Muscle structure normal

A molecule called succinylcholine is a competitive inhibitor of acetylcholine binding to the receptor and can be used as a muscle relaxant in surgical procedures. This compound has a structure that resembles acetylcholine closely enough that it can bind to the acetylcholine receptor. However, it does not have the ability to stimulate muscle contraction. The result is that muscles relax. Normal muscle contraction resumes after infusion of the drug ceases. 

Somlyo AP, Somlyo, AV (1968a) Vascular smooth muscle I. Normal structure, pathology, biochemistry, and biophysics. Pharmacol Rev 20 197-272 Somlyo AP, Somlyo AV (1994) Signal transduction and regulation in smooth muscle. Nature 372 231-236... 

Muscle phosphorylase (EC 2.4.1.1) deficient. Glycogen structure normal. Glycogen accumulates only in muscle. Exercise causes muscle cramps myoglobin from damaged muscle may appear in urine. Patients symptomless if they refrain from strenuous exercise. Prognosis favorable. 

CONTEXT The secondary structure of a protein is crucial to its biological activity, whether for good or ill. Snake venoms consist of saliva with a high proportion of toxic proteins. Cobra venom in particular acts on the victim by means of neurotoxins, proteins that attack the nervous system, in this case by blocking the acetylcholine receptors on the membranes of muscle cells. Normally, when acetylcholine... 

AH of these are apparently for short durations under normal circumstances. They are examples of the adaptations affecting the structure and function of the body. However, dysfunction occurs when there is either persistence past the point of usefulness, inappropriate activation, a reflex loop pattern or any combination. The activation of any portion can be primary, secondary, or tertiary. The body responds to stress with vasoconstriction of all of the arteries as a means of shunting blood to the muscles. A normal reaction by the coronary vessels is to dilate, not because of an apparent paradoxical effect or receptor difference, but because the sympathetic stimulation increases the inotropic and chronotropic effects on the heart. The increased pressure, because of the rate and force of contraction, typically results in greater capacitance and perfusion of the heart itself. Partial or total occlusion by atherosclerosis or thromboembolic phenomena results in ischemia and possible infarction. The resultant pain and pressure contributes to... 

Methods Muscle weakness was produced in one year old, female New Zealand white rabbits by injecting botulinum toxin type-A (BTXA) into the quadriceps musculature for times ranging from 1-6 months [7]. Contralateral limbs served as saline injected controls while other animals served as normal controls. Strength, muscle mass, muscle structure and knee histology (Mankin score) were evaluated to determine if muscle weakness caused joint degeneration. 

Both the G- and V-agents have the same physiological action on humans. They are potent inhibitors of the enzyme acetylcholinesterase (AChE), which is required for the function of many nerves and muscles in nearly every multicellular animal. Normally, AChE prevents the accumulation of acetylcholine after its release in the nervous system. Acetylcholine plays a vital role in stimulating voluntary muscles and nerve endings of the autonomic nervous system and many structures within the CNS. Thus, nerve agents that are cholinesterase inhibitors permit acetylcholine to accumulate at those sites, mimicking the effects of a massive release of acetylcholine. The major effects will be on skeletal muscles, parasympathetic end organs, and the CNS. 

Amylo-1 —> 6-glucosidase obtained by Cori and Larner218 from rabbit muscles, and R-enzyme isolated by Hobson, Whelan and Peat219 from potatoes and broad beans, are typical debranching enzymes, which will hydrolyze the 6 — 1-a-D-glucosidic linkage rather than the normal 4 —> 1-a-D linkage. These enzymes will therefore be particularly important in determinations of the fine structure of amylopectin, if they can be sufficiently well purified. 

Smooth muscle is distributed throughout the body, largely around hollow structures such as blood vessels, the gastrointestinal tract and the genitourinary system. Normal function requires that the smooth muscles contract and relax at appropriate times, and abnormalities of contraction underlie such important pathologies as hypertension, incontinence and abnormal childbirth. Since contraction is initiated by an increase of cytoplasmic Ca2+ concentration then normal function requires appropriate Ca2+ handling. 

Transverse relaxation of musculature is relatively fast compared with many other tissues. Measurements in our volunteers resulted in T2 values of approximately 40 ms, when mono-exponential fits were applied on signal intensities from images recorded with variable TE. More sophisticated approaches for relaxometry revealed a multi-exponential decay of musculature with several T2 values." Normal muscle tissue usually shows lower signal intensity than fat or free water as shown in Fig. 5c. Fatty structures inside the musculature, but also water in the intermuscular septa (Fig. 5f) appear with bright signal in T2-weighted images. 

When solutions of directly acting choUnomimetics are applied to the eye (i.e., conjunctival sac), they cause contraction of the smooth muscle in two important structures, the iris sphincter and the ciliary muscles (Fig. 12.3). Contraction of the iris sphincter decreases the diameter of the pupil (miosis). Contraction of the circular fibers of the ciliary muscle, which encircles the lens, reduces the tension on the suspensory ligaments that normally stretch and flatten the lens, allowing the highly elastic lens to spontaneously round up and focus for near vision (accommodation to near vision). 

At both these times, thigh muscle contained a higher concentration of 2-PAM I than abdominal muscle, but a lower concentration of III. Dogs and rabbits appear, therefore, to tolerate repeated daily intravenous doses of 2-PAM I at 30 mg/kg or of III at 10 mg/kg during a period of 6-8 wk when the dally doses are suspended during each weekend. Because in this and the other studies reviewed the animals were killed at or soon after the end of the period of administration of an oxime, there has been no opportunity to judge whether repeated administration of an oxime may initiate some alteration in normal structure or function that will result eventually in a definite lesion. No truly chronic study of the toxicity of an oxime has been found. Thus, possible cryptic toxic effects of this type of compound have never been assessed. 

Diacylglycerol, on the other hand, is lipid soluble and remains in the lipid bilayer of the membrane. There it can activate protein kinase C (PKC), a very important and widely distributed enzyme which serves many systems through phosphorylation, including neurotransmitters (acetylcholine, a,- and P-adrenoceptors, serotonin), peptide hormones (insulin, epidermal growth hormone, somatomedin), and various cellular functions (glycogen metabolism, muscle activity, structural proteins, etc.), and also interacts with guanylate cyclase. In addition to diacylglycerol, another normal membrane lipid, phos-phatidylserine, is needed for activation of PKC. The DG-IP3 limbs of the pathway usually proceed simultaneously. 

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