I believe that local controls are what causes reactive hyperemia to increase tissue perfusion. Reactive hyperemia or venous hyperemia is the transient increase in organ blood flow that occurs following a brief period of ischaemia.
Tissue perfusion is the decrease in oxygen resulting in the failure to nourish the tissues at the capillary level. Local blood flow regulation involves the rapid control of arterial vasomotion based on the metabolic needs of the surrounding tissues and cells.
Answer:
astro,bio,and celluar
Explanation:
there are many diiferent types of scientists
Answer:A law is a factual statement., and A law cannot be changed or replaced.
Explanation: idk cuz i did it -_-
Answer:
They are sections of DNA that produce the proteins that control an organism's characteristics.
Explanation:
- <em><u>Genes are units of heredity found in a certain place on a chromosome and that codes for a certain product.</u></em>
- A trait of an organism is a characteristic that an organism can pass on to its offspring through its genes
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- Genes are sections of DNA that contains information which controls a trait. Therefore, a trait depends on genes. Therefore; genes are the sections or segments of DNA that code for a specific trait in organisms.
Answer:
1. T
2. T
3. NP
4. F
5. F
Explanation:
In somatic cells, the cell cycle can be divided into 1-the interphase, 2-the mitotic phase or M phase, and 3-the G₀ phase. In turn, the interphase of the cell cycle can be divided into three phases: 1-the gap 1 (G1) phase or growth 1 phase, 2-the S phase (DNA replication or DNA synthesis), and 3-the gap 2 (G2) phase or growth 2 phase. During the G1 phase, the cell synthesizes key enzymes which are required during DNA replication (S phase) and cell division (M phase). Cytoplasmic factors are proteins and messenger RNAs (mRNAs) that control cell functions during the cell cycle. This cycle is modulated by proteins known as control factors, i.e., cyclins and cyclin-dependent kinases (Cdks) that work together to control the progression through different phases of the cell cycle. The transition from S to G2 occurs after DNA replication. This transition (S to G2) is controlled by a DNA damage checkpoint orchestrated by the ATM (Ataxia telangiectasia mutated) and ATR (Ataxia Telangiectasia and Rad3 related) kinases which are recruited to DNA damage sites. Moreover, the transition from G2 to M phase is mediated by the accumulation of mitotic inducers, which lead to an increase in the activity of mitotic kinase and finally trigger mitotic entry.
