Answer:
False
Explanation:
The papillary muscles of both right and left ventricles began to contract shortly before the other ventricular muscles (systole) so that they can take up the slack on the chordae tendineae as the full force of ventricular contractions sends blood against the atrioventricular (AV) valve flaps.
They prevent the backward flow of blood to atria from ventricles. So if they contract after the ventricle systole they would not be able to perform their job.
This is true they are the products of photosynthesis and the reactants for aerobic respiration.
Answer:
Endocrine and Cardiovascular system
Explanation:
Excess fat intake leads to different health hazards. They affect the body and cause lipids to clog the arteries thereby preventing blood from quickly delivering oxygen to the body parts.
Excess fat intake causes fatty pancreas and decreases its function.
It also causes series of cardiovascular diseases such as heart attack; elevated cholesterol/atherosclerosis,abnormal heart rhythms, hypertension, stroke etc
Answer:
A. 21 rad/s
B. 200.5 rpm
C. 26.46 rad/s2
D. 0.299 Hz
Explanation:
Parameters given are:
Tangential velocity,v = 1.26m/s
Diameter (outer edge) = 0.120m
Outer edge radius, ro = 0.12/2
= 0.06m
A. Calculate Angular velocity
Angular velocity, w = v/r
= v/ro
= 1.26/0.06 = 21 rad/s
In rpm,
2pi/60 rad/s = 1 rpm
1 rad/s = 60/2pi rpm
Sp, 21 rad/s = 60 * 21/2pi rpm
= 200.5 rpm
B. Calculate the inner edge radius, ri given w = 500 rpm
Converting rpm to rad/s,
= 2pi/60 * 500 rad/s
= 52.34 rad/s
ri = v/w
= 1.26/ 52.36
= 0.024m
C. Calculating centripetal acceleration, a from the outer edge, ro
a = v2/r = w2r
= (1.26)2/0.06
= 26.46 rad/s
D. Calculate the frequency, f of the outer edge angular velocity, w = 21 rad/s
f = 2pi/w
= 2pi/21
= 0.299 Hz (or per second)
A neuromuscular junction (or myoneural junction) is a chemical synapse formed by the contact between a motor neuron and a muscle fiber.[1] It is at the neuromuscular junction that a motor neuron is able to transmit a signal to the muscle fiber, causing muscle contraction.
Muscles require innervation to function—and even just to maintain muscle tone, avoiding atrophy. Synaptic transmission at the neuromuscular junction begins when an action potential reaches the presynaptic terminal of a motor neuron, which activates voltage-dependent calcium channels to allow calcium ions to enter the neuron. Calcium ions bind to sensor proteins (synaptotagmin) on synaptic vesicles, triggering vesicle fusion with the cell membrane and subsequent neurotransmitter release from the motor neuron into the synaptic cleft. In vertebrates, motor neurons release acetylcholine (ACh), a small molecule neurotransmitter, which diffuses across the synaptic cleft and binds to nicotinic acetylcholine receptors (nAChRs) on the cell membrane of the muscle fiber, also known as the sarcolemma. nAChRs are ionotropic receptors, meaning they serve as ligand-gated ion channels. The binding of ACh to the receptor can depolarize the muscle fiber, causing a cascade that eventually results in muscle contraction.
Neuromuscular junction diseases can be of genetic and autoimmune origin. Genetic disorders, such as Duchenne muscular dystrophy, can arise from mutated structural proteins that comprise the neuromuscular junction, whereas autoimmune diseases, such as myasthenia gravis, occur when antibodies are produced against nicotinic acetylcholine receptors on the sarcolemma.
