by David M. Panchision*

Diseases of the nervous system, including congenital disorders, cancers, and degenerative diseases, affect millions of people of all ages. Congenital disorders occur when the brain or spinal cord does not form correctly during development. Cancers of the nervous system result from the uncontrolled spread of aberrant cells. Degenerative diseases occur when the nervous system loses functioning of nerve cells. Most of the advances in stem cell research have been directed at treating degenerative diseases. While many treatments aim to limit the damage of these diseases, in some cases scientists believe that damage can be reversed by replacing lost cells with new ones derived from cells that can mature into nerve cells, called neural stem cells. Research that uses stem cells to treat nervous system disorders remains an area of great promise and challenge to demonstrate that cell-replacement therapy can restore lost function.

The nervous system is a complex organ made up of nerve cells (also called neurons) and glial cells, which surround and support neurons (see Figure 3.1). Neurons send signals that affect numerous functions including thought processes and movement. One type of glial cell, the oligodendrocyte, acts to speed up the signals of neurons that extend over long distances, such as in the spinal cord. The loss of any of these cell types may have catastrophic results on brain function.

Although reports dating back as early as the 1960s pointed towards the possibility that new nerve cells are formed in adult mammalian brains, this knowledge was not applied in the context of curing devastating brain diseases until the 1990s. While earlier medical research focused on limiting damage once it had occurred, in recent years researchers have been working hard to find out if the cells that can give rise to new neurons can be coaxed to restore brain function. New neurons in the adult brain arise from slowly-dividing cells that appear to be the remnants of stem cells that existed during fetal brain development. Since some of these adult cells still retain the ability to generate both neurons and glia, they are referred to as adult neural stem cells.

These findings are exciting because they suggest that the brain may contain a built-in mechanism to repair itself. Unfortunately, these new neurons are only generated in a few sites in the brain and turn into only a few specialized types of nerve cells. Although there are many different neuronal cell types in the brain, we now know that these new neurons can quot;plug inquot; correctly to assist brain function.1 The discovery of these cells has spurred further research into the characteristics of neural stem cells from the fetus and the adult, mostly using rodents and primates as model species. The hope is that these cells may be able to replenish those that are functionally lost in human degenerative diseases such as Parkinson's Disease, Huntington's Disease, and amyotrophic lateral sclerosis (ALS, also known as Lou Gehrig's disease), as well as from brain and spinal cord injuries that result from stroke or trauma.

Scientists are applying these new stem cell discoveries in two ways in their experiments. First, they are using current knowledge of normal brain development to modulate stem cells that are harvested and grown in culture. Researchers can then transplant these cultured cells into the brain of an animal model and allow the brain's own signals to differentiate the stem cells into neurons or glia. Alternatively, the stem cells can be induced to differentiate into neurons and glia while in the culture dish, before being transplanted into the brain. Much progress has been made the last several years with human embryonic stem (ES) cells that can differentiate into all cell types in the body. While ES cells can be maintained in culture for relatively long periods of time without differentiating, they usually must be coaxed through many more steps of differentiation to produce the desired cell types. Recent studies, however, suggest that ES cells may differentiate into neurons in a more straightforward manner than may other cell types.

Figure 3.1. The NeuronWhen sufficient neurotransmitters cross synapses and bind receptors on the neuronal cell body and dendrites, the neuron sends an electrical signal down its axon to synaptic terminals, which in turn release neurotransmitters into the synapse that affects the following neuron. The brain neurons that die in Parkinson's Disease release the transmitter dopamine. Oligodendrocytes supply the axon with an insulating myelin sheath.

2001 Terese Winslow

Second, scientists are identifying growth (trophic) factors that are normally produced and used by the developing and adult brain. They are using these factors to minimize damage to the brain and to activate the patient's own stem cells to repair damage that has occurred. Each of these strategies is being aggressively pursued to identify the most effective treatments for degenerative diseases. Most of these studies have been carried out initially with animal stem cells and recipients to determine their likelihood of success. Still, much more research is necessary to develop stem cell therapies that will be useful for treating brain and spinal cord disease in the same way that hematopoietic stem cell therapies are routinely used for immune system replacement (see Chapter 2).

The majority of stem cell studies of neurological disease have used rats and mice, since these models are convenient to use and are well-characterized biologically. If preliminary studies with rodent stem cells are successful, scientists will attempt to transplant human stem cells into rodents. Studies may then be carried out in primates (e.g., monkeys) to offer insight into how humans might respond to neurological treatment. Human studies are rarely undertaken until these other experiments have shown promising results. While human transplant studies have been carried out for decades in the case of Parkinson's disease, animal research continues to provide improved strategies to generate an abundant supply of transplantable cells.

The intensive research aiming at curing Parkinson's disease with stem cells is a good example for the various strategies, successful results, and remaining challenges of stem cell-based brain repair. Parkinson's disease is a progressive disorder of motor control that affects roughly 2% of persons 65 years and older. Triggered by the death of neurons in a brain region called the substantia nigra, Parkinson's disease begins with minor tremors that progress to limb and bodily rigidity and difficulty initiating movement. These neurons connect via long axons to another region called the striatum, composed of subregions called the caudate nucleus and the putamen. These neurons that reach from the substantia nigra to the striatum release the chemical transmitter dopamine onto their target neurons in the striatum. One of dopamine's major roles is to regulate the nerves that control body movement. As these cells die, less dopamine is produced, leading to the movement difficulties characteristic of Parkinson's disease. Currently, the causes of death of these neurons are not well understood.

For many years, doctors have treated Parkinson's disease patients with the drug levodopa (L-dopa), which the brain converts into dopamine. Although the drug works well initially, levodopa eventually loses its effectiveness, and side-effects increase. Ultimately, many doctors and patients find themselves fighting a losing battle. For this reason, a huge effort is underway to develop new treatments, including growth factors that help the remaining dopamine neurons survive and transplantation procedures to replace those that have died.

The strategy to use new cells to replace lost ones is not new. Surgeons first attempted to transplant dopamine-releasing cells from a patient's own adrenal glands in the 1980s.2,3 Although one of these studies reported a dramatic improvement in the patients' conditions, U.S. surgeons were only able to achieve modest and temporary improvement, insufficient to outweigh the risks of such a procedure. As a result, these human studies were not pursued further.

Another strategy was attempted in the 1970s, in which cells derived from fetal tissue from the mouse substantia nigra was transplanted into the adult rat eye and found to develop into mature dopamine neurons.4 In the 1980s, several groups showed that transplantation of this type of tissue could reverse Parkinson's-like symptoms in rats and monkeys when placed in the damaged areas.The success of the animal studies led to several human trials beginning in the mid-1980s.5,6 In some cases, patients showed a lessening of their symptoms. Also, researchers could measure an increase in dopamine neuron function in the striatum of these patients by using a brain-imaging method called positron emission tomography (PET) (see Figure 3.2).7

The NIH has funded two large and well-controlled clinical trials in the past 15 years in which researchers transplanted tissue from aborted fetuses into the striatum of patients with Parkinson's disease.7,8 These studies, performed in Colorado and New York, included controls where patients received quot;shamquot; surgery (no tissue was implanted), and neither the patients nor the scientists who evaluated their progress knew which patients received the implants. The patients' progress was followed for up to eight years. Unfortunately, both studies showed that the transplants offered little benefit to the patients as a group. While some patients showed improvement, others began to suffer from dyskinesias, jerky involuntary movements that are often side effects of long-term L-dopa treatment. This effect occurred in 15% of the patients in the Colorado study.7 and more than half of the patients in the New York study.8 Additionally, the New York study showed evidence that some patients' immune systems were attacking the grafts.

However, promising findings emerged from these studies as well. Younger and milder Parkinson's patients responded relatively well to the grafts, and PET scans of patients showed that some of the transplanted dopamine neurons survived and matured. Additionally, autopsies on three patients who died of unrelated causes, years after the surgeries, indicated the presence of dopamine neurons from the graft. These cells appeared to have matured in the same way as normal dopamine neurons, which suggested that they were acting normally in the brain.

Figure 3.2. Positron Emission Tomography (PET) images from a Parkinson's patient before and after fetal tissue transplantation. The image taken before surgery (left) shows uptake of a radioactive form of dopamine (red) only in the caudate nucleus, indicating that dopamine neurons have degenerated. Twelve months after surgery, an image from the same patient (right) reveals increased dopamine function, especially in the putamen. (Reprinted with permission from N Eng J Med 2001;344(10) p. 710.)

Researchers in Sweden followed the severity of dyskinesia in patients for eleven years after neural transplantation and found that the severity was typically mild or moderate. These results suggested that dyskinesias were due to effects that were distinct from the beneficial effects of the grafts.9 Dyskinesias may therefore be related to the ways that transplantation disturbs other cells in the brain and so may be minimized by future improvements in therapy. Another study that involved the grafting of cells both into the striatum (the target of dopamine neurons) and the substantia nigra (where dopamine neurons normally reside) of three patients showed no adverse effects and some modest improvement in patient movement.10 To determine the full extent of therapeutic benefits from such a procedure and confirm the reliability of these results, this study will need to be repeated with a larger patient population that includes the appropriate controls.

The limited success of these studies may reflect variations in the fetal tissue used for transplantation, which is of limited quantity and can not be standardized or well-characterized. The full complement of cells in these fetal tissue samples is not known at present. As a result, the tissue remains the greatest source of uncertainty in patient outcome following transplantation.

The major goal for Parkinson's investigators is to generate a source of cells that can be grown in large supply, maintained indefinitely in the laboratory, and differentiated efficiently into dopamine neurons that work when transplanted into the brain of a Parkinson's patient. Scientists have investigated the behavior of stem cells in culture and the mechanisms that govern dopamine neuron production during development in their attempts to identify optimal culture conditions that allow stem cells to turn into dopamine-producing neurons.

Preliminary studies have been carried out using immature stem cell-like precursors from the rodent ventral midbrain, the region that normally gives rise to these dopamine neurons. In one study these precursors were turned into functional dopamine neurons, which were then grafted into rats previously treated with 6-hydroxy-dopamine (6-OHDA) to kill the dopamine neurons in their substantia nigra and induce Parkinson's-like symptoms. Even though the percentage of surviving dopamine neurons was low following transplantation, it was sufficient to relieve the Parkinson's-like symptoms.11 Unfortunately, these fetal cells cannot be maintained in culture for very long before they lose the ability to differentiate into dopamine neurons.

Cells with features of neural stem cells have been derived from ES-cells, fetal brain tissue, brain tissue from neurosurgery, and brain tissue that was obtained after a person's death. There is controversy about whether other organ stem cell populations, such as hematopoietic stem cells, either contain or give rise to neural stem cells

Many researchers believe that the more primitive ES cells may be an excellent source of dopamine neurons because ES-cells can be grown indefinitely in a laboratory dish and can differentiate into any cell type, even after long periods in culture. Mouse ES cells injected directly into 6-OHDA-treated rat brains led to relief of Parkinson-like symptoms. Further investigation showed that these ES cells had differentiated into both dopamine and serotonin neurons.12 This latter type of neuron is generated in an adjacent region of the brain and may complicate the response to transplantation. Since ES cells can generate all cell types in the body, unwanted cell types such as muscle or bone could theoretically also be introduced into the brain. As a result, a great deal of effort is being currently put into finding the right quot;recipequot; for turning ES cells into dopamine neuronsand only this cell typeto treat Parkinson's disease. Researchers strive to learn more about normal brain development to help emulate the natural progression of ES cells toward dopamine neurons in the culture dish.

The recent availability of human ES cells has led to further studies to examine their potential for differentiation into dopamine neurons. Recently, dopamine neurons from human embryonic stem cells have been generated.13 One research group used a special type of companion cell, along with specific growth factors, to promote the differentiation of the ES cells through several stages into dopamine neurons. These neurons showed many of the characteristic properties of normal dopamine neurons.13 Furthermore, recent evidence of more direct neuronal differentiation methods from mouse ES cells fuels hope that scientists can refine and streamline the production of transplantable human dopamine neurons.

One method with great therapeutic potential is nuclear transfer. This method fuses the genetic material from one individual donor with a recipient egg cell that has had its nucleus removed. The early embryo that develops from this fusion is a genetic match for the donor. This process is sometimes called quot;therapeutic cloningquot; and is regarded by some to be ethically questionable. However, mouse ES cells have been differentiated successfully in this way into dopamine neurons that corrected Parkinsonian symptoms when transplanted into 6-OHDA-treated rats.14 Similar results have been obtained using parthenogenetic primate stem cells, which are cells that are genetic matches from a female donor with no contribution from a male donor.15 These approaches may offer the possibility of treating patients with genetically-matched cells, thereby eliminating the possibility of graft rejection.

Scientists are also studying the possibility that the brain may be able to repair itself with therapeutic support. This avenue of study is in its early stages but may involve administering drugs that stimulate the birth of new neurons from the brain's own stem cells. The concept is based on research showing that new nerve cells are born in the adult brains of humans. The phenomenon occurs in a brain region called the dentate gyrus of the hippocampus. While it is not yet clear how these new neurons contribute to normal brain function, their presence suggests that stem cells in the adult brain may have the potential to re-wire dysfunctional neuronal circuitry.

The adult brain's capacity for self-repair has been studied by investigating how the adult rat brain responds to transforming growth factor alpha (TGF), a protein important for early brain development that is expressed in limited quantities in adults.16 Injection of TGF into a healthy rat brain causes stem cells to divide for several days before ceasing division. In 6-OHDAtreated (Parkinsonian) rats, however, the cells proliferated and migrated to the damaged areas. Surprisingly, the TGF-treated rats showed few of the behavioral problems associated with untreated Parkinsonian rats.16 Additionally, in 2002 and 2003, two research groups isolated small numbers of dividing cells in the substantia nigra of adult rodents.17,18

These findings suggest that the brain can repair itself, as long as the repair process is triggered sufficiently. It is not clear, though, whether stem cells are responsible for this repair or if the TGF activates a different repair mechanism.

Many other diseases that affect the nervous system hold the potential for being treated with stem cells. Experimental therapies for chronic diseases of the nervous system, such as Alzheimer's disease, Lou Gehrig's disease, or Huntington's disease, and for acute injuries, such as spinal cord and brain trauma or stoke, are being currently developed and tested. These diverse disorders must be investigated within the contexts of their unique disease processes and treated accordingly with highly adapted cell-based approaches.

Although severe spinal cord injury is an area of intense research, the therapeutic targets are not as clear-cut as in Parkinson's disease. Spinal cord trauma destroys numerous cell types, including the neurons that carry messages between the brain and the rest of the body. In many spinal injuries, the cord is not actually severed, and at least some of the signal-carrying neuronal axons remain intact. However, the surviving axons no longer carry messages because oligodendrocytes, which make the axons' insulating myelin sheath, are lost. Researchers have recently made progress to replenish these lost myelin-producing cells. In one study, scientists cultured human ES cells through several steps to make mixed cultures that contained oligodendrocytes. When they injected these cells into the spinal cords of chemically-demyelinated rats, the treated rats regained limited use of their hind limbs compared with un-grafted rats.19 Researchers are not certain, however, whether the limited increase in function observed in rats is actually due to the remyelination or to an unidentified trophic effect of the treatment.

Getting neurons to grow new axons through the injury site to reconnect with their targets is even more challenging. While myelin promotes normal neuronal function, it also inhibits the growth of new axons following spinal injury. In a recent study to attempt post-trauma axonal growth, Harper and colleagues treated ES cells with a combination of factors that are known to promote motor neuron differentiation.20 The researchers then transplanted these cells into adult rats that had received spinal cord injuries. While many of these cells survived and differentiated into neurons, they did not send out axons unless the researchers also added drugs that interfered with the inhibitory effects of myelin. The growth effect was modest, and the researchers have not yet seen evidence of functional neuron connections. However, their results raise the possibility that signals can be turned on and off in the correct order to allow neurons to reconnect and function properly. Spinal injury researchers emphasize that additional basic and preclinical research must be completed before attempting human trials using stem cell therapies to repair the trauma-damaged nervous system.

Since myelin loss is at the heart of many other degenerative diseases, oligodendrocytes made from ES cells may be useful to treat these conditions as well. For example, scientists recently cultured human ES cells with a combination of growth factors to generate a highly enriched population of myelinating oligodendrocyte precursors.21,22 The researchers then tested these cells in a genetically-mutated mouse that does not produce myelin properly. When the growth factor-cultured ES cells were transplanted into affected mice, the cells migrated and differentiated into mature oligodendrocytes that made myelin sheaths around neighboring axons. These researchers subsequently showed that these cells matured and improved movement when grafted in rats with spinal cord injury.23 Improved movement only occurred when grafting was completed soon after injury, suggesting that some post-injury responses may interfere with the grafted cells. However, these results are sufficiently encouraging to plan clinical trials to test whether replacement of myelinating glia can treat spinal cord injury.

Amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig's disease, is characterized by a progressive destruction of motor neurons in the spinal cord. Patients with ALS develop increasing muscle weakness over time, which ultimately leads to paralysis and death. The cause of ALS is largely unknown, and there are no effective treatments. Researchers recently have used different sources of stem cells to test in rat models of ALS to test for possible nerve cell-restoring properties. In one study, researchers injected cell clusters made from embryonic germ (EG) cells into the spinal cord fluid of the partially-paralyzed rats.24 Three months after the injections, many of the treated rats were able to move their hind limbs and walk with difficulty, while the rats that did not receive cell injections remained paralyzed. Moreover, the transplanted cells had migrated throughout the spinal fluid and developed into cells that displayed molecular characteristics of mature motor neurons. However, too few cells matured in this way to account for the recovery, and there was no evidence that the transplanted cells formed functional connections with muscles. The researchers suggest that the transplanted cells may be promoting recovery in some other way, such as by producing trophic factors.

This possibility was addressed in a second study in which scientists grew human fetal CNS stem cells in culture and genetically modified them to produce a trophic factor that promotes the survival of cells that are lost in ALS. When grafted into the spinal cords of the ALS-like rats, these cells secreted the desired growth factor and promoted the survival of the neurons that are normally lost in the ALS-like rats.25 While promising, these results highlight the need for additional basic research into functional recovery in ALS disease models.

Stroke affects about 750,000 patients per year in the

U.S. and is the most common cause of disability in adults. A stroke occurs when blood flow to the brain is disrupted. As a consequence, cells in affected brain regions die from insufficient amounts of oxygen. The treatment of stroke with anti-clotting drugs has dramatically improved the odds of patient recovery. However, in many patients the damage cannot be prevented, and the patient may permanently lose the functions of affected areas of the brain. For these patients, researchers are now considering stem cells as a way to repair the damaged brain regions. This problem is made more challenging because the damage in stroke may be widespread and may affect many cell types and connections.

However, researchers from Sweden recently observed that strokes in rats cause the brain's own stem cells to divide and give rise to new neurons.26 However, these neurons, which survived only a couple of weeks, are few in number compared to the extent of damage caused. A group from the University of Tokyo added a growth factor, bFGF, into the brains of rats after stroke and showed that the hippocampus was able to generate large numbers of new neurons.27 The researchers found evidence that these new neurons were actually making connections with other neurons. These and other results suggest that future stroke treatments may be able to coax the brain's own stem cells to make replacement neurons.

Taking an alternative approach, another group attempted transplantation as a means to treat the loss of brain mass after a severe stroke. By adding stem cells onto a polymer scaffold that they implanted into the stroke-damaged brains of mice, the researchers demonstrated that the seeded stem cells differentiated into neurons and that the polymer scaffold reduced scarring.28 Two groups transplanted human fetal stem cells in independent studies into the brains of stroke-affected rodents; these stem cells not only survived but migrated to the damaged areas of the brain.29,30 These studies increase our knowledge of how stem cells are attracted to diseased areas of the brain.

There is also increasing evidence from numerous animal disease models that stem cells are actively drawn to brain damage. Once they reach these damaged areas, they have been shown to exert beneficial effects such as reducing brain inflammation or supporting nerve cells. It is hoped that, once these mechanisms are better understood, this stem cell recruitment can potentially be exploited to mobilize a patient's own stem cells.

Similar lines of research are being considered with other disorders such as Huntington's Disease and certain congenital defects. While much attention has been called to the treatment of Alzheimer's Disease, it is still not clear if stem cells hold the key to its treatment. But despite the fact that much basic work remains and many fundamental questions are yet to be answered, researchers are hopeful that repair for once-incurable nervous system disorders may be amenable to stem cell based therapies.

Considerable progress has been made the last few years in our understanding of stem cell biology and devising sources of cells for transplantation. New methods are also being developed for cell delivery and targeting to affected areas of the body. These advances have fueled optimism that new treatments will come for millions of persons who suffer from neurological disorders. But it is the current task of scientists to bring these methods from the laboratory bench to the clinic in a scientifically sound and ethically acceptable fashion.

Notes:

* Chief, Developmental Neurobiology Program, Molecular, Cellular & Genomic Neuroscience Research Branch, Division of Neuroscience and Basic Behavioral Science, National Institute of Mental Health, National Institutes of Health, Email: panchisiond@mail.nih.gov

Chapter 2|Table of Contents|Chapter 4

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Repairing the Nervous System with Stem Cells | stemcells ...

Editors Note: This article first appeared in the May2016edition of TTACsHeroes Against Cancermember newsletter.

Lack of adequate nutrition can lead to cancer growth on the other hand, the right nutrients can inhibit cancerous cells from multiplying.

Scientists have known for decades that cancer cells have the ability to repair themselves, multiply, differentiate, and escape normal cellular processes such as apoptosis or cell suicide. Only recently researchers have learned that cancer cells originate from stem cells. Stem cells are unspecialized cells in our body that can, given the right signal, be transformed into any specialized cell.

Stem cells are undifferentiated cells that, when given the right signal, can become any type of specialized cell

Stem cells found in adults are known as adult stem cells, which normally act as a repair system for the body, constantly replenishing our bodys tissues.

Researchers are also beginning to understand that our diet is perhaps the greatest tool in preventing and treating cancer. Specifically, regular consumption of freshly available, non-irradiated fruits and vegetables is associated with lowered risk of many chronic diseases, including cancer.

What is known as a pro-survival technique enables cancer cells to develop into the invasive and relentless disease that can wreak havoc on any tissue in our bodies. Unlike typical stem cells, cancer stem cells are self-sufficient, resistant to chemotherapeutic drugs and treatments, have the ability to self-renew, increase inflammation, and are not influenced by contact with other stem cells or anti-growth signals.

Cancer stem cells are also sustained by angiogenesis (the physiological process by which new blood vessels are formed, which cancer tumors use to feed themselves nutrients and grow), flawed cellular energy mechanisms, and their ability to evade normal cellular functions such as apoptosis or cell suicide.

Nutrient-rich plant foods typically contain phytochemicals, which have anti-cancer properties. Phytochemicals are chemical compounds that occur naturally in plants. Some are responsible for color such as the deep purple of blueberries, while others are responsible for smell. For example, the pungent fragrance of freshly squeezed garlic.

Phytochemicals can have specific actions on our body when we consume the plants containing them. It is estimated that there may be as many as 4,000 different phytochemicals in the plant world. Some of these phytochemicals not only target and kill cancer stem cells, but they also reverse the mechanical flaws in our body which cancer cells thrive on.

Consume the following 12 nutrients daily to equip your body with the cancer-fighting tools it requires to prevent and treat cancerous growth.

A dietary compound found in herbal medicines such as holy basil, as well as in the natural waxy coating of fruits like apples, ursolic acid has extraordinary anti-cancer potential. Ursolic acid has been shown to treat cancers of the skin, colon, breast, lung, cervix, prostate, esophagus, and pancreas.

Holy basil is a good source of ursolic acid, along with other common herbs such as lavender, peppermint, oregano, and thyme.

Specifically, ursolic acid reduced tumor size and distant organ metastasis of colorectal cancer cells, likely by blocking the expression of proteins needed for their survival, proliferation, and metastasis.

Researchers are aware of ursolic acids ability to reduce inflammation-promoting enzymes despite not having a full understanding of all biological functions which ursolic acid affects. Reducing the levels of these enzymes is critical to blocking abnormal cell cycles and preventing the expression of genes which turn off cellular apoptosis.

In other words, ursolic acid increases cancer cell apoptosis and prevents DNA replication, a typical characteristic of cancerous growth that would otherwise lead to metastasis.

Increasing the ursolic acid content of your daily nutrient intake can inhibit tumors from forming in your body. Many health practitioners supplement with a dose of 150-300 mg ursolic acid 3 times daily for optimal benefits. This is much more than you could get from using apple peels and holy basil which have between 5-10 mg of ursolic acid per serving. Waxy apple peels and holy basil do have other phytonutrients that are beneficial for the bodys immune system, however, and shouldnt be discarded.

Piperine is found in black pepper and is responsible for its pungent flavor

Every year colorectal cancer kills more than 639,000 individuals worldwide. One of the major causes likely to blame for such a high statistic is a bacterium known as H. pylori, which invades the gastrointestinal lining of more than half of the worlds population and is carcinogenic. Known as the King of Spices, piperine a compound found in black pepper helps reduce the incidence of cancers relating to the stomach and breast. Piperine has traditionally been used to treat symptoms of cold and fever. Most recently it has gained attention for its cancer fighting properties.

Direct research suggests that piperine has anti-inflammatory effects on H. pylori-induced gastritis and may potentially be useful in prevention of H. pylori-associated gastric carcinogenesis. Piperine appears to prevent H. pylori growth by preventing it from adhering to the gastrointestinal surface.

Piperine has also been shown to target cancer stem cells of breast tumors in testing. As a result of piperines actions, the H. pylori bacterium cannot release toxins, cause stress, raise inflammation levels, and promote cancer growth. The antimutagenic factors which piperine induces may be due to its ability to prevent proteins from binding which would normally stimulate cancer formation. Add piperine to your daily diet by including freshly ground high quality black pepper in marinades, salad dressings, sauces, dips, and soups.

Lycopene is found in fruits and vegetables with red flesh such as blood oranges and pink watermelon

Lycopene is a bioactive compound that destroys cancer cell activity. Foods rich in lycopene include red-fleshed colored fruits and vegetables such as tomatoes, watermelons, pink grapefruit, and even so-called blood oranges. In fact, red-fleshed sweet orange juice that contains high levels of beta-carotene and lycopene has been shown to have potential chemopreventive effects on leukemia cells in laboratory experiments.

Consuming a lycopene-rich diet is as easy as snacking on watermelon on hot summer days, or adding a bowl of grapefruit to your yogurt in the winter. Add pulp back into your beverage when juicing citrus foods containing lycopene. Increase the bioavailability of lycopene in foods by simmering tomato skins before consumption and enjoy homemade pasta sauce and salsa.

Lycopenes anti-cancer properties stem from its ability to increase cytotoxicity and apoptosis in cancer cells. This nutrient disrupts cancer stem cells communication signals which help a cancer cell to flourish and instead increases its risk of dying. Cancers which lycopene may be effective at preventing include cervix, colon, lung, and prostate cancer.

If you are looking to avoid carbohydrates and stay on a ketogenic diet, you may want to consider supplementing with 30-50 mg of lycopene, 1-2 times daily. This is about the same amount you would get from eating 2 servings of organic tomato sauce.

Three-day-old broccoli sprouts contain 10-100 times higher levels of sulforaphane than a mature head of broccoli

Isothiocyanates are derived from naturally occurring sulfur-containing compounds called glucosinolates. Cruciferous vegetables such as broccoli, cauliflower, kale, Brussels sprouts, wasabi, horseradish, mustard, radish, and watercress contain many types of glucosinolates, each of which forms a different isothiocyanate when hydrolyzed in our body.

Isothiocyanates such as sulforaphane may help to prevent cancer by eliminating potential carcinogens and by enhancing production of so-called tumor suppressor proteins. In other words, consuming isothiocyanates through cruciferous vegetable consumption may decrease cancer risk although boiling and microwaving cruciferous vegetables is known to reduce the bioavailability of isothiocyanates. Depending on the particular vegetable, either consume raw (eg. broccoli sprouts and watercress) or lightly steam (eg. Brussels sprouts, kale, and cauliflower) to retain the most nutrients.

Isothiocyanates promote detoxification, enhance immunity, activate cancer inhibiting agents, and prevent against tumor growth related to the breast, stomach, spleen, prostate, and colon. Isothiocyanates inhibit cancer in many ways. They:

You too can benefit from the many health benefits of isothiocyanates by adding them to your diet. Although cruciferous vegetables are excellent sources of these powerful compounds, it turns out their sprouts are far more powerful cancer fighting foods. For instance, did you know that cruciferous sprouts can contain up to 100 times more of the glucosinolate compounds needed for the body to produce isothiocyanates than an entire head of broccoli can provide?!

If choosing to supplement with sulforophane, many health practitioners advise taking 300-600 mg, 1-2 times daily. This is especially useful for complementing treatment against hormone-sensitive cancers, as isothiocyanates are very good estrogen detoxifiers.

Turmeric is a member of the ginger family that has been used for centuries in traditional Ayurvedic and Chinese medicine

Turmeric is a herbaceous perennial plant of the ginger family. The rhizomes of this plant are boiled, dried, and ground into a deep-orange-yellow powder that is used as a spice in Indian cuisine, for dyeing, and to impart color to mustard condiments. One active ingredient of this turmeric powder is curcumin.

Curcumin has antioxidant, anti-inflammatory, and anti-cancer properties. Curcumin prevents chronic inflammation and can also decrease risk of cancer development. Curcumin regulates various factors and substances involved with cancer stem cells and manipulates multiple signaling pathways that are necessary for cancer formation.

Curcumin has shown to target cancer cells by turning off factors which normally would suppress apoptosis, preventing angiogenesis which supplies nutrients and blood flow to cancer cells, and inhibiting tumor invasion and metastasis.

The following types of cancers have been shown to be suppressed by curcumin:

Many health practitioners recommend taking 500-1000 mg doses, 3-4 times daily with food. Curcumin should also be mixed with piperine from black pepper and taken with a fat-based meal for optimal absorption.

EGCG and other green tea antioxidants have been found to stop cancer cells from growing, kill cancer cells, and prevent the formation and growth of new blood vessels in tumors

Epigallocatechin-3-gallate, also referred to as EGCG, is a polyphenol found in green tea. EGCG is linked to numerous health benefits including its ability to treat cancer.

Did you know that sipping on green tea regularly can reduce your risk of breast, colon, prostate, and lung cancer? You could also make a green tea base instead of water to add to your smoothies.

EGCG prevents cancer cells from multiplying, causing inflammation, and invading new tissue and it also interrupts cancer stem cells communication pathways. Researchers have found that EGCG inhibits critical proteins required for cancer cell survival from binding and shuts off mechanisms which induce cancerous cell growth.

Matcha green tea is the most potent form of EGCG. One glass of Matcha is equivalent to 10 glasses of a commercial green tea in terms of its nutritional value and antioxidant content. One could also supplement with 400-800 mg of EGCG, 1-2 times daily. Always use this earlier in the day as it can be stimulating.

One caveat is that green tea does reduce folate absorption. If using green tea daily, it is advisable to consume extra raw green vegetables (that are rich in folate) in salads or juices or to supplement with an extra 500 mcg of methylfolate or calcium folinate.

Vitamin D3 deficiency is one of the most common factors associated with the development of cancer

Did you know that approximately 10,000 cancer cells are produced daily in your body and have the ability to invade, multiply, and spread to other areas? Vitamin D3 deficiency is one of the most common factors associated with the pathogenesis development) of cancer. Unfortunately, our lack of time spent outdoors in natural sunlight and the increase in use of synthetic drugs has lowered our bodys ability to absorb nutrients from the sun and vitamin D sources from food. Needless to say, proper intake of vitamin D3 daily is required for the prevention of cancer.

Vitamin D3 has been shown in doses of 20,000 IU to act as an effective therapy in delaying the onset of cancer and alleviating systemic inflammation. Perhaps most vital for D3 daily intake is the production of GcMAF, a protein which inhibits cancer cells and boosts the immune systems natural response to invasive agents such as cancer. GcMAF can eradicate tumors completely but requires adequate vitamin D3 levels for its activity.

Ideal levels for vitamin D3 (25-hydoxy vitamin D) are between 60-100 ng/ml with the ideal range between 80-100 ng/ml for individuals looking to prevent or slow cancer growth. As a general rule, take 1,000 IUs per 25 pounds (11.3 kg) of body weight to slowly raise your vitamin D levels into range or take 2,000 IUs per 25 pounds of body weight to quickly raise your vitamin D levels.

Because vitamin D is a fat-soluble nutrient, it is important to take the supplement with a fat-based meal for optimal absorption.

While grape skins are one of the highest sources of resveratrol, its nearly impossible to get enough of this nutrient through diet alone

Resveratrol is a natural phenol produced naturally by several plants in response to injury or when under attack by bacteria or fungi. Food sources of resveratrol include the skins of grapes (as well as wine made from grape skins), blueberries, raspberries, and mulberries.

This phenolic compound has a profound ability to prevent and heal metabolic conditions such as cancer. It is designed to protect our cells from damage and assist in extending their lifespan and improving normal cells processes which cause repair. The cancer-protective properties of resveratrol have been shown to prevent and heal cancers related to the prostate, liver, colon, pancreas, skin, and various other organs.

Adding a resveratrol supplement to your daily diet may be needed as getting enough of this cancer fighting nutrient solely from your diet is not possible given its low concentrations in foods and beverages. Patients combating cancer can take more than 200 mg of resveratrol daily. Non-cancer patients can take 20-100 mg of resveratrol every day to reap optimal anti-cancer benefits.

The unique fragrance and flavor of ginger come from its natural oils the most important of which is gingerol which has been studied for its powerful anti-inflammatory and antioxidant effects

Ginger is an excellent source of the phytonutrient 6-gingerol, which reduces nitric oxide production associated with inflammation and other cellular disturbances. 6-Gingerol protects against free radical damage and possesses powerful neuroprotective capabilities. Studies show that 6-gingerol stimulates antioxidant defenses and pharmacological pathways for healing.

To get the benefits of 6-gingerol, try sipping on ginger in your tea, add it to meat marinades, shave on vegetable dishes and include in your recipes for coleslaw and salad dressings to improve the chemoprotective properties of your meals. It is also advisable to consume fermented ginger, which is commonly used in Asian dishes such as sushi and in the Korean dish kimchi.

Silymarin is the main active ingredient in milk thistle. Silymarin is both an anti-inflammatory and antioxidant and is commonly used as a natural treatment for liver problems

Also known as milk thistle, Silymarin is a flavonoid which protects against skin and colon cancer. This healing nutrient acts as a strong detoxifying substance able to promote the function of the liver, kidneys, and gastrointestinal tract. Silymarin has shown therapeutic potential in preventing and treating cancers of the skin, prostate, cervix, and breast.

The ability of Silymarin to promote oxygenation to blood cells and increase enzymatic activity of antioxidants like glutathione and superoxide dismutase (SOD) are believed to contribute to its chemotherapeutic effects. Silymarin inhibits carcinogens from accumulating in organs of the body, which assists in detoxification processes and decreases the risk of cancerous cell growth.

Lower your risk of developing cancer by supplementing your diet with 200-600 mg of milk thistle daily to prevent against toxic waste build up and inflammation.

Primary dietary sources of the antioxidant quercetin include citrus fruits, apples, onions, parsley, sage, tea, and red wine

Quercetin is a dietary antioxidant found in fruits, vegetables, teas, and wine. Quercetin has been shown to specifically interfere with cancer stem cells by blocking communication to processes which stimulate free radical production. As a result, hazardous and cancer-stimulating free radicals such as reactive oxygen species are drastically reduced.

Quercetin exhibits anti-cancer properties which improve the production of other antioxidant levels such as glutathione and SOD, thereby further preventing free radical damage and cancer growth. High doses of quercetin may be used to impair the expression of cancer stem cell-activating genes linked to leukemia. Quercetin can relieve inflammation and acts as an antihistamine due to its impact on lowering immune cell responses.

Consuming organic apples (including the skin), red onions, green tea, raspberries, and dark colored tomatoes are great ways to increase quercetin in your diet and lower your risk of cancer. If choosing to supplement with quercetin, it is recommended to take 400-500 mg, 2-3 times per day.

The name anthocyanin is derived from cyan in Greek which means dark blue. The deep blue and purple colors of anthocyanins are created at the cellular level and provide sun protection for plants and us when we consume them

Over 600 types of anthocyanins are found naturally in plants such as berries (especially bilberries), grapes, red cabbage, red onions, eggplant, tea, and specific varieties of oranges. Anthocyanins increase the function of genes which act to inhibit tumor growth pathways in cancer stem cells. Anthocyanins are also equipped to trigger apoptosis by manipulating cell signaling between cancer stem cells and tumors.

Anthocyanins enable the body to naturally heal making them potentially useful in treating colorectal cancer, reducing breast cancer tumors, and limiting leukemia cells from spreading. These dietary components have the ability to control cancer stem cells which otherwise are uncontrollable. Anthocyanins enhance the productivity of genes which suppress tumors, induce apoptosis in colon cancer cells, and create dysfunction in leukemia cells.

Consuming nutrient-dense, anthocyanin-rich foods can help to protect your body from developing cancer and fight already present tumors. Having a handful of organic blueberries or blackberries each day is a fantastic way to get more of these nutrients into your system.

One of the best ways to get anthocyanins is to make fermented sauerkraut with red cabbage and red onions. The final product is rich in isothiocyanates, anthocyanins, and other sulfur compounds that boost glutathione and cancer stem cell-killing compounds.

The solution to killing cancer stem cells is found in our diets. This is a resolution which must be committed to for the long-term. Plant-based diets rich in nutrients which fight chronic inflammation, slow cellular aging, stimulate normal cellular functioning and most importantly, target and destroy cancer stem cells is vital to living a cancer-free life.

Shutting down the signaling pathways which stimulate pro-survival mechanisms in cancer stem cells is necessary to living a cancer-free life and can be accomplished with the 12 nutrients discussed in this article.

So how do you plan to implement these nutrients into your lifestyle on a regular basis to give you and your family the best cancer protection?

Lack of adequate nutrition can lead to cancer growth.

Nutrient-rich plant foods typically contain phytochemicals, which have anti-cancer properties.

12 nutrients to consume daily:

Read this article:
12 Nutrients that Target & Destroy Cancer Stem Cells

Weve all heard of NFL players suffering from serious ACL tears, but did you know thatyour dog is even more likely to experience a debilitating ACL injury? An estimated85% of all orthopedic canine injuriesrelate to the ACL.

A dog ACL tear doesnt just create temporary pain and discomfort; it triggers instability in the knee that leads to the development of chronic arthritis and joint degeneration. As a pet owner, its important to understand the signs of a dog ACL injury and viable treatment options to preserve your pets quality of life.

While surgery is necessary for severe canine ACL injuries, there are dog ACL surgery alternatives available for early injuries and partial tears. Read on to learn more about how to protect your pet from the dangerous implications of ACL damage.

ACL injuries, also known as cranial cruciate ligament (CCL) injuries, affect dogs of all breeds. In fact, they are the most common cause ofhind-limb lamenessin dogs. The ACL connects the bone above the knee with the bone below the knee, which makes it responsible for stabilizing the knee joint.

Although ACL ligaments are essential for a dogs range of motion, the unique anatomy of the canine body actuallytriggers accelerated degeneration of the ACL. If you take alook at your pet, youll notice that their natural physiology places extra strain on the knees and unusual tension on the kneecaps. This is why severe trauma isnt needed to cause damage to your dogs ACL; most dogs rip the ACL out of place simplyby catching a Frisbee wrong or trotting too quickly.

ACL injuries in dogscan be categorized as sprains or tears. ACL sprains are less severe injuries that can respond to alternative therapies, while ACL tears are more serious. An ACL tear occurs when the ACL separates from the bone. Surgery is the only way to treat a full ACL tear without causing degeneration of the knee jointin the future.

Developing an ACL injury is easy, but healing from the injury is not. Ligaments in both humans and dogs have very poor blood supply, which limits the tissues ability to heal. Humans can often bypass this lack of blood flow with a sling or brace that forces the ligament to stay straight for months at a time. However, canines cant be forced to stop moving around or putting weight on a certain leg.

This leaves surgery as theonly treatment optionfor full ACL tears in dogs:

TPLO:The tibial plateau leveling osteotomy (TPLO) procedure is an advanced surgery that addresses torn ligaments in a new way. It involves changing the joint angle to help dogs bear weight comfortably. During TPLO surgery, the head of the tibia is cut and rotated to eliminate the need for an ACL at all. A titanium plate and screws anchor the tibia together. After a few months of recovery, canine patients can walk with relative ease.

Stabilization therapy:Stabilization therapy occurs in a few different forms, all of which place a synthetic fiber or material into the knee to mimic how the ACL should function. The ultimategoal is to add strength and stability around the joint to restore the range of movement.

Since dogs develop ACL tears over time, rather than during one specific traumatic event, symptoms are often subtle. Lameness that lasts more than three or four days is the most common symptom that leads to the discovery of an ACL injury.

Other common symptoms include the inability to bear weight on the injured leg and swelling on the inside ofthe knee. Once these symptoms lead a pet owner to visit the veterinarian, specific tests are done to confirm the presence ofan ACL tear.

First, an X-ray of the leg may identify inflammation and swelling within the affected joint. Beyond a standard X-ray, veterinarians rely on the drawer sign to evaluate ACL injuries. Any dog with a healthy ACL wont be able to have its leg flexed beyond the natural limitations of the ligaments. However, in a dog with a torn ACL, the leg can slide back and forth easily, just like a drawer.

By the time that your dog has suffered a full ACL tear, surgery is the only real solution. The ACL is a highly specialized component of the joint that medical professionals havent yet mastered to replace. Only surgery can be used toaddress the damaged ACL and prevent future joint damage.

Many pet owners are eager to avoid surgery for their dogs at all costs, and some are tempted to skip ACL surgery in the hopes that the ligament will repair itself. This is a dangerous idea. The ACL injury creates instability within the joint itself, which in turntriggers arthritis.

After just one year of living with an untreated ACL tear, a dogs joints can age more than ten years. Arthritis accumulates in the joints rapidly until the dog cant walk, run, or live a normal, active life.

Astandard TPLO surgerycompletely alters the dynamics of a dogs knee. The bone is cut and rotated so that the tibial plateau can no longer slide backwards. This stabilizes the knee and eliminates any functional need for the ACL ligament at all. In fact, most dogs can return to bearing weight just a few days after surgery since the knee becomes efficiently stabilized.

The cost of TPLO surgery averages between $2,500 and $4,500. Due to the invasive nature of the surgery, anesthesia is required, along with a 12-week recovery period. This recovery time is critical for rehabilitation, and when done correctly it improves the likelihood of a safe and successful recovery. When done properly, TPLO surgery helps dogs resume full physical activity within six months.

There is no denying the importance of ACL surgery for dogs with full ACL tears, but stem cell therapy for dogs provides a viable alternative to surgery when treatment can occur before the ACL tear becomes too severe.

Stem cell therapy is an innovative medical treatment that harnesses the bodys existing healing mechanisms to treat injured areas of the body with stem cells. Veterinarians can place a large number of stem cells directly into a partially torn ACL to accelerate the natural healing process and minimize damaging inflammation.

However, not all stem cell therapies offer the same benefits and results. HUC-DT is a new and unique form of stem cell therapy proven tosafely and naturally decrease inflammation, speed up healing, and decrease pain in canine patients.

When HUC-DT is used to treat partial ACL tears, the healing process becomes expedited while pain and inflammation decrease. This offers valuable applications for dogs with ACL injuries:

You dont want to experience the heartbreak of watching your dog lose their ability to play their favorite games or run to the door to greet you, so its important to address their ACL injuries proactively.

Once evidence of limping and slow movements signal the possibility of an ACL tear, have your dog examined by a veterinarian to identify and treat any injuries immediately. A rapid response to your dogs symptoms increases your ability to take advantage of valuable dog ACL surgery alternatives like HUC-DT stem cell injections.

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Dog ACL Surgery Alternatives: How to Help Your Pet Heal ...

Stem cell therapy is a type of cell therapy wherein cells are introduced into the damaged tissue so as to treat the disorder or the injury. There are a number of medical researchers who believes that the stem cell therapy has the potential to change the treatment of human diseases and reduce the suffering people face when they have a disease. They believe that there are a lot of potential to replace the damaged and diseased tissues in the body without getting the risk of rejections.

The stem cells have the ability to self-renew and also give rise to further generation of cells that can multiply. There are a number of stem cell therapies that do exist but most of them are still in the experimental stages. The treatments are very costly with an exception of bone marrow transplant. However, researchers believe that one day they will be able to develop technologies from embryonic stem cells and also adult stem cells to cure type I diabetes, cancer, Parkinsons disease, cardiac failure, neurological disorders and many more such ailments.

The stem cell therapy however carries its own pros and cons and like any other therapy it cannot be said that the stem cell therapy is an advantageous package. Here are some of the pros and cons of the therapy.

Pros of the stem cell therapy include:

It offers a lot of medical benefits in the therapeutic sectors of regenerative medicine and cloning.

It shows great potential in the treatment of a number of conditions like Parkinsons disease, spinal cord injuries, Alzheimers disease, schizophrenia, cancer, diabetes and many others.

It helps the researchers know more about the growth of human cells and their development.

In future, the stem cell research can allow the scientists to test a number of potential medicines and drugs without carrying out any test on animals and humans. The drug can be tested on a population of cells directly.

The stem cell therapy also allows researchers to study the developmental stages that cannot be known directly through the human embryo and can be used in the treatment of a number of birth defects, infertility problems and also pregnancy loss. A higher understanding will allow the treatment of the abnormal development in the human body.

The stem cell therapy puts into use the cells of the patients own body and hence the risk of rejection can be reduced because the cells belong to the same human body.

The cons of the stem cell therapy include the following:

The use of the stem cells for research involves the destruction of the blastocytes that are formed from the laboratory fertilization of the human egg.

The long term side effects of the therapy are still unknown.

The disadvantage of adult stem cells is that the cells of a particular origin would generate cells only of that type, like brain cells would generate only brain cells and so on.

If the cells used in the therapy are embryonic then the disadvantage is that the cells will not be from the same human body and there are chances of rejection.

The stem cell therapy is still under the process of research and there are a number of things that needs to be established before it used as a treatment line.

View post:
Pros and Cons of Stem Cell Therapy | HealthGuidance

From the WebMD Archives

If you think your dog or cat has some bad habits, youre not alone. Ten to 15 percent of owners say that they have pet behavior issues, says certified applied animal behaviorist Stephen L. Zawistowski, PhD, science adviser to the ASPCA.

But does your animal need therapy? Yes, if his behavior puts him or others in danger.

Any time the safety or well-being of either the pet or human is in question, a professional should be brought in to determine the best course of action, says certified dog behavior consultant Michael Shikashio. It doesn't have to be as severe as aggression. An animal exhibiting 'quirky' behavior like excessive tail-chasing [could] be suffering from underlying issues.

The first step is seeing your veterinarian. There may be an underlying medical issue that needs to be treated. If you decide to meet with a certified pet behavior professional, be prepared to really work with your animal to get the problem corrected.

A pet owner shouldn't expect a quick fix, Shikashio says.

These are some of the behavior issues common in cats and dogs:

There are several reasons why a pet may become aggressive: He may be protective of his home or family; possessive of his food, bed or toys; fearful; or feel a need to be dominant.

In dogs, signs of aggression include growling, showing the teeth, charging, barking, snarling, snapping, nipping, and biting.

Going for a walk in the neighborhood provides so much stimulation in some dogs that it makes them feel more alert and aggressive. These are dogs that may benefit from "growl" classes, or reactive dog classes.

In these sessions, behaviorists put together two to four dogs in a controlled situation, to teach them social skills, Zawistowski says. The dogs and their owners are under strict supervision and given plenty of space. Each dog is slowly trained to be able to get closer to the other dogs without showing signs of aggression. These classes can help your pooch become more comfortable whenever other dogs or people are around. This will lead to more enjoyable walks for everyone.

An aggressive cat can bite and scratch. He may hiss, growl, howl, stare, flatten his ears, swish his tail or expose his teeth or claws.

Some cats don't like to be petted -- or petted for long periods of time. They may let you know by batting your hand away with a claw. Cats are territorial and may not want certain people or animals in their areas. Mother cats may act aggressively if they think their kittens are threatened. Other cats practice "redirected aggression" -- they may see another cat through a window, and scratch the people or animals that they can reach. Cats that are in pain, for any reason, can be aggressive.

If your cat is showing aggression and you cant figure out why, you should have her checked out by your vet to see if something physical may be causing the behavior. If pain is ruled out, a behaviorist who works with cats may be able to help.

Loud noises, being left alone, or even a change in routine can upset your pet.

Animals can show anxiety in several ways. A dog may pace and pant and whine. A cat may hide or meow. Both can also be destructive: relieving themselves where they shouldnt, and destroying things around the house. Some pets lick themselves so compulsively that their fur comes off and their skin is raw.

Is your dog bored?

Dogs are social animals, Zawistowski says. If you live alone and work long hours, your absence could upset your dog.

Animals who don't have their mental and physical enrichment needs met can display undesirable behaviors, Shikashio says.

If your dog is just bored, increasing walks and spending more time with him may help. But if he is truly afraid when you arent home, you may need to consult with a behaviorist.

Is your cat bothered?

Typical cat behavior issues can include litter box problems and clawing at personal belongings, Shikashio says.

A cat may become upset if you've moved the litter box, changed the litter, or started dating someone new.

Once the root of the problem is discovered, it's easier to address.

If you have a very high-anxiety dog or cat, it's difficult to do behavior modification without [the help of] prescription anxiety medications used to relax the animals, Zawistowski says. The medication can help get the animals comfortable with the behavior changes, and they can later be weaned off, he says.

To find an animal behavior consultant in your area, see the International Association of Animal Behavior Consultants (iiabc.org) or American College of Veterinary Behaviorists (dacvb.org).

SOURCES:

Michael Shikashio, certified dog behavior consultant, Connecticut; president, International Association of Animal Behavior Consultants.

Stephen L. Zawistowski, PhD, certified applied animal behaviorist, New York; science adviser, American Society for the Prevention of Cruelty to Animals.

International Association of Animal Behavior Consultants: Find an Animal Behavior Consultant.

American College of Veterinary Behaviorists: Member Directory.

Pagination

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Deciding if Animal Behavior Therapy Is Right for ... - WebMD

A PET scan is a nuclear medicine imaging test. It uses a form of radioactive sugar to create 3D colour images to see how your bodys cells are working.

PET uses a radioactive material (radiopharmaceutical) made up of a radioactive isotope that is attached to a material used in the body, usually sugar (glucose). It travels through the body and gathers in cells that are using a lot of energy, such as cancer cells. The radioactive material gives off tiny positively charged particles (positrons). A camera records the positrons and turns the recording into pictures on a computer.

A PET scan may be done to:

Combined PET-CT scanning joins a PET scan and a computed tomography (CT) scan into one test. It may provide a more complete image of a tumours location, growth or spread than either test alone.

Before you have any nuclear medicine test, it is important to tell the nuclear staff if you are breastfeeding or pregnant or think you may be pregnant.

Tell the nuclear medicine staff if you have diabetes. They may ask you to adjust your normal dose of diabetes medicine.

Before the scan, you may be told to:

You may be told to not wear clothes with metal zippers, belts or buttons on the day of the scan. Or you may change into a gown for the test. If you are wearing glasses, jewellery or objects that could interfere with the test, you will be asked to take them off.

Check with the nuclear medicine department to see if there is anything else you need to do before the test.

A PET scan is usually done as an outpatient procedure in the nuclear medicine department of a hospital or specialized PET scan centre. This means that you dont stay overnight. The test takes 45 minutes to 2 hours, depending on whether a single organ or the whole body is scanned.

The nuclear medicine staff will ask you if youve recently had surgery, a biopsy or cancer therapy (such as chemotherapy or radiation therapy). They may also check your blood sugar level before the test.

The radioactive material is injected into a vein in your hand or arm. It needs about 1 hour to travel throughout your body and get absorbed by the cells.

You will be asked to urinate just before the scan. Depending on the area being studied, a urinary bladder catheter or medicine (diuretic) may be used to help get rid of urine.

For the scan, you will sit or lie down on the exam table and will be asked to stay very still. The exam table moves through the PET scanner, which is shaped like a large doughnut. Detectors in the scanner pick up the signal from the radioactive material in the body. A computer analyzes the patterns and creates 3D colour images of the area being scanned.

If youre having a PET-CT scan, you will have one scan after the other during the same hospital visit.

The radioactive material passes out of the body through urine or stool (feces). It may take a few hours or days to completely pass out of the body. Drink lots of fluids after the test to help flush it out.

The dose of x-rays or radioactive materials used in nuclear medicine imaging can be different for every test. The dose depends on the type of procedure and body part being examined. In general, the dose of radioactive material given during a PET scan is small and you are exposed to low levels of radiation during the test. The benefits of having a PET scan outweigh the risk of exposure to the small amount of radiation received during the scan.

Allergic reactions to the radioactive material may occur, but they are extremely rare.

PET scans detect areas of activity (like cell growth) in the body. More radioactive material collects in cancer cells than normal cells and will appear brighter on the image.

Not all cancers show up on a PET scan. PET scan results are often used with other imaging and lab test results. Other tests are often needed to find out whether an area that collected a lot of radioactive material is non-cancerous (benign) or cancerous (malignant). Recent surgery, chemotherapy and radiation therapy and some medicines may affect the test results.

Your doctor may recommend more tests, procedures, follow-up care or treatment.

Preparing children before a test or procedure can help lower their anxiety, increase their cooperation and develop their coping skills. This includes explaining to children what will happen during the test, such as what they will see, feel and hear.

Preparing a child for a PET scan depends on the age and experience of the child. Find out more about helping your child cope with tests and treatments.

See the article here:
Positron emission tomography (PET) scan - cancer.ca

What is StemEnhance Ultra?

StemEnhance Ultra concentrates and combines extracts from natures most primitive superfoods, fresh watermicroalgae and marine macroalgae, proving the body with the ultimate in stem cell support.

StemEnhance Ultra assists the bodys inherent ability for long-term self-renewal by supporting the bodys natural release ofbone marrowstem cells.

StemEnhance Ultra provides the ultimate in stem cell support. It contains a proprietary blend of highly concentrated extracts, including Fucoidan and Cerules exclusive patented ingredients StemEnhance (AFA concentrate) & Mesenkine.

StemEnhance Ultra (AFA concentrate) is shown in studies to support the release of stem cells from the bone marrow.

Fucoidan (undaria pinnatifida) is a marinealgaewell known to support the immune system. Cerules fucoidan comes from undaria harvested from pristine environments like the Tasman Sea and Patagonia. Fucoidan from Undaria Pinnatifida has been documented to increase the number of circulatingstem cells.

Mesenkine is a unique extract from Spirulina, isolated through Cerules patented extraction process, that supports the release and homing of stem cells by balancing key messengers involved in stem cell function.

StemEnhance Ultra does not contain dairy, wheat, gluten, peanut, soy, corn, or allergens. There are no artificial flavors or colors. It is 100% vegetarian, non-GMO, and free from herbicides and pesticides.

The primary roles of adult stem cells in a living organism are to maintain and repair the tissue in which they are found. Stem cells released from the bone marrow can migrate to various tissues where they contribute to the process of tissue repair.

Suggested usage is 2 capsules 1 to 2 times daily.

The clinical studies were done using adults therefore we recommend StemEnhance Ultra for adult consumption, however there are no known contraindications for children.

StemEnhance Ultra is formulated for human consumption. We know of no reason that it may be harmful to pets. AFA and spirulina have been used in the pet nutrition industry for years. However, no studies have been done using the product for pet consumption. Please consult with your Veterinarian.

StemEnhance Ultra is the result of 16 years of research and constitutes the most efficacious and scientifically provenstem cell nutritionproduct on the market.

Through multiple clinical trials, StemEnhance Ultra was documented to optimize stem cell function in the body by increasing the number of bothstem cellsand and Endothelial Progenitor Cells (EPCs) in the bloodstream, supporting optimum renewal and repair of tissues and organs.

StemEnhance Ultra also contains Mesenkine, that was shown to increase the blood concentration of G-CSF that plays a key role in stem cell release.

See StemEnhance research here.

As stated on the label, the vegetarian capsule is made from hypromellose. Hypromellose is cellulose derivative or plant fiber.

StemEnhance Ultra ingredients are certified Kosher.It is not certified Halal.

There is an expiration date at the bottom of each bottle. StemEnhance Ultra has a shelf life of 3 years from date of manufacture. All bottles should be stored in a cool, dry place.

Yes! The Cerule products can be consumed together and were designed to enhance the beneficial effects of each other. We know of no concerning interaction between the Cerule products and other nutritional supplements.

Like many green foods, StemEnhance Ultra contains naturally occurring vitamin K, which could interfere with vitamin K blockers used to thin the blood, such as coumadin.

If you have any health condition and/or are using medication, then consult your attending health care provider before consuming any nutritional supplement.

For some people, due to their conditions and medications, they need to manage their intake of certain nutrients. Below are the amounts of naturally occurring nutrients found in the plant based ingredients within StemEnhance Ultra:

Vitamin K: around 20 ug per serving (2 capsules)Iron: 0.34 mg per serving (2 capsules)Iodine: around 4 ug per serving (2 capsules)Sodium: 9.66 mg per serving (2 capsules)PEA: >0.5%

Pregnancy and nursing are considered special conditions. We recommend that your attending Doctor(s) be made aware of any and all supplements consumed during this time. At this time, we do not advise StemEnhance Ultra consumption during pregnancy.

Go here to read the rest:
StemEnhance Ultra: The Best Stem Cell Supplement - Our ...

Active Comparator: Bortezomib + Lenalidomide + Dexamethasone (VRd) and Rd

Participants will receive bortezomib 1.3 milligram per square meter (mg/m^2) as subcutaneous (SC) injection twice weekly on Days 1, 4, 8, 11 for Cycles 1 through 8 (each cycle is of 21 days); lenalidomide 25 mg orally on Day 1 to Day 14 for Cycles 1 through 8 and on Days 1 to 21 for Cycle 9 (cycle of 28 days); dexamethasone 20 mg orally or intravenously on Days 1, 2, 4, 5, 8, 9, 11, 12 for Cycles 1 through 8 and 40 mg on Days 1,8, 15 and 22 during Cycle 9 and beyond (each cycle is of 28 days) followed by lenalidomide-dexamethasone (Rd) until disease progression or unacceptable toxicity.

Bortezomib 1.3 mg/m^2 will be administered by SC injection twice weekly on Days 1, 4, 8, and 11 of each 21-day cycle for Cycles 1-8.

Other Name: Velcade

Lenalidomide will be self-administered at a dose of 25 mg orally on Day 1 to Day 14 for Cycles 1 through 8 and on Days 1 to 21 for Cycle 9 and beyond until disease progression or unacceptable toxicity whichever occurs first.

Other Name: Revlimid

Dexamethasone will be self-administered orally, 20 mg on Days 1, 2, 4, 5, 8, 9, 11, 12 of each 21-day cycle for Cycles 1-8. During Cycle 9 and beyond dexamethasone, will be self-administered orally at a total dose of 40 mg on Days 1, 8, 15, 22 of each 28-day cycle.

Participants will receive daratumumab 1800 mg as SC injection once every week for Cycles 1 to 2, then every 3 weeks for Cycles 3 through 8 and every 4 weeks for Cycle 9 and beyond; bortezomib 1.3 mg/m^2 as SC injection twice weekly on Days 1, 4, 8, 11 for Cycles 1 through 8 (each cycle is of 21 days); lenalidomide 25 mg orally on Day 1 to Day 14 for Cycles 1 through 8 and on Days 1 to 21 for Cycle 9; dexamethasone 20 mg orally or intravenously on Days 1, 2, 4, 5, 8, 9, 11, 12 for Cycles 1 through 8 and 40 mg on Days 1,8, 15 and 22 during Cycle 9 and beyond followed by daratumumab-lenalidomide-dexamethasone (DRd) until disease progression or unacceptable toxicity.

Daratumumab (1800 mg) will be administered by SC injection once every week for Cycles 1 to 2, then every 3 weeks for Cycles 3-8. For Cycle 9 and beyond, participants will receive daratumumab 1800 mg SC once every 4 weeks until documented disease progression or unacceptable toxicity.

Bortezomib 1.3 mg/m^2 will be administered by SC injection twice weekly on Days 1, 4, 8, and 11 of each 21-day cycle for Cycles 1-8.

Other Name: Velcade

Lenalidomide will be self-administered at a dose of 25 mg orally on Day 1 to Day 14 for Cycles 1 through 8 and on Days 1 to 21 for Cycle 9 and beyond until disease progression or unacceptable toxicity whichever occurs first.

Other Name: Revlimid

Dexamethasone will be self-administered orally, 20 mg on Days 1, 2, 4, 5, 8, 9, 11, 12 of each 21-day cycle for Cycles 1-8. During Cycle 9 and beyond dexamethasone, will be self-administered orally at a total dose of 40 mg on Days 1, 8, 15, 22 of each 28-day cycle.

View original post here:A Study Comparing Daratumumab, VELCADE (Bortezomib ...

See the article here:
Pet Stem Cell Therapy

To our knowledge, The Institute is the first of its kind in the United States and it will primarily be housed here at Saint Francis Pet Care Center. Patients will experience the kind and thorough care that many of you have already come to know. Donations and grants received by our non-profit 501c3 Vets for Pets will be utilized to promote awareness and educate pet parents about Stem Cell Therapy. We will continue to collaborate with both veterinary and human researchers to assist with FDA approval and development of the most effective treatment protocols.

As I pour over the research, the possibilities of treatment are almost limitless. At this point, our treatment will be relegated to dogs, but we anticipate the ability to treat other species soon. Please click here to see what current and upcoming studies we are conducting. For patients who do not qualify for a study, we will have the ability to still employ stem cell therapy on an individual basis. If you would like to learn more about stem cell therapy in pets, please click the link to view Stem Cells 101.

For further inquiry, please feel free to contact us.

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About Us - The Pet Stem Cell Institute

Background

Pre-transplantation 18F-fluorodeoxyglucose (FDG) PET-negativity is one of the strongest predictors of outcome after high-dose therapy and autologous stem-cell transplant (HDT/ASCT) for patients with relapsed or refractory Hodgkin's lymphoma. In this study, we assessed the feasibility and activity of PET-adapted salvage therapy with brentuximab vedotin, followed by augmented ifosfamide, carboplatin, and etoposide (ICE).

In this non-randomised, open-label, single-centre, phase 2 trial, we enrolled patients with relapsed or refractory Hodgkin's lymphoma who had failed one previous doxorubicin-containing chemotherapy regimen. All patients received weekly infusions of 12 mg/kg brentuximab vedotin on days 1, 8, and 15 for two 28 day cycles. After completion of brentuximab vedotin treatment, patients received a PET scan. Patients who achieved PET-negative status (a Deauville score of 1 or 2) proceeded directly to HDT/ASCT; those with persistent abnormalities on PET received two cycles of augmented ICE (augICE; two doses of ifosfamide 5000 mg/m2 in combination with mesna 5000 mg/m2 continuous infusion over 24 h, days 1 and 2; one dose of carboplatin AUC 5, day 3; three doses of etoposide 200 mg/m2 every 12 h, day 1) before consideration for HDT/ASCT. Only patients with persistent abnormalities on PET after brentuximab vedotin received augICE; however, all patients in the intention-to-treat population were assessed for the primary outcome, which was the proportion of patients who were PET-negative after brentuximab vedotin alone or brentuximab vedotin followed by augICE. This study is registered with ClinicalTrials.gov, number NCT01508312, and is no longer accruing patients.

Between Jan 5, 2012, and Oct 4, 2013, we enrolled 46 patients. One patient was deemed ineligible, and not evaluable, before treatment initiation owing to having nodular, lymphocyte-predominant Hodgkin's lymphoma and thus 45 patients received treatment. After brentuximab vedotin, 12 patients (27%, 95% CI 1340) were PET-negative and proceeded to HDT/ASCT. 33 (73%, 95% CI 6086) patients were PET-positive after brentuximab vedotin; one PET-positive patient withdrew consent, therefore 32 PET-positive patients received augICE, 22 (69%, 95% CI 5385) of whom were PET-negative. Overall, 34 patients (76%, 95% CI 6289) achieved PET-negativity. All 44 patients who completed treatment as per protocol proceeded to receive HDT/ASCT. Brentuximab vedotin was well tolerated and associated with few grade 34 adverse events including hyperglycaemia (two [4%] patients, grade 3), nausea (one [2%], grade 3), hypoglycaemia (one [2%], grade 3 and one [2%], grade 4), and hypocalcaemia (one [2%], grade 3 and one [2%], grade 4).

PET-adapted sequential salvage therapy with brentuximab vedotin followed by augICE resulted in a high proportion of patients with relapsed or refractory Hodgkin's lymphoma achieving PET-negativity, and therefore could optimise the chance of cure after HDT/ASCT.

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PET-adapted sequential salvage therapy with brentuximab ...