Diabetic Nephropathy Animation 3D

Pterygium Excision with Auto Conjunctival Graft

MRI of Fetal Brain Development

How Smoking and Drinking Affect Your Body

How revolutionizing advancements helps patients with metastatic melanoma kick start the body’s immune system to increase survival.

Immunomodulating effect of autohaemotherapy (a literature review). PMID 3534085 [PubMed indexed for MEDLINE]

J Hyg Epidemiol Microbiol Immunol. 1986;30(3):331-6.

Immunomodulating effect of autohaemotherapy (a literature review).
Klemparskaya NN, Shalnova GA, Ulanova AM, Kuzmina TD, Chuhrov AD.

Abstract
An analysis is presented of experimental and clinical data from different authors on the stimulating effect of autohaemotherapy with regard to the immunological reactivity of humans and animals as well as in vitro experiments with lymphocytes. Erythrolysate has been found to exert a more powerful effect than intact erythrocytes. The stimulating effect of autohaemotherapy on both irradiated and non-irradiated animals manifests itself in an increase in resistance to infection (increased LD50 in experimental infection), enhanced production of antibodies to microbial and tissue antigens and activated functioning of cell-mediated immune defence mechanisms. The favourable influences on radioresistance and the antitumour effect of authohaemotherapy are described. Induced desensitization plays an important part in the mechanism of action of autohaemotherapy. The administration of large doses of erythrocytes or of erythrolysate results in immunosuppression. Autohaemotherapy does not cause side effects and is feasible both on an in-and out-patient basis.

PMID: 3534085

[PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/3534085

Autohemotherapy: an immunization with our own blood

http://www.geocities.ws/autohemoterapiabr/

http://autohemoterapia.fortunecity.com/

http://www.geocities.ws/autohemoterapiabr/aht_english.htm

http://autohemoterapia.fortunecity.com/aht_english.htm

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Auto-hemotherapy PDF files in GOOGLE sites:

https://sites.google.com/site/autohemotherapy/

Binding and Fusion: HIV begins its life cycle
when it binds to a CD4 receptor and one of two
co-receptors on the surface of a CD4+
Tlymphocyte. The virus then fuses with the host
cell. After fusion, the virus releases RNA, its
genetic material, into the host cell.

Reverse Transcription: An HIV enzyme
called reverse transcriptase converts the singlestranded HIV RNA to double-stranded HIV DNA.

Integration: The newly formed HIV DNA
enters the host cell's nucleus, where an HIV
enzyme called integrase "hides" the HIV DNA
within the host cell's own DNA. The integrated
HIV DNA is called provirus. The provirus may
remain inactive for several years, producing few or
no new copies of HIV

Transcription: When the host cell receives a
signal to become active, the provirus uses a host
enzyme called RNA polymerase to create copies of
the HIV genomic material, as well as shorter
strands of RNA called messenger RNA (mRNA).
The mRNA is used as a blueprint to make long
chains of HIV proteins.

Assembly: An HIV enzyme called protease cuts
the long chains of HIV proteins into smaller
individual proteins. As the smaller HIV proteins
come together with copies of HIV's RNA genetic
material, a new virus particle is assembled.

Budding: The newly assembled virus pushes out
("buds") from the host cell. During budding, the new
virus steals part of the cell's outer envelope. This
envelope, which acts as a covering, is studded with
protein/sugar combinations called HIV
glycoproteins. These HIV glycoproteins are
necessary for the virus to bind CD4 and coreceptors. The new copies of HIV can now move
on to infect other cells.

Pulmonary edema is a condition caused by excess fluid in the lungs. This fluid collects in the numerous air sacs in the lungs, making it difficult to breathe. In most cases, heart problems cause pulmonary edema. But fluid can accumulate for other reasons, including pneumonia, exposure to certain toxins and medications, trauma to the chest wall, and exercising or living at high elevations. Pulmonary edema that develops suddenly (acute pulmonary edema) is a medical emergency requiring immediate care. Although pulmonary edema can sometimes prove fatal, the outlook improves when you receive prompt treatment for pulmonary edema along with treatment for the underlying problem. Treatment for pulmonary edema varies depending on the cause but generally includes supplemental oxygen and medications.

What is an Aneurysm? A cerebral or intracranial aneurysm is an abnormal focal dilation of an artery in the brain that results from a weakening of the inner muscular layer (the intima) of a blood vessel wall. The vessel develops a "blister-like" dilation that can become thin and rupture without warning. The resultant bleeding into the space around the brain is called a subarachnoid hemorrhage (SAH). This kind of hemorrhage can lead to a stroke, coma, and/or death. Aneurysms are usually found at the base of the brain just inside the skull, in an area called the subarachnoid space. In fact, 90 percent of SAHs are attributed to ruptured cerebral aneurysms and the two terms are often used synonymously.

Selective immunoglobulin A deficiency (SIgAD) is a primary immunodeficiency disease and is the most common of the primary antibody deficiencies.[1] Total immunoglobulin A deficiency (IgAD) is defined as an undetectable serum immunoglobulin A (IgA) level at a value < 5 mg/dL (0.05 g/L) in humans. Partial IgAD refers to detectable but decreased IgA levels that are more than 2 standard deviations below normal age-adjusted means.[2, 3] IgAD is commonly associated with normal B lymphocytes in peripheral blood, normal CD4+ and CD8+ T cells, and, usually, normal neutrophil and lymphocyte counts. Anti-IgA autoantibodies of the IgG and/or IgE isotype may be present. Peripheral blood may also be affected by autoimmune cytopenias, eg, autoimmune thrombocytopenia,[4, 5] and patients may have other autoimmune phenomena. IgA was first identified by Graber and Williams in 1952; ten years later, the first patients with IgAD were described. IgAD is a heterogeneous disorder, and the results of intensive study are beginning to elucidate genetic loci and molecular pathogenesis that contribute to various subtypes of this disorder. Several lines of evidence suggest that, in many cases, IgAD and common variable immunodeficiency (CVID) have a common pathogenesis, which is discussed further in Pathophysiology. Other data indicate different genetic risk factors. Family studies show variable inheritance patterns. Familial inheritance of IgAD occurs in approximately 20% of cases,[6] and, within families, IgAD and CVID are associated.[7, 8] Many IgAD patients are asymptomatic (ie, "normal" blood donors) and are identified by finding a laboratory abnormality, without any apparent associated clinical disease. Some patients with IgAD may have the following associated conditions: (1) deficits in one or more immunoglobulin G (IgG) subclasses (this accounts for 20-30% of IgA-deficient patients, many of whom may have total IgG levels within the normal range) or (2) a deficient antibody response to pneumococcal immunization (specific polysaccharide antibody deficiency [SPAD]). Some patients with IgAD later develop CVID, and family members of patients with CVID may have only selective IgAD. Characterization of the receptor for the transmembrane activator and calcium-modulator and cyclophilin ligand interactor (TACI), encoded by the gene TNFRSF13B ( tumor necrosis factor receptor superfamily member 13B), suggests that people with the C104, A181E, and ins204A variants may be at risk for IgAD that progresses to CVID.[9] Primary IgAD is permanent, and below-normal levels have been noted to remain static and persist after 20 years of observation.[10] A recent report documents a rare case of reversion.[11] Environmental factors such as drugs or infections can cause IgAD, but this form is reversible in more than half the cases (see Causes). Although individuals with IgAD have largely been considered healthy, recent studies indicate a higher rate of symptoms. A 20-year follow-up study that compared 204 healthy blood donors with incidentally identified IgAD to 237 healthy subjects with normal IgA levels demonstrated that 80% of IgAD donors and 50% of control subjects had episodes of infections, drug allergy, or autoimmune or atopic disease. Severe respiratory tract infections occurred in 26% of IgAD subjects, in 24% of subjects with decreased IgA levels, and in 8% of control subjects; however, the incidence of life-threatening infections was not increased. IgAD is more common in adult patients with chronic lung disease than in healthy age-matched control subjects.[12] Patients with IgAD are at some increased risk of developing severe reactions after receiving blood products.[13, 14, 15] IgG anti-IgA antibodies may cause severe transfusion reactions if patients with IgAD are given whole blood; therefore, IgA-poor blood or washed red cells are preferred for those patients. IgA-deficient patients with immunoglobulin E (IgE)–class anti-IgA antibodies are at risk for anaphylaxis if they receive blood or intravenous immunoglobulin, but this situation is extremely rare. Individuals with such an unusual profile should receive only low IgA intravenous immunoglobulin preparations. However, caution must be used when administering IGIV to patients with IgAD if their anti-IgA status is unknown. A history devoid of previous blood product administration does not exclude the possibility of anti-IgA antibodies or adverse reactions. Fortunately, appropriate precautions can significantly reduce morbidity (see Treatment). Blood banks can use a simple ELISA screening approach to establish an IgAD blood donor poo

What Causes Chest Pain ?

A cornea transplant, also called keratoplasty, is a surgical procedure to replace part of your cornea with corneal tissue from a donor. Your cornea is the transparent, dome-shaped surface of your eye that accounts for a large part of your eye's focusing power. A cornea transplant can restore vision, reduce pain and improve the appearance of a damaged or diseased cornea. Most cornea transplant procedures are successful. But cornea transplant carries a small risk of complications, such as rejection of the donor cornea.

Pulmonary fibrosis is a lung disease that occurs when lung tissue becomes damaged and scarred. This thickened, stiff tissue makes it more difficult for your lungs to work properly. As pulmonary fibrosis worsens, you become progressively more short of breath. The scarring associated with pulmonary fibrosis can be caused by a multitude of factors. But in most cases, doctors can't pinpoint what's causing the problem. When a cause can't be found, the condition is termed idiopathic pulmonary fibrosis. The lung damage caused by pulmonary fibrosis can't be repaired, but medications and therapies can sometimes help ease symptoms and improve quality of life. For some people, a lung transplant might be appropriate.

IV Dose Calculations

Cardiac arrest is the abrupt loss of heart function in a person who may or may not have diagnosed heart disease. The time and mode of death are unexpected. It occurs instantly or shortly after symptoms appear. Each year, more than 350,000 emergency medical services-assessed out-of-hospital cardiac arrests occur in the United States

Personality disorders are a group of mental illnesses. They involve long-term patterns of thoughts and behaviors that are unhealthy and inflexible. The behaviors cause serious problems with relationships and work. People with personality disorders have trouble dealing with everyday stresses and problems. They often have stormy relationships with other people. The cause of personality disorders is unknown. However, genes and childhood experiences may play a role. The symptoms of each personality disorder are different. They can mild or severe. People with personality disorders may have trouble realizing that they have a problem. To them, their thoughts are normal, and they often blame others for their problems. They may try to get help because of their problems with relationships and work. Treatment usually includes talk therapy and sometimes medicine.

This video: Claudication is pain caused by too little blood flow, usually during exercise. Sometimes called intermittent claudication, this condition generally affects the blood vessels in the legs, but claudication can affect the arms, too. At first, you'll probably notice the pain only when you're exercising, but as claudication worsens, the pain may affect you even when you're at rest. Although it's sometimes considered a disease, claudication is technically a symptom of a disease. Most often, claudication is a symptom of peripheral artery disease, a potentially serious but treatable circulation problem in which the vessels that supply blood flow to your legs or arms are narrowed. Fortunately, with treatment, you may be able to maintain an active lifestyle without pain.

A heart attack occurs when the flow of blood to the heart is blocked, most often by a build-up of fat, cholesterol and other substances, which form a plaque in the arteries that feed the heart (coronary arteries). The interrupted blood flow can damage or destroy part of the heart muscle. A heart attack, also called a myocardial infarction, can be fatal, but treatment has improved dramatically over the years. It's crucial to call 911 or emergency medical help if you think you might be having a heart attack

Chest pain is a frequent complaint of patients seeking urgent medical assistance, and accounts for an estimated 2-4 per cent of all A&E visits in the UK (Becker, 2000). Generally, acute chest pain should be considered cardiovascular in origin until proven otherwise and it is common in clinical practice to err on the conservative or ‘safe’ side when evaluating people with chest pain. Individuals with suspected ischaemic chest pain must be evaluated rapidly for several reasons: - Myocardial ischaemia, if prolonged and severe, can cause myocardial infarction (necrosis); - Treatment strategies that achieve myocardial salvage (thrombolytic therapy or primary coronary angioplasty) are available for patients with acute coronary syndromes and these treatments reduce morbidity and mortality;

This video: Sickle cell anemia is an inherited form of anemia which is a condition in which there aren't enough healthy red blood cells to carry adequate oxygen throughout your body. Normally, your red blood cells are flexible and round, moving easily through your blood vessels. In sickle cell anemia, the red blood cells become rigid and sticky and are shaped like sickles or crescent moons. These irregularly shaped cells can get stuck in small blood vessels, which can slow or block blood flow and oxygen to parts of the body. There's no cure for most people with sickle cell anemia. However, treatments can relieve pain and help prevent further problems associated with sickle cell anemia.