It is an hydrophilic substance....<span>Substances that have charge or polarity are </span>hydrophilic<span>, and are likely to dissolve because they have either full or partial charge areas to form hydrogen bonds with water molecules.</span>
Answer:
Reflexes are not a function of the spinal cord.
Explanation:
The spinal cord is part of the central nervous system and is made up of neurons that go along it (from the end of the brain stem almost to the bottom of the spine).
The spinal cord receives incoming messages from the peripheral nervous system (including the sensory neurons) and pass on messages from the brain to efferent neurons (motor neurons at muscles).
The spinal cord contributes to learning as it passes on the info received from sensory neurons (that there is an obstacle in the path) to the brain and passes on the response from the brain to the muscles (to lift the foot up higher).
The spinal cord is essential for integration as it passes on sensory information to the brain to determine motor output.
Reflexes are when sensory information is quickly sent straight to motor neurons to move. It does not need to go to the brain (hence does not need to go to the spinal cord) for the reaction as it would be too slow. This is seen when someone who is paraplegic (paralysed at lower torso) can still move their leg in response to the doctor tapping their knee even when they cannot forcibly move their legs.
Therefore reflexes are not a function of the spinal cord.
Answer:
PFFT this might help? sorry if not mate
Explanation:
Cell cycle checkpoint controls play a major role in preventing the development of cancer [see Sherr, 1994, for a more detailed discussion]. Major checkpoints occur at the G1 to S phase transition and at the G2 to M phase transitions. Cancer is a genetic disease that arises from defects in growth-promoting oncogenes and growth-suppressing tumor suppressor genes. The p53 tumor suppressor protein plays a role in both the G1/S phase and G2/M phase checkpoints. The mechanism for this activity at the G1/S phase checkpoint is well understood, but its mechanism of action at the G2/M phase checkpoint remains to be elucidated. The p53 protein is thought to prevent chromosomal replication specifically during the cell cycle if DNA damage is present. In addition, p53 can induce a type of programmed cell death, or apoptosis, under certain circumstances. The general goal of p53 appears to be the prevention of cell propagation if mutations are present. The p53 protein acts as a transcription factor by binding to certain specific genes and regulating their expression. One of these, WAF1 or Cip1, is activated by p53 and is an essential downstream mediator of p53-dependent G1/S phase checkpoint control. The function of p53 can be suppressed by another gene, MDM2, which is overexpressed in certain tumorigenic mouse cells and binds to p53 protein, thus inhibiting its transcriptional activation function. Other cellular proteins have been found to bind to p53, but the significance of the associations is not completely understood in all cases. The large number of human cancers in which the p53 gene is altered makes this gene a good candidate for cancer screening approaches.
