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Galant Reflex

Anatomy of The Orbit

Histology of Kidney

Histology of Vocal Cords

Administering a Subcutaneous Injection

Renal Failure Treatment Options

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Human body circulatory system and respiratory system, 3D MOA (Mechanism of Action) animation, designed for Beijing Natural History Museum.

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Heart failure, sometimes known as congestive heart failure, occurs when your heart muscle doesn't pump blood as well as it should. Certain conditions, such as narrowed arteries in your heart (coronary artery disease) or high blood pressure, gradually leave your heart too weak or stiff to fill and pump efficiently. Not all conditions that lead to heart failure can be reversed, but treatments can improve the signs and symptoms of heart failure and help you live longer. Lifestyle changes — such as exercising, reducing salt in your diet, managing stress and losing weight — can improve your quality of life. One way to prevent heart failure is to control conditions that cause heart failure, such as coronary artery disease, high blood pressure, diabetes or obesity.

Interstitial cystitis is a clinical syndrome characterized by daytime and nighttime urinary frequency, urgency, and pelvic pain of unknown etiology. Interstitial cystitis has no clear etiology or pathophysiology, and diagnostic criteria for the syndrome remain undefined. Despite considerable research, universally effective treatments do not exist; therapy usually consists of various supportive, behavioral, and pharmacologic measures. Surgical intervention is rarely indicated. The International Continence Society has coined the term painful bladder syndrome (suprapubic pain with bladder filling associated with increased daytime and nighttime frequency, in the absence of proven urinary infection or other obvious pathology) and reserves the diagnosis of interstitial cystitis for patients with characteristic cystoscopic and histologic features of the condition.[1] An international consensus panel was able to generally agree on the following definition of interstitial cystitis/bladder pain syndrome (IC/BPS): unpleasant sensation (pain, pressure, discomfort) perceived to be related to the urinary bladder and associated with lower urinary tract symptoms of more than 6 weeks duration, in the absence of infection or other identifiable causes. American Urological Association (AUA) guidelines published in 2011 and amended in 2014 use an evidence-based approach to provide a clinical framework for the diagnosis and management of this condition.[2, 3, 4] In 1887, Skene initially described a condition characterized by inflammation that destroyed the urinary bladder "mucous membrane partly or wholly and extended to the muscular parietes." Guy Hunner popularized the disease with the description of characteristic bladder wall ulcers in association with a symptom complex of chronic bladder inflammation.[5] The first comprehensive epidemiologic description of interstitial cystitis is credited to Hand, who in 1949 described the widespread, small, submucosal bladder hemorrhages and the significant variation in bladder capacity characteristic of the condition. Despite years of intensive research, there are no specific clinical or urinary markers currently clinically available; no absolutely specific radiographic, laboratory, or serologic findings; and no biopsy patterns that are pathognomonic for interstitial cystitis. Some research suggests that the following may all play a role in the disease pathophysiology: (1) pelvic floor dyfunction, (2) dysregulated immune or inflammatory signals, (3) neural hypersensitivity, and (4) disruption of the proteoglycan/glycosaminoglycan (GAG) layer.[6] Interstitial cystitis, howerver, remains a diagnosis of exclusion (see Presentation, DDx, and Workup.) Intensive study has been done to attempt to identify biomarkers for IC/BPS. Some interesting studies have shown that bladder nitric oxide is an accurate marker for Hunner lesions, but these are not present in all patients, and the test requires specific equipment, which has limited widespread clinical use.[7] Differences in levels of cytokines and chemokines, specifically CXCL-10, have shown some ability to differentiate patients with and without Hunner lesions.[8] Other studies of ulcerative IC/BPS have shown that numerous other cytokines and chemokines are up-regulated as well, heralding a possible urinary test to identify patients.[9] An additional substance shown to be up-regulated in IC/BPS patients is antiproliferative factor (APF). This small 8–amino-acid peptide has been associated with suppression of cell growth, increases in transcellular permeability, and lowering of levels of proteins that form intercellular junctional complexes. It is synthesized and secreted from bladder epithelial cells from patients with IC/BPS and may play a key role in pathophysiology.[10] In vitro studies have shown that removal of APF from cell culture media restored cell proliferation and membrane integrity.[11] Studies have also suggested APF in the therapeutic effect of hydrodistension in patients with IC/BPS, although further confirmatory studies are necessary.[12] The most important element in treating patients with interstitial cystitis is education and emotional support. Periodic exacerbations are managed as they occur because no long-term therapy has been shown to prevent or delay recurrent episodes. Therefore, the purpose of treatment is to palliate and alleviate symptoms. Because no discrete pathognomonic pathologic criteria exist for assessing and monitoring disease severity, indications and goals for treatment are based on the degree of patient symptoms. Assessing patient response to treatment is also complicated because of the subjective nature of symptoms; the waxing and waning nature of symptoms without treatment; and the lack of objective serologic, physical, or histopathologic findings. Conservative measures and oral or intravesical treatments are considered first-line treatment. (See Treatment.)

Migraine treatments can help stop symptoms and prevent future attacks. Many medications have been designed to treat migraines. Some drugs often used to treat other conditions also may help relieve or prevent migraines. Medications used to combat migraines fall into two broad categories: Pain-relieving medications. Also known as acute or abortive treatment, these types of drugs are taken during migraine attacks and are designed to stop symptoms. Preventive medications. These types of drugs are taken regularly, often on a daily basis, to reduce the severity or frequency of migraines. Your treatment strategy depends on the frequency and severity of your headaches, the degree of disability your headaches cause, and your other medical conditions. Some medications aren't recommended if you're pregnant or breast-feeding. Some medications aren't given to children. Your doctor can help find the right medication for you

Tetralogy of Fallot (teh-TRAL-uh-jee of fuh-LOW) is a rare condition caused by a combination of four heart defects that are present at birth. These defects, which affect the structure of the heart, cause oxygen-poor blood to flow out of the heart and to the rest of the body. Infants and children with tetralogy of Fallot usually have blue-tinged skin because their blood doesn't carry enough oxygen. Tetralogy of Fallot is often diagnosed during infancy or soon after. However, tetralogy of Fallot might not be detected until later in life, depending on the severity of the defects and symptoms. With early diagnosis followed by appropriate surgical treatment, most children who have tetralogy of Fallot live relatively normal lives, though they'll need regular medical care and might have restrictions on exercise.

Benign paroxysmal positional vertigo (BPPV) is one of the most common causes of vertigo — the sudden sensation that you're spinning or that the inside of your head is spinning. Benign paroxysmal positional vertigo causes brief episodes of mild to intense dizziness. Benign paroxysmal positional vertigo is usually triggered by specific changes in the position of your head. This might occur when you tip your head up or down, when you lie down, or when you turn over or sit up in bed. Although benign paroxysmal positional vertigo can be a bothersome problem, it's rarely serious except when it increases the chance of falls. You can receive effective treatment for benign paroxysmal positional vertigo during a doctor's office visit

Less than a decade ago, corneal transplantation took a big leap forward with the introduction of Descemet’s stripping endothelial keratoplasty (DSEK), which removes only Descemet’s membrane and the diseased endothelium and replaces them with a thin, tripartite donor graft of posterior corneal stroma, Descemet’s membrane, and healthy endothelium. Then came DSAEK, in which the donor graft is prepared with an automated microkeratome, allowing for easier donor preparation and reproducible results by surgeons and eye bank technicians.1 DSAEK has proved to have many advantages over penetrating keratoplasty (PK) and its endothelial predecessors (see “A Brief History of Endothelial Keratoplasty”). Now DSAEK is being compared with a newer technique, Descemet’s membrane endothelial keratoplasty (DMEK), which has emerged as a promising alternative—grafting only Descemet’s membrane and endothelium, allowing for a pure anatomical replacement of only what was removed and the possibility of even better vision with quicker healing.1 Although indications for these procedures are similar, each has unique benefits and drawbacks. Five cornea surgeons offer their perspectives on the procedures and their thoughts on whether it may be time to move to the newer surgery.

A traumatic brain injury (TBI) is defined as a blow or jolt to the head, or a penetrating head injury that disrupts the normal function of the brain. TBI can result when the head suddenly and violently hits an object, or when an object pierces the skull and enters brain tissue. Symptoms of a TBI can be mild, moderate or severe, depending on the extent of damage to the brain. Mild cases (mild traumatic brain injury, or mTBI) may result in a brief change in mental state or consciousness, while severe cases may result in extended periods of unconsciousness, coma or even death. The 4th International Conference on Concussion in Sport held in Zurich, Switzerland in 2012 defined concussion, a subset of mTBI, as the following: Concussion is the historical term representing low velocity injuries that cause brain ‘shaking’ resulting in clinical symptoms and that are not necessarily related to a pathological injury. Concussion is a subset of TBI and will be the term used in this document. It was also noted that the term commotio cerebri is often used in European and other countries. Minor revisions were made to the definition of concussion, which is defined as follows: Concussion is a brain injury and is defined as a complex pathophysiological process affecting the brain, induced by biomechanical forces. Several common features that incorporate clinical, pathologic and biomechanical injury constructs that may be utilised in defining the nature of a concussive head injury include: 1. Concussion may be caused either by a direct blow to the head, face, neck or elsewhere on the body with an "impulsive" force transmitted to the head. 2. Concussion typically results in the rapid onset of short-lived impairment of neurological function that resolves spontaneously. However, in some cases, symptoms and signs may evolve over a number of minutes to hours. 3. Concussion may result in neuropathological changes, but the acute clinical symptoms largely reflect a functional disturbance rather than a structural injury and, as such, no abnormality is seen on standard structural neuroimaging studies. 4. Concussion results in a graded set of clinical symptoms that may or may not involve loss of consciousness. Resolution of the clinical and cognitive symptoms typically follows a sequential course. However, it is important to note that in some cases symptoms may be prolonged. To view peer reviewed literature related to sports concussions, the Sports Concussion Library can be found here. Incidence The U.S. Consumer Product Safety Commission (CPSC) tracks product-related injuries through its National Electronic Injury Surveillance System (NEISS). According to CPSC data, there were an estimated 446,788 sports-related head injuries treated at U.S. hospital emergency rooms in 2009. This number represents an increase of nearly 95,000 sports-related injuries from the prior year. All of the 20 sports noted below posted increases in the number of injuries treated in 2009, except for trampolines, which posted 52 fewer injuries in 2009. Sports that exhibited substantial increases from 2008 to 2009 included water sports (11,239 to 28,716*), cycling (70,802 to 85,389), baseball and softball (26,964 to 38,394) and basketball (27,583 to 34,692). *Four categories were tabulated by the AANS in the current analysis that were not reflected in the 2008 injury data analysis, but together, these account for only 1,397 injuries. The actual incidence of head injuries may potentially be much higher for two primary reasons. 1). In the 2009 report, the CPSC excluded estimates for product categories that yielded 1,200 injuries or less, those that had very small sample counts and those that were limited to a small geographic area of the country; 2). Many less severe head injuries are treated at physician's offices or immediate care centers, or are self-treated. Included in these statistics are not only the sports/recreational activities, but the equipment and apparel used in these activities. For example, swimming-related injuries include the activity as well as diving boards, equipment, flotation devices, pools and water slides. The following 20 sports/recreational activities represent the categories contributing to the highest number of estimated head injuries treated in U.S. hospital emergency rooms in 2009.

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