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Author Topic: Musclular distrophy/HIV effect by same protein same gene Vitamins help  (Read 3265 times)

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Offline bimazek

  • Member
  • Posts: 781
heck all diseases are related in a way, they all happen inside the body, the body has genes that produce proteins,  i recently did a search for new hiv articles that came out only in 2007 in peer reviewed science..

isnt this interesting the exact protein that hiv needs and uses and the gene that produce it,  the protein  called emerin, if blocked or knocked out stops hiv entering nucleus,  we know that hiv can damage muscle tissue...
this  exact protein that hiv needs and uses and the gene that produce it,  the protein  called emerin... is key in Musclular distrophy also... so hiv research may help solve this and this may be a way to stop wasting

SO THEN I ASK MYSELF, WELL Musclular distrophy has been around alot longer, I had a carnival fundraiser for Musclular distrophy in 1973, 33 years ago, so, with all the ideas about vitamins and HIV and i discover
Follow an anti-inflammatory diet is advise for Mus. Distrophy and this new

molecules that might inhibit the ability of HIV to interact with emerin might provide a new pathway to fighting HIV

 May 08, 2006
Protein Permits HIV Invasion
By David Biello
   Science Image: HIV, human immunodeficiency virus
   
The human immunodeficiency virus (HIV) that causes AIDS prospers by hijacking our immune system cells and forcing them to manufacture more copies of itself rather than tend to their infection-fighting duties. But in order to hijack these T cells or macrophages HIV must first penetrate their innermost walls. New research shows that HIV requires a particular protein in the envelope surrounding a macrophage's nucleus in order to slip in and reconfigure the cell's DNA.

Mario Stevenson and Jean-Marc Jacque of the University of Massachusetts first studied macrophages--literally big eaters, which consume infectious agents and other detritus in the body--because they rarely divide. Therefore, the walls of this cell could be studied without having to inhibit it from its natural processes. The scientists knocked out a protein--emerin--and unleashed HIV (seen in a schematic cross-section above) on the cells to see what would happen.In the absence of emerin, HIV found it difficult to enter its prospective host's nucleus and nearly impossible to effectively insert itself into the nuclear DNA, or chromatin.

Without such insertion, the HIV failed to replicate and thus failed to do much of its damaging work. "Our study provides evidence that [HIV DNA], on entering the nucleus, must interact with emerin to contact chromatin," the researchers write in a paper published online yesterday by Nature.
Study of pharmaceuticals or other molecules that might inhibit the ability of HIV to interact with emerin might provide a new pathway to fighting the scourge, the scientists argue. They also note that Emery-Dreifuss muscular dystrophy results from mutations in the gene that codes for emerin. Sufferers of that disease might reveal compelling evidence of HIV-resistance.
\

FROM THE MUSCULAR Dystrophy websearch on vitamins that help treat it...

Nutrition

Follow an anti-inflammatory diet, including organic whole foods such as whole grains, vegetables, fruit, legumes, sea vegetables, and essential fatty acids (nuts, seeds, and cold-water fish). Avoid refined foods, saturated fats (dairy and other animal products), and all known food allergens.

Potentially beneficial nutrient supplements include the following.

    * Essential fatty acids (for example, flax, borage, evening primrose, cod liver) 1,000 to 1,500 mg two to three times per day
    * Vitamin E (400 to 800 IU per day), selenium (100 to 200 mcg per day), coenzyme Q10 (100 mg one to three times per day)
    * L-carnitine (320 mg one to two times per day)
    * B-complex vitamins, especially B12 (1,000 mcg per day) and B6 (100 mg per day), and minerals, such as calcium (1,000 mg per day), magnesium (500 mg per day), and potassium (100 mg per day)
    * N-acetyl cysteine (500 mg twice a day)
    * Creatine (5 to 7 g per day)






AND GOD LOOK AT THIS.... I JUST FOUND AFTER AN HOUR OF SEARCHING

Sunshine exposure is an important source of vitamin D.
Children and young people with muscular dystrophy may
HAVE spend less time exposed to sunshine than their peers. Parents
should be encouraged to ensure that the children
have exposure to sunlight and diets rich in calcium and
vitamin D  ...
UK, January 16th 2004.
muscular dystrophy; its prevalence, treatment and prevention



what this says is that, to me, vitamin D, may help supress that nasty gene that causes  muscular dystrophy!!!

I have a friend who is long term survivor and always lays out in sun

who knows

20 min of vitamin D may help

ALSO

HERE ARE SOME MORE STUDIES


 - Web Search

Nutritional inadequacy in adults with muscular dystrophy. -
- Muscle Nerve, 2005 - ncbi.nlm.nih.gov
... certain individual nutrients (eg, copper and water-soluble vitamins). These data
indicate that a substantial number of adults with muscular dystrophy do not ...


Tolerance of high-dose (3,000 mg/day) coenzyme Q10 in ALS - group of 4 »
 Neurology, 2005 - AAN Enterprises
Muscular Dystrophy Association...  co-enzyme Q10/vitamin E wafers ...

Understanding the importance of selenium and selenoproteins in muscle function - group of 3 »
M Rederstorff, A Krol, A Lescure - Cellular and Molecular Life Sciences (CMLS), 2006 - Springer
... Corresponding author. Key words. Selenium; selenoprotein; muscle disorders;
congenital muscular dystrophy; SEPN1. Introduction ...


MUSCLE DAMAGE IN MDX (DYSTROPHIC) MICE: ROLE OF CALCIUM AND REACTIVE OXYGEN SPECIES - group of 6 NP Whitehead, EW Yeung, DG Allen - Clinical and Experimental Pharmacology and Physiology, 2006 - Blackwell Synergy  ... Duchenne muscular dystrophy (DMD) is a lethal, degenerative muscle disease caused
by a genetic mutation that leads to the complete absence of the cytoskeletal

REACTIVE OXYGEN SPECIES ... MEANS treat with anti oxidants HERE AGAIN WE HAVE THE OXIDATIVE STRESS MODEL OF A BAD GENE ACTIVATED


Clinical Case:: Outbreak of White Muscle Disease or Nutritional Muscular Dystrophy in Calves - group of 3 »
PA CONTRERAS, E PAREDES, F WITTWER… - 2005 - serbi.luz.edu.ve
... Disease, WMD, or Nutritional Muscular Dystrophy is reported ... were eosinophilic and
irregular muscular cells, with ... deficiency of Selenium or vitamin E. Surviving ...



The role of free radicals in muscular dystrophy - group of 2 »
JG Tidball, M Wehling-Henricks - Journal of Applied Physiology, 2006 - Am Physiological Soc
... 2003. 30. Fitzgerald G, and McArdle B. Vitamins E and B6 in the treatment of muscular
dystrophy and motor neuron disease. Brain 6



Selenium and vitamin E status correlated with myopathies of horses reared in farms in the Czech … - group of 3 »
E Ludvikova, P Jahn, L Pavlata, M Vyskocil - Acta Veterinaria Brno, 2005 - vfu.cz
... P, DVO¤ÁK V 1980: Fluorometric determination of vitamins A and ... Blood glutathione
peroxidase activity in horses in relation to muscular dystrophy and selenium ...
what is a myopathy??



SELENIUM CONCENTRATION IN MUSK RAT, HARE, COW TISSUES AND IN COW’S MILK, AS AN INDICATOR OF ITS …
B Debski, A Krynski, K Skrzymowska - Animals and environment, Volume 2: Proceedings of the XIIth …, 2005 - isah-soc.org
... Sparing effect of Se on vitamin E and delays the onset of ... muscle disease” (nutritional
muscular dystrophy) in cattle, exadutive diathesis and pancreatic



THIS IS FUN... I AM FINDING ALL KINDS OF GOOD STUFF....
HERE IS LINK TO SE   muscular dystrophy

Despite of analyzed material, the lowest level of Se in all analyzed samples originated
from Olsztyn province in north-eastern Poland. Grzebula (5) observed in south-eastern part of
Poland appearance of the nutritional muscular dystrophy in horses, sheep and cattle, as well as
disturbances in reproduction, typical for Se deficiency. It is possible that whole eastern part of
Poland is Se deficient.
          Several metabolic disorders relate to Se deficiency: “white
muscle disease” (nutritional muscular dystrophy) in cattle, exadutive diathesis and pancreatic
degeneration in poultry, hepatosis dietetica
http://scholar.google.com/scholar?num=100&hl=en&lr=&q=cache:7UyRR96ybrMJ:www.isah-soc.org/documents/2005/sections/104_vol_2.pdf+muscular+dystrophy+vitamins

F'ING SELENIUM DIFFICIENCY ALONE CAN CAUSE THAT DANG GENE TO EXPRESS AND CAUSE MUSCULAR DYSTROPHY!!!!!!!

THEY PROBABLY ONLY DISCOVERED THIS GENE IN MUSCULAR DISTROPHY A FEW YEARS AGO...

SCIENCE IS EXPLODING RIGHT NOW, GENES PROTEINS

VR Preedy - Journal of Nutritional & Environmental Medicine, 2005 - Taylor & Francis
... vitamins B1, 2, 6 and 12, magnesium and zinc should help. Oxidative stress may be
involved in Alzheimer’s disease, muscle fatigue, and muscular dystrophy.

THIS SEEMS TO SAY THAT EXERCISE ALONE CAN HELP KEEP THE GENE/PROTEIN

Reactive oxygen species and redox-regulation of skeletal muscle adaptations to exercise - group of 3 »
MJ Jackson - Philosophical Transactions: Biological Sciences, 2005 - journals.royalsoc.ac.uk
... Pre-supplementation with vitamin C reduced these responses, supporting the possibility ...
protein in the most common form, Duchenne muscular dystrophy (DMD), is a ...

a) Muscular dystrophies

The muscular dystrophies are a group of inherited disorders of muscle characterized by significant muscle degeneration and weakness (Partridge 1993). Dystrophin, the defective protein in the most common form, Duchenne muscular dystrophy (DMD), is a component of a complex set of proteins and glycoproteins associated with the cell membrane, several of which may cause other forms of muscular dystrophy if defective or absent (Durbeej & Campbell 2002). The functions of many components of the DGC complex are unclear. The skeletal muscle isoform of nNOS, termed nNOSmu (or muNOS), is associated with the complex (Brenman et al. 1995). Loss of dystrophin protein (as occurs in DMD patients or in the mdx mouse model) leads to complete loss of the DGC and nNOS from the sarcolemma (Durbeej & Campbell 2002). nNOS is also lost from the sarcolemma in mice deficient in other components of the DGC (Crosbie et al. 2002). Loss of nNOS from the sarcolemma leads to redistribution of nNOS to the cytosol. Estimates of the residual nNOS present in the cytosol in dystrophin-deficient muscle vary greatly from an overall decrease to a 75% increase (Brennan et al. 1995; Chang et al. 1996). There is evidence that reversal of this loss of nNOS by overexpression of the protein in mdx mice partially ameliorates the degeneration in this model (Wehling et al. 2001), providing strong support that changes in redox regulation may be important in this disorder.

(b) ROS generation in muscle of ageing mice

There is evidence that abnormalities in muscle NO/superoxide interactions play a role in ageing-related muscle dysfunction. Loss of muscle strength and muscle wasting are characteristic of ageing


he apparent inconsistency between the large increase in ROS generation during exercise and the lack of a deleterious effect of muscle activity on muscle ageing appears to be due to the ability of skeletal muscle to adapt to the ROS generated during exercise by increasing the expression of protective proteins (McArdle & Jackson 2000). An increase in these proteins helps protect the tissue against subsequent exposure to exercise-induced increases in ROS generation (McArdle et al. 2004a). This ability to respond to oxidative stress does not appear to be maintained in ageing animals and humans (Rao et al. 1999; Vasilaki et al. 2002), but surprisingly is associated with an increase in the resting SOD, catalase, glutathione peroxidase (GPx) and glutathione reductase activities in the muscle of aged compared with adult mice (Leeuwenburgh et al. 1994). Muscle nNOS activities have been reported to be either elevated (Capanni et al. 1998) or decreased (Richmonds et al. 1999) in aged animals. Whether these changes are associated with any aberrant NOS activity in old muscle is also unclear although there is some evidence for a relocation of nNOS to the muscle cytosol in aged animals (Cappani et al. 1998).

The net effect of these changes in ROS activity in aged muscle is unclear as is the potential for any amelioration of age-related muscle dysfunction by reduction or modification of ROS levels. Despite this, our recent data indicate that transgenic approaches to express high levels of a protein that protects against oxidative damage (HSP70) can improve muscle function in old mice (McArdle et al. 2004b).

http://www.journals.royalsoc.ac.uk/media/hpb9jdrgmj2wwjunfv5q/contributions/l/2/0/0/l200741j9k587775_html/fulltext.html

exercise helps the body remain at homeostasis, keeps the bad genes down??

he apparent inconsistency between the large increase in ROS generation during exercise and the lack of a deleterious effect of muscle activity on muscle ageing appears to be due to the ability of skeletal muscle to adapt to the ROS generated during exercise by increasing the expression of protective proteins (McArdle & Jackson 2000). An increase in these proteins helps protect the tissue against subsequent exposure to exercise-induced increases in ROS generation (McArdle et al. 2004a). This ability to respond to oxidative stress does not appear to be maintained in ageing animals and humans (Rao et al. 1999; Vasilaki et al. 2002), but surprisingly is associated with an increase in the resting SOD, catalase, glutathione peroxidase (GPx) and glutathione reductase activities in the muscle of aged compared with adult mice (Leeuwenburgh et al. 1994). Muscle nNOS activities have been reported to be either elevated (Capanni et al. 1998) or decreased (Richmonds et al. 1999) in aged animals. Whether these changes are associated with any aberrant NOS activity in old muscle is also unclear although there is some evidence for a relocation of nNOS to the muscle cytosol in aged animals (Cappani et al. 1998).

SEE MY RECENT POSTS ABOUT

A, B, C, D, E!!!!!!!!!!!!

KIND OF EXCITING.



Offline bimazek

  • Member
  • Posts: 781
Re: Musclular distrophy/HIV effect by same protein same gene Vitamins help
« Reply #1 on: January 31, 2007, 04:49:20 AM »
I MUST EMPHASIZE THAT THIS NEW PROTEIN GENE IS A NEW DISCOVERY THAT IT EFFECTS HIV INSERTION

SO THIS IS A NEW AREA OF RESEARCH AND INSIGHTS

I FOUND SOME MORE INFO...


The involvement of oxidative stress in determining the severity and progress of pathological ...
I Niebrój-Dobosz, I Hausmanowa-Petrusewicz - Acta Biochimica Polonica, 2005 - actabp.pl
... such conditions as ischemia, exhaus- tive exercise, and vitamin E deficiency ... STRATEGY
OF MUSCULAR DYSTROPHY TREATMENT BASED ON PREVENTION OF OXIDATIVE STRESS .


http://scholar.google.com/scholar?as_q=muscular+dystrophy+vitamins&num=100&btnG=Search+Scholar&as_epq=&as_oq=&as_eq=&as_occt=any&as_sauthors=&as_publication=&as_ylo=2005&as_yhi=2006&as_allsubj=all&hl=en&lr=



Coenzyme Q10 - group of 4 »
RA Bonakdar, E Guarneri - Am Fam Physician, 2005 - aafp.org
... II trials underway to clarify its potential contribution in the treatment of conditions,
such as Duchenne's muscular dystrophy, breast cancer ... Olay vitamins. ...
Coenzyme Q10
ROBERT ALAN BONAKDAR, M.D., and ERMINIA GUARNERI, M.D.
Scripps Center for Integrative Medicine, La Jolla, California
Coenzyme Q10 is a vitamin-like substance used in the treatment of a variety of disorders primarily related to suboptimal cellular energy metabolism and oxidative injury. Studies supporting the efficacy of coenzyme Q10 appear most promising for neurodegenerative disorders such as Parkinson's disease and certain encephalomyopathies for which coenzyme Q10 has gained orphan drug status. Results in other areas of research, including treatment of congestive heart failure and diabetes, appear to be contradictory or need further clarification before proceeding with recommendations. Coenzyme Q10 appears to be a safe supplement with minimal side effects and low drug interaction potential. (Am Fam Physician 2005

Migraine. A preliminary open label trial17 of 32 patients taking 150 mg of coenzyme Q10 daily demonstrated efficacy in reducing the frequency of migraine attacks. A recent randomized double-blind, placebo-controlled trial18 of 42 patients taking coenzyme Q10 at 300 mg a day found similar benefit. The response rate (i.e., decrease in headache frequency by 50 percent or more) was 47.6 percent in the coenzyme Q10 group and 14.4 percent in the placebo group. The number needed to treat was three.
Contraindications, Adverse Effects, and Interactions
No absolute contraindications are known for coenzyme Q10,

Key Points About Coenzyme Q10
Efficacy
   
Parkinson's disease and mitochondrial cytopathies: preliminary evidence for benefit
Congestive heart failure, hypertension, and ischemic heart disease: conflicting or preliminary evidence

Diabetes: conflicting evidence for improvement in glycemic control






Preventing oxidative stress in rats with aldosteronism by calcitriol and dietary calcium and … - group of 4 »
KD Goodwin, RA Ahokas, SK Bhattacharya, Y Sun, IC … - Am J Med Sci, 2006 - amjmedsci.com
... skin exposed to the ultraviolet B component of sunlight, vitamin D enters ... of skeletal
muscle that is a characteristic feature of Duchenne muscular dystrophy.



Oxidative stress resistance in skeletal muscle cells: role of vitamin C and redox sensitive …
L Avigliano, G Duranti - 2005 - dspace.uniroma2.it
... 1.1 DIFFERENT TYPE OF MUSCULAR FIBRE ... deleterious species are mostly removed by cellular
antioxidant systems, which include antioxidant vitamins, protein and non ..




http://scholar.google.com/scholar?q=muscular+dystrophy+vitamins&num=100&hl=en&lr=&as_ylo=2005&as_yhi=2006&start=100&sa=N

 


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