Friday, 30 August 2013

Biofeedback | learn to control your body's functions

Biofeedback is a technique you can use to learn to control your body's functions.
Biofeedback is a technique that trains people to improve their health by controlling certain bodily processes that normally happen involuntarily, such as heart rate, blood pressure, muscle tension, and skin temperature. 
Electrodes attached to your skin measure these processes and display them on a monitor. Electrical sensors help you receive information (feedback) about your body (bio). This feedback helps you focus on making subtle changes in your body, With help from a biofeedback therapist, you can learn to change your heart rate or blood pressure, for example. 
At first you use the monitor to see your progress, but eventually you will be able to achieve success without the monitor or electrodes. 
Biofeedback is an effective therapy for many conditions, but it is primarily used to treat high blood pressure, tension headache, migraine headache, chronic pain, and urinary incontinence.

Are there different types of biofeedback?
The three most commonly used forms of biofeedback therapy are:
  • Electromyography (EMG), which measures muscle tension
  • Thermal biofeedback, which measures skin temperature
  • Neurofeedback or electroencephalography (EEG), which measures brain wave activity
How does biofeedback work?
Researchers aren’t sure exactly how or why biofeedback works. However, there does seem to be at least one common thread: most people who benefit from biofeedback have conditions that are brought on or made worse by stress. For this reason, many scientists believe that relaxation is the key to successful biofeedback therapy. When your body is under chronic stress, internal processes like blood pressure become overactive. Guided by a biofeedback therapist, you can learn to lower your blood pressure through relaxation techniques and mental exercises. When you are successful, you see the results on the monitor, which encourages your efforts.

What is biofeedback good for?
Biofeedback seems to be effective for a range of health problems. For example, it shows promise for treating urinary incontinence, which is a problem for more than 15 million Americans. Some people choose biofeedback over drugs because of the lack of side effects. Based on findings in clinical studies, the Agency for Health Care Policy and Research has recommended biofeedback therapy as a treatment for urinary incontinence. It may also help people with fecal incontinence.
Research also suggests that thermal biofeedback may ease symptoms of Raynaud's disease (a condition that causes reduced blood flow to fingers, toes, nose, or ears) while EMG biofeedback has been shown to reduce pain, morning stiffness, and the number of tender points in people with fibromyalgia. A review of scientific clinical studies found that biofeedback may help people with insomnia fall asleep. Other studies suggest it may even reduce the risk of cardiac events by lowering blood pressure levels and reducing the body's "sympathetic" response during times of stress.
Biofeedback can also be used effectively in children. For example, EEG neurofeedback (especially when combined with cognitive therapy) has been reported to improve behavior and intelligence scores in children with attention deficit hyperactivity disorder (ADHD). Biofeedback, combined with a fiber rich diet, may help relieve abdominal pain in children. Thermal biofeedback helps relieve migraine and chronic tension headaches among children and teens as well.
Biofeedback may also be useful for the following health problems:
  • Anorexia nervosa
  • Anxiety
  • Asthma
  • Autism
  • Back pain
  • Bed wetting
  • Chronic pain
  • Constipation
  • Depression
  • Diabetes
  • Epilepsy and related seizure disorders
  • Headaches and migraines
  • Head injuries
  • High blood pressure
  • Learning disabilities
  • Motion sickness
  • Muscle spasms
  • Sexual disorders, including pain with intercourse
  • Spinal cord injuries

Read More:
Biofeedback | University of Maryland Medical Cente

Deep Brain Stimulation

Deep brain stimulation (DBS) is a surgical treatment involving the implantation of a medical device called a brain pacemaker which sends electrical impulses to specific parts of the brain. DBS in select brain regions has provided therapeutic benefits for otherwise treatment-resistant movement and affective disorders such as chronic pain, Parkinson's disease, tremor and dystonia. Despite the long history of DBS, its underlying principles and mechanisms are still not clear. DBS directly changes brain activity in a controlled manner, its effects are reversible (unlike those of lesioning techniques) and is one of only a few neurosurgical methods that allows blinded studies.

The FDA approved DBS as a treatment for essential tremor in 1997, for Parkinson's disease in 2002, and dystonia in 2003. DBS is also routinely used to treat chronic pain and has been used to treat various affective disorders, including major depression. While DBS has proven helpful for some patients, there is potential for serious complications and side effects.
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AUTOIMMUNITY is an immune response that is directed against self-antigen(s);
Autoimmune Diseases are conditions where the autoimmune response is responsible for the tissue or organ damage.

A. Mechanisms of breakdown in tolerance. Autoimmunity requires a breakdown in the mechanism of self-tolerance. During the development of the lymphocyte repertoire in the bone marrow and thymus, T and B cells with self-reactive receptors are eliminated or rendered anergic (unresponsive) to prevent immune system self-reactivity. Additional mechanisms of peripheral tolerance are also involved in controlling self-reactive lymphocytes.
1. Genetic factors. Autoimmune diseases tend to run in families. The genetic contribution to autoimmune diseases often involves multiple genes; however, there are some genetic components that are associated with increased risk for the development of certain autoimmune disorders.
Many of the strongest and best characterized genetic associations with autoimmune disorders involve different variants of MHC/HLA: HLA-B27 and increased risk of ankylosing spondylitis, HLA-DR3 or -DR4 and increased risk of insulin-dependent diabetes mellitus (IDDM), HLA-DR4 or -DR1 and increased risk of rheumatoid arthritis, and HLA-DR2 and a protective effect for the development of IDDM.

2. Hormonal influences. There is a general trend for autoimmune disease to occur more frequently in women than in men, probably due to differences in hormone profiles. The precise mechanism is unknown.

3. Infection. Molecular mimicry, or shared/similar epitopes in pathogen antigens and self-antigens, can elicit autoimmune disorders (e.g., immune reactivity to group A streptococcal M proteins and the development of rheumatic fever). Additionally, infection in a target organ induces the expression of co-stimulatory molecules and the presentation of pathogen and self-antigens through the action of IFN-g.

B. Organ-specific autoimmune disorders usually affect a single organ, most often an endocrine gland.
1. Hashimoto thyroiditis involves the infiltration of mononuclear cells, including lymphocytes, macrophages, and plasma cells, into the thyroid, resulting in destruction of follicular cells and a general breakdown in the architecture of the thyroid. The immune mechanisms involve antibody and cell mediated components. The resulting hypothyroidism is treated with synthetic thyroid hormone replacement (levothyroxine sodium also known as Synthroid, Levoxyl, Levothroid, or Unithroid).

2. Graves disease is the result of antibodies that act as agonists of thyroid-stimulating hormone (TSH) by binding to the TSH receptor and stimulating the release of thyroid hormones. The resulting hyperthyroidism is treated by antithyroid drugs (e.g., propylthiouracil or methimazole) or thyroid ablation by radiation or surgical removal, which would then be treated with synthetic thyroid hormone replacement therapy.

3. Rheumatic fever is due to the production of antibodies directed against the M proteins of group A streptococci (GAS), which are cross-reactive to antigens present in the heart. Early identification and antimicrobial treatment during an infection with GAS is important to prevent the formation of the antibodies. Repeated streptococcal infections can lead to further damage to the heart tissue (rheumatic heart disease).

4. Autoimmune-hemolytic anemia (erythrocyte), -thrombocytopenia (platelet), -neutropenia (neutrophil), and -lymphopenia (lymphocyte) are mediated by antibodies directed against antigens intrinsic to the cell surface of the affected blood cell. It is important to discriminate between type II hypersensitivity-mediated cellular destruction, which is often due to the transient presence of extrinsic antigens on the surface of the cell, and autoimmune disease, which would be due to immune activity toward self-antigens. Autoimmune responses may need immunosuppressant therapy to halt the destruction, whereas hypersensitivity is often self-limiting and resolves when the extrinsic antigen is no longer present. For autoimmune hemolytic anemia, transfusions may be required. Plasmaphoresis to remove self-reactive antibodies or splenectomy can slow the erythrocyte destruction in severe cases.

5. With myasthenia gravis, antibodies are directed against the acetylcholine receptor (Ach-R) on the motor end plates of the muscle cells, blocking the binding of acetylcholine and mediating complement-dependent damage to the receptor and cell membrane. The patient experiences variable skeletal muscle weakness, often appearing first as drooping eyelids, double vision due to an impairment of extraocular eye muscles. Acetylcholinesterase inhibitors, neostigmine (Prostigmin), pyridostigmine (Mestinon and Regonol), and others are the first line of treatment, followed by corticosteroids for long-term control, or other immunosuppressants (e.g.,  cyclosporine or azathioprine) for more severe cases.

6. Insulin-dependent diabetes mellitus (IDDM or type I diabetes) is caused by the selective destruction of the islets of Langerhans of the pancreas. Destruction involves T cells and often antibodies directed against antigens in the pancreatic b-cell, the primary producer of insulin. Disease symptoms appear when the destruction is nearly complete and the insulin levels are low. Increased risk of developing IDDM is associated with HLA-DR3 and -DR4. Current therapy targets the replacement of the insulin. Immunotherapeutic approaches to consistently and safely prevent or reverse IDDM have not been developed in humans.

7. Goodpasture syndrome is characterized by progressive glomerulonephritis and frequently, pulmonary hemorrhage (particularly in those who smoke). The tissue damage is due to the production of antibodies directed against antigens of type IV collagen, which is present in the basement membrane in the lungs and glomeruli. The risk of developing Goodpasture’s is strongly associated with certain variants of HLA-DRB1. Patients are treated by plasmaphoresis, followed by systemic corticosteroids, and often cyclophosphamide.

 8. Multiple sclerosis (MS) is an inflammatory, demyelinating neurodegenerative, autoimmune disease of the central nervous system. The exact immune mechanism is not completely understood; however, TH1 cells and the inflammatory cytokines that they secrete (e.g., IFN-g) are strongly implicated. The clinical features, which include sensory disturbance and motor dysfunction, can be highly variable and dependent on many factors, such as the sites of pathological lesions and the rate of new lesion formation. Treatment strategies focus on reducing the inflammation within the CNS, and include interferon b-1b (Betaseron and Extavia), interferon b-1a (Avonex and Rebif), glatiramer acetate, mitoxantrone, fingolimod, and natalizumab.

C. Non-organ specific or systemic autoimmune diseases affect multiple organs, usually associated with antigens found throughout the body.
1. Sjögren syndrome (SjS) is a complex, chronic autoimmune disease, which is characterized by mononuclear cell infiltration of exocrine glands resulting in reduced or loss of secretory function. SjS may present as either primary SjS or as secondary, occurring in association with other autoimmune diseases, such as rheumatoid arthritis, systemic lupus erythematosus, or other connective tissue disorders. The precise immune mechanism is not completely understood. Mild cases are treated with artificial tears, medications for dry eyes (cyclosporine ophthalmic emulsion and hydroxypropyl cellulose ophthalmic inserts), medications for dry mouth (cevimeline, and pilocarpine hydrochloride), and frequent drinking of water. Systemic manifestations often require immunosuppressive therapy, such as systemic corticosteroids, to treat internal organ manifestations or severe flares.

 2. Rheumatoid arthritis (RA) is a chronic, recurrent, systemic inflammatory disease that principally involves the joints. It is characterized by the presence of rheumatoid factors (autoantibodies directed against the Fc portion of IgG) in the serum and synovium, infiltration of lymphocytes and activated macrophages into involved joint synovium, and local production of TNF-a and other proinflammatory cytokines in involved synovium. Therapy is generally aimed at reducing synovial inflammation in order to improve symptoms and preserve joint function. Specific therapeutic interventions are required.

3. Systemic lupus erythematosus (SLE) is a systemic autoimmune disorder directed to self-antigens that are present in all or nearly all cells of the body, most typically nuclear components, such as nucleic acids and nucleoprotein particles. The immune complex formation initiates inflammatory reactions leading to cell and tissue destruction. Symptoms are variable depending on the site of immune complex formation and may be intermittent, which complicates diagnosis. 
Joint pain and swelling are the most common symptoms. Other symptoms include fatigue, fever with no other cause, malaise, hair loss, mouth sores, skin rashes (described as a butterfly rash on the face in some patients), sensitivity to sunlight, and swollen lymph nodes. For individual patients, the course of the disease is highly variable in terms of severity, the organs and tissues involved, and the progression of the disease. Mild disease may be treated with nonsteroidal anti-inflammatory drugs (NSAIDs) and corticosteroid creams for the skin rashes. Hydroxychloroquine (Plaquenil, an antimalarial medication) is sometimes useful in patients whose symptoms have not improved with other interventions. Belimumab (Benlysta), a monoclonal antibody inhibitor of B cells, is a newly FDA-approved drug for use in SLE.  
More severe cases of SLE are often treated with high-dose corticosteroids or cytotoxic drugs (e.g., cyclophosphamide). When flares have subsided, the dose can often be lessened to reduce side effects.  
Drug-induced lupus erythematosus is similar to SLE in terms of the clinical presentation; however, it is caused by a hypersensitivity reaction to a medication (e.g., chlorpromazine, hydralazine, isoniazid, methyldopa, penicillamine, procainamide, quinidine, and sulfasalazine). Symptoms tend to occur after taking the drugs for at least 3 to 6 months, and they tend to resolve when the medication is discontinued.

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Sunday, 25 August 2013

Children With Allergy, Asthma May Be at Higher Risk for ADHD

 The number of children being diagnosed with attention-deficit disorder (ADHD), allergy and asthma is increasing in the United States. And according to a new study, there might be a link between the growth of these three conditions.
The study, published in the August issue of Annals of Allergy, Asthma & Immunology, the scientific journal of the American College of Allergy, Asthma and Immunology (ACAAI), found there is an increased risk of ADHD in boys that have a history of allergy or asthma.
"ADHD, a chronic mental health disorder, is most commonly found in males, while asthma is also more common in young boys than girls," said Eelko Hak, lead study author. "We found there is an increased risk of ADHD in boys with a history of asthma and an even stronger risk associated with milk intolerance."
Researchers in the Netherlands and Boston studied 884 boys with ADHD and 3,536 boys without the disorder. Of the children with ADHD, 34 percent had asthma and 35 percent had an allergic disorder. The study suggests medications used to treat these conditions may be associated with an increased ADHD risk.
"Further research is needed to understand why there appears to be an increased risk of developing ADHD in children with allergy and asthma," said Gailen Marshall, MD, editor-in-chief of Annals of Allergy, Asthma & Immunology. "Medications for these conditions far outweigh the risks, and can be life-saving in some conditions. Treatment should not be stopped, unless advised by a board-certified allergist."
According to the ACAAI, allergy and asthma often run in families. If both parents have an allergy a child has a 75 percent chance of being allergic. If neither parent has allergy, the chance of a child developing an allergy is only 10 to 15 percent. Allergists also know allergies and asthma are linked. An estimated 60 to 80 percent of children with asthma also have an allergy. While the cause of ADHD is unknown, this disorder is also thought to run in families.


Saturday, 24 August 2013

Omega-3 Reduces ADHD Symptoms in Rats

 Researchers at the University of Oslo have observed the behaviour of rats and have analyzed biochemical processes in their brains. The results show a clear improvement in ADHD-related behaviour from supplements of omega-3 fatty acids, as well as a faster turnover of the signal substances dopamine, serotonin and glutamate in the nervous system. There are, however, clear sex differences: a better effect from omega-3 fatty acids is achieved in male rats than in female.
Unknown biology behind ADHD
Currently the psychiatric diagnosis ADHD (Attention Deficit/Hyperactivity Disorder) is purely based on behavioural criteria, while the molecular genetic background for the illness is largely unknown. The new findings indicate that ADHD has a biological component and that the intake of omega-3 may influence ADHD symptoms.
"In some research environments it is controversial to suggest that ADHD has something to do with biology. But we have without a doubt found molecular changes in the brain after rats with ADHD were given omega-3," says Ivar Walaas, Professor of Biochemistry.
The fact that omega-3 can reduce ADHD behaviour in rats has also been indicated in previous international studies. What is unique about the study in question is a multidisciplinarity that has not previously been seen, with contributions from behavioural science in medicine as well as from psychology, nutritional science and biochemistry.
Hyperactive rats
The rats used in the study are called SHR rats -- spontaneously hypertensive rats. Although this is primarily a common type of rat, random mutations in their genes have resulted in genetic damage that produces high blood pressure. It is therefore first and foremost blood-pressure researchers who have so far been interested in these rats.
However, the rats do not suffer from high blood pressure until they have reached puberty. Before that age they present totally different symptoms -- namely hyperactivity, poor ability to concentrate and impulsiveness. It is exactly these three criteria that form the basis for making the ADHD diagnosis in humans. The animals also react to Ritalin, the central nervous system stimulant, in the same way as humans with ADHD: the hyperactive responses are stabilized. SHR rats are therefore increasingly used in research as a model for ADHD.
Supplements as early as the fetal stage
Researchers believe that omega-3 can have an effect from the very beginning of life. Omega-3 was therefore added to the food given to mother rats before they were impregnated, and this continued throughout their entire pregnancy and while they fed their young. The baby rats were also given omega-3 in their own food after they were separated from their mother at the age of 20 days. Another group of mother rats were given food that did not have omega-3 added, thus creating a control group of SHR offspring that had not been given these fatty acids at the fetal stage or later.
The researchers started to analyze the behaviour of the offspring some days after they were separated from the mother. They studied behaviour driven by reward as well as spontaneous behaviour. Substantial differences were noted for both types of behaviour between the rats that had been given the omega-3 supplement as foetuses and as baby rats and those that had not.
Rewards made male rats more concentrated
The reward-driven behaviour was such that the rats were allowed access to a drop of water each time they pressed an illuminated button. The ADHD rats that had not been given omega-3 could not concentrate on pressing the button, whereas the rats that had been brought up on omega-3 easily managed to hold their concentration for the seconds this takes and were able to enjoy a delicious drop of water as a reward.
Surprisingly enough, it was only male rats that showed an improvement in reward-driven behaviour. However, with regard to the rats' spontaneous behavior, the same type of reduction in hyperactivity and attention difficulties was noted in both male and female rats that had been given the omega-3 supplement.
Changes in brain chemistry
Professor Walaas and his research group became involved in the study at this point in order to analyze the molecular processes in the rats' brains.
The group analyzed the level of the chemical connections in the brain, the so-called neurotransmitters that transfer nerve impulses from one nerve cell to another. The researchers measured how much of the neurotransmitters such as dopamine, serotonin and glutamate was released and broken down within the nerve fibres. A key player in this work was Kine S. Dervola, PhD candidate, who reports clear sex differences in the turnover of the neurotransmitters -- just as there had been in the reward-driven behaviour.
"We saw that the turnover of dopamine and serotonin took place much faster among the male rats that had been given omega-3 than among those that had not. For serotonin the turnover ratio was three times higher, and for dopamine it was just over two and a half times higher. These effects were not observed among the female rats. When we measured the turnover of glutamate, however, we saw that both sexes showed a small increase in turnover," Ms Dervola tells us.
Transferrable to humans?
The researchers are cautious about drawing conclusions as to whether the results can be transferred to humans.
"In the first place there is of course a difference between rats and humans, and secondly the rats are sick at the outset. Thirdly the causes of ADHD in humans are in no way mapped sufficiently well. But the end result of what takes place in the brains of both rats and humans with ADHD is hyperactivity, poor ability to concentrate and impulsiveness," says Professor Walaas, and concludes:
"Giving priority to basic research like this will greatly increase our detailed knowledge of ADHD."

Friday, 23 August 2013


A. Overview. Under some circumstances, immune responses produce damaging and sometimes fatal results, known collectively as hypersensitivities. 
Hypersensitivity reactions differ from protective immune responses in that they are exaggerated or inappropriate and damaging to the host. Hypersensitivity reactions are classified by the immune mechanism.

B. Type I hypersensitivity reaction (also known as immediate hypersensitivity) occurs upon the reaction of allergen (an antigen that elicits an allergic response) with specific IgE antibody that is bound to high affinity receptors on the surface of mast cells and basophils.

1. Sensitization phase. Initial contact with the allergen leads to proliferation and differentiation of the specific TH and B-cell populations. This is known as sensitization and does not generate allergic symptoms. After sensitization, IgE associates with mast cells and allergic reactions can be elicited upon reexposure to the allergen. All normal individuals can make IgE specific for a variety of different antigens; however, some individuals (atopic) are more prone to developing IgE and experiencing allergic responses. The tendency to develop IgE-mediated responses does appear to have a genetic component. The pattern of inheritance is not yet understood, although MHC-linked genes appear to be involved in some cases.

2. Activation phase. Cross-linking and clustering of the mast cell–bound IgE by the presence of allergen leads to the rapid release of mast cell granules containing many preformed inflammatory mediators (histamine, proteases, and TNF-a "Tumor necrosis factor alpha") and the synthesis of longer acting agents (leukotrienes, prostaglandins, and cytokines) that mediate the late phase response. The initial degranulation occurs within minutes, whereas the late phase response usually begins within 4 to 6 hrs and can last 24 hrs. Direct activation of mast cells via non–IgE-mediated events can also lead to the clinical features resulting from rapid mast cell degranulation. Complement components (C3a and C5a) act directly on mast cells, as do some food additives and certain drugs (e.g., aspirin, angiotensin-converting-enzyme [ACE] inhibitors, opioids) in some sensitive patients.

3. Effector phase. The symptoms of the type I hypersensitivity reactions are due to the inflammatory mediators released by the activated mast cells.
a. Histamine binds rapidly to a variety of cells via histamine receptors; H1 and H2 receptors are chiefly involved in the type I hypersensitivity reaction. Histamine binds to H1 receptors on smooth muscles (airway constriction, gastric muscular contractions) and endothelial cells (vascular permeability). Binding of histamine to H2 receptors, chiefly present at mucosal surfaces, results in increased mucous secretion and increased gastric acid production.
b. Cytokines and chemotactic factors are important for the growth and differentiation of leukocyte cell types, such as TH2s and eosinophils, as well as recruitment of leukocytes, including eosinophils and neutrophils.
c. Leukotrienes and prostaglandins, which are both synthesized as part of the late phase response, lead to prolonged constriction of smooth muscle (bronchoconstriction) and continued vascular permeability.

4. Clinical presentations of type I hypersensitivities
a. Allergic rhinitis is the most common atopic disorder worldwide. Airborne allergens react with IgE-sensitized mast cells in the nasal mucosa and conjunctiva, resulting in degranulation of these mast cells, increased mucous secretion, localized vasodilation, and increased vascular permeability. Typical respiratory allergens include grass, tree, and weed pollens; fungal spores; dust mite allergens; and pet dander.
b. Asthma is a syndrome characterized by a generalized but reversible airway obstruction, bronchial hyperresponsiveness, and airway inflammation. Asthma cannot be explained solely based on IgE-mediated mast cell processes; however, most cases occur in patients who also show immediate hypersensitivity to defined environmental allergens. Airway inflammation plays a major role in the pathogenesis of asthma; recruitment of inflammatory cells, particularly eosinophils, can ultimately lead to remodeling of the respiratory tissue.
c. Food allergies are caused by the intake of certain foods that then interact with sensitized mast cells of the GI tract. Mast cell degranulation and mediator release leads to smooth muscle contraction (nausea and vomiting) and increased mucous and acid secretion. Typical food allergens include nuts, eggs, milk, and shellfish. In some cases, the food can be absorbed systemically, leading to mast cell degranulation in the skin (hives or atopic urticaria) or anaphylaxis from systemic mast cell degranulation.
d. Anaphylaxis is due to a generalized degranulation of IgE-sensitized mast cells following allergen exposure and is characterized by bronchospasm and cardiovascular collapse. Common allergens associated with anaphylaxis include bee and wasp stings, certain foods, and drugs (most notably, penicillin).

5. Clinical tests for allergies and intervention. Sensitivity is normally assessed by the introduction of small amounts of allergen into the skin either via skin prick (scratch test) or intradermal injection, followed by assessment for the wheal and flare (swelling and redness) reaction within 30 mins. Alternatively, allergen-specific serum IgE can be measured by radioallergosorbent test (RAST) or the enzyme-linked immunosorbent assay (ELISA). Skin tests and antigen-specific IgE blood tests are not always an accurate assessment for food allergies.

6. Treatments
a. For some patients, the easiest means to control allergies or asthma is to avoid exposure to known allergens or asthma triggers.
b. Modulation of the immunologic response or desensitization by injection of small amounts of allergen can lessen the hypersensitivity reaction to those specific allergens. Desensitization is thought to occur via a stimulation of TH1 cells rather than TH2 cells and, in some cases, a production of increased amounts of IgG rather than IgE. Recent desensitization clinical trials using oral introduction of allergen shows promise, particularly with respect to food allergies, and is thought to occur via the stimulation of TREG cells. Sublingual immunotherapy (SLIT, currently used in Europe for desensitization to environmental allergies) and specific oral tolerance induction (SOTI, used in investigational studies) are not currently approved by the U.S. Food and Drug Administration (FDA) and are considered experimental.
c. Another strategy in the treatment of severe, persistent, allergic asthma uses an anti-IgE monoclonal antibody (omalizumab) to inhibit the binding of IgE to the mast cell.
d. Mast cell stabilization. Cromolyn sodium (sodium cromoglycate) renders mast cells more resistant to triggering and activation.
e. Mediator antagonists. Antihistamines (ethanolamines, most notably diphenhydramine) are H1-receptor competitive antagonists of histamine. Cimetidine and ranitidine competitively inhibit histamine H2 receptors. Specific treatments for asthma will be discussed later. Epinephrine acts through its alpha-agonist and beta-agonist effects and is the most important drug for the treatment of anaphylaxis.

C. Type II hypersensitivities are antibody mediated and are due to the production of IgM or IgG antibodies directed to foreign antigens associated with cell surfaces. The targeted cell is either damaged or destroyed by complement activation, either direct lysis or opsonization; antibody-dependent, cellmediated cytotoxicity via NK cells or eosinophils; or opsonization by antibody, followed by phagocytosis by neutrophils and macrophages. Certain drugs, as well as blood group antigens (e.g., ABO incompatible transfusion reactions or Rh hemolytic disease), may act as type II hypersensitivity antigens.
1. Type II drug reactions. Drugs acting as haptens may become associated with cells or other components of the body and initiate antibody formation. When associated with the surface of red blood cells, drugs (e.g., penicillins, cephalosporins, and quinidine) can result in hemolytic anemia. Other drugs (e.g., quinine) more often attach to platelets and produce thrombocytopenia. The sensitization phase of a type II hypersensitivity reaction to a drug requires approximately 7 to 10 days after the initiation of drug therapy, at which point, antibody production will be sufficient for cell lysis and inflammation. Subsequent exposure to the drug will result in symptoms more rapidly (approximately 3 days or less). Withdrawing the drug typically resolves the symptoms.
2. The Rhesus blood group (Rh antigen) is a protein antigen, most often the D polypeptide; anti-Rh antibodies are the leading cause of hemolytic disease of the newborn (HDN). During pregnancy of an Rh-negative mother with an Rh-positive child, the mother may become sensitized to the D antigen of the child’s blood. Sensitization usually occurs at or near delivery and does not affect the source child. However, subsequent Rh-positive children may develop HDN when maternal IgG, including anti-D antigen antibodies, are passed across the placenta into the neonate during the third trimester. Rh-negative women are administered RhoD immune globulin (RhoGAM) during the latter part of pregnancy and within 72 hrs of delivery of an Rh-positive child in an effort to prevent sensitization. The passive immunization with the anti-RhoD antibodies acts by binding fetal blood cells that may be in the maternal circulation.

D. Type III hypersensitivity reactions are mediated by immune complexes of foreign antigen together with IgG, or occasionally IgM antibodies. The presence of the immune complexes results in activation of complement, including the generation of chemotactic and vasoactive factors. The classic immune complex allergic disorders include the Arthus reaction, serum sickness, and hypersensitivity pneumonitis (farmer’s lung).
1. Arthus reactions are localized cutaneous inflammatory reactions due to the immune complexes and inflammation that form in dermal blood vessels following the localized injection of large amounts of antigen into a sensitized individual. Antigen sources for Arthus reactions include drug injections (e.g., b-lactam–based antibiotics, heparin, incidental foreign proteins in injectable products such as fetal calf serum), vaccines, insect stings, and spider bites. Arthus reactions are characterized by an edematous and erythematous reaction, occurring within 3 to 8 hrs at the site of the antigen injection. The reaction will resolve without intervention, although hemorrhagic ulceration at the site is not uncommon. A limited form of Arthus reaction occurs commonly at the site of allergy desensitization and usually subsides in less than 24 hrs.
2. Serum sickness is a systemic immune complex reaction that occurs after injection of large quantities of foreign material. The antigen–antibody complexes deposit in small blood vessels, where complement-generated inflammation gives rise to the clinical features: fever, joint pain, urticaria, and splenomegaly. Typical antigens for serum sickness include heterologous antiserum (e.g., antivenin for snake, scorpion, and spider bites), antitoxins, intravenous human gamma globulin, and intravenous drugs. After initial injection, symptoms of primary serum sickness begin to appear as the antibody response develops (usually 7 to 10 days). In patients already sensitized to the antigen, symptoms appear more quickly (usually 2 to 4 days after injection). Complications of serum sickness are rare, and the symptoms usually resolve as the antibody response increases and the immune complexes are more efficiently removed from the body. Treatment is largely symptomatic.
3. Inhalation of antigenic particles or fumes can result in a hypersensitivity pneumonitis due to antigen–antibody complexes and the subsequent inflammation that forms in the lungs. Inhalation of environmental fungal spores or other organic particles, especially Aspergillus spores in farmer’s lung, appears to generate both IgE and IgG to the inhaled antigens as well as TH1 cells. The combination of the IgE- and IgG-mediated reactions, together with the action of proinflammatory cytokines, leads to tissue damage, inflammation, and the typical symptoms, which could be described as asthma symptoms superimposed with fever, cough, and sometimes chronic lung damage. Avoidance of antigen exposure is an important feature of management; repeated episodes lead to bronchial wall weakening and pulmonary fibrosis. High-dose systemic corticosteroid therapy is necessary to resolve the acute allergic inflammation and prevent long-term lung damage.

E. Type IV hypersensitivities (delayed-type hypersensitivities) are mediated by specific effector T cells. Examples of type IV hypersensitivities include the immune response to some infections (tuberculosis) and contact dermatitis, most often associated with metals or haptenic chemicals.
1. One of the best known examples of a type IV hypersensitivity is the tuberculin skin test (Mantoux skin test). Injection of purified protein derivative (PPD) into the skin of an individual previously infected with Mycobacterium tuberculosis recruits and activates those cells currently or previously employed in response to the tubercule bacillus (i.e., T cells and macrophages). A positive tuberculin skin test will present with redness and a palpable induration at 48 to 72 hrs after administration.

2. Many chemical substances, natural and synthetic, can be the source of contact hypersensitivity, which is typically a type IV hypersensitivity reaction. Common allergens include metals (nickel and chromate), plastics, rubber, lanolin, latex, plant chemicals, and medications such as neomycin and phenothiazines. The plant oil urushiol is the immunogenic hapten that is responsible for the contact dermatitis associated with poison ivy. The reaction is characterized by a red rash within a few days of contact, bumps, patches of weeping blisters on the skin, swelling of the area, and intense itching. Effective treatment focuses on suppressing the T-cell response: topical steroids such as triamcinolone or clobetasol. If the affected area involves more than 20% of the body or is particularly severe, systemic corticosteroid therapy may be required. Inhalation of the allergen when the plants are burned can lead to severe allergic respiratory issues.

3. Celiac disease, also known as gluten-sensitive enteropathy, is considered an autoimmune disorder that is triggered by a cell-mediated, adaptive immune response to ingested gluten, such as that found in wheat gluten and related proteins in rye and barley. In genetically susceptible individuals (i.e., HLA-DQ2 or -DQ8), gliadin, gluten’s main antigen, associates with host proteins.
Development of the symptoms of the disease is associated with TH and TC lymphocytic infiltration in the gut epithelial membrane and lamina propria, expression of proinflammatory cytokines, and production of IgA and IgG antibodies directed against the gluten as well as host components (e.g., tissue transglutaminase). Inflammation, villous atrophy, and crypt hyperplasia in the small intestine are all characteristic of celiac disease. Extraintestinal symptoms can include bone and skin disease, anemia, endocrine disorders, and neurological deficits. Gluten-free diet is the only effective intervention for celiac disease.

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Wednesday, 14 August 2013

How Do Happiness and Sadness Circuits Contribute to Bipolar Disorder?

Prior research has clearly shown that brain emotion circuitry is dysregulated in individuals diagnosed with bipolar disorder. It is thought that these disturbances impair one's ability to control emotion and contribute to mood episodes.
Continuing this line of research, the January 15th issue of Biological Psychiatry reports the results of a study conducted by scientists from Indiana University School of Medicine. These investigators used functional magnetic resonance imaging (fMRI) to investigate which areas of the brain showed abnormal activation while patients in different mood phases of bipolar disorder tried to control their response to emotional and non-emotional material.
This allowed them to analyze brain activation patterns based on patient mood (manic, depressed, or euthymic) and stimuli type (emotion versus no emotion and happy versus sad). Because medication effects on brain activation have been observed in some studies, the researchers recruited only unmedicated volunteers.
They found that bipolar depressed patients abnormally activated brain areas when they had to withhold responses to sad faces. Manic patients, on the other hand, had abnormal activation regardless of whether they were trying to withhold response to sad faces, happy faces or non-emotional material. Even the euthymic bipolar subjects showed abnormal activation of cortical areas of the brain while withholding responses to emotional faces.
These findings suggest that distinct circuit dysfunctions may contribute to different features of emotion dysregulation in bipolar disorder.
Professor and senior author Dr. Amit Anand said, "This study provides important information regarding brain areas that may be important in controlling response to emotional material and the functional abnormalities in these areas in mood disorders."
"It is interesting that subtly different circuits distinguish symptomatic and non-symptomatic patients with bipolar disorder when they are suppressing their happy and sad reactions," commented Dr. John Krystal, Editor of Biological Psychiatry. "These findings may have implications for the refinement of circuit-based treatments for bipolar disorder including neurostimulation and psychotherapy."

Bipolar disorder is a severe mood disorder characterized by unpredictable and dramatic mood swings between the highs of mania and lows of depression. These mood episodes occur among periods of 'normal mood', termed euthymia.

Saturday, 10 August 2013

Brain Molecule Regulating Human Emotion, Mood Uncovered

A research team has discovered an enzyme called Rines that regulates MAO-A, a major brain protein controlling emotion and mood. The enzyme is a potentially promising drug target for treating diseases associated with emotions such as depression.

Monoamine oxidase A (MAO-A) is an enzyme that breaks down serotonin, norephinephrine and dopamine, neurotransmitters well-known for their influence on emotion and mood. Nicknamed the "warrior gene" a variant of the MAOA gene has been associated with increased risk of violent and anti-social behavior.

While evidence points to a link between MAO-A levels and various emotional patterns, however, the mechanism controlling MAO-A levels in the brain has remained unknown.
Now, a research team headed by Jun Aruga at the RIKEN Brain Science Institute has shown for the first time that a ligase named Rines (RING finger-type E3 ubiquitin ligase) regulates these levels. Their research shows that mice without the Rines gene exhibit impaired stress responses and enhanced anxiety, controlled in part through the regulation of MAO-A levels. The study is published today in Journal of Neuroscience.

As the first study to demonstrate regulation of MAO-A protein via the ubiquitin proteasomal system, this research presents a promising new avenue for analyzing the role of MAO-A in brain function. Further research promises insights into the treatment of anxiety, stress-related disorders and impaired social functions.

Tuesday, 6 August 2013

Psychosomatic disorders; brain is the key

Some physical diseases are thought to be particularly prone to be made worse by mental factors such as stress and anxiety. Your current mental state can affect how bad a physical disease is at any given time.
When a psychiatric problem, such as depression, anxiety or another disturbance, manifests itself as seemingly unrelated physical symptoms, we call that Psychosomatic disorders.

It is well known that the mind can cause physical symptoms. For example, when we are afraid or anxious we may develop: a fast heart rate, palpitations, feeling sick, shaking (tremor), sweating, dry mouth, chest pain, headaches, a knot in the stomach, and fast breathing. These physical symptoms are due to increased activity of nervous impulses sent from the brain to various parts of the body, and to the release of adrenaline into the bloodstream when we are anxious.

However, the exact way that the mind can cause certain other symptoms is not clear. Also, how the mind can affect actual physical diseases (rashes, blood pressure, etc) is not clear. It may have something to do with nervous impulses going to the body, which we do not fully understand. There is also some evidence that the brain may be able to affect certain cells of the immune system, which is involved in various physical diseases.
Some physical diseases are believed to have a mental component derived from the stresses and strains of everyday living. This is the case, for example, of lower back pain and high blood pressure, which appear to be partly related to stresses in everyday life. Psychiatry has found it difficult until relatively recently to distinguish somatoform disorders, disorders in which mental factors are the sole cause of a physical illness, from psychosomatic disorders, disorders in which mental factors play a significant role in the development, expression, or resolution of a physical illness.
For instance, while peptic ulcer was once thought of as being purely caused by stress, later research revealed that Helicobacter pylori caused 80% of ulcers. However 4 out of 5 people colonised with Helicobacter pylori do not develop ulcers, and an expert panel convened by the Academy of Behavioral Medicine Research concluded that ulcers are not merely an infectious disease and that mental factors do play a significant role. One likelihood is that stress diverts energy away from the immune system, thereby stress promotes Helicobacter pylori infection in the body.
It is still difficult to classify some disorders as purely physical, mixed psychosomatic, or purely somatoform. One example is Irritable Bowel Syndrome (IBS) that was considered formerly as having purely mental causes, while subsequent research showed significant differences in the behaviour of the gut in IBS patients. On the other hand, there are no actual structural changes in IBS patients and research shows that stress and emotions are still significant factors in causing IBS.

However, while it is necessary to identify if an illness has a physical basis, it is recognized more and more that the effort to identify disorders as purely physical or mixed psychosomatic is increasingly obsolete as almost all physical illness have mental factors that determine their onset, presentation, maintenance, susceptibility to treatment, and resolution.
Addressing such factors is the remit of the applied field of behavioral medicine. In modern society, psychosomatic aspects of illness are often attributed to stress making the remediation of stress one important factor in the development, treatment, and prevention of psychosomatic illness.

Psychosomatic medicine is an interdisciplinary medical field studying the relationships of social, psychological, and behavioral factors on bodily processes and quality of life in humans and animals.
The academic forebear of the modern field of behavioral medicine and a part of the practice of consultation-liaison psychiatry, psychosomatic medicine integrates interdisciplinary evaluation and management involving diverse specialties including psychiatry, psychology, neurology, surgery, allergy, dermatology and psychoneuroimmunology. Clinical situations where mental processes act as a major factor affecting medical outcomes are areas where psychosomatic medicine has competence.


Sunday, 4 August 2013


Nifuroxazide is an oral nitrofuran antibiotic, patented since 1966 and used to treat colitis and diarrhea in humans and non-humans. 
 It is sold under the brand names Ambatrol, Antinal, Bacifurane, Diafuryl (France), Diax (Egypt), Nifrozid, Ercefuryl, Erfuzide (Thailand), Endiex (Slovakia), Ercefuryl (Czech Republic), Nifuroksazyd (Poland), Pérabacticel (France), Pentofuryl (Germany), Topron (Latin America), Antinal (Egypt), Apazid (Morocco) and Septidiaryl. It is sold in capsule form and also as a suspension
The pharmaceutical group SmithKline Beecham claims that nifuroxazide is highly effective and the consumers' group Healthy Skepticism says that SmithKline Beecham's claims have no scientific support. 

Nifuroxazide is an antibacterial that is poorly absorbed from the gastrointestinal tract.

Nifuroxazide is an effective therapy for acute diarrhea and can be prescribed from the onset of diarrhea without waiting for stool culture results which can be late or negative.

It is given orally in a dose of 800 mg daily in divided doses in the treatment of colitis and diarrhoea.
The treatment course is 5 - 7 days.

Side effects
Nifuroxazide has no side effects and is well tolerated. 

some effects may be occasionally observed:
Gastrointestinal disorders: short-term abdominal pain, nausea, aggravation of diarrhea.
Hypersensitivity reactions: (require discontinuation of the drug):
Respiratory disorders: asthma;
Skin disorders: rash, pruritus.


Saturday, 3 August 2013

Miswak for Ultimate Dental Hygiene

Studies have shown that the health benefits of miswak are greater than those of toothbrush/toothpaste combination. Eliminate the need for toothbrush AND toothpaste by carrying a Miswak (2-in-1 deal!). Learn how to use it here : 


A. Primary immunodeficiencies are inherited or congenital, and are generally rare.
1. Phagocytic cell defects. Patients with defects in phagocytic cells have frequent bacterial infections.
a. Chronic granulomatous disease (CGD) is a group of disorders that involves the inheritance of defects in the NADPH (nicotinamide adenine dinucleotide phosphate) oxidase, which is essential for the production of the reactive oxygen species during the respiratory burst that accompanies phagocyte activation. Patients with CGD experience severe recurrent bacterial and fungal infections, often resulting in the formation of granulomas that can obstruct the gastrointestinal and urogenital systems. Early diagnosis and treatment, typically with prophylactic antibacterial and antifungal agents, as well as administration of IFN-g, can be effective, although at present, the only long-term cure is allogenic hematopoetic cell transplant (bone marrow transplantation).

b. Leukocyte adhesion deficiency (LAD) is a group of rare inherited disorders that is due to a defect in adhesion molecules of neutrophils, and often other leukocytes, that are necessary for leukocytes to enter the tissue from the blood. LAD patients should receive early antimicrobial therapy; allogenic hematopoietic stem cell transplantation has been successful in many LAD patients.

2. Complement system deficiencies
a. Complement component C3 is common to all pathways of complement activation, and as such, deficiencies in C3 have the most dramatic effect. Patients with C3 deficiency suffer from recurrent, and often severe, bacterial infections involving the upper respiratory tract, meninges, and bloodstream. Patients lacking the fluid phase control proteins (factor H and factor I) experience a similar pattern of recurrent infections due to the uncontrolled activation and thus depletion of C3.
b. Patients with immunodeficiencies in the lectin pathway of complement activation experience recurrent bacterial infections, typically in early childhood, prior to establishing an efficient antibody repertoire.
c. Lacking the early components of the classical pathway leads to an increase in the incidence of immune complex diseases and some autoimmune diseases, such as systemic lupus erythematosus and glomerulonephritis.
d. Patients lacking the late-acting complement components (C6–C9) are unable to form the MAC (Complement membrane attack complex); however, they are competent for opsonic function, immune clearance, and initiating inflammation via the complement cascade. Lacking any of these terminal complement components increases the patient’s susceptibility to infections with Neisseria.
e. Treatment. Complement deficiencies that lead to recurrent bacterial infections should be managed with antimicrobial therapy. Supplementation with purified complement components has had some success, although the half-life of most complement components is short, and frequent infusions would be required.

3. Antibody-related deficiencies
a. X-linked agammaglobulinemia (XLA) is due to mutations in the Bruton tyrosine kinase gene, which is important for BCR (B-cell receptor) signaling. XLA patients lack mature B cells, plasma cells, and all five classes of antibody. Patients with XLA have recurrent infections usually beginning at 5 to 6 months of age, when maternal antibody transferred prior to birth is waning. Treatment involves antimicrobial therapy as well as periodic injections of intravenous immunoglobulin containing large amounts of IgG.
b. Selective IgA deficiency is the most common primary immunodeficiency disorder and is characterized by a reduced level of IgA in the presence of normal levels of the other antibody isotypes. Many patients are asymptomatic or experience a slight increase in the frequency of respiratory tract infections. The genetic basis for selective IgA deficiency is not yet defined and is likely to be a heterogeneous group of genetic abnormalities. The foundation of treatment for IgA deficiency is the treatment of the associated infections, and no specific immunotherapy is required.
c. X-linked hyper-IgM (XHIM) syndrome is characterized by high levels of serum IgM and very low levels of serum IgG, IgA, and IgE. The B cells from these patients are functionally normal; however, their T-helper cells lack a ligand (CD40 ligand) that is important for signaling to the B cells to undergo isotype switching and generate memory B cells. The CD40 ligand is also important for T-cell interaction with dendritic cells and macrophages. XHIM presents with recurrent bacterial infections; some patients also have recurrent neutropenia and anemia. It is important to treat the associated bacterial infections; the infusion of immunoglobulin for intravenous use (IVIG) is the traditional therapy. Bone marrow transplantation can be performed in certain situations and will reconstitute the immune system with functional T cells, thereby improving antibody and leukocyte function.

4. T-cell–associated immunodeficiencies
a. DiGeorge syndrome or congenital thymic aplasia is a T-cell deficiency that is due to the failure of the thymus to develop normally during embryogenesis. Cell-mediated immune responses are undetectable in DiGeorge patients, and they present with multiple recurrent or chronic infections with viruses, bacteria, fungi, and protozoa. Additional features of DiGeorge patients include cardiac anomalies, renal anomalies, eye anomalies, hypoparathyroidism, and skeletal defects. Patients with partial hypoplasia often recover thymic function and need no immunologic treatment. Transplantation of postnatal allogeneic cultured thymus tissue has successfully reconstituted immune function in DiGeorge patients with severe T-cell deficiency.
b. Severe combined immunodeficiency (SCID) is a phenotypic term for a wide range of congenital and inherited immunologic defects that include the loss of both B- and T-cell systems. Most patients experience severe, recurrent infections that begin in the first few months of life. Some of the genetic defects result in defective T-cell signaling through cytokine receptor mutations or kinases involved in cytokine signaling (JAK3 kinase). Still other defects are in genes important for TCR complex signaling (CD3) or genes encoding recombinase enzymes required for gene rearrangement in TCR and BCR generation. Mutations in genes that control class II MHC expression result in a condition known as bare lymphocyte syndrome, which functionally presents as SCID, because class II MHC expression is necessary for TH cell development in the thymus. Most SCID patients will not survive the first year of life unless the immune system is reconstituted by hematopoietic stem cell transplantation.

B. Secondary immunodeficiencies. Defects in immunity that are secondary to another cause are more common than primary causes.
1. Malnutrition is the most common cause of immunodeficiency disorders worldwide, and malnourished individuals often experience an increased incidence of infectious diseases, an impaired response to vaccination, defects in cell-mediated immunity, and defective phagocyte function, all of which reverse following adequate nutritional support.
2. Patients with lymphoproliferative diseases, such as leukemia and myeloma, are also prone to infection. These patients experience varying degrees of hypogammaglobulinemia and impaired antibody responses; some lymphoproliferative diseases also lead to defective cell-mediated immune function.
3. In developed countries, immunodeficiency is often due to specific medical treatment. Therapeutic agents such as x-rays, cytotoxic drugs, and corticosteroids can have dramatic effects on the immune system. Immunosuppressive drugs, such as used to prevent organ transplant rejection or used to suppress autoimmune reactions, can also affect lymphocyte and neutrophil activity.
4. Some microorganisms suppress the immune response, particularly cytomegalovirus, measles, rubella, Epstein-Barr virus, and some bacterial infections, such as tuberculosis, leprosy, and syphilis.
5. AIDS is a late stage of a progressive infection with HIV. HIV (either HIV-1 or HIV-2, although HIV-1 is more common in the United States) selectively infects CD4-bearing cells leading to a gradual depletion of TH cells. AIDS is defined by the presence of certain opportunistic infections and cancers including Pneumocystis pneumonia; disseminated cryptococcosis; histoplasmosis; toxoplasmosis; mycobacterial disease; persistent, ulcerative herpes simplex virus infection; Kaposi sarcoma; and disseminated cytomegalovirus infection
There are many specific targets for antiretroviral therapy, including reverse transcriptase inhibitors, protease inhibitors, integrase inhibitors, and fusion inhibitors (reviewed more specifically later). Early intervention using a combination of drugs, while monitoring CD41 cell count and viral load, allows for tailored treatment regimens to achieve the best results for individual patients (i.e., highly active antiretroviral therapy or HAART). There are no known cures and no effective vaccines available for HIV, although there are clinical vaccine trials ongoing.

Ref: Comprehensive Pharmacy Review

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