Disruption of axonal transport would be a good target for his drug.
<h3>What is disruption of axonal transport?</h3>
- Axonal transport defects are among the early molecular events leading to neurodegeneration in mouse models of amyotrophic lateral sclerosis (ALS).
- Gene expression profiles indicate that dynactin-1 mRNA is downregulated in degenerating spinal motor neurons of autopsied patients with sporadic ALS.
- Disruption of axonal transport also underlies the pathogenesis of spinal muscular atrophy and hereditary spastic paraplegias.
- The neurotoxin β,β′-iminodipropionitrile (IDPN) selectively disrupts slow axonal transport without affecting fast anterograde or retrograde axonal transport.
- Impairment of slow axonal transport causes a proximal accumulation of neurofilaments.
- Because neurofilaments regulate axonal diameter, this accumulation leads to a marked swelling of the axon.
- Acrylamide causes decreased axonal transport, also causing proximal accumulations of neurofilaments and swelling.
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Metallic luster is your answer
Answer:
Last option
Explanation:
Mitochondria because they are smaller than cells and have membranes
B.To Understand group behavior through observation
Thickening of gill epithelia in rainbow trout, caused by chloride cell proliferation, could lead to an impairment of oxygen uptake under moderate to severe hypoxia (Thomas et al 1988; Bindon et al., 1994; Greco et al., 1995).
<h3>What results in an increase in AMS in interstitial lung disease?</h3>
The number of alveolar macrophages (AMs) can rise in interstitial lung disease. Precursor cells from the peripheral circulation may have been drawn in, and/or there may have been local lung growth, to create this.
<h3>What connection does sarcoidosis have between lymphocytes and proliferating cells?</h3>
Additionally, a strong association between the quantities of lymphocytes and proliferative cells in sarcoidosis and fibrosis was discovered in bronchoalveolar lavage (BAL). Eosinophil counts and proliferating cell counts were positively associated in fibrosis.
<h3>How do AMS patients and healthy controls differ in terms of propagating AMS?</h3>
With a substantial association between these two indices, there was a considerable increase in proliferating AMs in all patient groups when compared to healthy controls (4.2 versus 1.4% Feulgen, and 2.1 against 0.5% Ki67).
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