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Genetics Research Supports White supremacy
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[QUOTE]Originally posted by Narmerthoth: [QB] ^ As usual, you're wrong. As I stated, Human gnome is about correcting or repairing the devastating autosomal diseases that afflict Eurobino gentile and Jews who suffer from many many forms of genetic mutation resulting in everything from massive skin cancer susceptibility, to severe mental disorders, to an inability to sleep to extremely low reproduction rates where the ratio of deaths to births is affecting their very genetic survival. In all cases, EUROBINOS attempt to downplay the occurrence of these OCA related defects as characterizing them as, rare. However, in reality, they are as rare as the OCA mutation which is present in ALL EUROBINOS and Asians. Here is an prime example of the goal of genetics to allow Eurobinos to survive their mutation death toll. Note, that EUROBINOS will openly confess to the ATP7A defect, but will never ever confess to it's direct connection to OCA (their albinism). [b]Deadly genetic disease prevented before birth in zebrafish[/b] By injecting a customized "genetic patch" into early stage fish embryos, researchers at Washington University School of Medicine in St. Louis were able to correct a genetic mutation so the embryos developed normally. The research could lead to the prevention of up to one-fifth of birth defects in humans (EUROBINOS) caused by genetic mutations, according to the authors. Erik C. Madsen, first author and an M.D./Ph.D. student in the Medical Scientist Training Program at Washington University School of Medicine, made the groundbreaking discovery using a zebrafish model of Menkes disease, a rare, inherited disorder of copper metabolism caused by a mutation in the human version of the ATP7A gene. (THIS IS A OCA RELATED DEFECT WHICH PROVES OCA DOES NOT JUST NEGATIVELY AFFECT SKIN COLOR) Children who have Menkes disease have seizures, extensive neurodegeneration in the gray matter of the brain, abnormal bone development and kinky, colorless hair. Most children with Menkes die before age 10, and treatment with copper is largely ineffective. The development of organs in the fetus is nearly complete at a very early stage. By that time, the mutation causing Menkes disease has already affected brain and nerve development. The work is an important step toward personalized medicine, which can tailor treatment to an individual's genetic makeup. https://phys.org/news/2008-03-deadly-genetic-disease-birth-zebrafish.html#jCp [b]Cell-specific ATP7A transport sustains copper-dependent tyrosinase activity in melanosomes.[/b] To catalyse melanin synthesis, tyrosinase is subsequently reloaded with copper within specialized organelles called melanosomes. Copper is supplied to melanosomes by ATP7A, a cohort of which localizes to melanosomes in a biogenesis of lysosome-related organelles complex-1 (BLOC-1)-dependent manner. These results indicate that cell-type-specific localization of a metal transporter is required to sustain metallation of an endomembrane cuproenzyme, providing a mechanism for exquisite spatial control of metalloenzyme activity. Moreover, because BLOC-1 subunits are mutated in subtypes of the genetic disease Hermansky-Pudlak syndrome, these results also show that defects in copper transporter localization contribute to hypopigmentation, and hence perhaps other systemic defects, in Hermansky-Pudlak syndrome. [IMG]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2812007/bin/nihms132712f4.jpg[/IMG] Copper restores in vitro tyrosinase activity in melanosomes of BLOC-1-deficient melanocytes DOPA cytochemistry of BLOC-1− melan-mu (a–f) or BLOC-1R melan-mu:MuHA (g, h) cells in the absence or presence (+ Copper) of 20 µM copper sulfate in the reaction buffer. (a–d) Bright field microscopy analysis of cells treated for 4 h as indicated. Insets, boxed regions magnified 10X. Bars, 10 µm. Note the increased melanin deposits in BLOC-1− cells in the presence (c) compared to the absence (a) of copper. (e–h) EM analysis of thin sections of cells treated for 2 h. Note melanin deposits in the trans-most Golgi cisternae, but not in striated melanosomes, of BLOC-1− melan-mu cells in the absence of excess copper (e; inset), and the additional deposition of melanin in striated melanosomes in the presence of copper (f, stars; inset). GA, Golgi apparatus; TGN, trans-Golgi network; PM, Plasma membrane; II, III, IV, melanosome stages II and IV. Bars, 500 nm and inset, 200 nm [IMG]http://i32.photobucket.com/albums/d25/GoldenMenes/Screenshotat2012-06-05223825.png[/IMG] [/QB][/QUOTE]
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