Parkinson’s Disease

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Parkinson’s disease is a slow but relentlessly progressive neuron-degenerative disorder. The clinical decline Viz: bradykinesia, tremor, rigidity and gait dysfunctions, reflects ongoing nigrostriatal dopaminergic degeneration. The progressive degeneration ultimately results in severe motor, mental, and functional disability vendo viagra. You can fight and win Parkinson problem with Ayurvedic strategy of Vata Balancing. Parkin Oil and Herbs are effective and safe treatment to balance the Apana and Prana Vata. Read more…http://www.raipurnews.com/dr-mukesh-d-jain/parkinsons-ayurvedic-treatment

Ayurveda in CG

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Quality health care and low cost gives Indian Ayurveda a competitive advantage in the medical tourism industry.

Quality health care and low cost gives Indian Ayurveda  a competitive advantage in the medical tourism industry.   Raipur Nov 27, 2012 High quality health care and low cost gives Indian Ayurveda a competitive advantage in the medical tourism industry. People with uncontrolled medical neuro-muscular conditions such as Muscular dystrophy, myopathies, Multiple sclerosis, Myasthenia gravis, Parkinson’s disease and Autism are exploring possible ayurvedic treatment now in Chhattisgarh. Sergei 13 year, Damir 14 year and Dima – 8 year from Moscow are suffering from severe DMD and getting their simple and safe ayurvedic treatment in Sanjivani Wellness Centre in Bhilai Chhattisgarh. “DMD is not curable but can be treated to support patient condition” said Dr Mukesh D Jain, Program Director on NMD of Ayush Samiti. Muscular dystrophy is one of the most difficult disorders to treat. Conventional methods of coping with the disease include exercise and drugs that slow down or eliminate muscle wasting like anabolic steroids and supplementation. The current treatment of muscular dystrophies has evolved from electrical simulation to Gene Therapy and Cell Therapy. The goal of the treatment is (i) to correct the genetic defect, (ii) to restore functional expression of dystrophin, (iii) to slow disease progression, and (iv) to improve the quality of life of MD patients.  Read Full Raipur Story » http://www.raipurnews.com/chhattisgarh



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Autism is a complex dis-ability that affects the perception, processing and functioning of brain.  Autistic children have difficulties in verbal & non-verbal communication, and often have delayed language development. They also have mental retardation. About 10-20% autistic children begin to improve between 4 to 6 years of age and eventually attend an ordinary school and obtain work. But 10-20% can live at home but need to attend a special school or training centre and cannot work. Autism is a neuro-biological disorder affecting the neuron-anatomy & neuro-chemistry of the brain. CT scans have isolated a subgroup of autistic children with enlarged ventricles and MRI has identified a subgroup of autistic adults with hypoplasia of the cerebellar vernius. Some harmful substances ingested during pregnancy also have been associated with a risk of autism. An accurate diagnosis must be based on observation of the child’s communication, behaviour & developmental levels. The characteristic 4 behaviour of a child are suggestive of autism that needs further assessment:-

  • Does not gesture (point, wave, grasp) by 12 months
  • Does not say single words by 16months
  • Does not say two-word phrases on his/her own by 24 months
  • Has any loss of any language or social skill at any age

Autism can be diagnosed by following criteria:-Watch Full Movie Online Streaming Online and Download

(1)     Impairment in the social interactions and non-verbal behaviors such as eye-to-eye contact, and facial expression.

(2)      Lack of spontaneous seeking to share enjoyment, interests, or achievements with other people.

(3)     Persistent per-occupation and lack of emotional reciprocity.

(4)     Delay in the development of spoken language or repetitive use of language or idiosyncratic language.

(5)     stereotyped and repetitive motor mannerisms (e.g., hand or finger flapping or twisting, or body movements)

Treatments: Autism usually requires lifelong multidimensional approach of combined treatments such Behavior modification, Communication therapy, Dietary modifications and medicines. Other physical therapies such as ayurvedic massage, Panch karma procedures are used to help child control body movement.



Behavior modification Positive reinforcement to teach self care skills: Speech therapy (also sign language teaching) and structured class room training. (”special schooling”).

  • Development of regular routine with minimum or no changes
  • Behavioral techniques to encourage social & interpersonal interaction.



Medication Chemical or natural medicines may be used to treat various symptoms of autism e.g. attention difficulties, anxiety & can also be used to treat that may accompany the disorder (eg-epilepsy). Depression, obsessive-compulsive behavior & anxiety may be treated using antidepressants or Medhya Rasayana group of ayurvedic herbs. These medicines often reduce the frequency & intensity of repetitive behavior & irritability, tantrums & aggression & improve eye contact & responsiveness.


Communication therapy: this therapy is used to treat autistic patients who are unable to communicate verbally or to initiate language development. In young children with the disorder, speech therapy may be used to help the patients gain the ability to speak.

Dietary modification
Changing the diet or adding dietary supplements may improve digestion and eliminate food intolerances or allergies which may contribute to behavioural problems in autistic patients. Vitamin B, magnesium & cod liver oil supplements (contain A&D) may improve behaviour, eye contact, attention span & learning in autistic patients. Vitamin C improves depression.


Differential diagnosis:

    1. Child Schizophrenia: In infantile autism in contrast to children schizophrenia there is little or no period of normal development, mental retardation & epilepsy are common, have symptoms suggestive of negative symptoms of schizophrenia & there are no hallucination or delusions.
    2. Reactive attachment disorder of infancy: This disorder is characterized by a failure to establish normal attachment to a caregiver or an indiscriminate sociability. This is the result of psychosocial deprivation or abuse. These children have potentials for normal imaginative play & normal responses to the environment. There are no motor abnormalities & they are not mentally retarded.
    3. Elective mutism: There is absence of speech in some but not necessarily all environments. These children communicate via gesture, nodding or short monosyllabic utterances.
  • Others: The other disorders need to be differentiated are Tourette’s disorder, habit disorder’ obsessive compulsive disorder, attention deficit, specific developmental (language) disorder, acquired aphasia with convulsions, schizoid personality, neuron-degenerative diseases & Mental retardation.






DMD Treatment Options

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Duchenne muscular dystrophy is a genetic disorder that causes muscles to gradually weaken over time. A person with DMD will eventually lose the ability to walk and will have problems with breathing and his or her heart.  Children who have DMD make no or low amounts of a protein called dystrophin. Dystrophin acts like glue, holding muscles together by keeping the structure of muscle cells. Without it, muscles weaken over time and become unable to work properly. A simple and inexpensive blood test called creatine kinase (CK) can help make the diagnosis. If the test results are positive, you should confirm it by DNA finger printing and muscle biopsy.

Children with DMD  might:   

(i) Not be able to walk by 15 months of age

(ii) Walk with the legs apart, on the toes, or walk with the belly pointed out (also called Lordosis), or both

(iii) Fall frequently

(iv) Need help getting up from the floor with their hands in order to stand (also called Gowers manoeuvre)

(v) Have difficulty with motor skills such as running, hopping, jumping, or climbing stairs

(vi) Have larger calves than other children of the same size or age (also called pseudo-hypertrophy)

(vii) Frequently complain of having tired legs and have behavior and learning difficulties.

Treatment option: There is no 100% specific treatments that can reverse the progression of deterioration. Treatment is aimed at keeping the patient independent for as long as possible and preventing complications that result from weakness, reduced mobility, and cardiac and respiratory difficulties. Treatment may involve a combination of approaches, including physical therapy, drug therapy, and surgery. Assisted ventilation is often needed to treat respiratory muscle weakness. Obese patients with Duchenne MD may develop obstructive sleep apnea and require night-time ventilation. Patients on a ventilator may also require the use of a gastric feeding tube.

Synthetic Steroids may be prescribed to delay muscle degeneration. Steroids such as prednisone can slow the rate of muscle deterioration in Duchenne MD and help children retain strength and prolong independent walking by as much as several years. However, these medicines have side effects such as weight gain and bone fragility that can be especially troubling in children.

Natural Ayurvedic Drugs that may help delay the loss of muscle mass: Herbal preparations such as Mamsagni, Sukumar Guggal and Fulvia, either alone or in combination, are being studied to determine if they are able to increase strength and muscle mass. These nutritional supplements have been found to protect cell membranes from oxidative injury. It may also be essential for proper mitochondrial function and cellular energy production. Scientists are investigating the safety and efficacy of Ayurvedic ingredients when added to steroids as a treatment for boys with Duchenne MD.

Enhancing natural muscle repair mechanisms: Skeletal muscle has the ability to repair itself, but its regeneration and repair mechanisms are progressively depleted during the course of several types of MD. Understanding the repair mechanisms may provide new therapies to slow, and possibly stabilize, muscle degeneration. New studies are identifying points in the regeneration-repair pathways that can be targeted by either drug or gene therapy for muscle rescue. For example, researchers have shown that chronic blockade of the muscle growth inhibitor myostatin can enhance muscle repair in animal models of MD. Other study has found that increased expression of a muscle repair protein, dysferlin, can help offset muscle damage in dystrophic animals. And the strategy of enhancing natural muscle repair mechanisms with insulin-like growth factor 2 is being used in a clinical trial for myotonic dystrophy.

Cell-based therapy: The muscle cells of MD patients often lack a critical protein, such as dystrophin in Duchenne MD or sarcoglycan in the limb-girdle MDs. Scientists are exploring the possibility that the missing protein can be replaced by introducing muscle stem cells capable of making the missing protein in new muscle cells. Such new cells would be protected from the progressive degeneration characteristic of MD and potentially restore muscle function in affected persons.

The natural regenerative capacity of muscle provides possibilities for treatment of MD. Attempts to take muscle precursor cells from fathers of Duchenne patients and implant them into patients’ muscles originally failed. However, more recent studies have focused on using stem cells to try to restore missing proteins in MD patients.

Gene replacement therapy: A true cure for Duchenne, congenital, and limb-girdle MD might be obtained if the defective dystrophin gene could be replaced by a functional gene. The large size of the dystrophin gene and the early inability of gene-delivery systems (viral vectors) to target muscle have been substantive barriers to development of gene therapy for Duchenne MD.

Over the last several years, a mini-dystrophin gene (one that is small enough for a viral carrier to deliver it) has proven successful in animal models of Duchenne MD. Viral delivery systems are much better today. As a result, researchers have made important progress in delivering a dystrophin mini-gene to muscles of a mouse model of Duchenne MD.  Scientists also are using high-throughput screening (HTS) to find drugs that increase the muscle production of the protein utrophin, which is similar to dystrophin and can help compensate for its loss.

Genetic modification therapy to bypass inherited mutations: Approximately 80 percent of Duchenne MD patients have mutations in the dystrophin gene that causes it to function improperly and stop producing the dystrophin protein. By manipulating the protein synthesis process, production of a gene that “reads through” the genetic mutation that stops production can result in functional dystrophin.

Physical Therapy, Yoga & Diet Support:  These therapies can help prevent deformities, improve movement, and keep muscles as flexible and strong as possible. Options include passive stretching, postural correction, and exercise. An Ayurvedic program is developed to meet the individual patient’s needs. Therapy should begin as soon as possible following diagnosis, before there is joint or muscle tightness.

Passive stretching can increase joint flexibility and prevent contractures that restrict movement and cause loss of function. Passive stretching on children may be easier following a ayurvedic massage (TMP procedure), warm bath or shower.

Regular, moderate Yogic exercise can help MD patients maintain range of motion and muscle strength, prevent muscle atrophy, and delay the development of contractures. Persons with a weakened diaphragm can learn deep breathing exercises that are designed to keep the lungs fully expanded.

Dietary changes: Proper nutrition is essential, for overall health. Limited mobility or inactivity resulting from muscle weakness can contribute to obesity, dehydration, and constipation. A high-fiber, high-protein, low-calorie diet combined with recommended fluid intake may help. MD patients with swallowing or breathing disorders and those persons who have lost the ability to walk independently should be monitored for signs of malnutrition.

Support aids such as wheelchairs, splints and braces, other appliances, and overhead bed bars (trapezes) can help maintain mobility. Braces are used to help stretch muscles and provide support while keeping the patient ambulatory. Spinal supports can help delay scoliosis. Repeated low-frequency bursts of electrical stimulation to the thigh muscles can produce a slight increase in strength in boys with Duchenne MD.

If your child is diagnosed with DMD, there are many groups that can help you, including the Parent Project Muscular Dystrophy: http://www.parentprojectmd.org  and the Muscular Dystrophy Association: http://www.mda.org/ . For Ayurvedic treatment you can contact the Ayush Muscular Dystrophy Society (India) http://ayush-samiti.co.in






Cancer & Ayurveda

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Autism Treatment

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Agreement Signed on Ayurvedic Research

A multidimensional Autism project with an early intervention, teaching and behavior modification program for young children with autism and their families was signed jointly in Budapest by Dr Mukesh D Jain Director of Ayush Samiti, Bhilai, India, Prof Ivan Szalkai, Director of Oriental Medical Centre, and Ms Tivadar Radvanyine, Director of BHRG Foundation, Hungary. The agreement will facilitate several clinical & educational and research oriented activities. This includes: – (i) Information and counseling to patients and family members. (ii) Evaluation and analysis of the safe and efficacy of program, (iii) and Development of evidence-based treatment using Medhya Ayurvedic herbs and therapies.Review Android Smartphone

Read more:http://www.raipurnews.com/agreement-signed-autism-treatment

DMD & Exon Skipping

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The dystrophin protein is essential for the function of muscles. Muscle fibers stretch and contract with great force when a muscle is used. Dystrophin acts as a spring and a shock absorber between the muscle fiber surface and its internal motor made up of a protein called actin. In DMD, due to a mutation in the dystrophin gene, dystrophin is missing and as the actin motor causes the muscle to contract it damages the muscle 0 fiber’s surface membrane because the force-absorbing protection of dystrophin is missing. In small children with DMD, the force of muscle contraction is weak, so there is not much damage and repair can stay ahead of muscle damage. As children with DMD grow, their muscle strength increases and, eventually, muscle damage cannot be adequately repaired. Permanent muscle damage becomes more and more widespread and eventually becomes life threatening as the vital muscles for breathing (diaphragm) and the blood circulation (heart) are affected. Duchenne Muscular Dystrophy (DMD) is one of the most common fatal genetic disorders to affect children around the world.

The gene that encodes the information for the production of the dystrophin protein is the largest gene in the human body, containing 2.4 million base pairs of genetic information. DMD is caused by mutation of the dystrophin gene that prevents the production of dystrophin protein. The most common defects in the dystrophin gene leading to DMD are deletions, or missing pieces of DNA needed to properly direct the production of dystrophin. More specifically, the genetic mutations leading to DMD arise when a fragment of DNA is lost at a point in the gene that severely disrupts correct translation of the genetic information needed to direct dystrophin production.

Sometimes there is a less severe mutation that causes the loss of a small fragment of DNA at a point in the gene where the remaining information is not ruined and the cell has sufficient information to make a truncated, but still functional, form of dystrophin. In this case, although the dystrophin protein is smaller than dystrophin produced from the instructions of a whole gene, it can still perform some of the shock-absorbing tasks of dystrophin. Mutations leading to a shorter but functional dystrophin protein are seen in the milder, Becker form, of muscular dystrophy (BMD).Watch Full Movie Online Streaming Online and Download

Exon Skipping

Several years ago scientists identified a way to potentially restore the functionality of a gene containing a mutation resulting in DMD by a process called exon skipping. Through exon skipping it may be possible to realign the translation of genetic information in the dystrophin gene and promote synthesis of a shortened, but functional, version of the protein. We are developing exon skipping drug candidates with this potential. If these drugs are successful the course of DMD could be slowed down and the severity of the muscle disease could be reduced.

The relationship between exon skipping and the DMD deletions is shown below for some of the more frequent deletions in DMD. The deletions shown in the table are such that skipping of a single exon could be expected to repair the RNA and benefit the patients. There are also deletions  (not shown) that require skipping of more than one exon and therefore need more than one drug to be beneficial.

Exon skipped Potentially Repairable Deletions
51 45-50, 47-50, 48-50, 49-50, 50, 52
50 51, 51-53, 51-55
45 12-44, 18-44, 44, 46-47, 46-48, 46-49, 46-51, 46-53, 46-55
53 10-52, 45-52, 47-52, 48-52, 49-52, 50-52, 52
44 10-43, 19-43, 30-43, 35-43, 36-43, 40-43, 42-43, 45, 45-54
8 3-7, 4-7, 5-7, 6-7
55 47-54, 48-54, 49-54, 50-54, 52-54, 54, 56, 56-62
7 2-6, 8-11, 8-17, 8-43, 8-45
52 53, 53-55, 53-57, 53-59, 53-60
17 12-16, 18, 18-20, 18-22, 18-25, 18-27, 18-29, 18-33, 18-36, 18-38, 18-41, 18-44


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