Cerebral palsy is a disorder of movement, muscle tone or posture that is caused by damage that occurs to the immature, developing brain, most often before birth. Signs and symptoms appear during infancy or preschool years. In general, cerebral palsy causes impaired movement associated with abnormal reflexes, floppiness or rigidity of the limbs and trunk, abnormal posture, involuntary movements, unsteady walking, or some combination of these. People with cerebral palsy may have problems swallowing and commonly have eye muscle imbalance, in which the eyes don't focus on the same object. People with cerebral palsy also may suffer reduced range of motion at various joints of their bodies due to muscle stiffness. Cerebral palsy's effect on functional abilities varies greatly. Some affected people can walk while others can't. Some people show normal or near-normal intellectual capacity, but others may have intellectual disabilities. Epilepsy, blindness or deafness also may be present.

Future Technologies and Medical Advances That Will Change The World

Thrombotic thrombocytopenic purpura (TTP) is a rare blood disorder characterized by clotting in small blood vessels of the body (thromboses), resulting in a low platelet count. In its full-blown form, the disease consists of the pentad of microangiopathic hemolytic anemia, thrombocytopenic purpura, neurologic abnormalities, fever, and renal disease

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Basic well-male examination of the genitals and digital rectal exam.

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What are the symptoms of spinal meningitis in adults? Causes. The most common cause of viral meningitis is. ... Symptoms. Viral meningitis usually begins with symptoms of a viral infection, such as fever, a general feeling of illness (malaise), cough, muscle aches, vomiting, loss of appetite, and headache. ... Diagnosis. ... Treatment. ... Prognosis.

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• Define and use related medical terminology.
• Describe and demonstrate techniques for imaging the thyroid gland.
• Discuss functional abnormalities of the thyroid gland.
• Correlate laboratory data relevant to the thyroid and parathyroid glands.
• Describe, and recognize on images, pathologies of the thyroid gland.
• Identify the anatomy of the parathyroid glands on diagrams and sonograms.
• Describe and demonstrate techniques for imaging the parathyroid glands.
• Describe, and recognize on images, pathologies of the parathyroid glands.
• List and describe other neck masses.
• Follow relevant protocols when scanning.
• Differentiate the sonographic appearances of the female reproductive organs in relation to the menstrual cycle, the use of contraceptives and hormone replacement, and following chemotherapy.
• Explain the Patient Privacy Rule (HIPAA) and Patient Safety Act (see reference).

Hyperparathyroidism is an excess of parathyroid hormone in the bloodstream due to overactivity of one or more of the body's four parathyroid glands. These glands are about the size of a grain of rice and are located in your neck. The parathyroid glands produce parathyroid hormone, which helps maintain an appropriate balance of calcium in the bloodstream and in tissues that depend on calcium for proper functioning. Two types of hyperparathyroidism exist. In primary hyperparathyroidism, an enlargement of one or more of the parathyroid glands causes overproduction of the hormone, resulting in high levels of calcium in the blood (hypercalcemia), which can cause a variety of health problems. Surgery is the most common treatment for primary hyperparathyroidism. Secondary hyperparathyroidism occurs as a result of another disease that initially causes low levels of calcium in the body and over time, increased parathyroid hormone levels occur.

Neurotransmitter 3D Animation
on Tuesday, December 21, 2010




Neurotransmitters are endogenous chemicals which transmit signals from a neuron to a target cell across a synapse. Neurotransmitters are packaged into synaptic vesicles clustered beneath the membrane on the presynaptic side of a synapse, and are released into the synaptic cleft, where they bind to receptors in the membrane on the postsynaptic side of the synapse. Release of neurotransmitters usually follows arrival of an action potential at the synapse, but may also follow graded electrical potentials. Low level "baseline" release also occurs without electrical stimulation. Neurotransmitters are synthesized from plentiful and simple precursors, such as amino acids, which are readily available from the diet and which require only a small number of biosynthetic steps to convert. The chemical identity of neurotransmitters is often difficult to determine experimentally. For example, it is easy using an electron microscope to recognize vesicles on the presynaptic side of a synapse, but it may not be easy to determine directly what chemical is packed into them. The difficulties led to many historical controversies over whether a given chemical was or was not clearly established as a transmitter. In an effort to give some structure to the arguments, neurochemists worked out a set of experimentally tractable rules. According to the prevailing beliefs of the 1960s, a chemical can be classified as a neurotransmitter if it meets the following conditions: * There are precursors and/or synthesis enzymes located in the presynaptic side of the synapse. * The chemical is present in the presynaptic element. * It is available in sufficient quantity in the presynaptic neuron to affect the postsynaptic neuron; * There are postsynaptic receptors and the chemical is able to bind to them. * A biochemical mechanism for inactivation is present. There are many different ways to classify neurotransmitters. Dividing them into amino acids, peptides, and monoamines is sufficient for some classification purposes. Major neurotransmitters: * Amino acids: glutamate, aspartate, D-serine, γ-aminobutyric acid (GABA), glycine * Monoamines and other biogenic amines: dopamine (DA), norepinephrine (noradrenaline; NE, NA), epinephrine (adrenaline), histamine, serotonin (SE, 5-HT), melatonin * Others: acetylcholine (ACh), adenosine, anandamide, nitric oxide, etc. In addition, over 50 neuroactive peptides have been found, and new ones are discovered regularly. Many of these are "co-released" along with a small-molecule transmitter, but in some cases a peptide is the primary transmitter at a synapse. β-endorphin is a relatively well known example of a peptide neurotransmitter; it engages in highly specific interactions with opioid receptors in the central nervous system. Single ions, such as synaptically released zinc, are also considered neurotransmitters by some[by whom?], as are some gaseous molecules such as nitric oxide (NO) and carbon monoxide (CO). These are not classical neurotransmitters by the strictest definition, however, because although they have all been shown experimentally to be released by presynaptic terminals in an activity-dependent way, they are not packaged into vesicles. By far the most prevalent transmitter is glutamate, which is excitatory at well over 90% of the synapses in the human brain. The next most prevalent is GABA, which is inhibitory at more than 90% of the synapses that do not use glutamate. Even though other transmitters are used in far fewer synapses, they may be very important functionally—the great majority of psychoactive drugs exert their effects by altering the actions of some neurotransmitter systems, often acting through transmitters other than glutamate or GABA. Addictive drugs such as cocaine and amphetamine exert their effects primarily on the dop

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USMLE Step 2 CS - Acute Abdomen- This is just preview video. To get full access please visit our website : www.usmletutoring.com

There are two main types of influenza (flu) virus: Types A and B. The influenza A and B viruses that routinely spread in people (human influenza viruses) are responsible for seasonal flu epidemics each year. Influenza A viruses can be broken down into sub-types depending on the genes that make up the surface proteins. Over the course of a flu season, different types (A & B) and subtypes (influenza A) of influenza circulate and cause illness.

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How to diagnose digital ulceration in out patient clinic. part II