Answer:
Analogous structures
Explanation:
These structures are similar but not derived from the common ancestor like homologous structures. Analogous structures are formed as a result of convergent evolution-type of evolution in which organisms develop on similar way but independently. An example of analogous structures are wings. Birds, insects and bats all have wings, with the same purpose (flight) but they evolved in their own way.
Answer:
Check the areas that need excessive maintenance
Explanation:
Creatinine is a by-product of muscular metabolism. In the natural and normal scheme of things, this substance or waste product can be eliminated from the body. A high-serum creatinine level may cause kidney damage. In relation to the above question as to how high can creatinine levels go before death, it must be noted that kidneys have strong compensatory ability and by that as long as its still 50 percent functional, creatinine level won't be that high. Which leads us to a conclusion that, the lesser the kidney function level is, the higher the creatinine level.
On the other hand for the blood urea nitrogen (BUN) is the most stable blood constituent following death as it reaches antemortem (before death) levels and even after moderate decomposition.
Therefore, as long as the kidneys are functional, regardless of other factors such as the patient's condition/ diagnosis, these blood constituents are nearly normal.
Answer:
The correct answer is 3: "<em>High levels of Ca2+ are expected to be found </em><em>within the sarcoplasmic reticulum</em>".
Explanation:
Muscular contraction is a highly regulated process that depends on free calcium concentration in the cytoplasm. Amounts of cytoplasmic calcium are regulated by <u>sarcoplasmic reticulum</u> that functions as a storage of the ion.
When a nerve impulse reaches the membrane of a muscle fiber, through acetylcholine release, the membrane depolarizes producing the entrance of calcium from <u>extracellular space</u>. The impulse is transmitted along the membrane to the sarcoplasmic reticulum, from where calcium is released. At this point, <em>tropomyosin is obstructing binding sites for myosin on the thin filament</em>. The calcium channel in the sarcoplasmic reticulum controls the ion release, that activates and regulates muscle contraction, by increasing its cytoplasmic levels. When <em>calcium binds to the troponin C</em>, <em>the troponin T alters the tropomyosin by moving it and then unblocks the binding sites,</em> making possible the formation of <em>cross-bridges between actin and myosin filaments.</em> When myosin binds to the uncovered actin-binding sites, ATP is transformed into ADP and inorganic phosphate.
Z-bands are then pulled toward each other, thus shortening the sarcomere and the I-band, and producing muscle fiber contraction.
