Ultrasound Guided Sclerotherapy for Varicose Veins

this video is showing the laparoscopic transabdominal preperitoneal herina repair for direct inguinal herina

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

HD Hip Replacement Surgery

Vocal Cord Surgery HD

AZT Mechanism of Antiviral Activity

Basic CardioVascular Clinical Exam

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.

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What is Wallenberg syndrome? Wallenberg syndrome is a rare condition in which an infarction, or stroke, occurs in the lateral medulla. The lateral medulla is a part of the brain stem. Oxygenated blood doesn’t get to this part of the brain when the arteries that lead to it are blocked. A stroke can occur due to this blockage. This condition is also sometimes called lateral medullary infarction. The cause of the syndrome isn’t always clear, however.

Liposuction procedure under local anesthesia.

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

Heat stroke is the most serious form of heat injury and is considered a medical emergency. If you suspect that someone has heat stroke -- also known as sunstroke -- call 911 immediately and give first aid until paramedics arrive. Heat stroke can kill or cause damage to the brain and other internal organs. Although heat stroke mainly affects people over age 50, it also takes a toll on healthy young athletes. Heat stroke often occurs as a progression from milder heat-related illnesses such as heat cramps, heat syncope (fainting), and heat exhaustion. But it can strike even if you have no previous signs of heat injury. Heat stroke results from prolonged exposure to high temperatures -- usually in combination with dehydration -- which leads to failure of the body's temperature control system. The medical definition of heat stroke is a core body temperature greater than 105 degrees Fahrenheit, with complications involving the central nervous system that occur after exposure to high temperatures. Other common symptoms include nausea, seizures, confusion, disorientation, and sometimes loss of consciousness or coma

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

Hypothyroidism is a condition in which the body lacks sufficient thyroid hormone. Since the main purpose of thyroid hormone is to "run the body's metabolism," it is understandable that people with this condition will have symptoms associated with a slow metabolism. The estimates vary, but approximately 10 million Americans have this common medical condition. In fact, as many as 10% of women may have some degree of thyroid hormone deficiency. Hypothyroidism is more common than you would believe, and millions of people are currently hypothyroid and don't know it.

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.

The bones, ligaments and tendons that make up your shoulder joint are encased in a capsule of connective tissue. Frozen shoulder occurs when this capsule thickens and tightens around the shoulder joint, restricting its movement. Doctors aren't sure why this happens to some people, although it's more likely to occur in people who have diabetes or those who recently had to immobilize their shoulder for a long period, such as after surgery or an arm fracture.

Electrophysiology studies test the electrical activity of your heart to find where an arrhythmia (abnormal heartbeat) is coming from. These results can help you and your doctor decide whether you need medicine, a pacemaker, an implantable cardioverter defibrillator (ICD), cardiac ablation or surgery.