S Phase it is important that the cell develops properly
Joint hypermobility syndrome (JHS) and Ehlers-Danlos syndrome, hypermobility type (EDS-HT) are the tissue disorders which can be characterized by chronic pain, joint instability complications, and minor skin changes. During these, Fatigue and headache are the very common symptoms; though they can be diagnosed using specific criteria.
JHS/EDS-HT is a rare common condition that could not be diagnosed by most clinicians and pain specialists, resulting in interventions like symptomatic and non-satisfactory treatments, because there is a lack of reasonable pathophysiologic rationale.
Pain, fatigue, and headache in JHS/EDS are usually treated with the help of certain symptoms or on the basis of doctors’ experience.
<span>Therefore, in order to the cure of such symptoms, doctors suggest pathogenic mechanisms. The major aim of the re-writing of the natural history of JHS/EDS-HT is to raise awareness among clinical geneticists and specialists treating chronic pain conditions about pain and other complications of JHS/EDS-HT.</span>
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Hello!
✧･ﾟ: *✧･ﾟ:* *:･ﾟ✧*:･ﾟ✧
❖ Blood in the veins carries wastes away from the cells of the body and back to the heart.
~ ʜᴏᴘᴇ ᴛʜɪꜱ ʜᴇʟᴘꜱ! :) ♡
~ ᴄʟᴏᴜᴛᴀɴꜱᴡᴇʀꜱ
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.
