Our Research II

Ruff Life Charities

rufflife.org

Julie Nickerson

In 2015, The Clarke Family Foundation gave a $9700 grant to Julie Nickerson, CEO & President of Ruff Life Charities and Ruff Life (pet skin carewith aloe vera and apparel). Their mission is helping pets of elderly and/or sick people to receive emotional & physical care, so they can transition into a new home and family.

Julie Nickerson, has been assessing the needs of her customers for the past few years and noting the growing issues related to dog skin allergies. Many of her customers have had complaints that their vet's solution for skin-related allergies was to place the dog on steroids and hope for the best. They all came back with the same results, “it got better and then it got worse”.

In 2014, Julie developed a skin cream she named "Ruff Spots" for dogs (and humans). The créme formula provides relief for itchy skin, hot spots, paws, rashes, bug bites and skin allergies. Her customers have had astonishing results. Soon to follow in 2015, she developed an Aloe Vera Dog Shampoo called "Ruff It Up" which is a perfect companion to "Ruff Spots" and with all natural ingredients. The shampoo formula doesn't have the bubbles that you get with over-the-counter formulas because there are no sulfurs. But, it does the job of getting your dog clean and fresh. It took most of the summer to develop by partnering with a Laboratory in St. Petersburg. And, a lot of research was performed with her dog "Bella" (who had terrible skin allergies) and others. Julie feels that she's finally developed something that she can be proud of and works!

Julie, spent the majority of the grant on the development and introduction of "Ruff It Up" Aloe Shampoo and donations of free products to families, rescue organizations, shelters and rescue dogs in need of treatment before they were adopted.

Julie has a new mission for her charity to grow. She hopes to use the remaining money to help more rescue dogs and families when they are seeking a health treatment and/or dealing with a terminal disease. She hopes to develop other solutions for pet owners who are in need when sick or dying. Julie feels confident that she will find more solutions with Aloe Vera and continue to grow.

Ruff Life Charities

rufflife.org

Julie Nickerson

In July 2013 Ruff Life Charities was officially recognized as a non-profit. Julie Nickerson founded this charity on one basic principle to “pay it forward”. Julie had been shown great kindness by a complete stranger to raise money for a surgery her dog Jack desperately needed. As a result of this act of great kindness Julie has made it her mission to show the same compassion to many others through Ruff Life Charities.

The Clarke Family Foundation has partnered with Ruff Life Charities to distribute “Ruff Spots”, an aloe vera-based cream for dog’s skin ailments, to various animal shelters and dog rescue organizations. Ruff Life Charities is a non-profit organization that seeks to provide safety and health for dogs though both financial and emotional support. With the help of The Clarke Family Foundation, Ruff Life Charities has been given the opportunity to get their product, “Ruff Spots”, out to animals in need.

Ruff Life Charities and The Clarke Family Foundation share common values and goals in the pursuit of using the benefits of the aloe plant for health and wellness. Julie Nickerson, founder of Ruff Life Charities, says, “I think we are on the cusp of the natural health path for our animals and giving a product that shares animals, nature, and healing is a step in a much better direction”.

The Clarke Family Foundation has offered Ruff Life Charities a great deal beyond just grant money. Through their clear mission and experience in establishing their own non-profit over the past 17 years, The Clarke Family Foundation has offered mentorship to advise Ruff Life Charities on how to develop and grow as an organization.

North Texas Medical Associates

Ivan E. Danhof, Ph.D, M.D

Abstract

Diabetes mellitus type 2 (formerly termed non insulin-dependent diabetes mellitus (NIDDM) or adult-onset diabetes) is a metabolic disorder that is characterized by high blood glucose in the context of insulin resistance and relative insulin deficiency. This is in contrast to diabetes mellitus type 1, in which there is an absolute insulin deficiency due to destruction of the islet cells in the pancreas. The classic symptoms are excessive thirst, frequent urination, and constant hunger. Type 2 diabetes makes up about 90% of cases of diabetes with the other 10% due primarily to diabetes mellitus type 1 and gestational diabetes. Obesity is thought to be the primary cause of type 2 diabetes in people who are genetically predisposed to the disease. Type 2 diabetes is initially managed by increasing exercise and dietary modification.

Rates of type 2 diabetes have increased markedly over the last 50 years in parallel with obesity. As of 2010 there were approximately 285 million people with the disease compared to around 30 million in 1985. (SmithS, Heron A: Diabetes and obesity: the twin epidemics. Nature Medicine 12(1):75-80, 2006). Long-term complications from high blood sugar can include heart disease. strokes, diabetic retinopathy where eyesight is affected, kidney failure which may require dialysis, and poor circulation of limbs leading to amputations.

Dextrol

Dietary Supplement for Type II Diabetes Mellitus Test Product

The test product is called Dextrol derived from Dextrose Control. Dextrose is another name for blood sugar (glucose) and the name reflects what the product does, i.e., it regulates the level of blood sugar or glucose in the blood.

Most fluid products derived from Aloe Vera contain about 2,000 milligrams per 100 milliliters of long chains of molecules called methanol precipitable solids. The concentration of Dextrol is 10,000 milligrams per 100 milliliters.

Dosage

The usual dosage is one tablespoon (15 mls) taken before breakfast in the morning and before the evening meal, either alone or with a small amount of water. The dosage may need to be increased in persons who are over-weight to normalize the blood glucose and triglyceride (fat) levels. The final beneficial dosage may require a few days, but can usually be achieved without any undesirable side-effects. Persons on oral hypoglycemic agents may need to reduce the amount of these medications taken daily as the Dextral supplement contributes its share toward normalization of the carbohydrate and lipid metabolic processes. Some persons have been able to stop taking their oral hypoglycemic medications entirely.

How Dextrol Works

• 1. Aloe leaves were dried, pulverized, and extracted with aqueous MeOH (1:1). The extracted material was concentrated, filtered, dialyzed against distilled water, reconstituted and dried. Two kilograms of pulverized leaves yielded 4.9 grams of brown, powdery polysaccharide (yield = 0.245%). The material was found to consist of two separate glycans, termed arborans A and B. The glycans, when tested in normal and alloxanized mice, elicited a marked hypoglycemic effect. The fact that the plasma glucose was decreased in the alloxanized animal model, which is incapable of producing insulin, suggests that other mechanisms (than insulin action) must be considered as being responsible.
• 2. When the energy production in the cells is disturbed, fat is mobilized from adipose tissue storage areas and is used as the fuel for energy production.
• 3. As a result, the Type II Diabetes Mellitus patient shows the following:
• a. An elevated level of blood glucose
• b. An elevated insulin level
• c. An elevated level of blood fats (triglycerides)
• 4. Dextral, over a period of time, corrects these problems.

In 2012, The Clarke Family Foundation continued to partner with the FFB to support cutting edge research on age-related macular degeneration (AMD).

This disease, which is the most common cause of blindness among people 55 years of age and older, affects nearly two million people in the U.S. and some ten million more are at risk for developing this condition. Globally, the numbers affected and at risk are staggering. Despite these grim statistics, the research we support offers real hope to those affected and those at risk that we will overcome this vision-robbing disease. The following are examples of some of the promising AMD research that The Clarke Family Foundation helps a blood test to determine AMD risk.

Factors such as age, smoking, overall health, and inheritance of certain genes are known to affect a person’s risk of developing AMD. Unlike the familiar blood tests to determine an individual’s risk of developing diabetes (blood sugar test) or heart disease (cholesterol), there is no test that can provide an early indication of AMD risk.

Foundation-funded researchers led by Dr. John W. Crabb are making significant progress in rectifying this situation. They have developed blood tests for several indicators of AMD risk that they are now evaluating in hundreds of patients and in people unaffected by AMD to confirm their earlier results and to assess the utility of the tests in a more diverse patient population. Having relatively simple blood tests to determine AMD risk would enable patients and retina specialists to implement timely measures to slow retinal degeneration patient population. Having relatively simple blood tests to determine AMD risk would enable patients and retina specialists to implement timely measures to slow retinal degeneration.

Retinal Inflammation

Enhancing the understanding of retinal inflammation in AMD Postmortem examination of retinas from AMD patients frequently reveals that the retinas have been infiltrated by cells that are more typically observed during the early development of the retina and brain.

These cells are considered to be part of the immune system, but are usually associated with the nervous system, which includes the retina and brain. Corresponding cells in other parts of the body are key players in inflammatory reactions. A team headed by Dr. Joe G. Hollyfield, director of the retinal disease research center at Cole Eye Institute, is investigating the roles that these cells play in AMD. By studying retinas donated by AMD patients, they are attempting to learn if the inflammatory cells originate exclusively in the retina or if they have traveled to the retina from other parts of the body.

The team also is developing laboratory mice with retinal inflammation. As a model of human retinal inflammation, studies in these animals are likely to yield more definitive information about the source of the inflammatory cells, which would be of considerable importance in guiding future research on possible interventions.

A new approach to understanding AMD

The cells of the retina, like those throughout the body are arrayed in a thin matrix called the EMC that helps to support the cells, segregate tissues, and regulate interactions between cells.

Changes in the EMC have been associated with various diseases and there is evidence that mutations in an EMC-related gene called TIMP causes Sorsby Fundus Dystrophy, an early onset retinal degeneration that is somewhat similar to AMD. Dr. Bela Anand-Apte’s research group is investigating whether an imbalance between TIMP proteins and proteins produced by other EMC- related genes might impair the function of certain retina cells, thus triggering some of the early changes associated with AMD. Their studies employ mice that are unable to produce a particular type of TIMP protein, or that produce a form of the protein that is present in patients with Sorsby Fundus Dystrophy. This ground-breaking project could potentially identify novel therapeutic targets leading to possible treatments for AMD.

$70,000

The Clarke Family Foundation continues to partner with the Foundation Fighting Blindness to support cutting edge research on age-related macular degeneration (AMD). This disease, which is the most common cause of blindness among people 55 years of age and older, affects nearly two million people in the U.S. and some ten million more are at risk for developing this condition.

Globally, the numbers affected and at risk are staggering. Despite these grim statistics, the research we support offers real hope to those affected and those at risk that we will overcome this vision-robbing disease. The following are examples of some of the promising AMD reseach that The Clarke Family Foundation helps support.

Researchers at Johns Hopkins University are investigating oxidative injury to the retina, which may contribute to the development of AMD. The team is focusing on three molecules found in the retina whose activities may be increased by oxidative stress. They're determining if oxidative stress alters the location or amount of each protein in the retina. They also found that a certain antioxidant protected the retinal cells of mice from oxidative injury. Similarly, a synthetic form of a molecule present in a traditional Chinese medicine used to treat eye and other ailments transiently preserved retina cell function and appearance, and slowed retinal degeneration. These finding add to the evidence that antioxidants may have therapeutic potential for treating AMD.

Light-sensitive photoreceptors in the retina overlie specialized RPE cells that provide nutrients to and remove wastes from the former. RPE cells rest on a structure known as Bruch's membrane. At Columbia University scientists are studying age-related changes in Bruch's membrane and RPE cells relative to treating macular degeneration with transplanted retinal cells. They note that RPE cell survival declines when grown on Bruch's membranes from older donors or donors with AMD. The investigators are identifying the specific changes in RPE cell function that imperil cell survival. Characterizing both age- and disease-related changes in Bruch's membranes and in RPE cell function will enable them to evaluate treatments that might enhance the survival and growth of transplanted RPE cells. This may lead to treatments that preserve or restore Bruch's membranes, which may limit RPE cell degeneration or promote the survival of transplanted RPE cells.

Like most cells in our bodies those in the retina contain tiny structures that provide the energy they need to function properly Photoreceptors require a lot of energy, so if the supply is compromised the cells stop working, causing them to degenerate and die. Researchers at the Medical University of South Carolina are screening 50,000 compounds to identify those that stimulate energy production by injured retinal cells. They initially evaluate each compound's ability to protect photoreceptors from injury caused by exposure to damaging chemicals. After a series of more rigorous evaluations the most promising are used to treat laboratory mice with retinal degenerative diseases. Already, one compound has been found to increase retinal sensitivity six-fold in mice with retinal disease; another is undergoing further evaluation. Finding ways to protect retina cells from degeneration and death would be an important advance in clinical management of AMD patients and may preserve their vision until sight-restoring interventions like gene therapy or cell transplantation become available.

$70,000

Retinal Disease Research

Your support has aided the Foundation's ongoing commitment to funding research to save and restore sight to over 10 million Americans.

Our grant has helped fund various research projects that may lead to the discovery and development of promising preventions, treatments, and cures for age-related macular degeneration. Such advances will make a tremendous difference not only to those affected by this devastating disease, but also to future generations of their families that also may be at risk for developing age-related macular degenteration.

The Clarke Family Foundation's commitment to the Foundation is a reflection of FFB's solid reputation as a leader in the field of retinal disease research, ability to attract top scientific talent, and ability to identify and fund high quality scientific projects.

• At the Cleveland Clinic, Dr. Joe Hollyfield has discovered a way to produce AMD-like changes in the retinas of lab mice. This breakthrough will help researchers in evaluating treatments in future AMD therapies.
• At the University of Dentistry and Medicine in New Jersey, Dr. Zarbin is developing ways to transplant retinal cells in mice with geographic atrophy, Dry AMD, and learning how to slow the rejection of the implanted cells.
• At the Medical University of South Carolina, Dr. Rohrer is developing a designer protein to block inflammation associated with capillary growth. Her work is pointing to a whole new approach to treating wet AMD.
• Also at the Cleveland Clinic, Dr. Hagstrom has isolated two genes that direct the production of proteins that participate in immune reactions. She has found that these genes most likely are affected by HDL in the blood!
• At Duke University, Dr. Katsan has confirmed that HDL could be related to the risk of developing AMD. His work will help scientists and clinicians be able to make better diagnoses of the disease.