Additionally specifically in regards to ELLs the supreme court ruling Lau v. Nichols (1974) stated that equal treatment in school did not mean equal educational opportunity. Thus if a school teaches a lesson in a language that students do not understand then they are effectively worthless. This ruling is also supported by English language development services provided in schools, but these rulings do not require the individuals that teach and provide services to have any specific training nor is licensing different from a typical teacher or services provider. Critique of the medical model
Learning disability theory is founded in the medical model of disability, in that disability is perceived as an individual deficit that is biological in origin. Researchers working within a social model of disability assert that there are social or structural causes of disability or the assignation of the label of disability, and even that disability is entirely socially constructed. Since the turn of the 19th century, education in the United States has been geared toward producing citizens who can effectively contribute to a capitalistic society, with a cultural premium on efficiency and science. More agrarian cultures, for example, do not even use learning ability as a measure of adult adequacy, whereas the diagnosis of learning disabilities is prevalent in Western capitalistic societies because of the high value placed on speed, literacy, and numeracy in both the labor force and school system.
This trend may be accelerated by anagrelide. This increase in fibrosis appeared to be linked to a drop in hemoglobin as it progressed. Stopping anagrelide (and switching patients to hydroxyurea) appeared to reverse the degree of marrow fibrosis. Thus, patients on anagrelide may need to be monitored on a periodic basis for marrow reticulin scores, especially if anemia develops, or becomes more pronounced if present initially.Less common side effects include: congestive heart failure, myocardial infarction, cardiomyopathy, cardiomegaly, complete heart block, atrial fibrillation, cerebrovascular accident, pericarditis, pulmonary infiltrates, pulmonary fibrosis, pulmonary hypertension, pancreatitis, gastric/duodenal ulceration, renal impairment/failure and seizure. Due to these issues, anagrelide should not generally be considered for first line therapy for essential thrombocytosis. Mechanism of action
Anagrelide works by inhibiting the maturation of platelets from megakaryocytes. The exact mechanism of action is unclear, although it is known to be a phosphodiesterase inhibitor. It is a potent (IC50 = 36nM) inhibitor of phosphodiesterase-II. It inhibits PDE-3 and phospholipase A2. Synthesis
Phosphodiesterase inhibitor with antiplatelet activity. Condensation of benzyl chloride 1 with ethyl ester of glycine gives alkylated product 2. Reduction of the nitro group leads to the aniline and reaction of this with cyanogen bromide possibly gives cyanamide 3 as the initial intermediate. Addition of the aliphatic would then lead to formation of the quinazoline ring (4). Amide formation between the newly formed imide and the ester would then serve to form the imidazolone ring, whatever the details of the sequence, there is obtained anagrelide (5).