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I go by the name Cristina Yang. I am a doctor. My best friend is Meredith Grey. I am married to Dr. Owen Hunt. I have B.A. from Smith College . I also have a Ph.D in Biochemistry from the University of California, Berkeley. I will be the best surgeon there is.
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Many amino acid and organic acid disorders are associated with spongy myelinopathy (SM). This is a poorly understood, non-progressive lesion of central myelin, characterized by fluid filled vacuoles in the myelin sheath, which impart a spongy appearance to the white matter. 
Instability of myelin due to abnormal lipid composition of cell membranes may play a role in the pathogenesis of SM. Some amino acid disorders have different neuropathological lesions. Thus, Alzheimer type II astrocytes are seen in the urea cycle disorders, and vascular lesions are the key finding in homocystinuria. Hypoxic and ischemic changes (cortical and basal ganglia atrophy) are also seen in several amino acid disorders.
The clinical, biochemical, and pathological findings in the most common amino acid disorders are summarized in the table.
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Image: Functional magnetic resonance imaging (fMRI) and other brain imaging technologies allow for the study of differences in brain activity in people diagnosed with schizophrenia. The image shows two levels of the brain, with areas that were more active in healthy controls than in schizophrenia patients shown in orange, during an fMRI study of working memory.

Schizophrenia is associated with subtle differences in brain structures, found in 40 to 50% of cases, and in brain chemistry during acute psychotic states. Studies using neuropsychological tests and brain imaging technologies such as fMRI and PET to examine functional differences in brain activity have shown that differences seem to most commonly occur in the frontal lobes, hippocampus and temporal lobes. Reductions in brain volume, smaller than those found in Alzheimer’s disease, have been reported in areas of the frontal cortex and temporal lobes. It is uncertain whether these volumetric changes are progressive or preexist prior to the onset of the disease. These differences have been linked to the neurocognitive deficits often associated with schizophrenia. Because neural circuits are altered, it has alternatively been suggested that schizophrenia should be thought of as a collection of neurodevelopmental disorders.
Particular attention has been paid to the function of dopamine in the mesolimbic pathway of the brain. This focus largely resulted from the accidental finding that phenothiazine drugs, which block dopamine function, could reduce psychotic symptoms. It is also supported by the fact that amphetamines, which trigger the release of dopamine, may exacerbate the psychotic symptoms in schizophrenia.The influential dopamine hypothesis of schizophrenia proposed that excessive activation of D2 receptors was the cause of (the positive symptoms of) schizophrenia. Although postulated for about 20 years based on the D2 blockade effect common to all antipsychotics, it was not until the mid-1990s that PET and SPET imaging studies provided supporting evidence. The dopamine hypothesis is now thought to be simplistic, partly because newer antipsychotic medication (atypical antipsychotic medication) can be just as effective as older medication (typical antipsychotic medication), but also affects serotonin function and may have slightly less of a dopamine blocking effect.
Interest has also focused on the neurotransmitter glutamate and the reduced function of the NMDA glutamate receptor in schizophrenia, largely because of the abnormally low levels of glutamate receptors found in the postmortem brains of those diagnosed with schizophrenia,[58] and the discovery that glutamate-blocking drugs such as phencyclidine and ketamine can mimic the symptoms and cognitive problems associated with the condition.[59] Reduced glutamate function is linked to poor performance on tests requiring frontal lobe and hippocampal function, and glutamate can affect dopamine function, both of which have been implicated in schizophrenia, have suggested an important mediating (and possibly causal) role of glutamate pathways in the condition. But positive symptoms fail to respond to glutamatergic medication.
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BioDigital Human


I may have stumble across something awesome, super awesome.

It’s a site where you can look up anything about the human anatomy and various conditions. Everything’s in 3D, you can zoom in and out to see various anatomy, you can even select various body systems and body parts. (That includes clicking on something extremely detailed, like say…your left 4th rib or something)

This is freaking awesome, hours of entertainment, knowledge, and fun. :)

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