Happy Birthday Original Diva!

Happy Birthday, Diva. Today is My Mothers Birthday. And I would like to celebrate all the things she is to me. My fashion Icon, among other things. I also share some of the life events. That was happening ion the day she was born. She is definitely 76 years old and amazing.

Self Publishing? My 5 Mistakes

Planting Seeds

Planting your own seeds are necessary. When you realize you are not everyone's cup of tea. Waiting for others to water, nurture and feed your seed. May only delay your own Growth toward full Bloom. Until you find y9our people remember. To always fertilize your own ground. Because you are planting seeds.

My take on International Women's Day

Honoring International Women's Day. It was celebrated on March 8th. Which is the same date every year. And is the focal point for women's rights. I highlight the right to express ourselves through writing. Bring to the forefront.

Choosing the side effects and the cure

In choosing to undergo IVIG Infusions. IVIG is Intravenous Immunoglobulin. It is harvested from the plasma of approximately a thousand or more blood donors. I also choose the Possible Side Effects. Headaches, blood pressure changes, nausea, vomiting, fever, fatigue, and chills.

I am Just no Ordinary Girl

I am Just no Ordinary Girl with Myasthenia Gravis. I am #MGStrong. I fly above my circumstances. With the use of my mind. Removing my self mentally from the pain and unhappiness. One way I do this is through music. As I receive my monthly IVIG treatment. I stumbled on music by Leela James. I also express my self creatively. WITH THE USE OF FASHION. NOT LETTING MY OUTSIDE TOTALY REFLECT MY INSIDE.

SOME GREAT THINGS ARE HAPPENING

 BOOK SIGNING

I

Have a little Faith in Me

Have a little Faith in Me. Is what you hear when God answers your prayers. You hear God confirming his blessing.And the test and trials that have brought so much anguish. Is now finally clear to you. It was only a matter of opening your eyes. 

LOTS A SUPPORT FROM FRIENDS

MY FRIENDS SHOWED UP WITH LOADS OF SUPPORT.

 Just completed an Awesome Live interview. With The Logan Power Show​ #exhausted
#AfricanAmericanswithMG

THE SUPPORT OF MY FAMILY FOR MY BOOK

HOW SUPPORT IS SHOWN  BY FAMILY

MY DAUGHTER

ME AND MY MOTHER

All the way from Ludwigshafen Germany. To get his Autographed copy of my Book. It's My Dad.

My Support Group is for Support.

THE SUPPORT OF FRIENDS AND FAMILY.

 Sharing with members of my Local Myasthenia Gravis support group.

\

THE MARKETING OF THE BOOK

SO EXCITED I COMPLETED MY FIRST RADIO INTERVIEW.

MY STORY MY WAY

If you would like to donate today.please give online at www.myasthenia.org

THE STORY BEHIND MY SMILE MIRED IN THE TERROR OF THE INSIDIOUS LURKING DISEASE.

"THE MIRRORED IMAGE OF ME" A PHYSICAL AND SPIRITUAL JOURNEY WITH CHRONIC ILLNESS.

• THIS REAL LIFE TALE PROVIDES INFORMATION TO TAKE YOU THROUGH THE PROCESS OF HEALING 
• DIAGNOSING MYASTHENIA GRAVIS AN AUTOIMMUNE NEUROMUSCULAR DISEASE
  
  
• THE INCLUSION OF GOD IN ALL HEALTH DECISIONS BY WAY OF FAITH.
• THE IMPORTANCE OF FAMILY SUPPORT
• QUALIFIED MEDICAL PERSONNEL GUIDING THE CARE.

TO PURCHASE YOUR COPY OF THIS BOOK TODAY:

http://amzn.to/2nyAQxw

The traumas of self publishing

Self Publishing your first book is very complicated. Finally resolving some printing issues. And the Book will be back into publication soon. Thank you to those who have purchased. I look forward to sharing my journey with you.

The Mirrored Image of Me: A Physical and Spiritual Journey with Chronic Illness

https://www.amazon.com/dp/1978149689/ref=cm_sw_su_dp

The Mirrored Image of Me: A Physical and Spiritual Journey with Chronic Illness Paperback – October 31, 2017

by Lenora Angela Cash (Author)

This Journey started as early as 2008. It was then She became painfully aware of her plummeting overall physical health. Frantically witnessing the then crippling loss of muscle strength. And the devastating plunge into respiratory collapse. Blinded by the warning signs of Myasthenia Gravis Crisis. Mired in terror of the insidious lurking disease. But it would only be the beginning, of the complete tailspin her life was taking. And the miraculous vision set in motion towards her healing. As her Faith in God. Takes her beyond her physical image revealing a Spiritual Being.

Rare Insight: A Physician’s Perspective on Myasthenia Gravis

- As a physician specializing in the treatment of myasthenia gravis (MG), a rare, debilitating neurological disorder, I witness on a daily basis the adversities my patients face. Imagine being a hard-working, active adult—a mom who drove her kids to school every day, who liked to garden and exercise—suddenly faced with a disease that makes it difficult to see, walk or even talk. This is the reality of MG. It steals muscle strength to the point where those living with the disorder can no longer do the things they love. But many fight back, and I am consistently inspired by the strength and perseverance my patients exhibit to overcome these challenges and to not let their disease define them.

June is an important month for the MG community because it marks Myasthenia Gravis Awareness Month—a time when the community can come together, share experiences, and increase awareness for this rare, debilitating disorder. For me, this month provides a key opportunity to leverage my experiences seeing and treating patients with MG to elevate the public’s understanding of the disease and call attention to the special challenges faced by those living with it, including the need for improved diagnostic approaches and new, effective treatment options.Diagnosing and Treating MG

In the United States, a rare disease is one that affects fewer than 200,000 patients.1 While the number of patients affected may be small, the impact of rare diseases on patients, their families, and society is profound.

Like other rare diseases, people living with MG often face a long road to diagnosis since many physicians are unfamiliar with the signs and symptoms of MG. As a result, it may take patients several years before they are accurately diagnosed with MG and can begin treatment.2

Even then, there is no cure for MG, meaning people living with this disease cope with it over the course of their lives. While there are treatment options available that can help manage symptoms in many patients, some patients find that their disease is not adequately controlled with therapies. In fact, as many as 15 percent of MG patients have refractory MG—meaning that despite current treatment, they continue to suffer from debilitating muscle weakness that severely impairs their ability to engage in simple daily activities.3Living with MG

Significant muscle weakness is the hallmark symptom of MG, but no two people experience MG exactly the same way. Basic functions that many take for granted—like chewing, swallowing and walking —become difficult. Other common symptoms include drooping eyelids, blurred vision, slurred speech, and weakness in the arms and legs. Between 15 and 20 percent of MG patients will experience a “myasthenic crisis”—difficulty breathing that can require hospitalization and may be life-threatening.4

While the physicality of this disorder is debilitating, the emotional strain MG patients experience can be just as devastating. Many MG patients feel isolated and worry they are losing their identity. Because of their symptoms, many have had to give up their careers and may feel like a burden to their families both financially and socially. Relationships and friendships can suffer since any day can bring debilitating symptoms that force patients to cancel plans. The ability to travel, or even take a quick trip to the grocery store, may diminish, further compounding feelings of isolation.What’s Next for MG

For MG patients, learning to cope with a lifelong disease can be daunting, so it’s important to focus on cultivating a support system to help overcome challenges. Family, friends, fellow MG patients, and physicians all play a role in helping patients get through difficult times and cheering them on through the great times.

Today, I am optimistic about what the future holds for people living with MG. Unlike some rare diseases, MG is an active area of research, with new clinical trials under way. I am especially hopeful that new research may benefit patients with refractory MG—who continue to suffer without adequate treatment options.

My hope for the MG community is that the scientific advances over the past 30 years—and particularly today’s research—will lead to a better quality of life for patients with this disorder. Please join me today, and every day during the month of June, in celebrating Myasthenia Gravis Awareness Month and spreading the word about this rare disease.

For more information about MG, including education, support, and resources for people living with MG and their families, visit the Myasthenia Gravis Foundation of America website at www.myasthenia.org.

James F. Howard Jr., M.D., is a Distinguished Professor of Neuromuscular Disease and Professor of Neurology & Medicine at the University of North Carolina at Chapel Hill School of Medicine.

Study explores two new antibodies believed to cause myasthenia gravis

A study of patients from across the nation with myasthenia gravis is helping determine the incidence of two new antibodies believed to cause the disease, and whether these patients need different treatment strategies.
Researchers are examining the blood of patients from 22 centers specializing in the treatment of mysathenia gravis, the most common communication problem between brain and muscle, to determine what percentage of patients have one or both of the new antibodies and to characterize their clinical symptoms, said Dr. Lin Mei, chairman of the Department of Neuroscience and Regenerative Medicine at the Medical College of Georgia at Augusta University.
About 10 percent of patients have no evidence of two other antibodies already known to cause the disease, although they have classic clinical symptoms such as drooping eyelids, generalized muscle weakness and problems breathing, and electrical studies of their brain-muscle communication indicate a problem.
These so-called double-negative patients are the target for the new study, which is testing their blood for antibodies to two proteins, agrin and LRP4, that Mei's lab has shown are also critical to healthy brain-muscle communication.
Antibodies to agrin and LRP4 have already been found in some patients, and LPR4 antibodies cause myasthenia gravis-like symptoms when injected into lab animals.
"We want to know whether these patients have any unique symptoms so we can diagnose them early then confirm their diagnosis with a blood test," said Mei, Georgia Research Alliance Eminent Scholar in Neuroscience and principal investigator on the new $3 million National Instiutes of Health grant. He notes that several companies already are interested in developing agrin and LRP4 antibody tests.
"These patients may very well have slightly different symptoms because of where these antibodies are acting," said Dr. Michael H. Rivner, MCG neurologist specializing in neuromuscular disease who directs the Electrodiagnostic Medicine Laboratory at Augusta University Medical Center and follows about 250 patients with myasthenia gravis. "Obviously if you get a blood test that shows something, you feel much better about the diagnosis," added Rivner, co-investigator on the new grant.
Two antibodies already considered causative include one for the receptor for acetylcholine, a chemical released by neurons, which activates muscle cell receptors. The other is an antibody to MuSK, an enzyme that supports the clustering of these receptors on the surface of muscle cells.
Mei's lab found a link between agrin and LRP4 in 2008, reported LRP4 antibodies as a new cause of myasthenia gravis in 2013 and that agrin antibodies were associated with the disease the next year. Those findings have already filled in some important knowledge blanks in how the brain and muscle connect during development and continue to interact lifelong.
During development, agrin is released by motor neurons to direct construction of the nerve-muscle contact, or synapse, and MuSK, an enzyme on the muscle cell surface, enables a clustering of receptors, which are activated by acetylcholine. While agrin and MuSK work together, they don't directly communicate, which is where LRP4 comes in. Mei's lab has shown that agrin communicates with LRP4 on the muscle cell surface, then recruits MuSK to join the conversation. LRP4 and MuSK become major components of the receptor needed for the muscle cell to receive the message agrin is sending throughout life.
Mei and his colleagues first identified the antibodies to agrin and LRP4 in the blood of patients who were double-negative. They went back to the laboratory and showed the antibodies to LRP4 cause myasthenia gravis symptoms in animal models. The new grant has them looking at animal models again to learn more about how LRP4 and agrin antibodies cause disease. This includes removing the two antibodies from patients then giving those to lab animals to see if both cause disease. They theorize the antibodies diminish signaling between agrin, LRP4 and MuSK and/or stimulate an immune attack against the neuromuscular junction.

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Nearly 900 of the 4,500 patients with myasthenia gravis being followed at centers across the nation, such as Augusta University Medical Center, are double-negative. Over the next five years, more than 600 of those patients will have their blood tested for the two new antibodies. Similar studies will be done on the blood of healthy individuals as well as patients with other neurological problems such as Alzheimer's and stroke, both to ensure that the antibodies' presence is not random and to begin to collect evidence about whether they also contribute to other maladies, Mei said.
Thorough physical exams will look for any clinical distinctions in patients who test positive for the new antibodies. Research also will document their response to treatment.
Study participants will have other specialized testing, including single fiber electromyography, which looks at the electrical response of a single muscle fiber instead of the group of fibers controlled by a single motor neuron. Patients typically get this type of detailed analysis to help establish a diagnosis.
"Every time there is an action potential in this motor neuron, you should see a response occur within a certain amount of time. But if you have a defective neuromuscular junction, it may take longer for it to fire, or it won't happen at all," Rivner said, noting there tends to be plenty of neurotransmitter but too few receptors for a proper response.
When the MCG researchers immunize mice, rabbits and other animals to induce LRP4 antibodies, the animals show classic signs of myasthenia gravis and tend to be less active, although they can survive for long periods, Mei said. When they examine the neuromuscular junction, they can see its disentegration. An EMG shows the poor communication, which Mei likens to a personal relationship with no communication. "Things don't go well," he said.
Since word has spread of the previous studies identifying the new antibodies, the medical school has gotten numerous requests for testing of double-negative patients. Other centers have started doing limited testing, and early reports of the incidence of the newest antibodies vary dramatically in patients who are double-negative, another reason to consistenly look at incidence in a large number of patients, Mei said.
Whatever the cause, disease symptoms tend to respond well to therapy, which typically includes chronic use of drugs that suppress the immune response, Rivner said. However, immunosuppressive drugs carry significant risk, including infection, cancer and weight gain. "We would definitely like to have better treatments than we have now," Rivner said.
Removal of the thymus, a sort of classroom where directors of the immune response, called T cells, learn early what to attack and what to ignore, is another common therapy for myasthenia gravis. While the gland usually atrophies in adults, patients with myasthenia gravis tend to have enlarged glands. Rivner is part of another NIH-funded study to determine whether gland removal really benefits patients. Other therapies include a plasma exchange for acutely ill patients.

Source:

Medical College of Georgia at Augusta University

Myasthenia Gravis Overview, Types, Incidence and Prevalence October 13, 2015 Lussy williams

Overview of Myasthenia Gravis

Myasthenia gravis (MG) is a chronic autoimmune disorder that results in progressive skeletal muscle weakness. Skeletal muscles are primarily muscle fibers that contain bands or striations (striated muscles) that are connected to bone. MG causes rapid fatigue (fatigability) and loss of strength upon exertion that improves after rest.

In early stages, myasthenia gravis primarily affects muscles that control eye movement (extraocular muscles) and those that control facial expression, chewing, and swallowing. If untreated, the disorder may affect muscles that control breathing (respiration), causing acute respiratory failure.

Types of Myasthenia Gravis

pr> Myasthenia gravis can be classified according to which skeletal muscles are affected. Within a year of onset, approximately 85–90 percent of patients develop generalized myasthenia gravis, which is characterized by weakness in the trunk, arms, and legs.

About 10–15 percent of patients have weakness only in muscles that control eye movement. This type is called ocular myasthenia gravis.

Other types of MG include congenital, which is an inherited condition caused by genetic defect, and transient neonatal, which occurs in infants born to mothers who have MG. Congenital MG develops at or shortly after birth and causes generalized symptoms.

Transient neonatal MG is a temporary condition that develops in 10–20 percent of infants born to mothers who have MG. Transient neonatal MG is caused by circulation of the mother’s antibodies through the placenta and it lasts as long as the mother’s antibodies remain in the infant (usually a few weeks after birth).

Incidence and Prevalence of Myasthenia Gravis

Myasthenia gravis affects approximately 2 out of every 100,000 people and can occur at any age. It is most common in women between the ages of 18 and 25. In men, the condition usually develops between 60 and 80 years of age.

 

Why Myasthenia Gravis An Autoimmune Disorder?

Artem is a doctor of veterinary medicine and has taught science and medicine at the college level.

This lesson will go over a condition called myasthenia gravis. We’ll talk about why it occurs, how your immune system is involved, how it can be treated, if it’s curable, and what typical signs it produces in a person.October 15, 2015 Smith

 

Autoimmune Disease

Most every one of us has played a game called ‘monkey in the middle’, or something along those lines. It’s basically where at least one person stands in between at least two other people who throw or kick an object like a ball to one another. The role of the monkey in the middle is to block the ball from getting through to the other person. Typically, as was the case when I was the monkey in the middle, the person in the middle has a hard time intercepting the ball.

But in some cases of autoimmune diseases, diseases where your own body attacks itself, the monkey in the middle is devastatingly effective. So effective, in fact, that it causes serious problems, as this lesson will address.

What is Myasthenia Gravis?

The terrible game that our body plays with us isn’t called monkey in the middle, it’s called myasthenia gravis. This is an incurable autoimmune disease that leads a person to develop severe muscle weakness and fatigue.

Although, as with many diseases, myasthenia gravis can occur at almost any age, it seems to affect more women under 40 and more men over 60 years of age, and in the United States affects about 20 individuals for every 100,000 members of the population.

Some of the most famous people in the world have suffered from this terrible disease, such as Aristotle Onassis, the billionaire Greek shipping magnate who married Jackie Kennedy after JFK’s assassination.

Why Does Myasthenia Gravis Occur?

Scientists are still working out the details of why myasthenia gravis may occur. We know that everything from genetics to immune reactions to drugs may increase the likelihood of developing this condition. Some researchers also believe the thymus , an organ located underneath your breastbone that is responsible for the proper development of the immune system, may play a role in the aberrations that occur in this disease. It has been noted that certain individuals with myasthenia gravis have a thymoma, or a tumor of the thymus.

What we do understand a bit better is the end result of most cases of myasthenia gravis. In this condition, your own body produces little proteins called autoantibodies, which are antibodies that target an individual’s own body, organs, cells, and receptors for destruction or inactivation.

Normally, antibodies are supposed to target foreign invaders such as bacteria and viruses for destruction or inactivation. But in an autoimmune condition such as myasthenia gravis, the antibodies become directed against auto, or self.

Specifically, these autoantibodies attach themselves to the receptors on the skeletal muscles of your body; these are the muscles responsible for locomotion. By doing so, the antibodies prohibit the receptors on the muscles from receiving a specific signal or destroy the receptors outright. Namely, this signal comes from nerves innervating the skeletal muscles. These nerves release a neurotransmitter that activates muscles of locomotion, called acetylcholine.

Under normal conditions, the nerves release this acetylcholine and it lands on its receptor on the muscle the nerve innervates. Once it lands on the receptor on this muscle, the muscle gets all excited, contracts, and allows you to move. The release of acetylcholine occurs at the neuromuscular junction, the place where nerves meet the muscles they innervate. The space between the nerve ending and the muscle it controls is known as the synaptic cleft.

That’s what happens normally. However, in people with myasthenia gravis the autoantibodies bind to the receptors on the muscle cells and thereby destroy or inactivate them.

You can liken the autoantibodies to our monkey in the middle, the nerve and muscle to our two players, the space between the two players as the synaptic cleft, the acetylcholine to our ball, and the receptors on the muscle cells to the hands of our player called ‘the muscle.’

The nerve player wants to pass the ball to the muscle player, but the monkey latches onto the hands of the muscle player and blocks the muscle player from ever catching the ball. If the ball can’t pass from one end to the other and can’t land in the muscle’s hands because those hands are blocked by the monkey, then the muscle player cannot become all excited about catching the ball, becomes depressed instead, and refuses to move because the game is no fun anymore.

Clinical Signs, Symptoms, and Diagnostics

Since the muscles are no longer excited to move, you shouldn’t be shocked by the typical signs and symptoms associated with myasthenia gravis, which means ‘grave muscle weakness’ through its ancient Latin and Greek roots. These signs include:

• Difficulty walking, eating, speaking, smiling, and swallowing
• Droopy eyelids and double vision
• In serious cases, respiratory failure, when the muscles of respiration can no longer work.

Genetic Research Reveals Possible New Targets For Treatment Of Myasthenia Gravis October 15, 2015 Smith

NEW YORK – A new genome-wide association study suggests that immunomodulating drugs already approved by the U.S. Food and Drug Administration (FDA) could benefit patients with myasthenia gravis.

Dr. Bryan Traynor, chief of the Neuromuscular Diseases Research Section at the National Institutes of Health in Bethesda, Maryland, and colleagues, found three different disease-associated loci in myasthenia gravis patients. One locus was at CTLA4, and the FDA has approved two CTLA4-targeting treatments, abatacept and belatacept, for treating rheumatoid arthritis and renal transplant patients, respectively.

The findings also showed two distinct, but overlapping, disease-associated loci for the early- and late-onset forms of the illness
 

“The discovery of a genetic locus is always an exciting thing, but often times it can take 10 to 15 years between the discovery of a particular locus and a first-in-humans clinical trial,” Dr. Traynor told Reuters Health in a telephone interview. The fact that drugs targeting CTLA4 are already FDA approved should accelerate that timeline, he added.

In their study, published online February 2 in JAMA Neurology, Dr. Traynor and his colleagues looked at DNA from more than 1,000 white, North American patients with acetylcholine-receptor antibody positive myasthenia gravis and nearly 2,000 controls.

They investigated associations between more than 8 million variants and myasthenia gravis risk. Significant association signals were found at CTLA4 (odds ratio, 1.37); HLA-DQA1 (OR, 2.31) and TNFRSF11A (OR, 1.31).

The CTLA4 and HLA-DQA1 associations were replicated in a cohort of 423 myasthenia gravis patients and 467 controls from Italy.

The analysis also confirmed past observations that myasthenia gravis strikes younger patients, who are usually female, as well as patients 60 and older who are usually male.

We were able to find different genetic loci that drive genetic susceptibility in each case,” Dr. Traynor said. “We genetically proved that they are two fundamentally different conditions, but overlapping conditions as well.”

The CTLA4 associations were seen in both early- and late-onset patients, the researcher noted. It’s likely, he added, that clinical trials testing CTLA4-targeting drugs in myasthenia gravis would enroll all patients with the illness, regardless of their genotype.

Even in patients who don’t have the CTLA4 variants he and his colleagues identified, Dr. Traynor noted, “it’s possible that in the other patients there are other variants in that region that are altering CTLA4 function, but we are not powered to pick it up.”

While effective therapy for myasthenia gravis is available, the researcher added, some patients with the disease do wind up having significant problems. “I think there is considerable room to grow new treatments,” Dr. Traynor said.

Dr. Robert Lisak of Wayne State University School of Medicine in Detroit co-authored an editorial accompanying the study.

“As in other complex immune-mediated disorders, there is an important influence of minor changes in multiple genes, likely interacting with the environment and with one another and their protein products, in the pathogenesis of myasthenia gravis,” Dr. Lisak told Reuters Health by email. “And in an autoimmune disease it is not surprising that the minor changes occur in genes for proteins that are critical in the immune response.”

“Identifying changes in genes in patients with different types of myasthenia gravis has the potential to help us understand which molecules and pathways in the immune system are the most important in development of disease,” he added. “In theory that might help in development of more-focused treatments for patients with myasthenia gravis. Only time will tell if this ultimately happens.”