Look Your Best, Feel Your Best, and Be Your Best With AAIClinics
Call Us
(866) 224-5698
Mon-Fri: 10am-6pm
Sat-Sun: Closed
December 27, 2015 by Joseph Fermin 0 Comments

Sleep Disturbance and the link Between Hormones 0 (0)

Sleep Disturbance and the link Between Hormones

Sleep disturbance affects every facet of our existence. Many sleep-related problems can be overcome with testosterone therapy. Men with lower testosterone levels have lower sleep efficiency, with increased nocturnal awakenings and less slow-wave (REM) sleep. Studies have even shown that sleep disturbances caused by sleep apnea, a chronic breathing problem, may be linked to low testosterone levels.

In a 2011 study published in the Journal of the American Medical Association (JAMA), ten men volunteered to have their testosterone levels checked during eight nights of Sleep Disturbance restriction. They were only allowed five hours of sleep per night. The study found their daytime testosterone levels decreased by 10 to 15 percent. The lowest testosterone levels were in the afternoon and evening. The study also found a progressive loss of energy over the course of the week.

The Danger of Low Testosterone, Risks Associated with Low hGH in Men, HGH Side Effects, What Causes Low Testosterone, testosterone therapy preventive medicine

Thus, there appears to be a direct correlation between testosterone levels and Sleep quantity and quality. Here at AAI Rejuvenation Clinic, we’re ready to help. Our services are discrete and confidential. Contact us today or fill out our medical history form. Our trained wellness team is eager to get you started on the path to a better night’s sleep.

Sleep Studies

There have been an array of medical studies pointing to the fact that Sleep Disturbance, or lack thereof, has a direct correlation to our energy levels, cognitive functions and even organ and cellular health. Most commonly, adults are expected to sleep around 9 hours a day in order to get the adequate amount necessary for optimal systemic function. Unfortunately, the great majority of people get far less sleep than is necessary and recommended. Moreover, the number of people that are getting poor quality of sleep is slowly but surely increasing, leaving us to walk around in a world full of sleep-deprived, moody zombies.

Let’s talk about scary numbers:

– 60% of adults are not getting enough sleep
– The average American is in bed 7.5 hours but only asleep about 6.1.

Recommended sleep requirements:

– Toddlers   = 14 – 12 hours
– Children   = 11 – 10 hours
– Adults     = 9 – 7 hours

  • Sleep just 6 hours a night and increase the chances of being overweight by 27% (about 14lbs a year).
  • Sleep 6 hours a day and increase the possibility of heart disease by 48%.
  • Sleep only 5 hours and increase this risk to 73%.
  • Sleeping less than 5 hours a day reduces your hormonal production by 27% and interferes with other endocrine functions so complex, you cannot measure them by a simple % indication.
  • Sleep only 4 hours a night and you will increase daily calorie intake by 22%.
  • Reducing your average night sleep by 1.5 hours impairs alertness by 32%.
  • If you only sleep 6 hours a night for 2 weeks straight your cognitive equivalence to blood alcohol level will be .10%.
  • Driving while sleepy can be equally, if not more dangerous than driving while drunk.
  • Driving while sleepy accounts for 20% of all annual car accidents.
  • There is a gene that allows people to function well only 6 hours of sleep but, it only exists in 3% of the population.

Positive sleeping points:

  • Sleeping more is not an option? Take a nap: a 20-minute nap increases cognitive function by 40%, enhancing concentration, alertness and motor skills.
  • A 45-minute nap with REM sleep enhances creative thinking and boosts sensory processing.
  • Naps over 45 or 90 minutes will leave you groggy and disoriented.
  • Complete darkness stimulates melatonin – sleep hormone.

AAI Clinics can help you with Sleep Disturbance issues. If you find that you are not acquiring the adequate amount of sleep necessary to really promote your best potential and healthiest self, contact us for assistance. Despite the fact that well-balanced hormone levels significantly aid and promote restful quality of sleep, there are other nutraceuticals that we can provide needing patients with in order to promote real deep, quality sleep that isn’t induced by synthetic drug absorption.

Depending on your particular issues and life circumstances, you will want to click on the below medications to read the herbal facts and medicinal details of each of the below body-and-mind calming options to see which one of these, or combination of these, will best aid you in your quest for real quality sleep.

        • L-Tryptophan
        • Sereniten Plus
        • Relora ®-Plex
        • Seditol ® Plus
        • Brain CALM
        • Valerian Root Max-V
        • Valsed
        • Melatonin (3 mg)
        • Controlled-Release Melatonin


**NOTE**  The content contained in this blog is subject to interpretation and is the opinion of the content writer.  We do not claim it to be fact.  We encourage you to consult a medical doctor before taking any prescribed medications or supplements.

December 27, 2015 by Joseph Fermin 1 Comment

Fast Recovery from Wounds and Illness 0 (0)

Recovery from Wounds and Illness

The use of growth hormone and growth hormone factors can dramatically accelerate the healing process in people age forty and above. In studies, injections of growth hormone stimulated the formation of collagen (the glue that holds tissue together), increased the tensile strength of wounds, and made wounds close faster. With HGH therapy, cells regenerate and repair at a much faster pace, wounds heal more quickly, and bones knit more rapidly.

The healing properties of growth hormone have been used in many instances, recovery from wounds.

What can hGH do

Recovery from surgery, particularly muscle atrophy and weakness Injury or burn including:

  • Severe malnourishment
  • Leg ulcers in elderly people

Here at AAI Rejuvenation Clinic, we’re ready to help. Our services are discrete and confidential. Contact us today or fill out our medical history form. Our trained wellness team is eager to get you started.

HGH is the ultimate anti-aging therapy. It affects almost every cell in the body, rejuvenating the skin and bones, liver, regenerating the heart, lungs, and kidneys, bringing organ and tissue function back to youthful levels. HGH Is an anti-disease medicine that revitalizes and recharges the immune system, lowers the many risk factors for heart attack and even stroke, improves oxygen uptake in emphysema patients and prevent osteoporosis. It is under investigation for a host of different diseases from osteoporosis to post-polio syndrome two aids. HGH is cosmetic surgery in a bottle: smoothing out facial wrinkles, restoring elasticity in the skin. Its thickness and contours the skin; reversing the loss of extracellular water that makes old people look like a dried-up prune. Growth Hormone has healing powers that close ulcerated wounds and regrows burned skin.

Effects of Administration (high-frequency, low dose) in 20 patients L. Cass Terry, M.D., PH.D., and Edmund Chein, M. D., Medical College of Wisconsin and Palms Springs Life Extension Institute Healing, Flexibility and Resistance:

  • Healing of Old Injuries 55%
  • Healing of Other Injuries 61%
  • Healing Capacity 71%
  • Back Flexibility 83%
  • Resistance to Common Illness 73%

1 Mean self-assessment time was 180 days after HGH therapy initiation: range = 15 – 720 days.

Think about your children or yourself when you are a child. Remember how many times you fell down and scraped your knee? Your arms and legs always seemed to be wearing red badges of courage. Most relevantly, practically overnight, a scab would form and that wound would soon disappear, leaving absolutely no trace. The thing is when you are young, cells regenerate and repair at a much faster pace, wounds heal more quickly, and bones knit more rapidly. All these processes are under the control of Growth Hormone and growth factors. The use of Growth Hormone and Growth Hormone factors won’t restore the repair rate of an eight-year-old’s, but it can dramatically accelerate the healing process in those aged 40 and above.

The healing properties of Growth Hormone have already been used for patients who are injured, severely burned, recovering from surgery or severely malnourished. In animals and human studies of wound healing, injections of Growth Hormone-stimulated the formation of collagen (the glue that holds tissue together), increased the tensile strength of wounds and made the wound close faster. Growth Hormone and growth factors have also been used successfully to treat leg ulcers in elderly people. Studies in rats showed that it healed incisions considerably much faster. It even strengthened bones after fracture and helped reverse muscle atrophy and weakness after surgery. In one study of burn patients, Growth Hormone evidently stimulated the protein synthesis needed for healing in the body and increased blood flow. Other studies have shown that Growth Hormone increases the positive nitrogen balance that is needed for the formation of new tissue.

That same study showed that daily injections of Growth Hormone were exceptionally effective for increasing the nutritional status of patients that had experienced severe fractures, severe infection or gastrointestinal surgery. In a double-blind trial, patients who were receiving IV feedings were also given injections of either Growth Hormone or a saline solution. The patients on Growth Hormone were able to conserve protein while the patients who received saline lost protein.

The healing properties of Growth Hormone are now under intense investigation. Of course, the most effective dosage and length of time that Growth Hormone should be given must be determined and orchestrated by a medical professional studied and experienced in the art that is regenerative processing, which can only be achieved through biological, internal healing, promoted by the medical, miracle solution that is HGH. Fill out our Medical History Form or call us so we can help you regress old physical problems and accelerate the healing of any new ones.

HGH Injections – Curious about HGH injections Therapy? Read more about what you can expect from this treatment and contact us for more information (866) 224-5698

**NOTE**  The content contained in this blog is subject to interpretation and is the opinion of the content writer.  We do not claim it to be fact.  We encourage you to consult a medical doctor before taking any prescribed medications or supplements.

December 27, 2015 by Joseph Fermin 1 Comment

Osteoporosis and Bone Mass, As We Get Older 0 (0)

Osteoporosis and Bone Mass

Bone Mass and Osteoporosis. As we get older, it appears that time flies. When you’re young you can’t wait to be a grown-up and then in an instant you’re researching information about the health of your bones as we age. This is an important inevitability we all face whether we like it or not. There have been plenty of advancements in the 21st Century that enables you to maintain a healthier lifestyle and stay youthful longer. Take a proactive approach and control your well being.

Why are we concerned about aging? We don’t want to be brittle. We want to remain self-sufficient while maintaining our strength and vigor. We don’t want to waste time worrying about whether we can complete normal tasks without the possibility of falling and sustaining an injury.

Unfortunately, approximately 2 million men already have Osteoporosis. the gradual thinning that makes bones brittle and porous which in turn makes them more prone to fracture. As discussed above, over two million men in America are at risk and have experienced early signs of bone loss and low bone density, called osteopenia.

Testosterone replacement therapy is now commonly used to treat and prevent Osteoporosis in men who have low testosterone levels. Extensive clinical research has shown that TRT may improve bone thickness, especially in the bones of the spine (vertebrae), which is incredible news if you’re interested in taking charge of our health and well-being.

The most common cause in men is testosterone deficiency. There’s a clear consensus that when you’re evaluating men, you should always check for low levels of testosterone. This is the main reason that doctors will advise on testosterone replacement options to help build bone mass in men hoping to avoid the side effects of suffering from Osteoporosis.

Call us for a full evaluation so we can help you to understand where you currently stand in terms of your overall health and hormone levels. Let AAI put you on the path to the newfound vitality that remains through your lifetime. Fill out our Medical History Form or call us directly to speak with a caring and educated Wellness Advisor. We are eager to get you started on becoming the best you.

Human Growth Hormone (HGH) Testosterone and Bone Mass

Calcium is a fundamental component of bones since it provides the strength and thickness. As we get older, hormonal changes begin occurring inside the body. These changes tend to reduce the absorption and deposition of calcium in addition to other vital minerals needed by our bones. This change in processing and absorption makes bones thinner, more porous, lighter and more brittle. The end result is that this change is increasing the probability of developing fractures and injuries in our future. Growth hormone plays an important role in sustaining good bone density for the most of us up to the age of 30 – 40. Regardless, without question, after age 30, hGH levels in the body do unfortunately begin to drop. The older we get, the greater the rate of decline. By age 40, you can rest assured your HGH levels have dropped considerably, and you want to take into account that this affects bone mineralization to a life-impacting extent. Interestingly enough, regularly, bone density is healthy up to the age of 30 in most men and women. Sound familiar? That’s correct! Right around the time in which it been scientifically documented that your natural GH levels begin to decline, your bone density and sustaining minerals begin to descend as well. Situations in which this condition becomes severe, the patient usually ends up being diagnosed with ‘bone’. In such conditions, supplementation with calcium and Vitamin D becomes invaluable essential.

Osteoporosis is a disease characterized by low bone mass and loss of bone tissue that may lead to weak and fragile bones. If you have osteoporosis, you have an increased risk for fractured bones (broken bones), particularly in the hip, spine, and wrist.

Osteoporosis is often considered to be a condition that frail elderly women develop. However, the damage from osteoporosis begins much earlier in life. Because peak bone density is reached at approximately 25 years of age, it is important to build strong bones by that age, so that the bones will remain strong later in life. Adequate calcium intake is an essential part of building strong bones.

In the United States, many people already have osteoporosis. A large number of people also have a low bone mass that places them at an increased risk for developing osteoporosis. As our population ages, these numbers will increase. A majority of those with osteoporosis are women. Of people older than 50 years of age, one in two women and one in eight men are predicted to have an osteoporosis-related fracture in their lifetime.

Significant risk has been reported in people of all ethnic backgrounds. White and Asian racial groups, however, are at greatest risk.

Osteoporosis occurs when there is an imbalance between new bone formation and old bone resorption. The body may fail to form enough new bone, or too much old bone may be reabsorbed, or both. Two essential minerals for normal bone formation are calcium and phosphate. Throughout youth, the body uses these minerals to produce bones. Calcium is essential for proper functioning of the heart, brain, and other organs. To keep those critical organs functioning, the body reabsorbs calcium that is stored in the bones to maintain blood calcium levels. If calcium intake is not sufficient or if the body does not absorb enough calcium from the diet, bone production and bone tissue may suffer. Thus, the bones may become weaker, resulting in brittle and fragile bones that can break easily.

Usually, the loss of bone occurs over an extended period of years. Often, a person will sustain a fracture before becoming aware that the disease is present. By then, the disease may be in its advanced stages and damage may be serious.

The leading cause of osteoporosis is a lack of certain hormones, particular estrogen in women and androgen in men. Women, especially those older than 60 years of age, are frequently diagnosed with the disease. Menopause is accompanied by lower estrogen levels and increases a woman’s risk for osteoporosis. Other factors that may contribute to bone loss in this age group include inadequate intake of calcium and vitamin D, lack of weight-bearing exercise, and other age-related changes in endocrine functions (in addition to the lack of estrogen).

Other conditions that may lead to osteoporosis include overuse of corticosteroids (Cushing syndrome), thyroid problems, lack of muscle use, neck pain bone cancer, certain genetic disorders, use of certain medications, and problems such as low calcium in the diet.

Early in the course of the disease, osteoporosis may cause no symptoms. Later, it may cause dull pain in the bones or muscles, particularly low back neck pain.

Later in the course of the disease, sharp pains may come on suddenly. The pain may not radiate (spread to other areas); it may be made worse by activity that puts weight on the area, may be accompanied by tenderness, and generally, begins to subside in one week. Pain may linger more than three months.

People with osteoporosis may not even recall a fall or other trauma that might cause a broken bone, such as in the spine or foot. Spinal compression fractures may result in loss of height with a stooped posture (called a dowager’s hump).


**NOTE**  The content contained in this blog is subject to interpretation and is the opinion of the content writer.  We do not claim it to be fact.  We encourage you to consult a medical doctor before taking any prescribed medications or supplements.

Testosterone Therapy Information

What Is Testosterone?
Testosterone Therapy Info
Testosterone Injections
symptoms of Low Testosterone
causes of Low Testosterone
Low Testosterone in Men
Low Testosterone in Women
Low Testosterone
Testosterone Cypionate
Testosterone Propionate
Testosterone Enanthate
Testosterone Patches
Testosterone Gels
Testosterone Boosters
Side Effects of Testosterone

December 22, 2015 by admin 0 Comments

How is Testosterone Produced? 4 (1)

Testosterone Produced

Testosterone produced by the human body is chemically and functionally similar to the kind produced by synthetic manufacturing processes. Only the kind that’s manufactured is used as a therapeutic material in hormone therapy. No effective therapy depends on using the same exact chemical form produced in the body. One process is completely natural, part of what happens in a healthy person, the other process is artificial and yields the only forms of testosterone that are used in effective anti-aging medications. Both processes involve chemical steps and end up with the same end result, testosterone that’s usable by the body.


December 3, 2015 by admin 0 Comments

Regrowth Neurons also called Neuro-Regeneration 0 (0)

Regrowth Neurons also called Neuro-Regeneration

Regrowth neurons… also called Neuro-Regeneration is one of the most complicated issues in the field of medical/science. The subject matter concerns the repair and regrowth of nerve cells called neurons. The long body of the neuron is called the Axon.

This issue is divided into two imperative groups…. Peripheral Nervous System (PNS) and the Central Nervous System (CNS) characterized by the brain and spinal cord.

PNS has a method of regeneration to the injured neurons followed by the quick release of white blood cells to fight infection. Schwann cells release neurotrophic factors, which enhance regrowth of PNS Regrowth Neurons in several ways. The Schwann cells prevent too much cytotoxicity, which is generally part of the healing process but elicits far too much inflammation for regeneration to proceed normally. Schwann cells also set up tubes alongside the damaged neuron. These tubes are even connected to the injured degraded PNS neuron and a host of healing biochemicals are released by the tube to stop neural degradation and provide healing repair to the affected injured neuron.

There is a host of outside interventions that can make this process go faster but I will save them for Regeneration of the brain and spinal cord, which please remember is still thought in many universities, even taught to this day, that CNS Regrowth Neurons cannot regenerate!

Regeneration and Repair of the Central Nervous System (Brain and Spinal Cord. There are two types of cells meant to serve and protect CNS Regrowth Neurons from injury. They are called Astrocytes and Glial cells. It may be hard to believe but there are much more astrocytes in the brain then there are brain Neurons and there are some 15 to 18 billion brain Regrowth Neurons. Normally, after an injury to brain neurons, astrocytes support Regrowth Neurons by providing antioxidant protection.

 The Good the Bad and the Ugly

 While the Astrocytes bring in many antioxidants to prevent free radical oxidative toxic damage to the brain Regrowth Neurons, they also over-react and allow for too much inflammation and cytotoxins from white blood cell production of Interleukin-2 and 6. This is called up-regulation of immune cell activity. It can destroy brain neurons faster than the initial injury to a brain or spinal neurons. This process brings about, even more, inflammation to try and carry away all of the dead cells, including neurons and astrocytes as well as white blood cell waste deposits.

Unfortunately, the brain is limited in size and too much inflammation causes intracranial pressure to the point where brain infarct is possible without making a surgical opening in the cranium to release the pressure….that is the bad and the ugly.

 How do we solve the above dire situation and bring about brain cell neuron regeneration?

In some cases, like bacterial or viral Encephalitis of the brain and spinal cord, many Regrowth Neurons can be killed or injured due to massive white blood cell proliferation. The white blood cells kill the bacteria and virus that causes Encephalitis, but the situation is so dramatic that in order for the brain to survive the infection killing neurons, the message which signals the white blood cells to enter the brain becomes so up-regulated that it cannot down-regulate to a normal response thus further killing both infected Regrowth Neurons and the infected brain cells both. Many people die from this berserk super up-regulated immune response stuck on full throttle. It is a vicious repetitive cycle.

We can stop this deathly cycle by giving the patient large intravenous doses of Gamma Globulin. Gamma Globulin consists of every type of antibody the human body can make. Scientists are not exactly certain how and why this has such a profound normalizing effect immunologically but it does. It is called Immuno-modulation to the normal set point.

 In both Stroke patients and infection based Encephalitis of the brain, Immuno-Modulation to a normal set point is a must in order for neuron cell death to stop and for regeneration to begin.

Certain biochemical factors play a vital role to decrease astrocytes! Cyclin Kinase decreases astrocyte proliferation, increasing neuron function and recovery. Caffeic acid, alpha- melanocyte stimulating hormone and cilostazol are all highly beneficial. They are considered essential to an improved condition by reducing astrocyte production. This treatment shows a decrease in neuron injury, the decrease in astrocyte high levels of production is associated with a more positive and improved outcome moving toward CNS neuron regeneration.

In 1984, I experienced a life/death illness called Herpetic Viral Encephalitis. It was misdiagnosed my Manhattans most elite doctors…virtually always fatal, I lived and due to the fact the death rate is so nearly complete I spent 3 years in bed and several more in a wheelchair. There was no internet, no smart phones, just a nearly destroyed brain with pain so blinding it felt as if two ice picks were being run through both eyes… and trying to escape by pushing through the back of my skull. Luckily for me the feelers I sent out daily… resulted in a call from Nobel Prize winning doctor and scientist, Dr. Rita Levi Montalcini who won the Nobel Prize for the discovery of Embryonic Fetal Nerve Growth Factor in 1986. I was the first human to ever get shots of Fetal Nerve Growth Factor in 1988 to grow back and regenerate my damaged brain Regrowth Neurons. Then this magnificent woman became my mentor. I still live speaking to her shadow every day as she passed over at the age of almost 104.

Rita Levi-Montalcini’s discovery of a protein called ‘fetal nerve growth factor,’‘ which fosters the growth of nerve fibers and also plays a role in the brain and the immune system, is one of the most important steps taken so far toward understanding how the fantastically complex system of nerves is laid down and linked to the tissues in a developing embryo. Her account of the adventures leading to this discovery, for which she won a Nobel Prize in Physiology and Medicine in 1986, has a special contemporary interest. We now know her discovery is how the brain grows all of its Regrowth Neurons when one is an embryo inside one’s mother’s womb until birth and sustains, protects and regenerates brain Regrowth Neurons if one is fortunate to be born with a large amount of FNGF .  Thank goodness she was able to scale it up through a deal with a large cutting edge biotechnology lab in Montreal. They are the ONLY Lab in the world to this day that makes Dr. Rita’s original formulations.

We at AAI are indeed incredibly fortunate to be able to have access to her formulations at all times.

We combined her fetal nerve growth factors with very youthful blood levels of HGH (human growth hormone…levels that would be normal for the average healthy 16-year-old. Eighteen months later, I was completely better in every way, brain regeneration wise, and in every other health manner. The addition of HGH was my inspiration as it has been known for many decades that it is HGH which mobilizes all of the fetal tissue growth factors such as cardiac tissue growth factor…to do protein synthesis and thus regeneration of the heart AND all other tissues contained within the human body. Without youthful blood levels of HGH (say blood levels normal for a healthy 26 year old to 30 year old) and credible levels of fetal nerve growth factor, regrowth Neurons is unlikely in the extreme, BUT with these safe and effective blood levels of both regrowth of every type of Neuron is probably in and that brings amazing hope. The only Regrowth we cannot master yet is CNS spinal cord cut in half…but the army medical scientists are getting very close.

Imagine how old we would all look if we did not have adequate cell levels of epithelial (skin tissue growth factor) to regenerate our SKIN? So, just like hormones, as we age we lose our tissue growth factors…and if they cannot be replaced to the optimal level from exogenous sources we will all be subject to the ravages of age-related illness.

Gratefully, here at AAI we have all critical tissue growth factors available to you, our beloved family of clients.                  


  1. Lloyd-Jones D, Adams RJ, Brown TM, Carnethon M, Dai S, De Simone G, Ferguson TB, Ford E, Furie K, Gillespie C, Go A, Greenlund K, Haase N, Hailpern S, Ho PM, Howard V, Kissela B, Kittner S, Lackland D, Lisabeth L, Marelli A, McDermott MM, Meigs J, Mozaffarian D, Mussolino M, Nichol G, Roger VL, Rosamond W, Sacco R, Sorlie P, Roger VL, Thom T, Wasserthiel-Smoller S, Wong ND, Wylie-Rosett J. Heart disease and stroke statistics–2010 update: a report from the American Heart Association.Circulation. 2010;121:e46–e215. [PubMed]
  2. Blakeley JO, Llinas RH. Thrombolytic therapy for acute ischemic stroke. J. Neurol. Sci. 2007;261:55–62.[PubMed]
  3. Marder VJ, Jahan R, Gruber T, Goyal A, Arora V. Thrombolysis with plasmin: implications for stroke treatment. Stroke. 2010;41:S45–S49. [PMC free article] [PubMed]
  4. Bernard SA, Gray TW, Buist MD, Jones BM, Silvester W, Gutteridge G, Smith K. Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. N. Engl. J. Med.2002;346:557–563. [PubMed]
  5. Howells DW, Porritt MJ, Rewell SS, O’Collins V, Sena ES, van der Worp HB, Traystman RJ, Macleod MR. Different strokes for different folks: the rich diversity of animal models of focal cerebral ischemia. J. Cereb. Blood Flow Metab. 30:1412–1431. [PMC free article] [PubMed]
  6. Kettenmann H, Ramson BR. Neuroglia. New York: Oxford University Press; 1995.
  7. Nedergaard M, Ransom B, Goldman SA. New roles for astrocytes: redefining the functional architecture of the brain. Trends Neurosci. 2003;26:523–530. [PubMed]
  8. Sofroniew MV, Vinters HV. Astrocytes: biology and pathology. Acta Neuropathol. 2010;119:7–35.[PMC free article] [PubMed]
  9. Goldberg MP, Choi DW. Combined oxygen and glucose deprivation in cortical cell culture: calcium-dependent and calcium-independent mechanisms of neuronal injury. J. Neurosci. 1993;13:3510–3524.[PubMed]
  10. Swanson RA, Ying W, Kauppinen TM. Astrocyte influences on ischemic neuronal death. Curr. Mol. Med. 2004;4:193–205. [PubMed]
  11. Dringen R, Hirrlinger J. Glutathione pathways in the brain. Biol. Chem. 2003;384:505–516. [PubMed]
  12. Wilson JX. Antioxidant defense of the brain: a role for astrocytes. Can. J. Physiol. Pharmacol.1997;75:1149–1163. [PubMed]
  13. Rossi DJ, Brady JD, Mohr C. Astrocyte metabolism and signaling during brain ischemia. Nat. Neurosci.2007;10:1377–1386. [PubMed]
  14. Nedergaard M, Dirnagl U. Role of glial cells in cerebral ischemia. Glia. 2005;50:281–286. [PubMed]
  15. Ouyang YB, Voloboueva LA, Xu LJ, Giffard RG. Selective dysfunction of hippocampal CA1 astrocytes contributes to delayed neuronal damage after transient forebrain ischemia. J. Neurosci.2007;27:4253–4260. [PMC free article] [PubMed]
  16. Xu L, Emery JF, Ouyang YB, Voloboueva LA, Giffard RG. Astrocyte targeted overexpression of Hsp72 or SOD2 reduces neuronal vulnerability to forebrain ischemia. Glia. 2010;58:1042–1049.[PMC free article] [PubMed]
  17. Anderson MF, Blomstrand F, Blomstrand C, Eriksson PS, Nilsson M. Astrocytes and stroke: networking for survival? Neurochem. Res. 2003;28:293–305. [PubMed]
  18. Giffard RG, Swanson RA. Ischemia-induced programmed cell death in astrocytes. Glia. 2005;50:299–306. [PubMed]
  19. Almeida A, Delgado-Esteban M, Bolanos JP, Medina JM. Oxygen and glucose deprivation induces mitochondrial dysfunction and oxidative stress in neurones but not in astrocytes in primary culture. J. Neurochem. 2002;81:207–217. [PubMed]
  20. Xu L, Sapolsky RM, Giffard RG. Differential sensitivity of murine astrocytes and Regrowth Neurons from different brain regions to injury. Exp. Neurol. 2001;169:416–424. [PubMed]
  21. Zhao G, Flavin MP. Differential sensitivity of rat hippocampal and cortical astrocytes to oxygen-glucose deprivation injury. Neurosci. Lett. 2000;285:177–180. [PubMed]
  22. Lukaszevicz AC, Sampaio N, Guegan C, Benchoua A, Couriaud C, Chevalier E, Sola B, Lacombe P, Onteniente B. High sensitivity of protoplasmic cortical astroglia to focal ischemia. J. Cereb. Blood Flow Metab. 2002;22:289–298. [PubMed]
  23. Bondarenko A, Chesler M. Rapid astrocyte death induced by transient hypoxia, acidosis, and extracellular ion shifts. Glia. 2001;34:134–142. [PubMed]
  24. Giffard RG, Monyer H, Choi DW. Selective vulnerability of cultured cortical glia to injury by extracellular acidosis. Brain Res. 1990;530:138–141. [PubMed]
  25. Swanson RA, Farrell K, Stein BA. Astrocyte energetics, function, and death under conditions of incomplete ischemia: a mechanism of glial death in the penumbra. Glia. 1997;21:142–153. [PubMed]
  26. Tombaugh GC, Sapolsky RM. Mechanistic distinctions between excitotoxic and acidotic hippocampal damage in an in vitromodel of ischemia. J. Cereb. Blood Flow Metab. 1990;10:527–535. [PubMed]
  27. Chen Y, Swanson RA. Astrocytes and brain injury. J. Cereb. Blood Flow Metab. 2003;23:137–149.[PubMed]
  28. Lee MH, Kim H, Kim SS, Lee TH, Lim BV, Chang HK, Jang MH, Shin MC, Shin MS, Kim CJ. Treadmill exercise suppresses ischemia-induced increment in apoptosis and cell proliferation in hippocampal dentate gyrus of gerbils. Life Sci. 2003;73:2455–2465. [PubMed]
  29. Li Y, Chopp M, Zhang ZG, Zhang RL. Expression of glial fibrillary acidic protein in areas of focal cerebral ischemia accompanies neuronal expression of 72-kDa heat shock protein. J. Neurol. Sci.1995;128:134–142. [PubMed]
  30. Schroeter M, Schiene K, Kraemer M, Hagemann G, Weigel H, Eysel UT, Witte OW, Stoll G. Astroglial responses in photochemically induced focal ischemia of the rat cortex. Exp Brain Res. 1995;106:1–6.[PubMed]
  31. Van Beek J, Chan P, Bernaudin M, Petit E, MacKenzie ET, Fontaine M. Glial responses, clusterin, and complement in permanent focal cerebral ischemia in the mouse. Glia. 2000;31:39–50. [PubMed]
  32. Yamashita K, Vogel P, Fritze K, Back T, Hossmann KA, Wiessner C. Monitoring the temporal and spatial activation pattern of astrocytes in focal cerebral ischemia using in situ hybridization to GFAP mRNA: comparison with sgp-2 and hsp70 mRNA and the effect of glutamate receptor antagonists. Brain Res.1996;735:285–297. [PubMed]
  33. Liu D, Smith CL, Barone FC, Ellison JA, Lysko PG, Li K, Simpson IA. Astrocytic demise precedes delayed neuronal death in focal ischemic rat brain. Brain Res. Mol. Brain Res. 1999;68:29–41. [PubMed]
  34. Dugan LL, Bruno VM, Amagasu SM, Giffard RG. Glia modulate the response of murine cortical Regrowth Neurons to excitotoxicity: glia exacerbate AMPA neurotoxicity. J. Neurosci. 1995;15:4545–4555. [PubMed]
  35. Rosenberg PA, Aizenman E. Hundred-fold increase in neuronal vulnerability to glutamate toxicity in astrocyte-poor cultures of rat cerebral cortex. Neurosci. Lett. 1989;103:162–168. [PubMed]
  36. Voloboueva LA, Suh SW, Swanson RA, Giffard RG. Inhibition of mitochondrial function in astrocytes: implications for neuroprotection. J. Neurochem. 2007;102:1383–1394. [PMC free article] [PubMed]
  37. Chen JC, Hsu-Chou H, Lu JL, Chiang YC, Huang HM, Wang HL, Wu T, Liao JJ, Yeh TS. Down-regulation of the glial glutamate transporter GLT-1 in rat hippocampus and striatum and its modulation by a group III metabotropic glutamate receptor antagonist following transient global forebrain ischemia. Neuro-pharmacology. 2005;49:703–714. [PubMed]
  38. Yeh TH, Hwang HM, Chen JJ, Wu T, Li AH, Wang HL. Glutamate transporter function of rat hippocampal astrocytes is impaired following the global ischemia. Neurobiol. Dis. 2005;18:476–483.[PubMed]
  39. Ito U, Hakamata Y, Kawakami E, Oyanagi K. Degeneration of astrocytic processes and their mitochondria in cerebral cortical regions peripheral to the cortical infarction: heterogeneity of their disintegration is closely associated with disseminated selective neuronal necrosis and maturation of injury.Stroke. 2009;40:2173–2181. [PubMed]
  40. Ito U, Hakamata Y, Kawakami E, Oyanagi K. Temporary focal cerebral ischemia results in swollen astrocytic end-feet that compress microvessels and lead to focal cortical infarction. J. Cereb. Blood Flow Metab. 2010 [PMC free article] [PubMed]
  41. Vangeison G, Rempe DA. The Janus-faced effects of hypoxia on astrocyte function. Neuroscientist.2009;15:579–588. [PMC free article] [PubMed]
  42. Bidmon HJ, Jancsik V, Schleicher A, Hagemann G, Witte OW, Woodhams P, Zilles K. Structural alterations and changes in cytoskeletal proteins and proteoglycans after focal cortical ischemia. Neuroscience.1998;82:397–420. [PubMed]
  43. Yasuda Y, Tateishi N, Shimoda T, Satoh S, Ogitani E, Fu-jita S. Relationship between S100beta and GFAP expression in astrocytes during infarction and glial scar formation after mild transient ischemia. Brain Res. 2004;1021:20–31. [PubMed]
  44. Smith GM, Strunz C. Growth factor and cytokine regulation of chondroitin sulfate proteoglycans by astrocytes. Glia. 2005;52:209–218. [PubMed]
  45. Gris P, Tighe A, Levin D, Sharma R, Brown A. Transcriptional regulation of scar gene expression in primary astrocytes. Glia. 2007;55:1145–1155. [PubMed]
  46. Martinez AD, Saez JC. Regulation of astrocyte gap junctions by hypoxia-reoxygenation. Brain Res. Brain Res. Rev. 2000;32:250–258. [PubMed]
  47. Lin JH, Weigel H, Cotrina ML, Liu S, Bueno E, Hansen AJ, Hansen TW, Goldman S, Nedergaard M. Gap-junction-mediated propagation and amplification of cell injury. Nat. Neurosci. 1998;1:494–500.[PubMed]
  48. Wang W, Redecker C, Yu ZY, Xie MJ, Tian DS, Zhang L, Bu BT, Witte OW. Rat focal cerebral ischemia induced astrocyte proliferation and delayed neuronal death are attenuated by cyclin-dependent kinase inhibition. J. Clin. Neurosci. 2008;15:278–285. [PubMed]
  49. Forslin Aronsson S, Spulber S, Popescu LM, Winblad B, Post C, Oprica M, Schultzberg M. alpha-Melanocyte-stimulating hormone is neuroprotective in rat global cerebral ischemia. Neuropeptides.2006;40:65–75. [PubMed]
  50. Fang SH, Wei EQ, Zhou Y, Wang ML, Zhang WP, Yu GL, Chu LS, Chen Z. Increased expression of cysteinyl leukotriene receptor-1 in the brain mediates neuronal damage and astrogliosis after focal cerebral ischemia in rats. Neuroscience. 2006;140:969–979. [PubMed]
  51. Ye YL, Shi WZ, Zhang WP, Wang ML, Zhou Y, Fang SH, Liu LY, Zhang Q, Yu YP, Wei EQ. Cilostazol, a phosphodiesterase 3 inhibitor, protects mice against acute and late ischemic brain injuries. Eur. J. Pharmacol. 2007;557:23–31. [PubMed]
  52. Zhou Y, Fang SH, Ye YL, Chu LS, Zhang WP, Wang ML, Wei EQ. Caffeic acid ameliorates early and delayed brain injuries after focal cerebral ischemia in rats. Acta Pharmacol. Sin. 2006;27:1103–1110.[PubMed]
  53. Chung JH, Lee EY, Jang MH, Kim CJ, Kim J, Ha E, Park HK, Choi S, Lee H, Park SH, Leem KH, Kim EH. Acupuncture decreases ischemia-induced apoptosis and cell proliferation in dentate gyrus of gerbils. Neurol. Res. 2007;29 Suppl 1:S23–S27. [PubMed]
  54. del Zoppo GJ. Inflammation and the neurovascular unit in the setting of focal cerebral ischemia.Neuroscience. 2009;158:972–982. [PMC free article] [PubMed]
  55. Kaur C, Ling EA. Blood brain barrier in hypoxic-ischemic conditions. Curr. Neurovasc. Res. 2008;5:71–81. [PubMed]
  56. Nawashiro H, Brenner M, Fukui S, Shima K, Hallenbeck JM. High susceptibility to cerebral ischemia in GFAP-null mice. J. Cereb. Blood Flow Metab. 2000;20:1040–1044. [PubMed]
  57. Li L, Lundkvist A, Andersson D, Wilhelmsson U, Nagai N, Pardo AC, Nodin C, Stahlberg A, Aprico K, Larsson K, Yabe T, Moons L, Fotheringham A, Davies I, Carmeliet P, Schwartz JP, Pekna M, Kubista M, Blomstrand F, Mara-gakis N, Nilsson M, Pekny M. Protective role of reactive astrocytes in brain ischemia. J. Cereb. Blood Flow Metab. 2008;28:468–481. [PubMed]
  58. Kinoshita A, Yamada K, Kohmura E, Hayakawa T. Effect of astrocyte-derived factors on ischemic brain edema induced by rat MCA occlusion. APMIS. 1990;98:851–857. [PubMed]
  59. Buchhold B, Mogoanta L, Suofu Y, Hamm A, Walker L, Kessler C, Popa-Wagner A. Environmental enrichment improves functional and neuropathological indices following stroke in young and aged rats.Restor. Neurol. Neurosci. 2007;25:467–484. [PubMed]
  60. Keiner S, Wurm F, Kunze A, Witte OW, Redecker C. Rehabilitative therapies differentially alter proliferation and survival of glial cell populations in the perilesional zone of cortical infarcts. Glia.2008;56:516–527. [PubMed]
  61. Popa-Wagner A, Badan I, Walker L, Groppa S, Patrana N, Kessler C. Accelerated infarct development, cytogenesis and apoptosis following transient cerebral ischemia in aged rats. Acta Neuropathol.2007;113:277–293. [PubMed]
  62. Li Y, Chen J, Zhang CL, Wang L, Lu D, Katakowski M, Gao Q, Shen LH, Zhang J, Lu M, Chopp M.