Cannabis maybe. Hope this is for school lol
If it’s 40% glucose then it will be 60% water
Covalent bonding occurs when pairs of electrons are shared by atoms. Atoms will covalently bond with other atoms in order to gain more stability, which is gained by forming a full electron shell. By sharing their outer most (valence) electrons, atoms can fill up their outer electron shell and gain stability
Answer:
It could be embreology. (I think i spelled that wrong)
Explanation:
It is a way to compare the embreos of two species to see the similarities between the two. If there are similarities then they have a common ancestor. If they don't have similarities then they arent from the same family.
Answer:
1. nerve stimulus
4. calcium channels open
10. acetylcholine vesicles move to endplate
7. exocytosis occurs releasing acetylcholine into synaptic cleft
3. acetylcholine binds to receptor
6. impulse rides along sarcolemma
9. impulse enters the cells via the t-tubule
5. sarcoplasmic reticulum releases calcium
8. calcium binds to troponin moving tropomyosin out of the way
2. myosin attaches to actin causing a twitch
Explanation:
The central nervous system generates an action potential (<u>1</u>) that travels to the muscle fiber activating the calcium channels (<u>4</u>). Calcium triggers vesicles fusion to the presynaptic membrane (<u>10)</u> releasing acetylcholine (Ach) into the synaptic space (<u>7</u>). Once there, Ach binds to its receptors (<u>3</u>) on the postsynaptic membrane of the skeletal muscle fiber, causing ion channels to open. Positively charged sodium ions cross the membrane to get into the muscle fiber (sarcoplasm) and potassium leaves the cell. The difference in charges caused by these ions transport charges positively the muscle fiber membrane (<u>6</u>). It depolarizes. The action potential enters the t-tubules (<u>9</u>) depolarizing the inner portion of the muscle fiber.
Contraction initiates when the action potential depolarizes the inner portion of the muscle fiber. Calcium channels activate in the T tubules membrane, releasing calcium into the sarcolemma (<u>5</u>). At this point, the muscle is at rest, and the tropomyosin is inhibiting the attraction strengths between myosin and actin filaments. <em>Tropomyosin is obstructing binding sites for myosin on the thin filament</em>. When calcium binds to troponin C, troponin T alters the tropomyosin position by moving it and unblocking the binding sites (<u>8)</u>. Myosin heads join to the uncovered actin-binding points forming cross-bridges <u>(2</u>), and while doing so, ATP turns into ADP and inorganic phosphate, which is released. Myofilaments slide impulsed by chemical energy collected in myosin heads, producing a power stroke. The power stroke initiates when the myosin cross-bridge binds to actin (<u>2</u>). As they slide, ADP molecules are released. A new ATP links to myosin heads and breaks the bindings to the actin filament. Then ATP splits into ADP and phosphate, and the energy produced is accumulated in the myosin heads, which starts a new binding cycle to actin. Finally, Z-bands are pulled toward each other, shortening the sarcomere and the I-band, producing muscle fiber contraction.
