from recovering, Margarethe M Bosma-den Boer*, Marie-Louise van Wetten and Leo Pruimboom, University of Girona, Plaça Sant Domènec, 3 Edifici Les Àligues, 17071, Girona, Spain, Published: 17 April 2012
Abstract:
Serhan and colleagues introduced the term "Resoleomics" in 1996 as the process of inflammation resolution. The major discovery of Serhan's work is that onset to conclusion of an inflammation is a controlled process of the immune system (IS) and not simply the consequence of an extinguished or "exhausted" immune reaction. Resoleomics can be considered as the evolutionary mechanism of restoring homeostatic balances after injury, inflammation and infection. Under normal circumstances, Resoleomics should be able to conclude inflammatory responses. Considering the modern pandemic increase of chronic medical and psychiatric illnesses involving chronic inflammation, it has become apparent that Resoleomics is not fulfilling its potential resolving capacity. We suggest that recent drastic changes in lifestyle, including diet and psycho-emotional stress, are responsible for inflammation and for disturbances in Resoleomics. In addition, current interventions, like chronic use of anti-inflammatory medication, suppress Resoleomics. These new lifestyle factors, including the use of medication, should be considered health hazards, as they are capable of long-term or chronic activation of the central stress axes. The IS is designed to produce solutions for fast, intensive hazards, not to cope with long-term, chronic stimulation. The never-ending stress factors of recent lifestyle changes have pushed the IS and the central stress system into a constant state of activity, leading to chronically unresolved inflammation and increased vulnerability for chronic disease. Our hypothesis is that modern diet, increased psycho-emotional stress and chronic use of anti-inflammatory medication disrupt the natural process of inflammation resolution ie Resoleomics.
Article at:
http://www.nutritionandmetabolism.com/content/9/1/32#
List of Autoimmune and Autoimmune-Related Diseases at American Autoimmune website. (160 diseases for autoimmune only, if you are curious)
Link at:
http://www.aarda.org/research-report/
Vitamin D deficiency and autoimmune disorders at Health Central
8 Facts About Vitamin D and Rheumatoid Arthritis
Lene Andersen Aug 15, 2013 (updated Apr 23, 2014)
Slide 1:
"A study has linked vitamin D deficiency with an increased risk for cancer and autoimmune diseases, such as rheumatoid arthritis MS, and lupus. Researchers found, through mapping vitamin D receptors binding throughout the human genome, that vitamin D deficiency is a major environmental factor in increasing the risk of developing these disorders"
Slide 2:
"1 billion people don't get enough vitamin D
It's been estimated that 70 percent of children and adults in the U.S. are vitamin D deficient. The cause of deficiency is a combination of not getting enough exposure to the sun and not having enough vitamin D in their diets."
Slide 3:
"Medications can affect vitamin D absorption
Hydroxychloroquine, or Plaquenil, and corticosteroids, which both can be prescribed for the treatment of rheumatoid arthritis, are among these. Even if you are taking one of these drugs, your doctor can adjust your vitamin D dose to correct the malabsorption."
Slide 4:
"A blood test can determine your vitamin D level
A blood test can determine your vitamin D level
You can ask your doctor to give you a simple blood test called, 25-hydroxy vitamin D test. It can tell you how deficient you might be in vitamin D."
Slide 5:
"You can add vitamin D by changing your diet
To increase your level of vitamin D through food, you should include more oily fish, such as salmon, mackerel and tuna. Egg yolks and mushrooms also provide vitamin D, You could also choose a cereal and milk fortified with vitamin D."
Slide 6:
"15 minutes of sun exposure can make a difference
Just 15 minutes of exposure to the sun gives you 20,000 IUs of vitamin D. However, this is without sunblock in the summer, and be aware that you need to be careful not to expose your skin to the sun without sunblock for long stretches of time. This can cause skin damage and increase your risk of skin cancer."
Slide 7:
"Vitamin D can lift moods and strengthen bones
Not only does vitamin D play a crucial role in the absorption of calcium, but it can stave off osteoporosis, which can be a risk for people with RA. It also protects those susceptible to seasonal affective disorder from becoming depressed."
Slide 8:
"Vitamin D can help you manage chronic pain
Vitamin D plays a role in managing musculoskeletal pain caused by rheumatoid arthritis and other diseases. It's common for people who live with chronic pain to have a vitamin D deficiency, so doctors routinely check their patients for their levels of vitamin D and often recommend vitamin D supplements as part of a treatment plan
Slides at:
http://www.healthcentral.com/rheumatoid-arthritis/cf/slideshows/10-facts-about-vitamin-d-and-rheumatoid-arthritis?ap=104#slide=1
I think you should reread the report(s). The Flint CRP study report is at the Free Library:
http://www.thefreelibrary.com/Star+Scientific+Announces+Successful+First+Look+at+the+%22Flint%22+CRP...-a0306202830
You may also be interested in the Thyroid study that got published in the Journal of Clinical Endocrinology amd Matabolism:
http://press.endocrine.org/doi/full/10.1210/jc.2013-2951
Inovio Pharmaceuticals Acquires Early Stage DNA Therapies to Treat Alzheimer's and Multiple Sclerosis in Fierce Biotech Research, May 14, 2014
Excerpt:
"BLUE BELL, PA, USA I May 13, 2014 I Inovio Pharmaceuticals, Inc. (NYSE MKT: INO) announced today it acquired worldwide rights (excluding China) for early preclinical therapies addressing Alzheimer's disease and multiple sclerosis based on the academic research of Dr. Bin Wang, a professor at Fudan University's Shanghai Medical College. Dr. Wang is a pioneer in the field of DNA therapies, having worked closely with Dr. David Weiner at the University of Pennsylvania. Dr. Wang was the primary author on some of the earliest DNA vaccine papers and patents. In consideration for these rights, Inovio will make clinical and regulatory milestone payments to the University.
These newly licensed technologies are based on patent-protected and published discoveries from Dr. Wang and his collaborator, who found a novel way to generate inducible regulatory T cells, or iTreg. iTreg cells are involved in shutting down immune responses after they have successfully eliminated invading organisms, and also in preventing autoimmunity or inflammatory diseases. In multiple published preclinical studies, this approach generated CD25-iTreg in an antigen-specific manner. These novel approaches could be used to develop therapies targeting major inflammatory diseases like multiple sclerosis and may be used to treat Alzheimer's disease.
Article at:
http://www.fiercebiotechresearch.com/press-releases/inovio-pharmaceuticals-acquires-early-stage-dna-therapies-treat-alzheimers#ixzz32GjxuHQg
Pancreatic cancer likely to become no. 2 cause of cancer deaths article in Mother Nature Network By: Rachael Rettner, LiveScience
Tue, May 20, 2014
Excerpts:
"A disease without a screening test, 94 percent of those eventually diagnosed with pancreatic cancer die within five years."
"Pancreatic cancer is projected to become the second most common cause of cancer-related death in the United States in 2030, overtaking deaths from breast and colon cancers, according to new research.
Currently, the top three causes of cancer-related death in the United States are lung, colorectal and breast cancers. Pancreatic cancer is fourth, followed by prostate and liver cancers. In 2030, lung cancer will remain the top killer, but pancreatic cancer will move to second, followed by liver cancer and colorectal cancer, according to the report from the Pancreatic Cancer Action Network (PCAN), a charity organization that advocates for pancreatic cancer research.
The reason for the increases in deaths from pancreatic and liver cancers is partly due to changes in demographics, including an increase in the number of people ages 65 and older, who are at greater risk for cancer in general, said study researcher Lynn Matrisian, vice president of scientific and medical affairs at PCAN. In addition, some minority groups, such as African Americans, are at greater risk for pancreatic cancer than whites, so changes in minority group populations also affect the risk of the disease."
Article at:
http://www.mnn.com/health/fitness-well-being/stories/pancreatic-cancer-likely-to-become-no-2-cause-of-cancer-deaths
Chronic inflammation and pancreatic cancer in PubMed by:
McKay CJ1, Glen P, McMillan DC. Lister Department of Surgery, Glasgow Royal Infirmary, Glasgow G31 2ER, Scotland, UK. cjmk3y@clinmed.gla.ac.uk dated 2008
Abstract:
"There is a proven association between carcinoma of the pancreas and both the sporadic and hereditary forms of chronic pancreatitis. In chronic pancreatitis the standardised incidence ratio for development of pancreatic cancer is 14-18 and is further increased by cigarette smoking. Underlying mechanisms are unclear but current theories point to the progressive accumulation of genetic mutations as a consequence of repeated DNA damage and cell regeneration in an environment favouring proliferation and neovascularisation. In patients who develop pancreatic cancer, there is interest in the role of the inflammatory response in the development of cancer cachexia and in determining prognosis. Furthermore, markers of a systemic inflammatory response have prognostic significance in both advanced, inoperable pancreatic cancer and in patients undergoing resection. Further understanding of the details of the relationship between inflammation, carcinogenesis and cancer prognosis may lead to new therapeutic possibilities as part of multi-modality management of this difficult disease.
Article at:
http://www.ncbi.nlm.nih.gov/pubmed/18206813
Bioresearch Monitoring Information System (BMIS) Database at:
http://www.fda.gov/Drugs/InformationOnDrugs/ucm135162.htm
Excerpt:
"In order to foster transparency and encourage information sharing within the clinical research community, FDA’s Center for Drug Evaluation and Research (CDER) maintains a bioresearch monitoring Web site that makes clinical research information available to the public. This Web site contains information that identifies clinical investigators, contract research organizations, and institutional review boards involved in the conduct of Investigational New Drug (IND) studies with human investigational drugs and therapeutic biologics. This information is extracted from IND-related documents submitted to the agency and made available to the public as the Bioresearch Monitoring Information System (BMIS) at http://www.accessdata.fda.gov/scripts/cder/bmis/"
My comments: When STSI files an NDI, it will show up here in the FDA dabase for NDI: Zip file and Search file links
Search Clinical Trials at Center Watch webpage at:
http://www.centerwatch.com/clinical-trials/listings/
My comments: Clinical trials listed by therapeutic area and location
Rosenkamp Clinical Trials Website:
"Roskamp Institute Clinical Trials Experience
Under the leadership of the Institute’s Scientific Director, Michael Mullan, MBBS, Ph.D., along with our clinical investigative team headed by Andrew Keegan, MD, a renowned neurologist, Roskamp has extensive expertise in a multitude of therapeutic areas and phases of pharmaceutical/nutraceutical clinical research. Our clinical research coordinators and nurses, many of whom are certified, are highly experienced in all aspects of clinical trials including regulatory issues, recruitment, and accurate record maintenance. Our goal is to provide excellent trial-related patient care, while meeting contract goals and sponsor timelines. Our research is conducted with strict adherence to Federal Drug Administration (FDA), International Conference of Harmonization (ICH), Good Clinical Practice (GCP) and HIPPA guidelines.
We perform primarily phase II - IV clinical research studies. Specific areas of study include:
Alzheimer's Disease (actively enrolling)
Elan Agitation Study
Accera AD Trial
TauRx AD Study
Multiple Sclerosis (actively enrolling)
RRMS Novartis Cognition study
RR<S Novartis PREFER Study
RRMS Novartis ASSESS study
Dementia Mild Cognitive Impairment (MCI)
Depression
Head and Traumatic Brain Injury
Migraine
Neurodegenerative disease
Neuromuscular disordersParkinson's Disease
Tourette's Syndrome
Other psychiatric and central nervous system conditions
Bipolar DisorderGeneral Anxiety Disorder
For more information on clinical trials, contact:
Roskamp Institute Clinical Trials
2040 Whitfield Avenue
Sarasota, FL 34243
Phone: 941-256-8018
Fax: 941-756-3681
Email: Clinical Trials Division
Roskamp Institute Memory Clinic
2040 Whitfield Avenue
Sarasota, FL 34243
Phone: 941-256-8018
Fax: 941-756-3681
Email: Clinical Trials Division
Webpage at:
http://www.rfdn.org/clinical_trials.html
Disappointing Results For Statins In Two NIH Trials article in Forbes Pharma and Healthcare, 5/18/2014 by Larry Husten
Excerpt:
"Two NHLBI studies have failed to find any benefit for statin therapy in patients with chronic obstructive pulmonary disease (COPD) and acute respiratory distress syndrome (ARDS). Previous observational studies had raised the possibility that statins, perhaps due to their anti-inflammatory effects, might improve outcomes in people with these serious diseases. But both trials were stopped early by their data and safety monitoring boards for futility. The results of the trials were presented at the annual meeting of the American Thoracic Society and published simultaneously in the New England Journal of Medicine."
Article at:
http://www.forbes.com/sites/larryhusten/2014/05/18/disappointing-results-for-statins-in-two-nih-trials/?ss=pharma
I Have UC, Ulcerative Colitis Stories and Solutions at:
http://www.ihaveuc.com/anatabloc-helped-my-uc/
SPARKPEOPLE, Hashimoto's Thyroiditis sub-group board at:
http://www.sparkpeople.com/myspark/team_messageboard_thread.asp?board=0x22376x51917998
Rosacea Support Community discussion board at:
http://rosacea-support.org/community/viewtopic.php?f=24&t=4097
A Study to Evaluate the Safety, Tolerability, and Effects of Anatabloc® Crème in Rosacea posted at ClincalTrials.gov
Excerpt:
"This study has been completed.
Sponsor:
Rock Creek Pharmaceuticals, Inc."
"ClinicalTrials.gov Identifier:
NCT01740934
First received: November 30, 2012
Last updated: April 29, 2014
Last verified: April 2014"
"Primary Outcome Measures:
Adverse Effects [ Time Frame: 8 to 16 weeks ] [ Designated as safety issue: No ]
Collected information of the safety, tolerability and adverse events, and subjective experience related to the use of Anatabloc Cream by subjects
Secondary Outcome Measures:
Change in the appearance of the facial skin [ Time Frame: 8 to 16 weeks ] [ Designated as safety issue: No ]
Change measured by comparison of questionnaire and rating scores over time
Enrollment: 117
Study Start Date: November 2012
Study Completion Date: August 2013
Primary Completion Date: August 2013 (Final data collection date for primary outcome measure)"
Report at:
http://clinicaltrials.gov/ct2/show/study/NCT01740934
SEC says ex-Penson execs violated securities lending rule, Reuters Business News, May 20, 2014 By Jonathan Stempel
Article:
"NEW YORK, May 19 (Reuters) - The U.S. Securities and Exchange Commission charged four former officials at a Penson Worldwide Inc unit with violations of a post-financial crisis rule on securities lending that was designed to help markets function by ensuring that trades are completed.
Rule 204 of Regulation SHO was adopted by the SEC in July 2009 to curb abuses in "naked" short sales, where investors sell shares short without first borrowing those shares or making sure they can be borrowed. An inability to deliver such shares in a timely manner is called a "fail."
According to the SEC, Thomas Delaney, once chief compliance officer at Penson Financial Services, knew the now-bankrupt clearing services firm's procedures for selling customer margin securities were causing rule violations, yet affirmatively assisted the violations and concealed them from regulators.
The SEC also said Charles Yancey, once the unit's chief executive, ignored "significant red flags" about Delaney's involvement in the violations, including the alleged concealment. Two other former Penson officials settled related charges, the SEC said.
According to the SEC, when Penson loaned stocks in customer margin accounts to third parties, and the customers then sold the stocks, the firm waited too long to recall the loans. It said this led to "serial failures to deliver," sometimes lasting several days.
"This enforcement action seeks to hold Penson executives responsible for choosing profits over compliance with Regulation SHO," SEC enforcement chief Andrew Ceresney said in a statement.
The SEC said it plans to litigate against Yancey and Delaney in administrative proceedings and settled with former Penson securities lending officials Michael Johnson and Lindsey Wetzig.
Without admitting or denying the findings, Johnson agreed to pay a $125,000 penalty and accept a five-year securities industry ban, while Wetzig agreed to a censure, the SEC said.
Kit Addleman, a lawyer for Yancey, said: "The SEC is attempting to hold the CEO of what was once the second-largest clearing firm in the country responsible for technical violations that he wasn't involved in. The SEC's claims are baseless, and we look forward to disproving them."
Brent Baker, a lawyer for Delaney, said his client is "confident that he will prevail."
Lawyers for Johnson and Wetzig did not immediately respond to requests for comment.
Before the case was announced, SEC Commissioner Kara Stein on Monday said gatekeepers like chief compliance officers should be held more accountable for oversight, and that the regulator could "provide guidance that sets clearer expectations on what it means to act appropriately." She spoke at a Compliance Week conference in Washington, D.C.
Penson Worldwide filed for Chapter 11 protection in January 2013 with the Delaware bankruptcy court. The court approved Penson's liquidation in July.
(Reporting by Jonathan Stempel in New York; Additional reporting by Sarah N. Lynch in Washington, D.C.; Editing by Cynthia Osterman)
Article at:
http://finance.yahoo.com/news/sec-says-ex-penson-execs-222034682.html;_ylt=AwrSyCShRHtTATcAyASTmYlQ
Read More About Medicines in Development for Alzheimer's Disease on the PHARMA website.
Excerpt:
"America’s biopharmaceutical research companies are investigating or developing 93 medicines to help the more than five million patients in the United States who are living with Alzheimer’s. The medicines in development – all in either clinical trials or under review by the Food and Drug Administration – include 81 for Alzheimer’s, 11 for cognition disorders and 2 for dementias, according to a new report released by the Pharmaceutical Research and Manufacturers of America (PhRMA).
Article at:
http://www.phrma.org/research/medicines-development-alzheimers-disease#sthash.tlDSJxIs.dpuf
Some drugs may slow Alzheimer’s in Visalia-Time Delta, May 19, 2014
Excerpt:
"Dr. Anton Porsteinsson, director of the Alzheimer’s Disease Care, Research and Education Program at the University of Rochester School of Medicine in New York, said Celexa seems to have a “not inconsequential” impact on levels of the protein.
But he cautioned that while Alzheimer’s researchers still tend to believe that too much beta amyloid is a bad thing, “every treatment intervention that directly targets beta amyloid has been ineffective or equivocal. So far, there is no absolute evidence in humans that lowering beta amyloid is a good thing from a therapeutic perspective.”
He also cautioned that the 60-mg dose of Celexa used in the study is high compared to the usual doses of 40 mg or 20 mg in older people. And, he added, it’s important to be aware that Celexa has a significant side effect: it can disrupt the heart’s rhythms.
In 2011, the U.S. Food and Drug Administration issued a warning that stated Celexa should not be given at doses greater than 40 mg a day since it can cause a dangerous irregular heartbeat at higher doses.
Article at:
http://www.visaliatimesdelta.com/story/life/2014/05/19/study-drugs-may-slow-alzheimers/9282263/
Mergers don't make good medicines by Scott Gotliebs, 09 May 2014
in The Independent
Excerpts:
"When Pfizer constructed a massive drug development facility in Groton, Connecticut, the 160-acre research site became a symbol of the perceived dominance of the big drug makers.
Built on the revenues from blockbuster drugs such as the cholesterol-lowering Lipitor, Groton was the largest drug research centre in the world when it opened in 2000. The sprawling campus had more than 5,000 employees at its peak and comprised 2.7 million square feet of research space.
The Groton lab was the most visible symbol of a new approach to drug discovery that employed massive tools, referred to as "high throughput screening". In its simplest form, the tactic used enormous machines to screen libraries of billions of compounds against a novel biological target.
Big Pharma expected that their scale would help them exploit a new generation of drug development tools that leveraged these scientific methods. Many of these tools were enabled by the mapping of the human genome, along with our ability to visualise the protein targets of new drugs. The aim was to find a molecule that could stick to a target in the right way – for example, turning off a cell receptor in order to alter the course of a disease.
It was said that only the big pharmaceutical companies could marshal the financial resources to erect these kinds of tools. Analysts crowed that these new methods would enable the big drug makers to flourish. Pfizer, with its Groton facility, was at the vanguard of these approaches.
There was one problem. The bigger is better tactic didn't work. It turns out that drug discovery isn't an enterprise that responds well to scale (leaving aside whether these endeavours will also respond poorly to big business mergers)."
"Discovering new and better medicines isn't merely a function of having the largest libraries of compounds, the fastest tools by which to screen them, or the most PhDs working in a laboratory. Sprawl, in fact, can reduce scientific productivity.
Nobody learnt these lessons harder than Pfizer. Over the two decades that it operated its massive facility in Groton, the only major drug to emerge from those labs was the smoking cessation medicine Chantix. Now Pfizer has largely mothballed the lab. Much of the centre's office space has been rented out, or sold off. There are reports that some of the buildings are being razed."
"In drug development, we've learned that focus matters more than scale. Knowledge around these distinct areas of biology isn't widely dispersed. It's often held in the hands of small teams of scientists who have worked with these targets for many years. The key to uncovering drugs is keeping scientists working together long enough so that they can learn from dead ends, and use their accumulating knowledge to make fundamental breakthroughs."
"The scale that results from big mergers helps drug makers run the large clinical trials that are required for global registrations. Scale improves their ability to commercialise new drugs, and manufacture them at low costs. But size alone doesn't lead to more scientific productivity. Evidence clearly shows that there are diminishing returns to scale in drug research. This is especially true when it comes to the earlier phases of drug development.
It's no coincidence that today, the big drug companies are rebuilding their pharmaceutical pipelines by realising that their research success isn't tied to the scale of those endeavours, but the precision of that work. While most observers focus on the drugs in the later stages of drug development, some of the most meaningful medical promise resides in the early pipelines of these big companies."
Article at:
http://www.independent.co.uk/news/business/comment/scott-gottlieb-mergers-dont-make-good-medicines-9341741.html
From morphine to Cipro: History of drug development chronicled in R&D News, Wed, 04/30/2014, Bill Hathaway, Yale Univ
Excerpts:
"Yale Univ.’s Michael Kinch spent his spare time in the last year creating a massive database that encompasses the entire history of drug development in the U.S. In a series of 20 articles scheduled to be published over the next year in Drug Discovery Today, Kinch mines the data and provides historical tidbits about the history of drug development and reveals trends on how—or whether—we will get new medicines in the future.
“The hope is that this data—such as when and what drugs were approved, what happened to companies that developed them, who did the clinical trials—will convey insight into trends that today are reshaping the biopharmaceutical industry,” said Kinch, managing director of the Yale Center for Molecular Discovery at West Campus."
"For instance, the second paper in the series, shows that the contributions of biotechnology companies to new drug development has been declining since 2000 and is at a level not seen since the early 1980s. Pharmaceutical companies now swallow up biotechnology organizations even before a company gains its first FDA approval, the analyses shows."
"An unexpected insight from this endeavor is that we might be able to actively prevent future problems by learning from the past,” Kinch said"
Article at:
http://www.rdmag.com/news/2014/04/morphine-cipro-history-drug-development-chronicled
Can Antidepressants Prevent Alzheimer? in publication Nigeria, 17 MAY 2014
My comments: Anatabloc is an MAOI. hmmm? can it have same effect as SSRI? (Monoamine oxidase inhibitors (MAOIs) are chemicals which inhibit the activity of the monoamine oxidase enzyme family. They have a long history of use as medications prescribed for the treatment of depression.-Wikipedia)
Article:
"The outcome of a new study on a common antidepressant is pointing to the possibility of it preventing Alzheimer's disease also known as dementia, which is not medically known to have a cure, but worsens as it progresses until it leads to death.
The study, published in Science Translational Medicine, included people and mice, found that the selective serotonin re-uptake inhibitor (SSRI) citalopram (Celexa) stopped growth of amyloid beta, a brain peptide that clumps into the plaques believed to trigger Alzheimer's.
According to the lead author of the study, Yvette Sheline, Professor of Psychiatry, Radiology and Neurology and Director of the Centre for Neuromodulation in Depression and Stress, at University of Pennsylvania's Perelman School of Medicine, "The study isn't evidence that this drug can slow Alzheimer's disease, but it's an exciting first step towards greater understanding of the capabilities of SSRIs, which offer promise as preventive measures".
Currently, Alzheimer's ranks as the sixth-leading cause of death in the US and the rates of the disorder are expected to more than triple over coming decades, unless a way to prevent it is discovered.
Since Alzheimer's symptoms begin about 15 years after plaques start to form, says Dr. Sheline, "the hope is that early treatment could slow or even prevent the disease."
However, it's too soon to tell if antidepressants can ward off the much-feared disorder, the doctor adds. Here's a closer look at the research.
The study is the first to identify a previously unknown effect of citalopram, which was approved by the FDA in 1998 for treatment of depression.
While the drug typically takes a few weeks to help relieve depression, the researchers discovered that it has an immediate - and significant - effect on amyloid beta, says Dr. Sheline.
In the double-blinded controlled study, 23 healthy adults, ages 18 to 50, who had no previous history of antidepressant use, received the drug. Compared to people who took a placebo, those treated with citalopram had a 38 percent lower level of amyloid beta in their cerebrospinal fluid, which was tested hourly over a 37-hour period.
In a parallel study with mice that are genetically predisposed to develop brain plaques, treatment with the drug reduced levels of the peptide by 25 per cent, compared to baseline levels.
In addition, over a two-month period, the treated mice had no new growth of plaques, compared to a control group of mice given sugar water.
The research builds on a 2011 study by Dr. Sheline and colleagues linking antidepressant use to reduced amyloid levels in the brains of elderly volunteers.
"That was an astonishing discovery, since depression is a risk factor for developing Alzheimer's," says Dr. Sheline. In that retrospective study, the team analysed PET scans of the brains of 186 cognitively normal adults with late-life depression.
During the analysis, the researchers didn't know which volunteers had taken antidepressants. After the results were un-blinded, the team found that volunteers who had taken citalopram during the previous five years had significantly less plaque development, compared to people who hadn't taken the drug.
What's more, the longer the volunteers had been treated with the antidepressant, the fewer plaques they had. The researchers also found that mice genetically predisposed to develop Alzheimer's had a 50 per cent reduction in brain plaques if they were treated with the drug, compared to mice given sugar water."
Article at:
http://allafrica.com/stories/201405191770.html
The Cost Of Creating A New Drug Now $5 Billion, Pushing Big Pharma To Change in Forbes Pharma and Healthcare, 8/11/2013 by Matthew Herper
Excerpts:
"There’s one factor that, as much as anything else, determines how many medicines are invented, what diseases they treat, and, to an extent, what price patients must pay for them: the cost of inventing and developing a new drug, a cost driven by the uncomfortable fact than 95% of the experimental medicines that are studied in humans fail to be both effective and safe."
"“This is crazy. For sure it’s not sustainable,” says Susan Desmond-Hellmann, the chancellor at UCSF and former head of development at industry legend Genentech, where she led the testing of cancer drugs like Herceptin and Avastin. “Increasingly, while no one knows quite what to do instead, any businessperson would look at this and say, ‘You can’t make a business off this. This is not a good investment.’ I say that knowing that this has been the engine of wonderful things.”"
"A 2012 article in Nature Reviews Drug Discovery says the number of drugs invented per billion dollars of R&D invested has been cut in half every nine years for half a century. Reversing this merciless trend has caught the attention of the U.S. government. Francis Collins, the director of the National Institutes of Health, in 2011 started a new National Center for Advancing Translational Sciences to remove the roadblocks that keep new drugs from reaching patients."
"“Great drugs build great franchises, but great franchises don’t necessarily build great drugs,” Perlmutter says. “If you are too prescriptive with your R&D, you can spend an awful lot of money and not be terribly productive because there may actually not be any new mechanisms that you can get to right now that will help you in a particular disease area.”
Article at:
http://www.forbes.com/sites/matthewherper/2013/08/11/how-the-staggering-cost-of-inventing-new-drugs-is-shaping-the-future-of-medicine/
Also look at:
How Much Does Pharmaceutical Innovation Cost? A Look At 100 Companies by Matthew Herper at:
http://www.forbes.com/sites/matthewherper/2013/08/11/the-cost-of-inventing-a-new-drug-98-companies-ranked/
Patent Expirations Through 2016 Predicted to Lower Brand Spending by $127 Billion at Drugs.com
Excerpts:
"The U.S. share of global drug spending is expected to decline from 41 percent in 2006 to 31 percent by 2016, primarily due to patent expiries and slower brand growth. In the U.S. and led by Lipitor, $103 billion (44%) of 2011 brand spending will shift to generics with substantially lower prices. Major U.S. brand products, including Plavix, Seroquel, Singulair, Actos and Viagra undergo patent expiration in 2012, with the “patent cliff” continuing through 2016. Patent expirations for over 36 major brands, slower market uptake for new molecular entities, and efforts from health plans and regulators to curtail drug spending shrink brand dollars in the U.S. market through 2016.
Patent expirations up to 2016 will reduce brand spending in worldwide developed markets by $127 billion, but will be counterbalanced by generic spending, resulting in a five-year global savings of close to $106 billion. In Japan, the UK, France and Germany, many of the same or similar brands that were impacted in the U.S. will also lose patent protection. For example, in Japan, the use of generics is expected to increase as the government promotes policies to use lower-cost alternatives, and major products face generic competition. [b]Overall, exclusivity loss in one or more developed markets will impact seven of the top 10 leading prescription drugs, including Lipitor, Plavix, Advair Diskus, Crestor, and Nexium."
"
Protection Expiry Year
2012
Plavix
Seroquel
Singulair
Actos
Lexapro
Diovan
Diovan HCT®
Geodon
Viagra
Boniva Nu Lotan
Myslee
Preminent Haigou
Seroquel
Lipitor
Amias
Seroquel
Aricept®
Singulair
Tahor
Singulair
Pariet
Ixprim
Aprovel
Seroquel
Atacand
Atacand Plus
Sortis
Aricept
2013
Oxycontin®
Aciphex
Zometa
Xeloda
Opana ER
Asacol
Diovan
Plavix
Livalo
Elplat
Viagra
Xeloda
Seretide
Coaprovel
Xeloda
Micardis
Viagra
Viani
Zometa
Atmadisc
Coaprovel
Viagra
2014
Nexium®
Cymbalta
Celebrex
Symbicort
Lunesta
Restasis
Evista
Sandostatin LAR
Actonel
Prograf
Glivec
Abilify
Abilify
Cipralex
Risperdal Consta
Seroplex
Abilify
Ebixa
Risperdal Consta LP
Axura
Risperdal Consta
Blopress Plus
2015 Abilify
Copaxone
Gleevec
Namenda
Provigil
Combivent
Zyvox
Prezista
Avodart
Zyprexa
Adoair
Alimta
Spiriva
Symbicort
Spiriva
Cymbalta
Alimta
Alimta
Spiriva
Copaxone
Protelos
Cymbalta
Spiriva
Copaxone
Alimta
Cymbalta
2016
Crestor
Benicar
Benicar HCT
Cubicin
Blopress
BaracludeA
Article at:
http://www.drugs.com/article/patent-expirations.html
Report: Pancreatic cancer second most deadly by 2030, By Jacque Wilson, CNN, Mon May 19, 2014
Excerpts:
"By 2030, the top cancer killers in the United States will be lung, pancreas and liver, according to a new report published Monday in the American Association for Cancer Research's journal.
Lung cancer is already the top killer overall, but pancreatic and liver cancer will surpass the cancers currently considered the second and third leading causes of death, researchers say. Right now, second most dangerous is breast cancer for women and prostate cancer for men; and third is colorectal cancer for both men and women.
Researchers looked at trends in cancer incidence and death rates between 2006 and 2010, and used that data -- combined with expected U.S. demographic changes -- to predict numbers for 2030.
Overall, the cancer-related death rate has been decreasing, researchers say, as a result of improved screening and treatment options. Yet while deaths from breast, prostate and colon cancers are projected to drop, deaths caused by liver, pancreatic, bladder and leukemia cancers are expected to increase.
In fact, liver and pancreatic cancers will surpass breast and prostate to become the second and third-leading causes of cancer-related deaths, the researchers say."
""Many Americans are not aware that the combination of obesity, high-caloric intake and lack of physical activity is the second-leading cause of cancer in the U.S.," Brawley said. "It is linked to at least 12 types of cancer, of which these are two. This is an American problem ... the rise in pancreatic cancer is not as severe as in Europe where obesity is less of an issue."
Obesity may affect cancer patients' outcomes
Overall, the number of cancer cases is expected to increase over the next 16 years, due to the rapidly aging population. In 2010, the United States had about 1.5 million cases of cancer; in 2030, researchers expect that number to reach 2.1 million.
"We're living much longer in the United States, so the number of people 65 age and older will be much greater," Matrisian said. "And that's, of course, one of the biggest risk factors for cancer: Age."
Lung, breast, prostate and colorectal cancers are currently the most common in the United States. Known as the "big four," these cancers have the highest incidence rates and receive the most research funding from the National Cancer Institute.
This is unlikely to change by 2030, the researchers say, except for colorectal cancer, which is expected to be surpassed by thyroid, melanoma and uterine cancers in total number of cases."
"The dramatic increase in thyroid cases is not a new epidemic, they say, but simply an increase in the number of cases being diagnosed. And while thyroid cancer has a 98% five-year survival rate, only 6% of pancreatic cancer patients are alive five years after diagnosis."
Article at:
http://www.cnn.com/2014/05/19/health/pancreatic-liver-cancer-deaths/
MY ANECDOTAL OPINION: Since there are those for and those against STSI posting on this board, my two bits. I'm for!
Re sales this last quarter--yes, disappointing but understandable. Selling mostly through GNC, STSI sells wholesale so their SALES are at the wholesale level. Their markup is signficantly less. When the bruhaha broke out about the FDA letter, I like many others stocked up. I bought 8 bottles, just in case. With little or no advertising, the chance of significant growth in the neutracutical area is daunting at best. Having said that, over a year ago the conversation was always about a pharmaceutical version and a broader application of anatabine citrate. (follow the money) Almost all small biotechs are a gamble and most of us investing here are not really looking at current profit but what may lie in the future. In the last two years, I have noticed a significant rise in interest on 'chronic inflammation' as a major target for autoimmune diseases, cardiovascular issues, and cancers related to chronic inflammation. With this rise in interest, I would bet that Dr Mullan is aware of Anatabloc's potential applications. He has put his future and reputation on it. If you don't believe the future possiblities Anatabloc has to offer, so be it. I am not in that count. After about a month of doing meta-searches on the subject, I am convinced STSI has potential and the profits will come when clinical trials prove it's efficacy. Though many of you poo poo anecdotal comments, I think the sheer quantity of people posting, both good and bad, should give investors a rough cut at what may lie in store. For those of you that don't believe in Anatabloc's potential, I wonder why you spend so much time trying to convince people like me with your ANECDOTAL comments and don't post research and findings that would negate Anatabloc's potential success and add weight to your arguement? I always thought stock prices were a gauge of future earnings and for small biotechs, that comes with the success (and potential thereof) of their product in the market place. If and when a merger, license, or teaming agreement occurs, it will be too late to buy long and too late for the shorts to get out. BTW, my thoughts on Anatabloc are more directed towards PREVENTION rather than post-disease application. Those complaining about the cost of Anatabloc should look at the cost when you get cancer, cardiovascular event, or contract an autoimmune disorder. It is really expensive! I personally want to live long healthy and not long sick.
You might be interested in reviewing the attached links to see what is happening in the pharmaceutical world, food for thought:
"Sure, We'll (Eventually) Beat Cancer. But Can We Afford To?"
http://www.forbes.com/sites/theapothecary/2014/05/16/sure-well-eventually-beat-cancer-but-can-we-afford-to/?ss=pharma
"An UnheAlthy AmericA: The Economic Burden of Chronic Disease"
http://www.milkeninstitute.org/healthreform/pdf/AnUnhealthyAmericaExecSumm.pdf
"Top 10 Drug Patent Losses of 2014"
http://www.fiercepharma.com/special-reports/top-10-drug-patent-losses-2014
Have a good day!
Please review effect of Anatabloc vs Celebrix and Aspirin :
http://www.rfdn.org/inflammaging3.html
An Immune System and Thyroid Upside for Tobacco?
Posted on March 7, 2013 by Mary Shomon in National Academy of HypoThyroidism, NAH (Repeat article, but read the anecdotal comments from those that follow Mary Shomon)
Article at:
http://nahypothyroidism.org/an-immune-system-and-thyroid-upside-for-tobacco/
Dr. Jonny Bowden "The Great Cholesterol Myth" Video, no need to buy the book. Well worth the watch.(little over an hour) Highlights the three major players in the heart disease paradigm:
Stress
Sugar (diet)
Inflammation
You need to take control of stress and sugar so inflammation doesn't become a factor. For those that ignore, Anatabloc is available to help.
See video at:
Mercury and Alzheimers---Food for thought
Two articles in Pubmed:
Mercury induced the Accumulation of Amyloid Beta (Aß) in PC12 Cells: The Role of Production and Degradation of Aß., Song JW, Choi BS., Dec 2013, Department of Preventive Medicine, College of Medicine, Chung-Ang University, Seoul, Korea.
Abstract
Extracellular accumulation of amyloid beta protein (Aß) plays a central role in Alzheimer's disease (AD). Some metals, such as copper, lead, and aluminum can affect the Aß accumulation in the brain. However, the effect of mercury on Aß accumulation in the brain is not clear. Thus, this study was proposed to estimate whether mercury concentration affects Aß accumulation in PC12 cells. We treated 10, 100, and 1000 nM HgCl2 (Hg) or CH3HgCl2 (MeHg) for 48 hr in PC12 cells. After treatment, Aß40 in culture medium increased in a dose- and time-dependent manner. Hg and MeHg increased amyloid precursor protein (APP), which is related to Aß production. Neprilysin (NEP) levels in PC12 cells were decreased by Hg and MeHg treatment. These results suggested that Hg induced Aß accumulation through APP overproduction and reduction of NEP.
Article at:
http://www.ncbi.nlm.nih.gov/pubmed/24578793
Does inorganic mercury play a role in Alzheimer's disease? A systematic review and an integrated molecular mechanism., 2010
Mutter J1, Curth A, Naumann J, Deth R, Walach H.,Department of Environmental and Integrative Medicine, Constance, Germany.
Abstract
"Mercury is one of the most toxic substances known to humans. It has been introduced into the human environment and has also been widely used in medicine. Since circumstantial evidence exists that the pathology of Alzheimer's disease (AD) might be in part caused or exacerbated by inorganic mercury, we conducted a systematic review using a comprehensive search strategy. Studies were screened according to a pre-defined protocol. Two reviewers extracted relevant data independent of each other. One thousand and forty one references were scrutinized, and 106 studies fulfilled the inclusion criteria. Most studies were case control or comparative cohort studies. Thirty-two studies, out of 40 testing memory in individuals exposed to inorganic mercury, found significant memory deficits. Some autopsy studies found increased mercury levels in brain tissues of AD patients. Measurements of mercury levels in blood, urine, hair, nails, and cerebrospinal fluid were inconsistent. In vitro models showed that inorganic mercury reproduces all pathological changes seen in AD, and in animal models inorganic mercury produced changes that are similar to those seen in AD. Its high affinity for selenium and selenoproteins suggests that inorganic mercury may promote neurodegenerative disorders via disruption of redox regulation. Inorganic mercury may play a role as a co-factor in the development of AD. It may also increase the pathological influence of other metals. Our mechanistic model describes potential causal pathways. As the single most effective public health primary preventive measure, industrial, and medical usage of mercury should be eliminated as soon as possible."
Article at:
http://www.ncbi.nlm.nih.gov/pubmed/20847438
FYI, Bad Drug List, Complete A-Z Bad Drug List Index
Lists side effects, warmings and recalls, use, and other names
List at:
http://www.sciencedaily.com/releases/2014/03/140313123233.htm
Scientists catch brain damage in the act, March 13, 2014, University of British Columbia
Summary:
"Scientists have uncovered how inflammation and lack of oxygen conspire to cause brain damage in conditions such as stroke and Alzheimer's disease, bringing researchers a step closer to finding potential targets to treat neurodegenerative disorders. Chronic inflammation and hypoxia, or oxygen deficiency, are hallmarks of several brain diseases, but little has been known about how they contribute to symptoms such as memory loss."
Excerpts:
"The discovery, published today in Neuron, brings researchers a step closer to finding potential targets to treat neurodegenerative disorders.
Chronic inflammation and hypoxia, or oxygen deficiency, are hallmarks of several brain diseases, but little was known about how they contribute to symptoms such as memory loss.
The study used state-of-the-art techniques that reveal the movements of microglia, the brain's resident immune cells. Brain researcher Brian MacVicar had previously captured how they moved to areas of injury to repair brain damage.
The new study shows that the combination of inflammation and hypoxia activates microglia in a way that persistently weakens the connection between neurons. The phenomenon, known as long-term depression, has been shown to contribute to cognitive impairment in Alzheimer's disease.
"This is a never-before-seen mechanism among three key players in the brain that interact together in neurodegenerative disorders," says MacVicar with the Djavad Mowafaghian Centre for Brain Health at UBC and Vancouver Coastal Health Research Institute.
"Now we can use this knowledge to start identifying new potential targets for therapy."
Article at:
http://www.sciencedaily.com/releases/2014/03/140313123233.htm
Nuclear factor kappa B (NF-?B) in multiple sclerosis pathology. in PubMed, 2013 Oct;19, Mc Guire C1, Prinz M, Beyaert R, van Loo G., 1Department for Molecular Biomedical Research, Unit of Molecular Signal Transduction in Inflammation, VIB, B-9052 Ghent, Belgium; Department of Biomedical Molecular Biology, Ghent University, B-9052 Ghent, Belgium.
Abstract"
"[b]The nuclear factor kappa B (NF-?B) signaling cascade plays a critical role in the regulation of immune and inflammatory responses and has been implicated in the pathogenesis of autoimmune demyelinating diseases such as multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE), the main animal model of MS. NF-?B is essential for peripheral immune cell activation and the induction of pathology, but also plays crucial roles in resident cells of the central nervous system (CNS) during disease development. Here we review recent evidence clarifying the role of NF-?B in the different cell compartments contributing to MS pathology and its implications for the development of therapeutic strategies for the treatment of MS and other demyelinating pathologies of the CNS."
Article at:
http://www.ncbi.nlm.nih.gov/pubmed/24007818
UPDATE 2-U.S. FDA approves Biogen's oral MS drug, Tecfidera
Wed Mar 27, 2013, in Reuters Health By Toni Clarke
Excerpts:
"* Tecfidera expected to become dominant oral MS treatment
* Sales of Tecfidera expected to top $3 billion by 2017
* Tecfidera expected to be launched within days
* Stock rises 3.2 percent to $182.68 (Adds analyst comment, background, stock price)"
"Shares of Weston, Massachusetts-based Biogen rose 3.2 percent to close at $182.68 on Wednesday. The shares have more than tripled over the past three years, mainly driven by high hopes for Tecfidera, known chemically as dimethyl fumarate.
Biogen already sells the MS drugs Avonex and Tysabri, which together account for about 30 percent of the market. Teva Pharmaceutical Industries Ltd's drug Copaxone is the current market leader, with a roughly 29 percent share and annual sales last year of more than $4 billion.
Unlike Copaxone, Avonex and Tysabri, which are injected or infused, Tecfidera comes in the more convenient form of a pill. As such, it will compete with Novartis AG's MS pill Gilenya, which, though first to market, has been dogged by heart safety concerns. Gilenya holds an 8.5 percent share of the market and generated worldwide sales of $1.2 billion last year.
Tecfidera will also compete with Sanofi's recently approved MS pill Aubagio. Aubagio's label carries a boxed warning -- the most serious kind of warning -- alerting physicians to a potentially heightened risk of liver problems."
Article at:
http://www.reuters.com/article/2013/03/27/biogen-tecfidera-idUSL2N0CJ1WJ20130327
Risk of serious illness climbs with psoriasis severity, BY ANNE HARDING, NEW YORK Thu Aug 15, 2013 in Reuters
Excerpts:
"(Reuters Health) - People with psoriasis have an increased risk of serious medical illness, and the more severe their skin disease, the more severe the risk for other conditions, new research finds.
Those with the most severe psoriasis - affecting more than 10 percent of the skin surface - are at nearly twice the risk of heart and blood vessel disease compared to people without psoriasis, Dr. Joel Gelfand, an associate professor of dermatology at the University of Pennsylvania Perelman School of Medicine in Philadelphia, and his colleagues report.
The researchers also found an increased risk of chronic lung disease, diabetes, kidney disease, joint problems and other health conditions among psoriasis patients."
"The researchers looked at electronic medical records from the UK for 9,035 psoriasis patients whose illness severity had been determined by how much of their skin surface area was affected by psoriasis.
Just over half had mild disease, meaning it affected less than 3 percent of their skin; 36 percent had moderate disease (up to 10 percent of skin area) and 12 percent had severe disease (more than 10 percent of skin affected).
The researchers then matched each patient to 10 similar people in the database without psoriasis for comparison.
Overall, the risk for any other type of serious illness was 11 percent higher for people with mild psoriasis than for their counterparts in the comparison group, 15 percent higher for patients with moderate psoriasis and 35 percent higher for those with severe psoriasis.
Patients with moderate psoriasis were 22 percent more likely to have diabetes than people without the skin condition, for example, while those with severe psoriasis had a 32 percent increased risk of diabetes.
Moderate psoriasis also conferred a 36 percent increased risk of diabetes with complications such as eye disease, while severe psoriasis conferred an 87 percent higher risk.
Moderate and severe psoriasis increased the risk of cardiovascular disease by 39 percent and 81 percent, respectively.
People with psoriasis are known to have more inflammation in their blood vessels, which probably accounts for some of their increased risk of other illnesses, Gelfand said."
"People with more severe psoriasis, he added, "need to take this information very seriously."
Article at:
http://www.reuters.com/article/2013/08/15/us-health-psoriasis-health-risk-idUSBRE97E0YC20130815