Anatomy of The Posterior Thorax

Histology of Placenta

Pediatric Febrile Seizures

TV interview with Dr. Mostafa Yakoot, MD discussing the published study for efficacy of a new local cream for diabetic foot ulcers. دكتور مصطفى ياقوت علاج جديد للقدم السكرى

35 year old women with breathing difficulties for 6 months and feels like fluid is leaking down her front and back. Was exposed to mold for a 2 years. Has a dog witch has persistent worm infection. Breast implants 10 years ago.

Brain Concussion Recognize and Report

Plastic Surgery New York Dr. Carlin Vickery of 5th Avenue Aesthetics Surgery in Manhattan
(http://www.5thavesurgery.com) speaks at a Fab Over 50 event on having great breasts after the age
of 50. In this presentation Dr. Carlin shares patient results by providing before and after pictures from
different types of breast surgeries including breast lifts, implants and reductions.

Sleepiness, tiredness and fatigue are complaints which must be thoroughly analyzed to eliminate blur and ambiguity.
Physiological sleepiness (“sleep pressure”) increases while being awake and additionally underlies the circadian rhythm with a lower threshold to fall asleep during night time.
Excessive daytime sleepiness (EDS) is considered normal only after sleep deprivation. Clinically, EDS manifests by frequents daytime napping and/or reduced alertness with automatic behavior or - in its extreme form - in recurrent attacks of sudden, uncontrollable compulsion to sleep also in inappropriate situations (= “sleep attacks”).
EDS is “objectively” addressed by measuring the mean sleep latency to four to five nap opportunities throughout the day using the multiple sleep latency test (MSLT) or the maintenance of wakefulness test (MWT).
EDS denotes both, a ready entrance into sleep as well as difficulty in staying awake during daytime or accordingly in inappropriate situations. These two partially independent aspects of EDS are separately assessed by the “passive” MSLT and the “active” MWT respectively.
For that reason the MSLT and MWT only weakly correlate with each other when tested over a broad range of patients with EDS. It is important to keep in mind, that these tests are importantly influenced by a great variety of factors such as mood, anxiety, and motivation.
“Vigilance” comprises wakefulness, alertness and attention and therefore is more than just the reciprocal to sleepiness. Cognitive performance tasks such as Steer Clear Reaction Time Test (SCRTT) or driving simulators require the complete integrity of vigilance to achieve normal results. Hypersomnia is usually broadly defined as the combination of abnormally prolonged night-time sleep (regularly >10 h) with EDS during ≥1 months.
On the other hand, the term hypersomnia has also been used in a narrower scene for the isolated abnormality of a prolonged night-time sleep need (>10 h). “Tiredness”, also in colloquial language often used for sleepiness, in a broader sense also describes the feeling of lack of energy, motivation and initiative.

These patients seek rest rather than sleep. They often cannot fall asleep when given the opportunity in spite of feeling tired, and hence, in an MSLT, do not show an abnormally short sleep latency. Furthermore, tiredness (and fatigue) as opposed to sleepiness has a mental (“central”) and physiological (bodily or “peripheral”) component, which the patients can readily distinguish. Patients with insomnia, mild sleep apnea syndrome, or depression rather suffer from mental tiredness than sleepiness during the day.
The simple subjective self-assessment using the Epworth Sleepiness Scale (ESS) quite reliably differentiates between sleepiness and mental tiredness (without sleepiness), which makes it a widely used test. The term “fatigue” is also heterogeneously used.
In physiology the “fatigue” implied a “time on task performance decrement” to describe decreasing muscle force during a sustained physical effort. In clinical medicine one distinguishes physical (“peripheral”) from mental (“central”) fatigue and the term usually denotes a chronic and more abnormal situation than tiredness.
In a broad sense “fatigue” implies a deficiency in coping satisfactorily with mental and physical work load. The chronic fatigue syndrome entails both mental as well as a physical fatigue (so called “leaden paralysis” of limbs). Depressive states are often associated with insomnia and fatigue, but there are also cases with hypersomnia rather than insomnia ( non organic hypersomnia , “atypical depression” or “hypersomnolent depression”)
Sometimes these patients have a tendency to spend much of the day lying in the bed without actually sleeping (so called clinophilia). The basic and clinical aspects of fatigu

http://www.landging.com/skeletal-system-animation-knee-surgery.html
This skeletal system animation demonstrates the new concept of knee surgery procedure.

A new approach to health care working with patients and doctors to streamline the process and makes it easier and more efficient to get health care they need.

Mal Di Stomaco Rimedi, Bruciore All Esofago, Come Combattere L Acidita Di Stomaco

http://reflusso-acido-rimedi.good-info.co

Le cause del reflusso acido

La sindrome da reflusso acido, nota anche come sindrome da reflusso gastro-esofageo (GERD), si verifica a causa della coesistenza di diversi disturbi medici e di stile di vita.

Fattori fisiologici che scatenano GERD includono l'ipotonia dello sfintere esofageo inferiore (LES) (il graduale indebolimento del LES), insieme con il flusso retrogrado del contenuto dello stomaco nell'esofago, e il livello di sensibilità del muco esofagea al contenuto riflusso.


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https://www.youtube.com/watch?v=InjDBmCwkUg
Mal Di Stomaco Rimedi, Bruciore All Esofago, Come Combattere L Acidita Di Stomaco
Mal Di Stomaco Rimedi,
rimedi contro reflusso,
bruciori di stomaco continui,
acidità e reflusso,
reflusso acido sintomi,
rimedi naturali per bruciore stomaco,
acidità stomaco sintomi,
sintomi ulcera stomaco,
cura del reflusso gastroesofageo,
dieta per il reflusso gastro esofageo,
bruciori stomaco,
reflusso di bile cause,
reflusso acido notturno,
reflusso gastroesofageo notturno,
alleviare il bruciore di stomaco,

Dr. Arthur Handal explains the differences patients can expect when their surgeon chooses to use either a needle or a cannula to inject facial fillers.

Dr. Arthur Handal discusses how injectable fillers can be used to restore a patient's youth.

HIV is spread only in certain body fluids from a person infected with HIV. These fluids are blood, semen, pre-seminal fluids, rectal fluids, vaginal fluids, and breast milk. In the United States, HIV is spread mainly by having sex or sharing injection drug equipment, such as needles, with someone who has HIV. To reduce your risk of HIV infection, use condoms correctly every time you have vaginal, oral, or anal sex. Don’t inject drugs. If you do, use only sterile injection equipment and water and never share your equipment with others. Pre-exposure prophylaxis (PrEP) is an HIV prevention option for people who don’t have HIV but who are at high risk of becoming infected with HIV. PrEP involves taking a specific HIV medicine every day. PrEP should always be combined with other prevention options, such as condoms.

The hip joint is formed between the 'ball' of the femoral head and the 'socket' of the acetabulum and a cartilaginous labrum. Strong supporting muscles, the fibrous joint capsule and ischiofemoral ligament make this a stable joint. Hip dislocations are either congenital or traumatic. Congenital dislocation of the hip is caused by dysplasia of the femoral head or acetabulum and is covered in the separate article Developmental Dysplasia of the Hip. This remainder of this article deals with traumatic dislocation. Traumatic hip dislocation is an orthopaedic emergency. Large forces are required to cause hip dislocation (except in prosthetic hips) and this means that such injury may be associated with other life-threatening injuries and other fractures. The condition is extremely painful. Accurate and swift diagnosis means appropriate management can reduce morbidity.

The term subclavian steal describes retrograde blood flow in the vertebral artery associated with proximal ipsilateral subclavian artery stenosis or occlusion, usually in the setting of subclavian artery occlusion or stenosis proximal to the origin of the vertebral artery. Alternatively, innominate artery disease has also been associated with retrograde flow in the ipsilateral vertebral artery, particularly where the subclavian artery origin is involved. Subclavian steal is frequently asymptomatic and may be discovered incidentally on ultrasound or angiographic examination for other indications, or it may be prompted by a clinical examination finding of reduced unilateral upper limb pulse or blood pressure. In some cases, patients may develop upper limb ischemic symptoms due to reduced arterial flow in the setting of subclavian artery occlusion, or they may develop neurologic symptoms due to posterior circulation ischemia associated with exercise of the ipsilateral arm.[1] Treatment has traditionally consisted of open subclavian artery revascularization, typically via carotid-subclavian bypass or subclavian artery transposition, which are generally durable procedures. Newer, less invasive options include endovascular intervention with recanalization as appropriate and angioplasty and stenting if required. The clinical relevance of subclavian steal was described in 1961 by Reivich, Holling and Roberts; however, the recognition of retrograde vertebral artery flow dates back another 100 years to Harrison and Smyth. Some papers, including a previous version of this article, advocate restricting the term subclavian steal to patients with neurologic symptoms only, but this is incorrect in view of the substantial literature using this term to describe the hemodynamic scenario of retrograde vertebral flow and proximal subclavian artery disease.

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 infection Drainage

Graves disease is an autoimmune disorder that leads to an overactive thyroid gland (hyperthyroidism). An autoimmune disorder is a condition that occurs when the immune system mistakenly attacks healthy tissue. Causes The thyroid gland is an important organ of the endocrine system. The gland is located at the front of the neck above where the collarbones meet. This gland releases the hormones thyroxine (T4) and triiodothyronine (T3), which control body metabolism. Controlling metabolism is important for regulating mood, weight, and mental and physical energy levels. When the body makes too much thyroid hormone, the condition is called hyperthyroidism. (An underactive thyroid leads to hypothyroidism.) Graves disease is the most common cause of hyperthyroidism. It is due to an abnormal immune system response that causes the thyroid gland to produce too much thyroid hormone. Graves disease is most common in women over age 20. But the disorder can occur at any age and can affect men as well. Symptoms Younger people may have these symptoms: Anxiety or nervousness, as well as problems sleeping Breast enlargement in men (possible) Problems concentrating Fatigue Frequent bowel movements Hair loss Heat intolerance and increased sweating Increased appetite, despite having weight loss Irregular menstrual periods in women Muscle weakness of the hips and shoulders Moodiness, including irritability and anger Rapid or irregular heartbeat Shortness of breath with activity Tremor Many people with Graves disease have problems with their eyes: The eyeballs may seem to be bulging out and may be painful. Eyes can feel irritated and be tearing. Double vision may be present. Older people may have these symptoms: Rapid or irregular heartbeat Chest pain Memory loss Weakness and fatigue

Atopic dermatitis (eczema) is a condition that makes your skin red and itchy. It's common in children but can occur at any age. Atopic dermatitis is long lasting (chronic) and tends to flare periodically and then subside. It may be accompanied by asthma or hay fever.