WIN A X FACTOR T SHIRT or EVEN A CYCLE!!!
- 11-15-2007, 03:31 PM
WIN A X FACTOR T SHIRT or EVEN A CYCLE!!!
Allright here's the deal! As promised, I'm goving away some goodies to my fellas. Because X Factor is the king of all anabolics, I will give you a chance to score a T Shirt, or even a CYCLE! Yeah, that's right! What you need to do is quite simple, answer the question:
What is inflamation, and how important is it to us, bodybuilders?
Make some research, and post it right in here, 5 shirts and 1 cycle will be given away!!!!!
Now go do some work!
- 11-15-2007, 03:37 PM
It's when your muscles blow up and swell to the size of watermelons from so much/Drive, similar to the look of jjhon. At that point, the muscles are able to absorb so many nutrients that they at a rate faster than ussual, therefore building huge amounts of new muscle almost over night.
- 11-15-2007, 03:38 PM
11-15-2007, 03:43 PM
Inflammation - is the complex biological response of vascular tissues to harmful stimuli, such as pathogens, damaged cells, or irritants. It is a protective attempt by the organism to remove the injurious stimuli as well as initiate the healing process for the tissue
Research in the next few years is going to confirm that inflammation is a critical aspect of building muscle mass. In particular, the ability to reduce inflammation as it goes hand in hand with muscle growth (hypertrophy). As we get older, a chronic inflammatory response manifests within our bodies that makes it increasingly difficult to build and/or maintain muscle as we get older. In directly, this also makes it more difficult to shed body fat.
This increased level of inflammation ultimately results in oxidative damage to our DNA within muscle cells. In particular, the DNA within the mitochondria within each cell. Most of you probably know that the mitochondria are the primary site of ATP (energy) production within cells. This energy comes from the metabolism of all macro-nutrients; fats, carbs and even protein. The mitochondria are the powerhouses in all cells that crank out the seemingly endless supply of energy.
The bottom line is science has revealed what causes the destruction of your hard earned muscle, therefore, we can start developing therapies to block/reduce this effect. This process is based on nutritional intervention with specific supplements.
More? I can go to books to this is off an internet source i read.
11-15-2007, 03:44 PM
11-15-2007, 03:44 PM
11-15-2007, 03:45 PM
11-15-2007, 03:45 PM
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11-15-2007, 03:47 PM
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11-15-2007, 03:51 PM
11-15-2007, 03:54 PM
Using resistance exercises to create hypertrophy causes an overload of the skeletal muscle - more force is exerted that what the muscle usually uses, therby causing an "injury" to that muscle. Immediately after there is an inflammatory response, including macrophages entering the muscles. Macrophages come from white blood cells, and one of their most important tasks is the removal of damaged tissue, and repair of existing tissue. IGF-1 release is also is also stimulated by the release of inflammatory cells.
Another piece of the inflammatory puzzle are prostaglandins. They are the chemicals that the body produces as a part of the COX cycle, promoting parts of the inflammatory response. They are involved in the sensation of pain, as well as the rise in body temperature associated with fevers. In a positive way, they are regulators of protein synthesis in skeletal muscles, as well as directly inhibiting adipogenesis.
On the flip side, anti-inflammatories such as ibuprofen (particularly any NSAIDs that target COX sites) have been show to reduce muscle hypertrophy by reducing the expression of cox-2 enzymes. The NSAIDs directly interefere with protein synthesis, and by blocking the prostaglandins from being produced also prevent them from helping protein synthesis. In animal studies, high doses of NSAIDs have been shown to reduce muscle gain vs a control set to virtually nothing in mice that were being trained.
11-15-2007, 03:57 PM
well i am no genius? or....am i?
redness, swelling, pain, tenderness, heat, and disturbed function of an area of the body, esp. as a reaction of tissues to injurious agents
x factor might go sweet with my dcp/leviathan reloaded im ordering today... cough cough
11-15-2007, 04:08 PM
isnt that when you get break outs form STD'S????
its when you breathe in smoke right???
haha goodluck people
11-15-2007, 04:20 PM
11-15-2007, 04:22 PM
Inflammation (Latin, inflammatio, to set on fire) is the complex biological response of vascular tissues to harmful stimuli, such as pathogens, damaged cells, or irritants. It is a protective attempt by the organism to remove the injurious stimuli as well as initiate the healing process for the tissue. Inflammation is not a synonym for infection. Even in cases where inflammation is caused by infection it is incorrect to use the terms as synonyms: infection is caused by an exogenous pathogen, while inflammation is the response of the organism to the pathogen.
In the absence of inflammation, wounds and infections would never heal and progressive destruction of the tissue would compromise the survival of the organism. However, inflammation which runs unchecked can also lead to a host of diseases, such as hay fever, atherosclerosis, and rheumatoid arthritis. It is for this reason that inflammation is normally tightly regulated by the body.
Inflammation can be classified as either acute or chronic. Acute inflammation is the initial response of the body to harmful stimuli and is achieved by the increased movement of plasma and leukocytes from the blood into the injured tissues. A cascade of biochemical events propagates and matures the inflammatory response, involving the local vascular system, the immune system, and various cells within the injured tissue. Prolonged inflammation, known as chronic inflammation, leads to a progressive shift in the type of cells which are present at the site of inflammation and is characterised by simultaneous destruction and healing of the tissue from the inflammatory process.
Acute inflammation is a short-term process which is characterised by the classic signs of inflammation - swelling, redness, pain, heat, and loss of function - due to the infiltration of the tissues by plasma and leukocytes. It occurs as long as the injurious stimulus is present and ceases once the stimulus has been removed, broken down, or walled off by scarring (fibrosis). The first four characteristics have been known since ancient times and are attributed to Celsus. Loss of function was added to the definition of inflammation by Rudolf Virchow in the 19th century.
The process of acute inflammation is initiated by the blood vessels local to the injured tissue, which alter to allow the exudation of plasma proteins and leukocytes into the surrounding tissue. The increased flow of fluid into the tissue causes the characteristic swelling associated with inflammation, and the increased blood flow to the area causes the reddened colour and increased heat. The blood vessels also alter to permit the extravasation of leukocytes through the endothelium and basement membrane constituting the blood vessel. Once in the tissue, the cells migrate along a chemotactic gradient to reach the site of injury, where they can attempt to remove the stimulus and repair the tissue.
Meanwhile, several biochemical cascade systems, consisting of chemicals known as plasma-derived inflammatory mediators, act in parallel to propagate and mature the inflammatory response. These include the complement system, coagulation system and fibrinolysis system.
Finally, down-regulation of the inflammatory response concludes acute inflammation. Removal of the injurious stimuli halts the response of the inflammatory mechanisms, which require constant stimulation to propagate the process. Additionally, many inflammatory mediators have short half lives and are quickly degraded in the tissue, helping to quickly cease the inflammatory response once the stimulus has been removed.
Chronic inflammation is a pathological condition characterised by concurrent active inflammation, tissue destruction, and attempts at repair. Chronic inflammation is not characterised by the classic signs of acute inflammation listed above. Instead, chronically inflammed tissue is characterised by the infiltration of mononuclear immune cells (monocytes, macrophages, lymphocytes, and plasma cells), tissue destruction, and attempts at healing, which include angiogenesis and fibrosis.
Endogenous causes include persistent acute inflammation. Exogenous causes are varied and include bacterial infection, especially by Mycobacterium tuberculosis, prolonged exposure to chemical agents such as silica, or autoimmune reactions such as rheumatoid arthritis.
In acute inflammation, removal of the stimulus halts the recruitment of monocytes (which become macrophages under appropriate activation) into the inflamed tissue, and existing macrophages exit the tissue via lymphatics. However in chronically inflamed tissue the stimulus is persistent, and therefore recruitment of monocytes is maintained, existing macrophages are tethered in place, and proliferation of macrophages is stimulated (especially in atheromatous plaques.)
Acute inflammation is characterised by marked vascular changes, including vasodilation, increased permeability, and the slowing of blood flow, which are induced by the actions of various inflammatory mediators. Vasodilation occurs first at the arteriole level, progressing to the capillary level, and brings about a net increase in the amount of blood present, causing the redness and heat of inflammation. Increased permeability of the vessels results in the movement of plasma into the tissues, with resultant stasis due to the increase in the concentration of the cells within blood - a condition characterised by enlarged vessels packed with cells. Stasis allows leukocytes to marginate along the endothelium, a process critical to their recruitment into the tissues. Normal flowing blood prevents this, as the shearing force along the periphery of the vessels moves cells in the blood into the middle of the vessel.
Plasma cascade systems
The complement system, when activated, results in the increased removal of pathogens via opsonisation and phagocytosis.
The kinin system generates proteins capable of sustaining vasodilation and other physical inflammatory effects.
The coagulation system or clotting cascade which forms a protective protein mesh over sites of injury.
The fibrinolysis system, which acts in opposition to the coagulation system, to counterbalance clotting and generate several other inflammatory mediators.
The cellular component involves leukocytes, which normally reside in blood and must move into the inflamed tissue via extravasation to aid in inflammation. Some act as phagocytes, ingesting bacteria, viruses, and cellular debris. Others release enzymatic granules which damage pathogenic invaders. Leukocytes also release inflammatory mediators which develop and maintain the inflammatory response. Generally speaking, acute inflammation is mediated by granulocytes, while chronic inflammation is mediated by mononuclear cells such as monocytes and lymphocytes.
An organism can escape the confines of the immediate tissue via the circulatory system or lymphatic system, where it may spread to other parts of the body. If an organism is not contained by the actions of acute inflammation it may gain access to the lymphatic system via nearby lymph vessels. An infection of the lymph vessels is known as lymphangitis, and infection of a lymph node is known as lymphadenitis. A pathogen can gain access to the bloodstream through lymphatic drainage into the circularitory system.
When inflammation overwhelms the host, systemic inflammatory response syndrome is diagnosed. When it is due to infection, the term sepsis is applied, with bacteremia being applied specifically for bacterial sepsis and viremia specifically to viral sepsis. Vasodilation and organ dysfunction are serious problems associated with widespread infection that may lead to septic shock and death.
Inflammation also induces high systemic levels of acute-phase proteins. In acute inflammation, these proteins prove beneficial, however in chronic inflammation they can contribute to amyloidosis. These proteins include C-reactive protein, serum amyloid A, serum amyloid P, vasopressin, and glucocorticoids, which cause a range of systemic effects including:
Increased blood pressure
Loss of appetite
Systemic inflammation and obesity
With the discovery of interleukins (IL), the concept of systemic inflammation developed. Although the processes involved are identical to tissue inflammation, systemic inflammation is not confined to a particular tissue but involves the endothelium and other organ systems.
High levels of several inflammation-related markers such as IL-6, IL-8, and TNF-α are associated with obesity. During clinical studies, inflammatory-related molecule levels were reduced and increased levels of anti-inflammatory molecules were seen within four weeks after patients began a very low calorie diet. The association of systemic inflammation with insulin resistance and atherosclerosis is the subject of intense research.
The outcome in a particular circumstance will be determined by the tissue in which the injury has occurred and the injurious agent that is causing it. There are three possible outcomes to inflammation:
The complete restoration of the inflamed tissue back to a normal status. Inflammatory measures such as vasodilation, chemical production, and leukocyte infiltration cease, and damaged parenchymal cells regenerate. In situations where limited or short lived inflammation has occurred this is usually the outcome.
Large amounts of tissue destruction, or damage in tissues unable to regenerate, can not be regenerated completely by the body. Fibrous scarring occurs in these areas of damage, forming a scar composed primarily of collagen. The scar will not contain any specialized structures, such as parenchymal cells, hence functional impairment may occur.
In acute inflammation, if the injurious agent persists then chronic inflammation will ensue. This process, marked by inflammation lasting many days, months or even years, may lead to the formation of a chronic wound. Chronic inflammation is characterised by the dominating presence of macrophages in the injured tissue. These cells are powerful defensive agents of the body, but the toxins they release (including reactive oxygen species) are injurious to the organism's own tissues as well as invading agents. Consequently, chronic inflammation is almost always accompanied by tissue destruction.
Overtraining refers to when a bodybuilder has trained to the point where his workload exceeds his recovery capacity. There are many reasons that overtraining occurs, including lack of adequate nutrition, lack of recovery time between workouts, insufficient sleep, and training at a high intensity for too long (a lack of splitting apart workouts). Training at a high intensity too frequently also stimulates the central nervous system (CNS) and can result in a hyper-adrenergic state that interferes with sleep patterns. To avoid overtraining, intense frequent training must be met with at least an equal amount of purposeful recovery. Timely provision of carbohydrates, proteins, and various micronutrients such as vitamins, minerals, phytochemicals, even nutritional supplements are acutely critical.
11-15-2007, 04:23 PM
11-15-2007, 04:25 PM
I'd love to buy some bulk X-Factor, but I like to 'try before I buy.' So, a bottle would sure do me good, especially during my upcoming cycle. That is, when I finally decide on what the hell I wanna run.
11-15-2007, 04:26 PM
11-15-2007, 04:28 PM
Inflammation-Redness, swelling, pain, tenderness, heat, and disturbed function of an area of the body, esp. as a reaction of tissues to injurious agents.
2. the act or fact of inflaming.
3. the state of being inflamed.
P.s. Guys that have this Eat cherries! I know from my Grandfather being in the Health and nutrution Movement since I was a young boy, he kind of got me into natural healing food and their mechanisms.
Follow me on facebook, twitter and youtube, where I share information and videos to help you achieve your physique goals, John Smeton Ftness
11-15-2007, 04:28 PM
11-15-2007, 04:30 PM
11-15-2007, 04:35 PM
Fish (ideally cold-water, such as salmon and trout) provide the best source of omega-3. Omega-3 is the most important EFA for bodybuilders as it counters muscular inflammation, thereby promoting recovery.
Inflammation and muscle growth (hypertrophy) go hand in hand. If muscles weren't able to 'wear and tear,' in turn causing inflammation, than muscle growth would not be possible. As the muscle fibers regenerate and grow, that in turn, sheds body fat. However, as we get older, a chronic inflammatory response manifests within our bodies that makes it very difficult, and increases with age, to build and/or maintain muscle as we get older. In directly, this also makes it more difficult to shed body fat.
11-15-2007, 04:36 PM
11-15-2007, 04:39 PM
11-15-2007, 04:44 PM
So, I'll just stop there, lol.
This X-Factor opportunity was just way too tempting to pass up.
How long is this 'contest' going on for?
11-15-2007, 04:46 PM
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11-15-2007, 05:00 PM
11-15-2007, 05:19 PM
Follow me on facebook, twitter and youtube, where I share information and videos to help you achieve your physique goals, John Smeton Ftness
11-15-2007, 05:39 PM
11-15-2007, 06:36 PM
Inflammation is any disturbed function of a body part, whether it be swelling, redness, heat, or any other form of irritation. There are several negative types of inflammation. One type is Naturally Inhibit Inflammation. In this case, the inflammation is caused by overproduction of free radicals in the body. Primarily caused by histamine, a biological agent that swells veins and capillaries so severely that they leak blood plasma into tissue, this can be harmful in the regulation of blood flow into muscle tissues.
Another type of inflammation is edema, or swelling. Edema is caused by the leakage of blood into surrounding tissues of the body, which leaves a person with a swollen look. Edema is also a medical condition which causes chronic puffy eyes. It's important to bodybuilders to reduce venous congestion in parts of the body so that there is no tenderness or pain during or post workout.
A third type of inflammation (most commonly found in workouts) is postoperative inflammation. Highly common in bodybuilders, athletes, and trainers, postoperative inflammation is similar to the other two types of inflammation, where muscles are swollen and veins are dilated. Sport-related injuries weaken vascular walls around muscle tissues, which hurts the blood flow of the body.
Just a side note: For bodybuilders, the best advice is to consume anti-oxidant nutrients and stay in healthy shape. Most of all, don't over-train. There's also a new study connecting nitric oxide to help reducing muscle inflammation. Nitric oxide in reasonable amounts is supposed to increase mind-muscle connection, memory, pain sensory and information processing.
All-in-all, inflammation is a condition to be wary of as a bodybuilder when working out. When your body says "no", you should listen to it. Pumps and vascularity are a treasured thing amongst weight-lifters, but there are also diabolical effects associated with it. Eat, sleep, and lift responsibly people
That's my take on it. May or may not be what you were looking for, but I tried to be thorough. Hope you guys learned something!
Oh, and if you didn't get it by reading the article, inflammation is very important to bodybuilders.
11-15-2007, 07:23 PM
oh yea brother!
The Role of Macrophages in Muscle Repair and Growth
When resistance exercise involves heavy eccentric muscular contractions (lowering the weight), it is associated with overloading skeletal muscle —that is, the force requirement of the muscle exceeds what it is accustomed too—and results in injury to skeletal muscle. It has traditionally been felt that the events following the initial injury, including inflammation, are necessary for optimal repair and growth of new muscle. Exercise-induced muscle damage stimulates an acute-phase inflammatory response, which includes infiltration into skeletal muscle by macrophages1. Macrophages (Greek: ‘big eaters’) are cells within the tissues that originate from specific white blood cells. One important role of macrophage is the removal of damaged tissue by heavy resistance exercise. Repairing damaged muscle cells is an important function of macrophages in the early stages of muscle damage and inflammation. This inflammatory response coincides with muscle repair, regeneration, and growth, which involves the activation of satellite cells (satellite cell activation is essential for muscle hypertrophy). The number of macrophages per square millimeter of muscle tissue is increased after heavy eccentric exercise compared to concentric exercise (lifting the weight) which may play an important role as to why eccentric contractions produce greater muscle hypertrophy2. Macrophages are also able to promote muscle growth and repair. In vitro studies (test tubes studies) show macrophages can increase muscle cell growth factors3,4, which indicates a role for macrophage-derived factors in muscle growth.
What happens if you suppress your ‘Healing Factor’?
The healing process that occurs during rest is an important adaptation to building muscle. You may be sore as hell after a heavy leg workout but that means your shocking your muscles into new growth. The inflammatory process although painful for a bodybuilder is an essential part of the muscle growth process. For instance, mediators such as IGF-1 are stimulated by the release of inflammatory cells5. So what happens if you suppress macrophages after injury? Just like Wolverine in the movies, if you lose your ‘healing factors’ you’re screwed in terms of building muscle. Researchers injected mice with an antibody that reduced macrophage concentrations after a couple of days of muscle overloading (86% reduction in macrophage concentration) and found that muscle fiber repair and growth was significantly impaired after muscle overload6. Macrophage-depletion also reduced muscle regeneration and prevented growth of muscle fibers that normally occurs with muscle overload. These findings suggest that macrophage first invades injured muscle serves to remove cellular debris, after which the subsequent invasive population participates in repair, regeneration and growth.
A strain of mice was recently genetically engineered to test the hypothesis of macrophage invasion to the site of injury is important for muscle regeneration and growth. A strain of mice was bred to be deficient in a protein called MCP-1 (Monocyte chemotactic protein-1), a potent activator for macrophage invasion and inflammation. Researchers damaged muscle fibers of these mice and compared them to normal mice; the mice that had impaired muscle macrophage activity due to a MCP-1 deficiency had impaired muscle regeneration and growth. The researchers speculated that the impaired muscle regeneration was due to macrophages not being able to repair the damaged muscle. Remember, muscle growth takes place during the recovery phase, lifting weights only serves as the stimulus. The research suggests that unless the damaged muscle fiber becomes invaded by macrophages and other repair mediators, it becomes stagnant and muscle repair is halted and the muscle tissue stays damaged. Interestingly, macrophages can increase nitric oxide which expands blood vessels and open up the muscle tissue to blood flow which allows for more macrophages to repair damaged muscle tissue10. NSAIDS Suppress Muscle Growth
You may feel the urge to take an Aleve or Ibuprofen tablet after an intense workout to reduce muscle soreness or you may suffer from a chronic knee or elbow injury from years of heavy lifting but only take NSAIDS when absolutely necessary. According to a new study in Medicine & Science in Sports & Exercise, taking ibuprofen can inhibit muscle hypertrophy. In the study, rats had surgeries performed in which their leg muscles are chronically overloaded to cause muscle hypertrophy. One group of rats received ibuprofen while the other group received nothing. At the end of the study, rats that were administered ibuprofen had a whopping 50% reduction in muscle hypertrophy8. Another study reported that when Non Steroidal Anti-Inflammatory Drugs (NSAIDS) were examined after muscle injury, not only was satellite cell (muscle stem cells) activity in muscle inhibited by their was a increase in myostatin (inhibits muscle growth) production. Examples of NSAIDs include Aspirin, indomethacin (Indocin), ibuprofen (Motrin), naproxen (Naprosyn), piroxicam (Feldene), and nabumetone (Relafen). Recent research suggests that regular use of NSAIDS or COX-2 inhibitors such as Celebrex or Vioxx can significantly reduce muscle hypertrophy by reducing expression of the enzyme COX-2. In conjunction with other research, the COX-2 pathway serves as an important mediator of the inflammation response after exercise serving to repair damaged tissue and is an essential for muscle hypertrophy to occur.
More recent findings have shown cyclooxygenase-2 (COX-2) oral administration of COX-2 inhibitors can slow muscle regeneration and reduce muscle growth after acute injury of muscle7. Interestingly, mice that are genetically engineered to be COX-2 deficient showed less macrophage invasion of injured muscle during regeneration7, which may indicate that macrophages normally promote muscle cell proliferation and muscle regeneration following injury. Alternatively, COX-2 may have a direct effect on muscle cells to affect muscle repair. Additionally, it is well known that in order to build muscle there must be an increase in muscle protein synthesis rates. Studies have reported that if the maximal dosage of ibuprofen or acetaminophen is taken before exercise that protein synthesis rates are blunted9. In that study, subjects performed 10 sets of eccentric exercise performed at 120% of a 1-RM, subjects that received a placebo had average of 76% increase in protein synthesis rates, whereas the subjects whom received either ibuprofen or acetaminophen had no increase in protein synthesis.
In conclusion, don’t take any NSAIDS unless it’s absolutely necessary for alleviating pain. NSAIDS reduce muscle protein synthesis and inhibit muscle hypertrophy. Muscle inflammation and repair is an essential part of hypertrophy process, and although you may be sore as hell, the benefits you will reap from the pain are bigger and stronger muscles.
1. Fielding, RA, Manfredi TJ, Ding W, Fiatarone MA, Evans WJ, and Cannon JG. Acute phase response in exercise. III. Neutrophil and IL-1 accumulation in skeletal muscle. Am J Physiol Regulatory Integrative Comp Physiol 265: R166-R172, 1993.
2. Stupka N, Tarnopolsky MA, Yardley NJ, Phillips SM. Cellular adaptation to repeated eccentric exercise-induced muscle damage. J Appl Physiol. 2001 Oct;91(4):1669-78.
3. Cantini M & Carraro U (1995). Macrophage-released factor stimulates selectively myogenic cells in primary muscle culture. J Neuropathol Exp Neurol 54, 121-128.
4. Cantini M, Giurisato E, Radu C, Tiozzo S, Pampinella F, Senigaglia D, Zaniolo G, Mazzoleni F & Vittiello L (2002). Macrophage-secreted myogenic factors: a promising tool for greatly enhancing the proliferative capacity of myoblasts in vitro and in vivo. Neurol Sci 23, 189-194.
5. Musaro A, McCullagh K, Paul A, Houghton L, Dobrowolny G, Molinaro M, Barton ER, Sweeney HL, Rosenthal N. Localized Igf-1 transgene expression sustains hypertrophy and regeneration in senescent skeletal muscle. Nat Genet. 2001 Feb;27(2):195-200.
6. Tidball JG, Wehling-Henricks M. Macrophages promote muscle membrane repair and muscle fibre growth and regeneration during modified muscle loading in mice in vivo. J Physiol. 2007 Jan 1;578(Pt 1):327-36.
7. Bondesen BA, Mills ST, Kegley KM, Pavlath GK. The COX-2 pathway is essential during early stages of skeletal muscle regeneration. Am J Physiol Cell Physiol. 2004 Aug;287(2):C475-83.
8. Soltow QA, Betters JL, Sellman JE, Lira VA, Long JH, Criswell DS. Ibuprofen inhibits skeletal muscle hypertrophy in rats. Med Sci Sports Exerc. 2006 May;38(5):840-6.
9. Trappe TA, Fluckey JD, White F, Lambert CP, Evans WJ. Skeletal muscle PGF(2)(alpha) and PGE(2) in response to eccentric resistance exercise: influence of ibuprofen acetaminophen. J Clin Endocrinol Metab. 2001 Oct;86(10):5067-70.
10. Nguyen HX, Tidball JG. Interactions between neutrophils and macrophages promote macrophage killing of rat muscle cells in vitro. J Physiol. 2003 Feb 15;547(Pt 1):125-32. Epub 2002 Dec 20.
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