New Ebola Vaccine Shows Promise in Human Trials

 

It appeared to provoke good immune response in Chinese study, but larger trials are needed

By Robert Preidt 

 

WEDNESDAY, March 25, 2015 (HealthDay News) -- An experimental Ebola vaccine shows promise in an early clinical trial, but requires much more testing, researchers report.

The trial included 120 healthy adults in China who received either a low or high dose of the vaccine, or a placebo. Twenty-eight days later, 38 of 40 people in the low-dose group and all 40 of those in the high-dose group showed an immune response to the vaccine.

No serious side effects occurred among the participants who received the vaccine.

While the results suggest the vaccine is effective and safe, more long-term testing is needed to determine whether it can actually protect people against Ebola, according to the authors of the study published March 25 in The Lancet.

The vaccine is based on the strain of Ebola that has been circulating in the West African outbreak. The researchers note that, until now, all tested Ebola vaccines have been based on the Ebola strain from the 1976 outbreak in Zaire.

The vaccine was developed by the Beijing Institute of Biotechnology and Tianjin CanSino Biotechnology in China. Both helped fund the study, along with China National Science and Technology.

"On the basis of our findings, we believe that the Ebola vaccine we assessed has some potential, and a significant advantage of this type of vaccine is that [it is] stable and much easier to store or transport in tropical areas with inadequate cold-chain capacity, such as Africa," research team leader Fengcai Zhu, from the Jiangsu provincial center for disease prevention and control in China, said in a journal news release.

"However, whether this candidate vaccine could become a final vaccine for widespread use against Ebola outbreaks is still uncertain," Zhu added. "Furthermore, these results only assess immune response up to 28 days, so we plan to assess the persistence of the specific immune response by following up the vaccine recipients of this study."

Still, two experts said the development of the vaccine is a testament to how scientists can effectively respond in a crisis.

This vaccine, "is an example of how quickly existing vaccine platforms can be modified to incorporate a new virus strain, and moved, with minimum testing in animals, into trials in humans during a crisis situation," Andrea Marzi, of the U.S. National Institute of Allergy and Infectious Diseases, and Darryl Falzarano, of the University of Saskatchewan in Canada, wrote in an accompanying commentary.

"However...ultimately, the effectiveness of all these vaccines will only become clear when they proceed to phase 2 efficacy trials in outbreak regions," they added.

The West African Ebola outbreak, while ebbing, is not yet over. According to the U.S. Centers for Disease Control and Prevention, almost 25,000 probable or confirmed cases have been detected in Guinea, Liberia and Sierra Leone, including more than 10,000 deaths.

SOURCE: The Lancet, news release, March 25, 2015

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Research in Retinal Disease The Foundation Fighting Blindness Invests 2 1 Million in Seven New Research Efforts

As I continually search the web for interesting news about new technologies for treating retinal diseases, I came across this news from the Foundation Fighting Blindness’ website  yesterday afternoon. It relates to some of the annual grants to researchers that the FFB will be funding this year. It includes better ways of looking at retinal cells (via use of the adaptive optics laser scanning ophthalmoscope) and several projects involving gene therapy, along with a couple looking at ways of, hopefully, stopping the progression of dry AMD.

The following write up is reprinted with permission of the FFB.

The Foundation Invests $2.1 Million in Seven New Research Efforts

The Foundation Fighting Blindness

August 15, 2013

The Foundation's Scientific Advisory Board (SAB) recently completed its annual grants review process, leading to the allocation of $2.1 million in funding for seven new research projects, including those for identifying new disease-causing gene mutations, developing cross-cutting gene therapies and advancing potential treatments for dry age-related macular degeneration. The three-year grants were awarded after the SAB reviewed 117 proposals submitted to the Foundation last October.

"Grants review is a rigorous, multi-step process that takes most of the year to complete," says Stephen Rose, Ph.D., chief research officer, Foundation Fighting Blindness. "Due to revenue limitations, we can only fund a fraction of the high-quality projects we'd like to fund. That makes the selection process even more challenging. We had to leave several excellent proposals on the table."

Here are brief descriptions of the new research projects:

AOSLO: Detecting Retinal Degeneration Before Vision is Lost

The adaptive optics laser scanning ophthalmoscope (AOSLO) is like a powerful microscope that enables retinal researchers to see structural changes in the retina well before vision is lost from a retinal disease. That power can enable researchers to more quickly determine if a treatment is working in a clinical trial. Austin Roorda, Ph.D., of the University of California, Berkeley, is performing studies of AOSLO to correlate changes in the retina (e.g., loss of photoreceptors) with changes in vision.

Enhancing AOSLO for Expanded Clinical Use

Like Dr. Roorda, Stephen Burns, Ph.D., of the University of Indiana, is working with AOSLO to study the correlation between retinal and vision changes. He is also making AOSLO more affordable by using newer camera technology. In addition, he's employing state-of-the-art computing technologies derived from video games to decrease image-processing times and costs. The new technology will make the imaging process more comfortable for the patient by tolerating more head and eye movement.

Figuring Out Why Severity of Vision Loss Varies for People with XLRP

Researchers have reported for many years that the severity of vision loss for people with X-linked retinitis pigmentosa (XLRP) can vary greatly, even for people within the same family. Stephen Daiger, Ph.D., of the University of Texas Health Science Center at Houston, will be looking at the role of a various biological, genetic and environmental factors in vision-loss variability for those with XLRP. The identification of a significant factor that modulates vision-loss severity - perhaps a protective protein - could lead to a potential treatment.

Finding New Genes Linked to ADRP

Researchers have identified almost two dozen genes linked to autosomal dominant retinitis pigmentosa (adRP), but many are yet to be found. Rui Chen, Ph.D., of Baylor College of Medicine, is on the hunt for those remaining adRP genes. With DNA from 118 adRP families, including 18 families with at least nine affected members, Dr. Chen is well positioned to identify additional genes linked to adRP. Finding the new genes will provide researchers with targets for treatments and cures.

Developing Neuroprotective Gene Therapies to Preserve Vision

John Ash, Ph.D., is developing gene therapies that have the potential to preserve vision in people affected by a broad range of retinal diseases. Unlike corrective gene therapies, which work only for conditions caused by a specific gene, Dr. Ash's proposed treatments are designed to keep the retina healthy independent of the underlying disease-causing gene. He also believes the proteins delivered by his treatments - PIM-1 and STAT3 - will be less likely to cause damaging inflammatory side effects than some previously investigated neuroprotective proteins.

Targeting Inflammation to Halt AMD

Thanks to previous Foundation-funded genetic studies, researchers have strong evidence that the progression of age-related macular degeneration is associated with an over-active immune system. This ultimately leads to inflammation and cell death in the retinal pigment epithelium (RPE), a layer of cells that provides critical waste and nutritional support to photoreceptors. Loss of the RPE subsequently leads to loss of photoreceptors and vision. Jayakrishna Ambati, M.D., of the University of Kentucky, is developing a gene therapy that preserves the RPE by preventing the harmful sequence of immune-system events.

Boosting Cells' Energy Supplies to Save Vision in AMD

Based on prior research, Deborah Ferrington, M.D., of the University of Minnesota, believes that mitochondrial dysfunction in the RPE plays a significant role in the development of AMD. Mitochondria are like miniature organs (organelles) within all cells that provide energy. When not working properly in retinal cells, they can lead to cell death and vision loss. Dr. Ferrington is evaluating compounds that help protect mitochondrial function in the RPE.

Aging Telomeres and Yoga New Study by Elizabeth Blackburn and Dean Ornish

by Baxter

Telomere Caps

A while back, we reported on an interesting potential marker in the body for aging of the cells connected to the genes called a telomere (see Stressed Mind, Stressed Cells and Science, Aging and Yoga). A telomere is like a tail on the end of DNA strands found in our cells, and an enzyme called telomerase influences the length and activity of the telomere. Studies done a few years ago by a Dr. Elizabeth Blackburn at UCSF in San Francisco began to show a connection between telomeres and cell longevity—the longer the telomere, the longer the cell life. Her work garnered her a Nobel Prize in Medicine.

Now Dr. Blackburn has teamed up with Dr. Dean Ornish to see what effect his life-style changes approach to prostate cancer has on telomeres and telomerase activity. Dr. Ornish has already shown that a combination of dietary changes (vegan diet with less than 10% fat per day), exercise in the form of walking for 30 minutes most days, and stress management tools that include regular yoga asana and breath work, mindfulness meditation and once a week group stress reduction sessions can reverse heart disease and diabetes, and can stabilize prostate cancer and stop its progression.

In their most recent study, published in Lancet Oncology (see Effect of comprehensive lifestyle changes on telomerase activity and telomere length in men with biopsy-proven low-risk prostate cancer: 5-year follow-up of a descriptive pilot study), the two researchers looked at how the lifestyle program impacted the cellular genetic level in regards to telomere length and enzyme activity. What they found was that the 10 men studied had longer telomeres in the short (as quickly as three months!) and long run, if they stuck to the program, and the 25 men who were controls had shorter telomeres. And they also looked at gene activity in their ten study subjects, and found that 500 genes were turned on, and all were beneficial, according to Ornish. 

Even though telomeres may be an indicator of longer cell life, and by extension, longer overall lifespan, this has not been definitively concluded, so more studies will need to be done, looking at much larger numbers of people. But the early evidence is promising, and even if the telomere/aging cell theory does not pan out, it seems evident that yoga, diet, exercise and stress management do have significantly positive impacts on health, disease progress or remission, and are therefore worth the effort. And as Dr. Ornish noted, his study participants found the lifestyle plan easy to follow, with 85-90% compliance, much better than most pharmaceutical based treatment plans. Why, you might ask? Well, has he says, it’s because it’s pleasant and comprehensive and “most people feel so much better they change their lifestyle.”

To read more, you can check out articles at ucsf.edu and today.com—among others—which reported these new findings.

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Iluvien Update 2 New Safety and Efficacy Data Presented at ARVO

In July 2010, I wrote a comprehensive report about Iluvien and its potential in the treatment of diabetic macula edema (DME) (Iluvien and the Future of Ophthalmic Drug Delivery Systems). It was anticipated at that time that the company would obtain marketing approval for its sustained release treatment of DME by the end of that year. However, as I wrote in early January, the company received a CRL (complete response letter) from the FDA instead, that requested additional information before approval could be granted. (Iluvien Update: FDA Marketing Approval Delayed).

Earlier this week, Alimera Sciences and pSivida Corporation jointly announced that one of the FAME Study investigators had presented on a subset of the FAME Study data at the ARVO Meeting in Fort Lauderdale, and that the company (Alimera) plans to submit this new subgroup data to the FDA in support of its New Drug Application. Iluvien is licensed by pSivida to Alimera Sciences, Inc.

Here are the details:

Alimera's New 36-Month Safety and Efficacy Results From the Phase 3 Fame Study of Iluvien in Patients With Diabetic Macular Edema Presented at the 2011 Arvo Annual Meeting

Alimera Plans to Submit This New Data to the FDA in Support of Its Pending New Drug Application

Alimera Sciences, Inc. announced that positive new data from the completed FAME Study of Iluvien were presented at the 2011 Association for Research in Vision and Ophthalmology (ARVO) Annual Meeting. The new data showed that 33.6% of patients in Trial A (p<0.001) and 42.4% of patients in Trial B (p<0.001) were observed achieving best corrected visual acuity (BCVA) improvement of 15 letters or more from baseline at month 30 in the identifiable subgroup of patients diagnosed with diabetic macular edema (DME) for three years or more at baseline. The new data were presented by Dr. Andrew N. Antoszyk, one of the FAME investigators and a practicing retina specialist at Charlotte Eye, Ear, Nose and Throat Associates in Charlotte, N.C.

The new data, presented by Dr. Andrew N. Antoszyk, analyzed the subgroup of patients who had been diagnosed with DME for three or more years at entry of the FAME Study (which comprises over 50% of patients in the Study).

The FAME Study consisted of two three-year, Phase 3 pivotal clinical trials (Trial A and Trial B) to assess the safety and efficacy of Iluvien in the treatment of DME. The 956 patients in the trials were randomized to receive either high dose Iluvien, low dose Iluvien or control treatment. The primary endpoint for efficacy in the trials was the difference in the percentage of patients whose BCVA improved by 15 or more letters from baseline on the Early Treatment Diabetic Retinopathy Study (ETDRS) eye chart at month 24 between the treatment and control groups.

As previously reported, the pre-specified primary endpoint for the FAME Study was met for the low dose Iluvien in both Trial A and Trial B. Based on these data, Alimera submitted a New Drug Application (NDA) to the U.S. Food and Drug Administration (FDA) on June 29, 2010 for approval of the low dose Iluvien. Therefore, only the low dose data is presented and discussed here.

In February 2011, Alimera presented positive results from the full patient population at month 36 of the FAME Study in Trial A (28.4%) and Trial B (29.0%) with demonstrated improvement in BCVA of 15 letters from baseline. Statistical significance was seen in both trials as late as month 33 with Trial A at 28.4% (p=0.042) and Trial B at 29.6% (p=0.046).

Dr. Antoszyk's ARVO presentation on May 3rd included additional data from a subgroup of study patients that was identifiable prior to administration of Iluvien. This subgroup reflected the duration of DME at baseline and across all patients randomized, with a median duration of DME at baseline of three years.

In the data reported for this subgroup at 36 months in Trial A, 31.8% of patients treated with Iluvien experienced an improvement in best corrected visual acuity (BCVA) of 15 or more letters from baseline compared with 13.6% of those in the control group (p=0.010), for a net benefit of Iluvien versus control of 18.2%.  In Trial B, 36.4% of Iluvien patients in this subgroup experienced improvement of 15 or more letters compared to 13.2% of control patients (p= 0.004), for a net benefit of Iluvien versus control of 23.2%.  On a combined basis for both Trials A and B, at three years the net benefit of Iluvien compared to control reported for patients in the subgroup was  20.6%, more than double that seen for the full patient population (9.8%).

In the subgroup, peak efficacy was seen at month 30, with 33.6% of Iluvien treated patients in Trial A gaining 15 or more letters in BCVA compared to 10.2 % of control (p < 0.001) and 42.4% of Iluvien treated patients in Trial B gaining 15 or more letters in BCVA Trial B compared to 11.3% of control (p< 0.001).

Consistent with the full patient population in the FAME Study, approximately 75% of the patients in this subgroup treated with Iluvien were reported to have received only one Iluvien insert over the 36 month study.

There was no statistically significant difference in BCVA improvement in the subgroup of patients with less than three years' duration of DME at entry compared to control.

"Throughout the FAME Study, Iluvien has shown significant potential for patients suffering with DME. This new data is particularly exciting with 34% of patients who've had DME for three years or more gaining three lines of vision after therapy," said Dr. Antoszyk. "If regulatory approval of Iluvien is obtained, we will be able to offer an additional option in the form of a long-term treatment to our patients who are dealing with this devastating disease."

Data for the subgroup was gathered from 536 patients who had been diagnosed with DME for three years or more and 416 patients who had been diagnosed with DME for less than three years. Alimera will provide these additional data in its response to the Complete Response Letter issued by the FDA in December 2010.

Safety was assessed among those patients within the subgroup who were treated with Iluvien in the study. Intraocular pressure (IOP) increases to 30 millimeters of mercury (mmHg) or greater at any time point were seen in 14.8% of these patients by month 36, compared to 18.3% in the full Iluvien treated patient population. By month 36, 5.3% of these patients had undergone an incisional surgical procedure to reduce elevated IOP, compared to 4.8% in the full patient population. The incidence of cataracts among patients with a natural lens in their eye at the start of the study was 86% at month 36, with 85% undergoing a cataract operation, compared to 80% and 74.9%, respectively, in the full patient population.

"We are pleased that this identifiable subgroup shows even greater benefit to risk than the full patient population through month 36 of the study, thereby further improving Iluvien's profile," said Dan Myers, Alimera's president and CEO. "This data spotlights the benefit that Iluvien, if approved, could bring to the patient population that retinal specialists are targeting for its use. We believe this data will be very valuable to the treatment of DME going forward."

Paul Ashton, president and chief executive officer of pSivida, said, "We are very pleased with the efficacy and safety results through month 36 in patients with chronic DME.  This subgroup comprised a majority of patients in the FAME Study.  We look forward to Alimera's filing of this data with the FDA in connection with the NDA for Iluvien."


About the FAME Study

Alimera conducted two 36-month, Phase 3 pivotal clinical trials (collectively known as the FAME Study) for Iluvien involving 956 patients in sites across the United States, Canada, Europe and India to assess the efficacy and safety of Iluvien with two doses of the corticosteroid fluocinolone acetonide (FAc), a high and low dose, for the treatment of DME. The primary efficacy endpoint for the FAME Study was the difference in the percentage of patients whose best corrected visual acuity improved by 15 or more letters from baseline on the ETDRS eye chart at month 24 between the treatment and control groups. The study concluded in September 2010 with the final patient visit at the three-year data point.

Following its NDA submission to the FDA, Alimera submitted a Marketing Authorization Application to the Medicines and Healthcare products Regulatory Agency in the United Kingdom. Applications have also been submitted to regulatory agencies in Austria, France, Germany, Italy, Portugal and Spain. Based upon the analysis of the FAME Study, all filings included the 24-month data. The FDA, in a December 2010 Complete Response Letter, requested further information including the month 36 data from the FAME Study.

About DME

DME, the primary cause of vision loss associated with diabetic retinopathy, is a disease affecting the macula, the part of the retina responsible for central vision. When the blood vessel leakage of diabetic retinopathy causes swelling in the macula, the condition is called DME. The onset of DME is painless and may go undetected by the patient until it manifests with the blurring of central vision or acute vision loss. The severity of this blurring may range from mild to profound loss of vision. The Wisconsin Epidemiologic Study of Diabetic Retinopathy found that over a 10-year period approximately 19% of people with diabetes studied were diagnosed with DME. As the population of people with diabetes increases, Alimera expects the annual incidence of diagnosed DME to increase, as well.

New Theory About the Purpose of Sleep and Why Its So Important to Get Sound Sleep

by Ram

Sleep by Francisco Goya

According to Ayurveda philosophy, sleep is one of three pillars that endow the body with strength, complexion, and healthy growth, which can continue through the full span of life. The Ayurvedic texts also describe the maladies that can result from poor-quality sleep, including but not limited to misery, emaciation, weakness, brain fog, memory loss, and fatigue. It is believed that good quality sleep is essential for the well-being of any individual as the body utilizes the sleep time to repair itself of damage sustained during the waking hours.

In this hypercompetitive world, many of us complain of a lack of good quality sleep. We’re a world of unhealthy sleepers. If one were to compare the world statistics of insomnia and poor quality sleep, it is interesting to note that the numbers are nearly similar throughout the world. Within the USA, 30 percent of us have trouble falling asleep (insomnia) and 50 percent can sleep but have trouble maintaining sound/quality sleep due to tension, work, stress and/or emotional upheaval. 

Nearly 10 million people in the U.S. use prescription sleep aids. Several recent studies have shown that lack of sleep or a discontinuous sleep during the night may be deleterious for the brain, and may trigger dementia and increase the risk of stroke symptoms. For more on sleep and suitable interventions, check our earlier posts on these topics including: sleep and memory by Nina Sleep, Alzheimer's Disease and Yoga and The Importance of Good Sleep and natural interventions for good sleep 5 Tips for Better Sleep. 

The type of sleep and how we are affected by it is of great interest to sleep researchers. Sleep researchers have provided a number of reasons for why we sleep. Sleep helps to maintain a healthy immune system, balance our appetites, makes us less susceptible to degenerative diseases or infections, improves memory, and enhances cognition. Recent research work points to another interesting fact about why we sleep. Published just a week ago, a pair of papers offers evidence for another theory: Ultrastructural evidence for synaptic scaling across the wake/sleep cycle and Homer1a drives homeostatic scaling-down of excitatory synapses during sleep. 

According to these researchers, sleep helps us to forget some of the things we learn each day. Learning requires new neuronal connections or neuronal branching in our brains, which help neurons to communicate with neighboring neurons quickly and efficiently. Furthermore, these new neuronal branches also store firsthand memories of impressions that we draw in each day through our five senses. However, some of this information is redundant and does not require being stored. For example, you do not need to know what clothes you wore to work on a Thursday couple of weeks ago. Similarly, the people you saw at the airport terminal is not a value for the brain. 

In the first study Ultrastructural evidence for synaptic scaling across the wake/sleep cycle scientists from the University of Wisconsin-Madison proposed that neuronal branches grow so wildly during the day with all our experiential learning that our neuronal circuits actually get “noisy” (in neuroscience, “noisy” refers to the constant bombardment of electrical activity in neurons that can be measured by sophisticated machines). These scientists further added that when we sleep soundly, the brain discards all the unnecessary noise and consolidates only the relevant signals. In one experiment, scientists grew neurons in a lab dish and fed the neurons with a drug that stimulates the excess noise (that is, growth of extra neuronal branches). Twenty four hours later, the neurons had pared backed some of the branches. In a follow up experiment, the scientists surveyed brain tissue slices from mice that slept soundly and compared them to tissue slices from mice that were forced to keep awake. The neuronal branches in the mice that slept were much smaller and far less “noisy” compared to neuronal branches from mice that were forced to stay awake.

The second study Homer1a drives homeostatic scaling-down of excitatory synapses during sleep, led by scientists from Johns Hopkins University, explored the same theory with a different set of experiments. In this case, the researchers created a tiny window through which they could peer into mouse brains. They added a chemical that would light up each time a new neuronal branch developed, suggesting a new learning had triggered electrical activity, resulting in a noise. 

Looking through the window, they found that the chemical lit up very few times in mice that were asleep, suggesting that the brain was discarding all the extra branches resulting in reduced noise. This suggested that sleep turned on the pruning machinery to pare back the excess neuronal branches. More importantly, this sleep-induced pruning of neurons helped in consolidating memories. Mice that were not allowed to sleep ended up with less pruning of the branches, more neuronal noise, and fuzzy memories. Interestingly, the pruning machinery was very specific; it did not prune the well-established old neuronal connections. 

To provide an analogy, I am reminded of what the computer folks always advise us when the computer starts functioning erratically. Before thinking of any expensive repairs, the first thing they do is to switch off the computer and reboot it. The reasoning is that the processor discards and clears the hard drive of all of the unnecessary and not-needed information. So the take-home message is that we do not need to harbor all the information that we encounter briefly on a day-day basis, especially the bad, unpleasant, sad, and negative events. 

Every day we encounter brief negative thoughts/experiences —when we typically experience a brief bout of anger—that do not need to be consolidated. For example, while driving you may have encountered someone who speeded wildly and overtook you without signaling, or maybe your waiter took a long time to bring the lunch order and you got delayed for your next important meeting. These situations need not be stored as it is not helpful—it is a noise that we need to erase by sleeping soundly.

If we cannot discard these negative experiences through sound sleep, these disharmonious memories can keep lurking in the brain for a long time, and create the excess noise through the numerous unwanted neuronal branches and erratic electrical activity that will have deleterious effects on the brain. 

Sleep experts are now busy trying to discover medicines that might precisely target the molecules to induce sleep, ensuring that neuronal branches get properly pruned and all the junk information is purged. However, as yogis we know what works better naturally than medicines: a good sleep. Remember, good sleep is essential for a person’s health and wellbeing and if you are experiencing sleep problems, there is quite a price to pay.

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Facts You Need To Know About Sleeve Gastrectomy New York

By Kimberly Brooks

If you intend to go through this procedure, you should first strive to find out more about it. You should make sure that you learn about what it entails, the cost, and the possible risks and benefits. Outlined below, are facts that you need to know regarding sleeve gastrectomy New York:

This procedure is classified under bariatric surgical procedures, which are done to aid significant weight loss. During this procedure, experts reduce the size of the stomach by at least eighty or ninety percent. This reduction, in turn, limits the amount of food that the stomach can hold. If performed effectively, this procedure can yield positive weight-loss results, within a short period.

This procedure is performed within a short period. If you want to have a surgery that will not take a lot of time, you can opt for this procedure. After undergoing this procedure, the post-operation check-ups that you are supposed to have are minimal.

Like other surgical procedures, this procedure has various complications. First, if patients do not undergo proper post-surgical checkups, they may succumb to deadly infections. If not treated, these infections can cause death. Second, this procedure can trigger serious heart-related diseases including thrombosis and pulmonary embolism. Third, this process can trigger severe internal hemorrhage that can cause death. To minimize the occurrence of these risks, you should ensure that you find credible and experienced doctors that will perform the procedure effectively.

This surgical procedure is pricey. However, to obtain fair deals, you can choose to visit different experts and ask for overall price estimates. It is advisable to undergo this procedure in a health facility that offers it at a fair cost. Some hospitals may accept insurance covers. Therefore, if you do not have a sufficient amount, you should check to see if hospitals accept insurance covers.

This operation is suitable for people that are at a high risk of contracting diseases caused by excess cholesterol. If you are susceptible to contracting these diseases, you should consider visiting your doctor and enquire about this procedure. Also, this operation is suitable for people that are overweight. If your body mass index is high, you should also consider having this surgery. Nonetheless, if you are not overweight, and you are not at a risk of contracting diseases caused by excess body fat, you need to seek advice from your doctor before carrying on with this procedure.

This procedure is suitable for people that have an extremely high body mass index. Also, this procedure is suitable for people that are at a high risk of contracting congenital heart diseases, or other diseases that are associated with excess body fat. If you are not vulnerable to diseases associated with excess fat and you do not have a high body mass index, you should first consult your doctor before deciding to undergo this procedure. Your doctor will help you to determine if this procedure is safe for you.

If you do not know anything regarding this operation, you should ensure that you find out more about it. To learn about this operation, you can refer to this article. The details discussed above will help you to learn more about this operation.

About the Author:

If you are looking for the facts about sleeve gastrectomy New York locals can pay a visit to our web pages online today. More details are available at http://www.lapspecialists.com/bariatric-weight-loss-surgery.html now.

Basic Overview Of Massage Therapy New Orleans

By Elsa Noel

Massage therapy involves the application of a set of manual techniques aimed at improving the well-being of people through hand movements on various tissues. Massage therapy New Orleans encompasses the skin, muscles, tendons and ligaments. These therapies aim to improve well-being (both physical and mental). The term massage covers a set of methods that, despite their philosophical differences and applications, share a number of principles.

The masseuse's fingers relieve stress points by percussion, kneading, friction. The technique is dictated by the patient's reactions. The type of massage is called anma by the Japanese. Amma massage chair is intended to lessen if not eliminate the accumulated stress. Chair massage was originally developed by David Palmer, an American who wanted an easy way to massage clients at Apple, Inc.

He was the first to develop in 1983 a kata (precise series of maneuvers), which is useful for relaxing the back, shoulders, arms, hands, head and neck in 15 minutes. The amma is given through clothing, catcher sitting in an ergonomic chair. Practiced in sessions of fifteen minutes, which makes it accessible to businesses, cafes and public locations, the amma sometimes called "acupuncture without needles" runs over all meridians (energy channels).

It entails use of various hand and elbow techniques on 140 specific points. The techniques include energy scans, stretching, pressure and percussion. The recipients are pressurized at nerves that go directly towards the hypothalamus, located inside the brain structure. The latter through massage will trigger the production of pleasure hormones, such as ocytocine. Abdominal massage is designed to relax by massaging the abdomen, especially the intestines. It is used to degas the gastrointestinal tract. Abdominal pain and stress disappear.

The masseuse holds his arm firmly and stretches it without pulling the person off the ground. He or she continues by shaking the arm up and down in a relatively low amplitude at an average speed of at least once per 30 seconds. It is called the active phase. This is followed by the passive phase where the arm is stretched for a second in a slightly steeper motion while raising it to a height of about 15 inches.

Throughout the Korean acupressure, the arm is raised from the ground to a height corresponding to the desired effect.

These two steps take place in a single cycle of all Korean massage processes. In most cases, at least three identical cycles are needed for a Korean movement that is actually very active. The great beauty of Korean relaxation is that the massage is very deep while being totally painless (except for existing pain).

These actions are useful for anyone tired that needs to reinvigorate their system. It is also useful for people with lymphatic edema, venous, to a lesser extent (but the handling is slightly different: no pumping and movement is slow and follows the venous system). This in addition to people with heavy legs. Marma Sanskrit is a place of joining or meeting of the five organs: ligaments, vessels, muscles, bones and joints. These points are the seats of vital energy or prana.

About the Author:

You can visit www.oldmetairiemassage.com for more helpful information about Basic Overview Of Massage Therapy New Orleans.

OCD Workshops for Parents at the Child Mind Institute in New York City

The Child Mind Institute let me know that they are offering a series of workshops for parents of children with OCD, with the last three being in January, February and March, 2012. All of the workshops in the series are free and open to the public. Here's a description of their mission:

Our Obsessive-Compulsive Disorder Parent Support and Information Group workshop series covers a range of issues affecting children with obsessive-compulsive disorder (OCD) and their support networks, from navigating friendships and family gatherings to the ins and outs of treatment and medication. This program is an opportunity to gain invaluable skills and learn how to help your children take control of their condition and thrive. Below you'll find the dates and topics of the 2011-2012 workshops; descriptions to follow.
This series is brought to you by the Child Mind Institute's Intensive Pediatric OCD Program. All workshops are held at the Child Mind Institute headquarters located at 445 Park Avenue (with entrance on 56th Street), New York, NY 10022.
The Nuts and Bolts of Exposure Therapy
Speaker: Jerry Bubrick, PhD, Senior Director, Anxiety & Mood Disorders Center; Director, Intensive Pediatric OCD Program
Date: Tuesday, January 10, 2012
Time: 6:00PM - 7:30PM
Location: Fascitelli Board Room at the Child Mind Institute
At first glance, the treatment for a child with OCD can seem illogical and difficult—why would my child want to do exactly what she fears? In this workshop, Jerry Bubrick, PhD, Senior Director of the Anxiety & Mood Disorders Center and Director of the Child Mind Institute's Intensive Pediatric Obsessive-Compulsive Spectrum Disorders Program explains why exposure therapy is the gold standard in OCD treatment and how it works to alleviate the extreme anxiety a child experiences around his or her symptoms. He explains how to help your child face the "bully in the brain" head-on and regain control over his or her life.
Is Medication Part of the Answer? Medication Approaches to OCD
Speaker: Roy Boorady, MD, Senior Director of the Child Mind Institute's Psychopharmacology Center
Date: Tuesday, February 7, 2012
Time: 6:00PM - 7:30PM
Location: Fascitelli Board Room
When deciding how to best treat a child with OCD, it is important to be aware of all of the options. Treatment for children with OCD will often involve cognitive-behavioral therapy, medication, or a combination of the two. Roy Boorady, MD, Senior Director of the Child Mind Institute's Psychopharmacology Center and one of the nation's foremost experts in the psychopharmacological treatment of children and teens, discusses medication approaches to treating OCD. You'll gain a deeper understanding of when and how medication should be used in the treatment of OCD as well as the benefits and drawbacks of the different classes of medication available.
Real Stories: Parents Speak
Date: Tuesday, March 6, 2012
Time: 6:00 PM - 7:30 PM
Location: Fascitelli Board Room at the Child Mind Institute
Join us for a very special Q&A panel of parents who've successfully led their children through the challenges of OCD. They will share personal stories—their struggles as well as the successes—of raising a child with OCD. You'll have the opportunity to ask questions and gain insight into how you can help your child while maintaining balance in your life.

AMD Update 6 An Overview of New Treatments for Dry AMD

Those of you who have been following this space know that I have been reporting on new drug and device treatments for wet age-related macular degeneration for the past several years. I haven’t paid much attention to the treatments under development for the dry form, basically because most are drug-related, and my knowledge of how drugs work is limited. However, I recently read an excellent overview of the new drugs that are being developed for dry AMD, written by Dr. Philip Rosenfeld (the father of Avastin for use in AMD) and John Legarreta, a medical student at State University of New York at Buffalo, which presents a clear picture of current developments in this important field.

I have previously written about the potential for the use of lasers to treat dry AMD by Iridex, but that attempt did not prove successful. I have also written about the Ellex 2RT (retinal regeneration) program that might hold potential in the early intervention in dry AMD. Links to both of these writeups are shown at the end of this posting.

With about 80% to 90% of newly diagnosed AMD cases being of the dry variety, and with no effective treatment currently in use, it is important to track the developmental work underway in this area. This review appeared in the November 2009 issue of Retinal Physician, and with the permission of the magazines publishers, here is the complete writeup:

Preclinical and Phase 1 Drugs in Development for Dry AMD: An Overview

Retinal Physician, November 2009

Philip J. Rosenfeld, MD, PhD ● John Legaretta, BFA

Philip J. Rosenfeld, MD, PhD, is professor of ophthalmology at the Bascom Palmer Eye Institute at the University of Miami Miller School of Medicine in Florida. He receives significant research support from Potentia and Alexion, and he has a minimal advisory relationship with Potentia. John Legarreta, BFA, is a medical student at the School of Medicine and Biomedical Sciences, State University of New York at Buffalo. He has no financial interest in any products mentioned in this article. Dr. Rosenfeld can be reached at prosenfeld@med.miami.edu.


The vast majority of AMD patients have the nonexudative or dry form of the disease, characterized by a constellation of clinical features, including drusen, disturbances of the retinal pigment epithelium (pigment clumping and/or dropout), and geographic atrophy (GA) of the macula. As defined by the Age-Related Eye Disease Study (AREDS), the severity of AMD can be classified into three categories: early, intermediate, and advanced.

[Editors Note: For a breakdown on the number of people in the three categories noted above in both dry and wet AMD in 2007, as estimated by Market Scope, please see the link to the table shown at the end of this posting.]

While drusen alone, particularly those of smaller size, do not seem to be associated with vision loss, at least one large druse measuring 125 μm in diameter is sufficient for the diagnosis of intermediate AMD. Dry AMD may remain static or progress slowly to produce a greater number and distribution of drusen with areas of GA. The increase in size or area of drusen or pigment abnormalities (focal hyper- or hypopigmentation of the retinal pigment epithelium [RPE]) predicts the likelihood of developing vision-threatening lesions in AMD, which include central GA and neovascularization, the advanced forms of AMD.(1)

CURRENT TREATMENT OPTIONS FOR DRY AMD

Antiangiogenic therapies have been developed to treat wet AMD. While drugs such as ranibizumab (Lucentis, Genentech) and bevacizumab (Avastin, Genentech) have revolutionized the care of patients with neovascular AMD, under the best of circumstances, treatment converts the neovascular form of AMD back to dry AMD. There is no evidence to suggest that these antiangiogenic drugs have any beneficial effect on the underlying degenerative process known as dry AMD. Currently, there is no proven drug treatment for dry AMD; however, the cessation of smoking and treatments based on nutritional recommendations and supplements can slow disease progression. Nutrient-based treatments for AMD were evaluated in the AREDS trial.(2)

TARGETING THE CAUSE OF AMD

The overall goal of treatment for dry AMD is to target the underlying cause of the disease and halt, or at least slow, the loss of vision. This approach has been hampered by two major issues. First, there are no reliable in vitro systems for testing the efficacy of any drug for dry AMD, and second, no true animal model exists for AMD. A well-developed macula is only found in primates and birds, and while numerous attempts have been made to develop nonprimate models for AMD, and these models highlight various pathological features of human AMD, none of these animal models truly replicates the disease process seen in humans. The only model that may be useful for potential drug testing is the naturally occurring monkey colonies that have been found to develop drusen.(3)

The second issue that has hampered drug development is the uncertainty surrounding the best molecular pathway to target for the treatment of dry AMD. However, several different strategies have evolved. These strategies have targeted three major therapeutic areas of investigation: preservation of photoreceptors and the RPE (neuroprotection), prevention of oxidative damage, and suppression of inflammation. Each strategy is supported by varying degrees of scientific evidence and will have to await validation based on clinical trial outcomes.

CLINICAL TRIAL ENDPOINTS IN DRY AMD

The most obvious study endpoint for dry AMD therapies would be the preservation of visual acuity; however, studies using visual acuity as an endpoint will take many years to complete. To decrease the time required to show a benefit from a drug, surrogate endpoints have been developed that might indicate a positive outcome without waiting the years required to show visual acuity benefit.

One surrogate endpoint is the prevention of disease progression from dry to wet AMD. This endpoint was first used in the study investigating anecortave acetate (Retaane, Alcon) for the treatment of dry AMD. While the drug failed to prevent progression of dry to wet AMD, the study demonstrated the feasibility of this study design. Another strategy is to assume that a treatment for dry AMD might also affect the underlying stimulus for neovascularization in wet AMD. If true, then a potential endpoint might be to demonstrate that a drug for dry AMD is able to decrease the need for retreatment with antiangiogenic therapy in wet AMD or improve the visual acuity outcome. This study design has not been tested.

A feature of dry AMD that could serve as a surrogate endpoint is the area of drusen in the macula. While drusen area as measured by fundus photography has already been explored as an endpoint in the failed laser-to-drusen trials, (4-6) the change in drusen volume in response to pharmacotherapy is a novel clinical trial endpoint that has not been explored previously. Spectral-domain optical coherence tomography has the potential to reliably and reproducibly identify drusen in the macula and provide truly automated volume quantification. The most likely surrogate clinical trial endpoint, based on a symposium held in Washington, DC, and sponsored by the National Eye Institute and the Food and Drug Administration, is an endpoint that assesses a drug’s effects on the growth of GA, since GA is a feature of dry AMD that directly causes loss of photoreceptors and the RPE. (7)

DRUGS TO PROMOTE SURVIVAL OF PHOTORECEPTORS AND THE RPE

No matter what the underlying cause of AMD, drugs that can preserve viable photoreceptors and maintain the RPE should preserve vision. One strategy to promote survival of photoreceptors and the RPE is to protect cells against ischemia and improve the choroidal circulation in patients with dry AMD. Two studies are currently using this strategy. In Europe, an ongoing multicenter, randomized, placebo-controlled study is investigating the use of an offlabel, generic drug known as trimetazidine (Vastarel MR, 35 mg tablet), a drug currently used for the treatment of angina pectoris. Trimetazidine improves myocardial glucose utilization by stopping fatty acid metabolism, and it is considered to have cytoprotective effects in ischemic conditions. Other uses for this drug include the treatment of vertigo, tinnitus, and vision loss and visual field loss due to vascular causes. The primary goal of this study is to slow the conversion of dry AMD to wet AMD.

Another drug being investigated for its vasodilatory effect is Alprostadil, also known as prostaglandin E1 (PGE1). The presumed rationale is based on the belief that improved circulation would slow the progression of AMD. This multicenter, randomized, placebo-controlled study is ongoing in Europe.

Another strategy to preserve the macular function is to prevent apoptosis by using neuroprotective agents. Ciliary neurotrophic factor (CNTF), a potent neuroprotective agent, has been shown to inhibit photoreceptor apoptosis in an animal model of retinal degeneration (8) and is being investigated as a treatment for dry AMD. Using encapsulated cell technology that permits CNTF-producing transfected cells to be implanted into the vitreous cavity, Neurotech Pharmaceuticals (Lincoln, RI) has developed a sustained-release platform that produces CNTF for a year or longer. The phase 2 study is completed and data analysis is currently under way. Other neuroprotective agents currently under investigation for dry AMD include a brimonidine tartrate intravitreal implant (Allergan, Irvine, CA) and topical tandospirone (Alcon, Fort Worth, TX).

Yet another strategy is to interfere with the normal visual cycle and preserve vision by decreasing the accumulation of toxic metabolites, such as lipofuscin and the retinal fluorophore A2E. This strategy is being pursued by Sirion Therapeutics (Tampa, FL) with the use of fenretinide - N-(4-hydroxyphenyl) retinamide - for the treatment of dry AMD. Fenretinide binds retinol-binding protein in the circulation and prevents uptake of retinol by the RPE, thus downregulating photoreceptor metabolism. The phase 2 study investigating fenretinide for the treatment of GA is fully enrolled and in its second year of follow-up.

Downregulation of photoreceptor activity is also being investigated using the drug ACU-4429 (Acucela, Bothell, WA). ACU-4429 is a small nonretinoid molecule that functions as a modulator of the isomerase (RPE65) required for the conversion of all transretinol to 11-cis-retinal in the RPE. By modulating isomerization, ACU-4429 slows the visual cycle in rod photoreceptors and decreases the accumulation of A2E. The ongoing phase 1 study has shown so far that the drug is safe and well tolerated in healthy volunteers. A phase 2 study for treatment of dry AMD is currently being planned.

A novel strategy for the preservation of photoreceptors and the RPE borrows a therapeutic strategy used for the treatment of Alzheimer's disease. An antibody against amyloid ß has completed a phase 1 study as an intravenous treatment for GA in AMD patients. This antibody, known as RN6G (Pfizer, New York, NY), was shown to decrease the amount of amyloid ß in the eye from a mouse model of AMD when given as a systemic therapy.(9) A phase 2 study is currently under way.

The therapies under investigation that seek to preserve photoreceptors and the RPE are summarized in Table 1.


(Note: I have reproduced the tables included with the article. By clicking on the tables they will open in a new window or tab in a larger more readable size. Or, go to the original online writeup for a clearer view of the table contents.)

DRUGS TO PREVENT INJURY FROM OXIDATIVE STRESS AND MICRONUTRIENT DEPLETION

In AMD, oxidative stress and the depletion of essential micronutrients are considered to be driving forces in disease progression. This disease paradigm assumes that AMD is caused by a lifelong exposure to free radicals - a byproduct of high oxygen consumption in the neural retina and RPE - combined with exposure to environmental toxins, such as those derived from smoking, in conjunction with inadequate levels of naturally occurring antioxidants. These exposures and deficits result in the accumulation of cellular debris - particularly oxidized lipids, which promote inflammation and may be directly toxic to the macular tissues - resulting in the clinical manifestations known as AMD. This paradigm is supported by epidemiologic studies showing that diets rich in antioxidants decrease the risk of AMD, while smoking was associated with an increased risk of AMD.(10)

Support for this nutrient-based paradigm was provided by the AREDS trial. This multicenter, NEI-sponsored study evaluated the effect of pharmacological doses of zinc and/or a formulation containing nutrients with antioxidant properties (vitamin C, vitamin E, and beta-carotene) on the rate of progression to advanced AMD and on visual acuity. The use of these vitamins and micronutrients reduced the risk of developing advanced AMD by about 25%.(2) The overall risk of moderate vision loss was reduced by 19% at five years. The theory of oxidative damage as a cause for AMD has also been supported by the findings that individuals have an increased risk of developing AMD if they carry a specific genetic polymorphism in mitochondrial DNA (A4917G), an organelle important for oxidative metabolism, and in nuclear DNA within the 5'-upstream region of a genetic locus important for DNA repair (ERCC6). DNA damage can be caused by oxidative stress.(11,12)

The AREDS2 trial, now under way, is designed to evaluate the effect of dietary xanthophylls (lutein/zeaxanthin) and/or omega-3 long-chain polyunsaturated fatty acids (LCPUFA), known as docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), on the progression to advanced AMD (www.areds2.org). These micronutrients are believed to function not only as antioxidants, but also as anti-inflammatory and antiangiogenic agents, according to epidemiologic and laboratory studies. In addition, AREDS2 will investigate the effects of eliminating betacarotene and the effects of reducing zinc in the original AREDS on the development and progression of AMD.

A topical antioxidant called OT-551 (Othera Pharmaceuticals, Exton, PA) was being explored as a treatment for dry AMD. OT-551 (4-cyclopropanoyloxy- 1-hydroxy-2,2,6,6-tetramethylpiperidine HCl) is a small lipophilic molecule that readily penetrates the cornea. OT-551 is converted by ocular esterases to TEMPOL-H (TP-H), the active metabolite that is a potent free-radical scavenger that does not penetrate the cornea. In animal studies, topical therapy has resulted in excellent ocular bioavailability, with significant levels of TP-H achieved in the retina.

The drug OT-551 was shown to possess antiinflammatory and antiangiogenic properties, as well as antioxidant properties. OT-551 was also shown to protect against oxidative damage in vitro, protect against light damage in vivo,(13) suppress photoreceptor cell death in animal models, and block angiogenesis stimulated by growth factors. Based on these preclinical data, OT-551 was being investigated as a therapy for GA in AMD. This two-year, phase 2 trial, known as the OMEGA (OT-551 Multicenter Evaluation of Geographic Atrophy) study, was stopped after 18 months, due to an apparent lack of efficacy in preventing the enlargement rate of GA in AMD.

The therapies under investigation that seek to prevent injury from oxidative stress and micronutrient depletion are summarized in Table 2.


DRUGS TO SUPPRESS INFLAMMATION

Genetic association studies using different populations have shown that inflammation appears to be the driving force behind AMD.(14) In 2005, four groups identified a genetic polymorphism in complement factor H (CFH), which was associated with an increased risk of developing AMD.(15-18) The documented risk-conferring single-nucleotide polymorphism (SNP) was a thymine (T) to cytosine (C) substitution at nucleotide 1277 in exon 9, which results in a tyrosine-to-histidine change at amino acid position 402 (Y402H) of the CFH protein.

Since complement is a system of serum proteins that comprise an important arm of the innate immune system, association studies have definitively linked AMD to the immune system. Also, two independent studies reported the association of the complement factor 3 gene with AMD, (19,20) as well as the complement factor B/component 2 gene.(21) An association between the complement factor 1 gene and AMD has been reported too.(22) Less robust associations have been reported between AMD and SERPING1, which regulates the first component of complement (C1), (23) and between AMD and C7 and mannose binding lectin 2 (MBL2) loci.(24) Protective alleles associated with the complement pathway have also been reported. Two of the five CFH-related genes (CFHR1-5), which lie within the regulators of complement activation (RCA) locus on chromosome 1q32, known as CFHR1 and CFHR3, are considered to be protective against AMD.(25)

These genetic association studies would imply that inhibition of complement activation would be a reasonable strategy for the treatment of AMD. However, after a lifetime of complement-mediated damage, such a strategy might have no effect on disease progression later in life. One drug being investigated is POT-4 (Potentia Pharmaceuticals, Louisville, KY), a cyclic peptide comprised of 13 amino acids, that is derived from compstatin. POT-4 binds reversibly to complement component 3 (C3) and prevents its proteolytic activation to C3a and C3b and the subsequent release of all downstream anaphylatoxins, as well as the formation of terminal membrane attack complex. As a C3 inhibitor, POT-4 inhibits all three major pathways of complement activation. POT-4 has unique slow-release properties due to the formation of an intravitreal gel at higher doses, which should permit less frequent intravitreal injections to achieve prolonged complement inhibition.

The phase 1 dose-escalation study, known as Assessment of Safety of Intravitreal POT-4 Therapy for Patients with Neovascular AMD (ASaP), was performed on patients with advanced neovascular lesions with the intention to pursue POT-4 as a treatment for dry AMD. To date, POT-4 appears safe up to a dose of 1.05 mg, with evidence of efficacy at the higher doses.

Another complement inhibitor under investigation is eculizumab (Soliris, Alexion Pharmaceuticals), a humanized monoclonal antibody derived from a murine antihuman C5 antibody. Eculizumab specifically binds the terminal complement protein C5, thereby inhibiting its cleavage to C5a and C5b during complement activation. The strategic blockade of the complement cascade at C5 prevents the release of the downstream anaphylatoxin C5a and prevents the formation of the cytolytic membrane attack complex.

Eculizumab is FDA-approved for the intravenous treatment of another complement-mediated disease known as paroxysmal nocturnal hemoglobinuria. At the Bascom Palmer Eye Institute, we are performing a phase 2 investigation with eculizumab for the treatment of patients with dry AMD, known as the COMPLement Inhibition with Eculizumab for the Treatment of Non-Exudative Age-Related Macular Degeneration (COMPLETE) Study. Patients with GA or high-risk drusen are being randomized 2:1 to receive intravenous infusions of eculizumab or placebo.

Ophthotech's ARC-1905 (Princeton, NJ), an anti-C5 aptamer, is another complement inhibitor being tested in AMD. ARC-1905 is being administered by intravitreal injection. The phase 1 dose-escalation study was performed in combination with ranibizumab therapy for the treatment of wet AMD. Genentech/Roche are developing an anti-Complement Factor D antibody Fab (FCFD4514S), which is in a phase 2 trial. Another phase 1 study using ARC1905 for dry AMD is currently under way.

Another complement inhibitor in preclinical studies is JPE1375 (Jerini Ophthalmic, New York, NY), a small, peptidomimetic molecular antagonist against the C5a receptor, which prevents binding of C5a, thus inhibiting the biological activity of C5a. Additional complement inhibitors are being pursued in preclinical studies by several companies, but details are not yet available.

More generalized immune suppression for the treatment of dry AMD is being pursued with the use of subcutaneous glatiramer acetate (Copaxone, Teva Pharmaceuticals, Kfar- Saba, Israel), intravitreal sustained-release fluocinolone acetonide (Iluvien implant, Alimera Sciences, Alpharetta, GA), and subcutaneous sirolimus (rapamycin), a macrolide fungicide with immunosuppressive properties.

The therapies under investigation that seek to suppress inflammation are summarized in Table 3.


SUMMARY

Several different strategies are being investigated, but it will take years before we know if any of them are successful. While we await positive outcomes, these clinical trials will produce a wealth of natural history data on the progression of dry AMD and provide us with extensive experience using several different imaging modalities to track disease progression. With this experience, our clinical trial designs will improve over time and the appropriate clinical trial endpoints should become obvious. With all the drugs in development, there is a good chance that a treatment breakthrough should occur within the next decade. RP

REFERENCES

1. Ferris FL, Davis MD, Clemons TE, et al. A simplified severity scale for agerelated macular degeneration: AREDS Report No. 18. Arch Ophthalmol. 2005;123:1570-1574.
2. A randomized, placebo-controlled, clinical trial of high-dose supplementation with vitamins C and E, beta carotene, and zinc for age-related macular degeneration and vision loss: AREDS report no. 8. Arch Ophthalmol. 2001;119:1417-1436.
3. Kaidzu S, Tanito M, Ohira A, et al. Immunohistochemical analysis of aldehydemodified proteins in drusen in cynomolgus monkeys (Macaca fascicularis). Exp Eye Res. 2008;86:856-859.
4. Laser treatment in patients with bilateral large drusen: the complications of age-related macular degeneration prevention trial. Ophthalmology. 2006;113:1974-1986.
5. Friberg TR, Musch DC, Lim JI, et al. Prophylactic treatment of age-related macular degeneration report number 1: 810-nanometer laser to eyes with drusen. Unilaterally eligible patients. Ophthalmology. 2006;113:622 e1.
6. Owens SL, Bunce C, Brannon AJ, et al. Prophylactic laser treatment hastens choroidal neovascularization in unilateral age-related maculopathy: final results of the drusen laser study. Am J Ophthalmol. 2006;141:276-281.
7. Csaky KG, Richman EA, Ferris FL 3rd. Report from the NEI/FDA Ophthalmic Clinical Trial Design and Endpoints Symposium. Invest Ophthalmol Vis Sci. 2008;49:479-489.
8. Tao W, Wen R, Goddard MB, et al. Encapsulated cell-based delivery of CNTF reduces photoreceptor degeneration in animal models of retinitis pigmentosa. Invest Ophthalmol Vis Sci. 2002;43:3292-3298.
9. Ding JD, Lin J, Mace BE, et al. Targeting age-related macular degeneration with Alzheimer's disease based immunotherapies: anti-amyloid-beta antibody attenuates pathologies in an age-related macular degeneration mouse model. Vision Res. 2008;48:339-345.
10. Risk factors associated with age-related macular degeneration. A case-control study in the age-related eye disease study: Age-Related Eye Disease Study Report Number 3. Ophthalmology. 2000;107:2224-2232.
11. Canter JA, Olson LM, Spencer K, et al. Mitochondrial DNA polymorphism A4917G is independently associated with age-related macular degeneration. PLoS One. 2008;3:e2091.
12. Tuo J, Ning B, Bojanowski CM, et al. Synergic effect of polymorphisms in ERCC6 5' flanking region and complement factor H on age-related macular degeneration predisposition. Proc Natl Acad Sci U S A. 2006;103:9256-9261.
13. Tanito M, Li F, Elliott MH, et al. Protective effect of TEMPOL derivatives against light-induced retinal damage in rats. Invest Ophthalmol Vis Sci. 2007;48:1900-1905.
14. Patel M, Chan CC. Immunopathological aspects of age-related macular degeneration. Semin Immunopathol. 2008;30:97-110.
15. Edwards AO, Ritter R, 3rd, Abel KJ, et al. Complement factor H polymorphism and age-related macular degeneration. Science. 2005;308:421-424.
16. Hageman GS, Anderson DH, Johnson LV, et al. A common haplotype in the complement regulatory gene factor H (HF1/CFH) predisposes individuals to age-related macular degeneration. Proc Natl Acad Sci U S A. 2005;102:7227-7232.
17. Haines JL, Hauser MA, Schmidt S, et al. Complement factor H variant increases the risk of age-related macular degeneration. Science. 2005;308:419-421.
18. Klein RJ, Zeiss C, Chew EY, et al. Complement factor H polymorphism in agerelated macular degeneration. Science. 2005;308:385-389.
19. Maller JB, Fagerness JA, Reynolds RC, et al. Variation in complement factor 3 is associated with risk of age-related macular degeneration. Nat Genet. 2007;39:1200-1201.
20. Yates JR, Sepp T, Matharu BK, et al. Complement C3 variant and the risk of age-related macular degeneration. N Engl J Med. 2007;357:553-561.
21. Gold B, Merriam JE, Zernant J, et al. Variation in factor B (BF) and complement component 2 (C2) genes is associated with age-related macular degeneration. Nat Genet. 2006;38:458-462.
22. Fagerness JA, Maller JB, Neale BM, et al. Variation near complement factor I is associated with risk of advanced AMD. Eur J Hum Genet. 2009;17;100-104.
23. Ennis S, Jomary C, Mullins R, et al. Association between the SERPING1 gene and age-related macular degeneration: a two-stage case-control study. Lancet. 2008;372:1828-1834.
24. Dinu V, Miller PL, Zhao H. Evidence for association between multiple complement pathway genes and AMD. Genet Epidemiol. 2007;31:224-237.
25. Hughes AE, Orr N, Esfandiary H, et al. A common CFH haplotype, with deletion of CFHR1 and CFHR3, is associated with lower risk of age-related macular degeneration. Nat Genet. 2006;38:1173-1177.


Links:

Laser Treatments for AMD Show Promise; Ocular Surgery News, January 15, 2000.

Ellex 2RT Retina Regeneration Therapy: A First Report

AMD Cases in the U.S. by Type and Stage in 20007

Preclinical and Phase 1 Drugs in Development for Dry AMD: An Overview

New Photo Galleries

by Nina

Bhavani Cooper, Age 56
barbara-e-cooper.healthcoach1.integrativenutrition.com

Our first photo contest (see Photo Contest and Friday Q&A: Why Only Women in Your Photo Contest?) has turned out to be a huge success. I have to say, I’m just thrilled. It’s taking me some time to go through all the photos submitted so far, but there are going to be a large number of prize-winning photos for sure!

So I’ve decided to create some new pages on the blog that are photo galleries of the prize-winning photos, one for women and one for men (that second photo contest is coming soon).

See Photo Gallery: Women Over 50 and Photo Gallery: Men Over 50.

The only reason I’m creating two separate pages for the genders is that I’m concerned that having too many photographs on a single page might cause technical problems on the blog. Later on, I may divide them up in some other way. Actually if you have suggestions for a better way of splitting them up, let me know.

Richard Rosen, Age 67, photographed by Melina Meza
richardrosenyoga.com

So far, I’ve only put up a few photos on these pages, but you can keep checking back. Basically, if your photo or photos “win,” you’ll eventually be in the gallery. If not, you’ll receive an email or Facebook reply from me explaining why I’ve rejected your photo. 

Reasons for rejection typically include:

• Photo is out of focus, partly out of focus, or too small (low resolution)
• Background is cluttered or unattractive
• The lighting is poor
• There is a very tiny image of you in a big landscape (that won't work on the blog)
• Body parts are cropped off (feet not showing, fingertips not in the frame, etc.)
• Face is shaded and dark, while background is bright (wearing hats definitely causes this problem as does strong back lighting) or your face doesn’t show at all (exceptions will be made for certain poses)
• Alignment of the pose looks unhealthy in my opinion, for example, the head and neck are not in line with the spine

Although I don’t by any means require professional photos, typically a quick snapshot done with your phone, unless it is really special, is not going to make the grade. So if you want your images to be seriously considered, take some time in creating them. Arrange the setting and move that plastic water bottle somewhere else. Have someone look at your alignment and give you some cues. Take multiple shots to get one good one. Take off your hat and sunglasses. Smile. Like these:

Judith Sims-Barlow, Age 72

Nancy LaNasa, Age 60

And if I reject your photo, you can always try again with a different photo. There are no deadlines for these contests.

But if you are interested in having your photo taken by our staff photographer, yoga teacher Melina Meza, she is available for hire. You can see her photographs of yoga practitioners on Flickr. To contact her, to the Contact page on her web site melinameza.com for her email information.

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A New Approach to Treating Chronic Kidney Disease Replenishing Your Nephrons

As some of you may know, I have chronic kidney disease (CKD). Thanks to my wife and the scare put into me by my nephrologist, that I would soon have to begin dialysis, I have managed to get my CKD  in remission, or at least under control. My GFR number (that indicates when you must start dialysis) has held steady, or actually gotten better since my wife put me on a strict diet and I have lost about 15 pounds – and my nephrologist took me off of lisinopril (for blood pressure control), which seemed to raise my GFR by about three points. So, it appears I won’t have to go on dialysis any time soon.

All that being said, and with my strong interest in the use of stem cells and gene therapy in treating retinal diseases in ophthalmology, I have been searching the web for research on the use of stem cells to treat kidney disease or to produce new nephrons, the kidney cells that filter the blood as it passes through the kidney – and that go bad or die causing CKD. I think I have found very early research of that possibility.

Earlier this week, I saw a news  release from the University of Queensland in Australia that said that Dr. Melissa Little and her research group at the Institute of Molecular Bioscience (IMB) have found a set of six genes that can prompt some types of adult kidney cells to regress to an earlier stage of development (stem cells) and act like the precursors to the cells of the nephron. Since it is death or damage of nephrons that causes chronic kidney disease, by forcing adult cells to act like early nephrons, they may have potentially found a way to trigger the growth of new filters in the kidney.

All of your nephron cells are formed before birth and people with fewer nephrons are at higher risk of kidney disease.

Note: Dr. Little is one of sources that I had found in my web search as she had published a paper on “Stem Cell Options for Kidney Disease” in 2008, and we had corresponded at the beginning of this year when I began my search for a stem cell answer.

"This discovery is the first of its kind and offers hope to patients with chronic kidney disease. If we can find a way to provide new nephrons to an adult or increase nephron numbers in babies at birth, we could potentially reduce the risk of disease progression," said Professor Little.

This landmark paper, “Direct Transcriptional Reprogramming of Adult Cells to Embryonic Nephron Progenitors”, by Caroline E. Hendry, Jessica M. Vanslambrouck, Jessica Ineson, Norseha Suhaimi, Minoru Takasato, under the supervision of Professors Fiona Rae and Melissa H. Little, was published June 14th in the Journal of the American Society of Nephrology, the world's leading nephrology journal.

Professor Little said, “There was still more work to be done to encourage these reprogrammed early nephron cells to function and integrate. While this is a beginning, we hope it will inspire industry leaders and researchers around the world to invest further in cellular and bioengineering approaches to kidney repair and regeneration."

Stem Cells Australia Program Leader and Chair of Stem Cell Science at The University of Melbourne, Professor Martin Pera welcomed the research findings. "This innovative study provides evidence that adult cells can be reprogrammed to resemble the cells in the embryo that give rise to the kidney. The results pave the way for future studies that will enable researchers to produce human kidney cells in the laboratory, for use in studies of renal disorders, and for testing new drugs. Eventually this technology might help to make cells for transplantation to treat kidney disease," said Professor Pera.

The Technology

I have attempted to read Dr. Little’s paper on reprogramming kidney cells, and with her assistance, this is what I understand she and her colleagues have done, which is a very early step in the long road to someday being able to replenish nephron cells in an adult kidney.

In an earlier paper written by Caroline Hendry and Dr. Little, “Reprogramming the kidney: a novel approach for regeneration”, they discussed the various approaches that might be taken to re-create viable cells within a diseased kidney, including using  induced pluripotent stem cells (iPSCs) derived from skin cells or other sites, or even the use of embryonic stem cells (ESCs) that would be introduced into the kidney to form new nephrons (?), if they could – as shown in the accompanying figure (but how would you control the formation of the new cells?). But they concluded that the best approach would be reprogramming existing kidney cells to the progenitor stage, with the hope that these would develop into the needed new cells, or in this case, nephrons, the approach they ultimately used in this new research.

Figure1 | The application of reprogramming to the kidney, indicating the feasible starting cells and target phenotypes.

(i) Reprogramming may involve the directed differentiation of human embryonic stem cells (hESCs)/induced pluripotent stem cells (iPSCs) to a renal lineage. The iPSCs may be recipient-derived and may be derived from adult kidney cells or any other available adult cell type using the same factors. Directed differentiation is likely to recapitulate development; hence, it is likely to require differentiation through a nephron progenitor intermediate (induced nephron progenitor cell; iNP) but may continue on to more specific mature renal cell types.

(ii) A specific renal lineage may also be achieved via lineage-instructive reprogramming directly to that state from an adult cell type. Again, this may be the renal epithelium, renal stroma, or any other available differentiated adult cell type; however, this is likely to be more successful if the attractor states of the starting and target cell type are as close as possible. Reprogramming may be to the iNP state or directly to a more mature renal cell fate.

(iii) Finally, reprogramming may use the classical Yamanaka factors until the cells pass the point of no return, after which a renal lineage may be reached via the application of the appropriate environmental cues. Such cues may once again target the iNP state or aim to directly induce a more mature renal cell type.

As previously stated, the nephron progenitor population of the embryonic kidney gives rise to all of the nephron cells that will be present in the adult kidney, prior to birth. So, currently, what you’ve got at birth is what you live with.

Using a screening technique, the researchers were able to identify a group of six genes, that activate a network of genes that can reprogram adult proximal tubule cells back to the nephron progenitor stage – which in turn can form adult nephron cells. Although the researchers believe that other factors are required, they concluded that these results suggest that re-initiation of kidney development (nephron cells) from a population of adult cells (proximal tubule cells) by generating embryonic progenitors may be feasible, opening the way for additional cellular and bioengineering approaches to renal repair and regeneration.

In their literature search, they could not find any previous reports of kidney cells being reprogrammed back to a progenitor cell type. Their hope is that this discovery will lead others to follow their lead and begin further work in the possible reprogramming of adult kidney cells for the repair and rejuvenation of diseased kidneys.

Sources:

News Releases:

Research reprograms future of kidney health, Institute for Molecular Bioscience and Stem Cells Australia, June 14, 2013

Papers:

Direct Transcriptional Reprogramming of Adult Cells to Embryonic Nephron Progenitors, Hendry et al, Jnl Am Soc. Nephrology, June 11, 2013

Reprogramming the kidney: a novel approach for regeneration, Hendry and Little, Kidney International, March 21, 2012

Stem Cell Options for Kidney Disease, Hopkins et al, Jnl of Pathology, October 20, 2008


Resource:

Healthline.com recently launched a free, interactive "Human Body Maps" tool. One of the “maps” is of the kidney, showing and explaining how the kidney works to cleanse the body of waste material carried by the blood. To see a "map" of the kidney, and read how it functions, please follow this link.

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