The White House held a background briefing Friday to discuss Obamacare implementation with a handful of journalists from liberal and progressive outlets.
Slate blogger Matthew Yglesias posted a photograph to Instagram Friday featuring himself and other liberal journalists at the White House, with the caption “#thistown.”
Yglesias’ photograph features American Prospect staff writer Jamelle Bouie and MSNBC’s Benjy Sarlin attending the briefing.
The announced one-year delay in enforcement brings with it an immediate revenue loss. But by further encouraging firms to drop coverage now—allowing businesses to privatize gains and socialize losses—the change could cause federal spending on Obamacare exchange subsidies to soar.
The Congressional Budget Office (CBO) estimated in May that the employer mandate would raise $10 billion in revenue in its first year. (Because the employer mandate is a tax penalty, firms will pay the penalties the following year—penalties for 2014 will be paid in 2015; penalties for 2015 will be paid in 2016, etc.) That $10 billion in employer mandate revenue projected for fiscal year 2015 will almost certainly disappear.
Then there’s the separate question of whether, when, and how employers will drop their health insurance plans and dump their workers on the exchanges. Here’s what we know on that front:
from: Ed Hiserodt and Rebecca Terrell
Worldwide, more than 2,700 people will die today because of a bureaucratic regulation instituted during the Nixon administration in 1972. The same number died yesterday and will again tomorrow, in an ever-growing tally of victims of that catastrophic policy. The regulation imposed by Nixon’s newly formed Environmental Protection Agency (EPA) banned DDT, an insecticide that had until then saved the lives of countless U.S. citizens. Leaders in Europe and the United Nations followed suit in a frenzy of misguided environmental zeal and bloodthirsty population control fervor.
“European nations and the United States used insecticides to rid themselves of disease and then pulled up the ladder, denying Africans, Asians and Latin Americans the benefits of those same insecticides,” explain Dr. Donald Roberts and Richard Tren in their 2010 exposé, The Excellent Powder: DDT’s Political and Scientific History. Wealthy nations merit this accusation because before the advent of DDT, parasitic diseases like malaria, typhus, and yellow fever had plagued their own shores for centuries. These infections are known as vector-borne diseases because insects (i.e., vectors) carry disease-causing parasites from person to person.
When DDT first came into use as a pesticide, many called it miraculous, which was hardly an exaggeration considered in perspective. Until then, yellow fever claimed so many lives it was known in the United States as the “Scourge of the South.” The French abandoned efforts in the 1880s to construct the Panama Canal because malaria killed so many workers. Typhus, the disease that took the life of diarist Anne Frank, was once feared as deadlier than any weapon of war in Europe. Yet in a period of three weeks in 1943, DDT wiped out one of history’s deadliest typhus outbreaks in Naples, Italy. In fact DDT’s effectiveness has made all these disease names as antiquated to our ears as scurvy and the plague.
Not so for unfortunates in developing countries. According to the Centers for Disease Control and Prevention (CDC), globally malaria kills approximately one million people every year, more than any other parasitic infection. Most victims are young children in sub-Saharan Africa. Names like typhus, yellow fever, leishmaniasis, dengue fever, and bancroftian filariasis are likewise too familiar to hundreds of thousands of those affected in Africa, Latin America, and the Middle East.
DDT’s life-saving properties are lost to them because the EPA’s 1972 ban sparked a global censure of the pesticide. The UN Environment Programme (UNEP) now classifies it as one of 12 “Persistent Organic Pollutants” (POPs), otherwise known as “The Dirty Dozen.” UNEP claims DDT is a danger to humans and the environment. Yet a closer look at the case reveals a terrifying reality: saving lives isn’t what policymakers are after.
Introducing a ‘glucose sensor’ by gene therapy eliminates the symptoms of the disease
Researchers from the Universitat Autònoma de Barcelona (UAB), led by Fàtima Bosch, have shown for the first time that it is possible to cure diabetes in large animals with a single session of gene therapy. As published this week in Diabetes, the principal journal for research on the disease, after a single gene therapy session, the dogs recover their health and no longer show symptoms of the disease. In some cases, monitoring continued for over four years, with no recurrence of symptoms.
The therapy is minimally invasive. It consists of a single session of various injections in the animal’s rear legs using simple needles that are commonly used in cosmetic treatments. These injections introduce gene therapy vectors, with a dual objective: to express the insulin gene, on the one hand, and that of glucokinase, on the other. Glucokinase is an enzyme that regulates the uptake of glucose from the blood. When both genes act simultaneously they function as a “glucose sensor”, which automatically regulates the uptake of glucose from the blood, thus reducing diabetic hyperglycemia (the excess of blood sugar associated with the disease).
As Fàtima Bosch, the head researcher, points out, “this study is the first to demonstrate a long-term cure for diabetes in a large animal model using gene therapy.”
This same research group had already tested this type of therapy on mice, but the excellent results obtained for the first time with large animals lays the foundations for the clinical translation of this gene therapy approach to veterinary medicine and eventually to diabetic patients.
The study was led by the head of the UAB’s Centre for Animal Biotechnology and Gene Therapy (CBATEG) Fàtima Bosch, and involved the Department of Biochemistry and Molecular Biology of the UAB, the Department of Medicine and Animal Surgery of the UAB, the Faculty of Veterinary Science of the UAB, the Department of Animal Health and Anatomy of the UAB, the Spanish Biomedical Research Centre in Diabetes and Associated Metabolic Disorders (CIBERDEM), the Children’s Hospital of Philadelphia (USA) and the Howard Hughes Medical Institute of Philadelphia (USA).
A safe and efficacious gene therapy
The study provides ample data showing the safety of gene therapy mediated by adeno-associated vectors (AAV) in diabetic dogs. The therapy has proved to be safe and efficacious: it is based on the transfer of two genes to the muscle of adult animals using a new generation of very safe vectors known as adeno-associated vectors. These vectors, derived from non-pathogenic viruses, are widely used in gene therapy and have been successful in treating several diseases.
In fact, the first gene therapy medicine ever approved by the European Medicines Agency, named Glybera®, makes use of adeno-associated vectors to treat a metabolic disease caused by a deficiency of lipoprotein lipase and the resulting accumulation of triglycerides in the blood.
Long-term control of the disease
Dogs treated with a single administration of gene therapy showed good glucose control at all times, both when fasting and when fed, improving on that of dogs given daily insulin injections, and with no episodes of hypoglycemia, even after exercise. Furthermore, the dogs treated with adeno-associated vectors improved their body weight and had not developed secondary complications four years after the treatment.
The study is the first to report optimal long-term control of diabetes in large animals. This had never before been achieved with any other innovative therapies for diabetes. The study is also the first to report that a single administration of genes to diabetic dogs is able to maintain normoglycemia over the long term (more than 4 years). As well as achieving normoglycemia, the dogs had normal levels of glycosylated proteins and developed no secondary complications of diabetes after more than 4 years with the disease.
Application in diabetic patients
There have been multiple clinical trials in which AAV vectors have been introduced into skeletal muscle, so the strategy reported in this study is feasible for clinical translation. Future safety and efficacy studies will provide the bases for initiating a clinical veterinary trial of diabetes treatment for companion animals, which will supply key information for eventual trials with humans. In conclusion, this study paves the way for the clinical translation of this approach to gene therapy to veterinary medicine, and eventually to diabetic patients.
Diabetes mellitus is the most common metabolic disease, and a large number of patients need insulin treatment to survive. In spite of the use of insulin injections to control the disease, these patients often develop serious secondary complications like blindness, kidney damage or amputation of limbs. Moreover, in order to achieve good blood glucose control, insulin has to be injected two or three times a day, which brings a risk of hypoglycemia episodes (lowering of blood sugar): an additional problem that comes on top of the other hardships of the treatment.
Attribution: Real Clear Science (02-07-2013)
A jab that uses electricity to blast its way into immune system cells could revolutionize the treatment of asthma.
The ‘supercharged’ vaccine enables the immune system to overcome dust mite allergy – one of the leading triggers of asthma attacks.
The attacks are triggered by the immune system overreacting to the droppings of the tiny bugs, and releasing the chemical histamine.
It is this rush of histamine that leads to swelling and irritation of the airways, causing breathing difficulties and asthma attacks.
The current ‘vaccine’ against asthma is immunotherapy, where the patient receives multiple injections of small amounts of the harmful dust mite protein.
The idea is that the immune system becomes used to the protein, so no longer overreacts.
This exposure also triggers the production of helper cells, which dampen down this overreaction. However, the treatment can be lengthy, and involves 50 to 80 injections over as long as five years.
As an alternative, scientists have developed vaccines that, rather than containing the actual dust mite protein, contain tiny amounts of the protein’s DNA.
This contains the instructions for ‘building’ the protein. With the new technique, the DNA is injected into the body, where it is absorbed by the immune cells. The cells then manufacture the protein themselves, using the instructions from the DNA.
This tiny exposure allows the immune system to acclimatise to the protein and produce helper cells. This confers protection in just one injection, rather than many.
However, all cells are covered by a protective layer, called the plasma membrane. Previous vaccines have struggled to get through this shield.
The electric vaccine, however, could be the solution. Scientists at Chulalongkorn University in Bangkok, Thailand, injected mice with dust mite allergies with a DNA vaccine immediately after firing electrical pulses through the skin.
These pulses temporarily break up the protective outer membrane that keeps immune system cells intact.
The results, published in the journal Immunology Letters, showed helper cell levels were 40 times higher after an electric jab than a conventional one.
The team are confident the technology will work on humans. Malayka Rahman, research officer at Asthma UK, says: ‘Nine out of ten people with asthma tell us dust triggers their symptoms, increasing their risk of asthma attack.
‘However, dust is notoriously difficult to avoid. Although this research is an important step forward towards more effective vaccines, it is in its early stages.’
Attribution: Daily Mail
A previously unknown layer of the cornea has been discovered in the human eye, a breakthrough experts say could ‘rewrite the opthalmology textbooks’.
Researchers from the University of Nottingham found the new layer – which is just 0.001 mm thick – within the cornea, the clear window at the front of the eye.
They say it could help surgeons dramatically improve outcomes for patients undergoing corneal grafts and transplants.
WHAT DOES THE DISCOVERY OF DUA’S LAYER MEAN?
- Knowledge of Dua’s Layer could improve outcomes for patients undergoing corneal grafts and transplants
- During surgery, tiny air bubble are injected into corneal stroma via the ‘big bubble technique’
- If the bubble bursts it causes damage to the eye.
- But if the air bubble is injected under Dua’s layer instead of above it, the layer’s strength reduces the risk of tearing
- Diseases of the cornea including acute hydrops, Descematocele and pre-Descemet’s dystrophies may be affected by the discovery of Dua’s layer
Problems with the layer could also explain many eye diseases that until now were elusive in origin.
The new layer has been dubbed the Dua’s layer, after Professor Harminder Dua who discovered it, reports journal Ophthalmology.
Professor Dua said: “This is a major discovery that will mean that ophthalmology textbooks will literally need to be re-written.
Having identified this new and distinct layer deep in the tissue of the cornea, we can now exploit its presence to make operations much safer and simpler for patients.
‘From a clinical perspective, there are many diseases that affect the back of the cornea which clinicians across the world are already beginning to relate to the presence, absence or tear in this layer.’
Scientists previously believed the cornea to be comprised of five layers, from front to back, the corneal epithelium, Bowman’s layer, the corneal stroma, Descemet’s membrane and the corneal endothelium.
The new layer that has been discovered is located at the back of the cornea between the corneal stroma and Descemet’s membrane.
Although it is just 15 microns thick – the entire cornea is around 550 microns thick or 0.5mm – it is incredibly tough and is strong enough to be able to withstand one and a half to two bars (21-29 psi) of pressure.
Researchers proved the layer existed by simulating human corneal transplants and grafts on eyes donated for research.
During these experiments, tiny bubbles of air were injected into the cornea to separate the different layers.
The scientists then subjected the separated layers to electron microscopy, allowing them to study them at many thousand times their actual size and revealing Dua’s layer.
The authors say that the discovery will have an impact on advancing understanding of a number of diseases of the cornea, including acute hydrops, Descematocele and pre-Descemet’s dystrophies
The scientists now believe that corneal hydrops, a bulging of the cornea caused by fluid build up that occurs in patients with keratoconus (conical deformity of the cornea), is caused by a tear in the Dua layer, through which water from inside the eye rushes in and causes waterlogging.
Attribution: Nicola Rowe, Mail Online
Louisiana State Senator Karen Carter Peterson took to the floor earlier this week to explain to everyone the real reason people are opposed to Obamacare and specifically the Medicaid expansion provision:
“…[I]t shouldn’t be about this administration at the state level, nor should it be about the federal administration when it comes to Obamacare. But in fact it is. And why is that? Why is that? I have talked to so many members in the House and the Senate, and you know what? You ready? You ready [for] what it comes down to? It’s not about how many federal dollars we can receive. It’s not about that. You ready? It’s about race. No, nobody wants to talk about that. It’s about the race of this African-American president, because this same thing has been offered by whom? By former Speaker Newt Gingrich in the past. Yeah, he had a similar bill to what President Obama has offered. Similar legislation was offered. It comes down to the race of the President of the United States, which causes people to disconnect and step away from the substance of the bill…”