Allergies, what causes them? This animated video reviews the pathophysiology of allergies, what causes them and why the symptoms occur. Food allergies, seasonal allergies and allergies to pollen all occur through a similar mechanism.

Vaccines are extremely safe. Adverse reactions are uncommon. The most common reaction is pain and swelling at the vaccine site, which is easily treated, and has no longterm problems. An allergic reaction to vaccines are rare. Dr. Michael Davis dispells this and other vaccine myths, including myths about autism and vaccines.

Urinary System Structure and Function

A video showing bone marrow biopsy

Umbilical Hernia Repair using the new device echnique Ventral Patch

The video will describe possible reasons of raised hemidiaphragm. It will also show some good examples. Please see my website for discalimer.

Arterial line insertion usually involves cannulation of the radial artery with a 20 gauge catheter for the purposes of beat-by-beat blood pressure monitoring all along with arterial blood gas monitoring.

The video will describe what is Tree in bud sign on CT scan of Chest. Please see disclaimer on my website www.academyofprofessionals.com

After watching our video on nasal irrigation for natural sinus relief, visit http://www.nasalcleanse.com/index.html. Learn how & why this natural sinus remedy really works! Unlike messy, old-fashioned neti pots or competitors with badly designed, backflow-prone squeeze bottles that can cause sinus infection, NasalCare has a patented nasal rinse system that delivers a comfortable, soothing formula throughout the nasal passages, preventing sinus infection, allergy and post nasal drip. A mix of sea salt and Aloe Vera extract washes away nasal irritants and the common causes of colds and flu while providing nasal congestion relief. NasalCare also acts as a sinus rinse for allergy treatment. Used for centuries in the Orient as a natural remedy and preventative measure for all sinus conditions, nasal irrigation is just catching on here.

A to Z in ecg arabic lesson 2

Vocal Cord Surgery HD

Anatomy of The Shoulder and Arm Muscles

Chronic Renal Failure

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

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.

Esophageal varices are abnormal, enlarged veins in the tube that connects the throat and stomach (esophagus). This condition occurs most often in people with serious liver diseases. Esophageal varices develop when normal blood flow to the liver is blocked by a clot or scar tissue in the liver. To go around the blockages, blood flows into smaller blood vessels that aren't designed to carry large volumes of blood. The vessels can leak blood or even rupture, causing life-threatening bleeding. A number of drugs and medical procedures can help prevent and stop bleeding from esophageal varices.

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

You might not notice signs or symptoms of Hashimoto's disease at first, or you may notice a swelling at the front of your throat (goiter). Hashimoto's disease typically progresses slowly over years and causes chronic thyroid damage, leading to a drop in thyroid hormone levels in your blood. The signs and symptoms are mainly those of an underactive thyroid gland (hypothyroidism). Signs and symptoms of hypothyroidism include: Fatigue and sluggishness Increased sensitivity to cold Constipation Pale, dry skin A puffy face Hoarse voice Unexplained weight gain — occurring infrequently and rarely exceeding 10 to 20 pounds, most of which is fluid Muscle aches, tenderness and stiffness, especially in your shoulders and hips Pain and stiffness in your joints and swelling in your knees or the small joints in your hands and feet Muscle weakness, especially in your lower extremities Excessive or prolonged menstrual bleeding (menorrhagia) Depression

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.