Butt implants are a popular plastic surgery procedure among those who wish to enhance the appearance, shape, and size of their rear ends. Buttock augmentation involves the surgical insertion of artificial body implants into a patient’s buttocks to create a larger, shapelier, and more sensuous rear end. Patients who have underdeveloped buttocks can achieve a more proportionate figure with butt implants. Women who wish to achieve an “hour glass” figure or are unhappy with the size of their buttocks can benefit from female butt implants. Men with flat or poorly developed buttocks can enhance the shape of the area to their liking with male butt implants. Many buttock augmentation patients say that their clothes fit better, they feel more attractive, and their confidence levels have improved.

Robotic-assisted prostatectomy

This video may contain images of a medical doctor providing emergency care for a patient.

Demonstration of deep dermal suturing technique for laceration repair or wound closure in the operating room.

Misgav Ladach - Joel Cohen approach for breech presentation

9 Months In The Womb: A Remarkable Look At Fetal Development Through Ultrasound

Laparotomy Closure Abdomen Animation

A new and safer method of inserting a Foley catheter suprapubically. The technique allows the insertion to be carried out in an Outpatient setting, thus saving time, cost and effort. By using the Seldinger technique, the product reduces the chances of bowel or bladder perforation and resultant morbidity.
The product has been chosen by The NHS National Technology Adoption Centre to help facilitate adoption of the product.
See www.mediplus.co.uk for more information

A pacemaker insertion is the implantation of a small electronic device that is usually placed in the chest (just below the collarbone) to help regulate slow electrical problems with the heart.

In emergencies (eg, asystole), transcutaneous pacing should be tried first. If transvenous pacing is tried, the catheter should be advanced during asynchronous pacing at maximum output until the ventricle has been captured and a palpable pulse is detected in the patient.

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Phlebotomy Drawing Blood from Veins

Watch that Ectopic Pregnancy Medical Abortion Procedure

Loyola Breast Examination part 2 Medical breast examination of a female from Loyola University,Chicago

HCG Injection Procedure

As more couples explore anal sex, understanding the risks, rewards, and proper strategy is important. Here's what you need to know about safety and more.

Loyola Full Male Exam Part 3 A video from Loyola medical school, Chicago showing the full examination of the male

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

Finger Abscess Incision and Drainage. Digital block with drainage.