Chronic Renal Failure

Diabetic Nephropathy Animation 3D

Pterygium Excision with Auto Conjunctival Graft

MRI of Fetal Brain Development

Baby Delivery

Congestive Heart Failure 3D Animation

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.

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.

each type of heart problem requires different treatment but may share similar warning signs. It is important to see your doctor so that you can receive a correct diagnosis and prompt treatment. Learn to recognize the symptoms that may signal heart disease. Call your doctor if you begin to have new symptoms or if they become more frequent or severe. Symptoms of Coronary Artery Disease The most common symptom of coronary artery disease is angina, or chest pain. Angina can be described as a discomfort, heaviness, pressure, aching, burning, fullness, squeezing, or painful feeling in your chest. It can be mistaken for indigestion or heartburn. Angina may also be felt in the shoulders, arms, neck, throat, jaw, or back. Other symptoms of coronary artery disease include: Shortness of breath Palpitations (irregular heart beats, or a "flip-flop" feeling in your chest) A faster heartbeat Weakness or dizziness Nausea Sweating

IV Dose Calculations

This video: Multiple myeloma is a cancer that forms in a type of white blood cell called a plasma cell. Plasma cells help you fight infections by making antibodies that recognize and attack germs. Multiple myeloma causes cancer cells to accumulate in the bone marrow, where they crowd out healthy blood cells. Rather than produce helpful antibodies, the cancer cells produce abnormal proteins that can cause kidney problems. Treatment for multiple myeloma isn't always necessary. If you're not experiencing signs and symptoms, you may not require treatment. If signs and symptoms develop, a number of treatments can help control your multiple myeloma.

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.

Intracranial pressure (ICP) is the pressure inside the skull and thus in the brain tissue and cerebrospinal fluid (CSF). ICP is measured in millimeters of mercury (mmHg) and, at rest, is normally 7–15 mmHg for a supine adult.

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.

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;