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The myosin heads have sites that can bind to actin and thereby form cross-bridges between the myosin and the actin filaments generic alfuzosin 10 mg without prescription mens health yellow sperm. The energy released when this happens changes the conformation discount alfuzosin 10 mg on-line man health 99, and therefore the orientation buy alfuzosin discount prostate cancer incontinence, of the myosin head. They are wrapped by chains of the polypeptide tropomyosin and studded at intervals with another protein,troponin. Together, these details explain the cycle of events that cause the actin and myosin filaments to slide past each other and shorten the sarcomere. Upon binding, the head changes its orientation with respect to the myosin filament, thus exerting a force that causes the actin filament to slide about 5 to 10 nm relative to the myosin filament. We have been discussing the cycle of contraction in terms of a single myosin head. That is why when a single myosin head breaks its contact with actin, the actin filaments do not slip backward. This fact explains why muscles stiffen soon after animals die, a condition known as rigor mortis. These events have regular time courses that differ somewhat for different regions of the body; therefore, an examination of the stiffness of the muscles of a corpse can help a coroner estimate the time of death. Actin-myosin interactions are controlled by calcium ions Muscle contractions are initiated by action potentials from motor neurons arriving at the neuromuscular junction (see Troponin has three subunits: one binds actin, one binds tropomyosin, and one binds Ca2+. Actin filament Actin monomer Tropomyosin Troponin Troponin has three subunits: one binds actin, one binds tropomyosin, and one binds Ca2+. Actin filament Actin monomer Tropomyosin Troponin Linear polypeptide chain Linear polypeptide chain Figure 44. The axons of motor neurons are generally highly branched and can synapse with up to a hundred muscle fibers each. All the fibers activated by a single motor neuron constitute a motor unit and contract simultaneously in response to action potentials fired by that motor neuron. Like neurons, muscle cells are excitable; that is, their plasma membranes can generate and conduct action potentials. In the case of skeletal muscle fibers (but not smooth or cardiac muscle fibers), all action potentials are initiated by motor neurons. When an action potential arrives at the neu- romuscular junction, the neurotransmitter acetylcholine is released from the motor neuron, diffuses across the synaptic cleft, binds to receptors in the postsynaptic membrane, and causes ion channels in the motor end plate to open. Most of the ions that flow through these channels are Na+, and therefore the motor end plate is depolarized. The depolarization spreads to the surrounding plasma membrane of the muscle fiber, which contains voltage-gated sodium channels. When threshold is reached, the plasma membrane fires an action potential that is conducted rapidly to all points on the surface of the muscle fiber. The plasma membrane is continuous with a system of tubules that descends into and branches throughout the cytoplasm of the muscle fiber (also called the sarcoplasm) (Figure 47. The action potential that spreads over the plasma membrane also spreads through this system of transverse tubules, or T tubules. The T tubules come very close to a network of intracellu-lar membranes called the sarcoplasmic reticulum. The sarcoplasmic reticulum forms a membrane-enclosed compartment that surrounds every myofibril. Calcium pumps in the sarcoplasmic reticulum cause it to take up Ca2+ ions from the sarcoplasm. Therefore, when the muscle fiber is at rest, there is a high concentration of Ca2+ in the sarcoplasmic reticulum and a low concentration of Ca2+ in the sarcoplasm. Spanning the space between the membranes of the T tubules and the membranes of the sarcoplasmic reticulum are two proteins. One protein, which is located in the T tubule membrane, is voltage- sensitive and changes its conformation when an action potential reaches it. When it is activated by an action potential, the voltage-sensitive protein opens the Ca2+ channel, and Ca2+ ions diffuse out of the sarcoplasmic reticulum and into the sar-coplasm surrounding the actin and myosin filaments. It is these Ca2+ ions that trigger the interaction of actin and myosin and the sliding of the filaments. An actin filament, as we have seen, is a helical arrangement of two strands of actin monomers. Lying in the grooves between the two actin strands is the two-stranded protein tropomyosin (see Figure 47. The troponin molecule has three subunits: One binds actin, one binds tropomyosin, and one binds Ca2+. When Ca2+ is sequestered in the sarcoplasmic reticulum, the tropomyosin strands block the sites on the actin filament where myosin heads can bind. When the T tubule system depolarizes, Ca2+ is released into the sarcoplasm, where it binds to troponin, changing its conformation. Because the troponin is bound to the tropomyosin, this conformational change of the troponin twists the tropomyosin enough to expose the actin-myosin binding sites. Thus the cycle of making and breaking actin-myosin bonds is initiated, the filaments are pulled past each other, and the muscle fiber contracts. When the T tubule system repolarizes, the calcium pumps remove the Ca2+ ions from the sarcoplasm, causing the tropomyosin to return to the position in which it blocks the binding of myosin heads to actin, and the muscle fiber returns to its resting condition. Motor neuron ffi An action potential (black arrows) arrives at the motor neuron terminal. Motor neuron ffi An action potential (black arrows) arrives at the motor neuron terminal. The muscle fiber plasma membrane generates an action potential that spreads down T tubules. Plasma membrane Sarcoplasmic reticulum The muscle fiber plasma membrane generates an action potential that spreads down T tubules. Calmodulin mediates Ca2+ control of contraction in smooth muscle Smooth muscle cells do not have the troponin-tropomyosin mechanism for controlling contraction, but Ca2+ still plays a critical role. A Ca2+ influx into the sarcoplasm of a smooth muscle cell can be stimulated by action potentials, by hormones, or by stretching. The calmod-ulin-Ca2+ complex activates an enzyme called myosin kinase, which can phosphorylate myosin heads. When the myosin heads in smooth muscle are phosphorylated, they can undergo cycles of binding and releasing actin, causing muscle contraction. As Ca2+ is removed from the sarcoplasm, it dissociates from calmodulin, and the activity of myosin kinase falls. In addition, another enzyme, myosin phosphatase, de-phosphorylates the myosin and helps stop the actin-myosin interactions. Single skeletal muscle twitches are summed into graded contractions In skeletal muscle, the arrival of an action potential at a neu-romuscular junction causes an action potential in a muscle fiber. The spread of that action potential through the T tubule system of the muscle fiber causes a minimum unit of contraction, called a twitch. A twitch can be measured in terms of the tension, or force, it generates (Figure 47.
The variatons of amperage and voltage electro acupuncture buy 10 mg alfuzosin otc mens health 10k edinburgh, injury repair generic alfuzosin 10 mg androgen hormone pregnancy, cellular regeneraton alfuzosin 10 mg discount prostate use, immune stmulaton, allergy testng, fow give us a way to measure capacitance and inductance. In America the system is designed for professional use on any and magnetc efects of bio-electricity. So frequency was lef out of The system can measure and repair the basic body electric health parameters of Volts, Amps, the one channel resistance systems of old. Resistance, Hydraton index, Oxidaton index, Proton and Electron Pressure, Reactve Speed and Changes in the voltage, amperage, and resistance together make up the reactance and susceptance Resonant Frequency. This incredible advancement in medicine measures subtle electrical factors of the body. Voltage lower lef quad on the operator to apply the probe to the acupuncture point. Voltage lower right quad probe delivery (not the pressure), the operator could infuence the outcome. Resistance lower right quad and here is where all of a sudden the apprehension and fear start. Proton pressure the inverse logarithim of the amount of protons versuses electron 24. Electron pressure the inverse logarithim of the amount of electrons versuses protons 25. Reactance 3 - “ This group of 57 is measured and or calculated with 4 diferent quadrants or 228 channels of informaton every millisecond. Reactance 4 - “ ” From these calculatons several other ramifcatons can be surmised. Reactance 6 - “ ” homeopathics, herbals, minerals, amino acids, enzymes, hormones, bacteria, fungus, parasites, 31. The resonance of the system is measured by determining the provoked reactve potental or reacton of the body to these 32. Susceptance 1 - Inverse of total reactance Provoked Reactve potental is the electrical reacton of a patent to a stmulus. Susceptance 2 - “ ” patents provoked reactve potental or change in the above 52 measures we can see the paterns of the energetc body of the patent. Biofeedback is also bioresonance as the feedback of a signal in a cybernetc loop is feedback. These devices also mostly all use point probes that depend on the therapist to apply to the skin. The applicaton of the point probe is subject to idiomotor or subtle muscle control. The same idiomotor control that makes the ouigi board appear to work, can efect the control of the energetc medical devices. If the point probe is applied slowly the reading will be lower than if the probe is applied quickly. It is the speed of delivery of the probe that controls the result more than the end all pressure. Even though there is a measure of operator interference, the system was measuring something. The next difculty with the antquated point probe devices was the limitaton of the tme of the test. This is the basis of reacton as electron transport or ionic exchange dictates the reacton. Reactvity = Delta Volts + Delta Amps + Delta Resistance The reacton dictates that there is a change in the Volts, Amps and Resistance variables. If there is a constant current and a change in resistance, means that there is no added energy. In animals they found that the voltage of the body was connected to the catecholamines. The amperage was connected to the indolamines or brain hormones like serotonin and melatonin. As patent start to die from chronic disease their life force or amperage slips away. In the fgures on reactvity the frst spike of reacton is just a variable of resistance change and thus no amperage change. If the resistance does not rebound but sustains, then there is a voltage resonance sustaining the reactvity. When there is an amperage change that then sustains the resonance, this indicates a more negatve response as the organism is prompted to move away from a potentally harmful stmuli. So the nature of the V A R reacton and it’s resonance or not is of great importance. Afer the body has it’s inital reacton,(one hundredths of a sec) the body will stll contnue to react to the item for a variety of reasons in a variety of paterns. When we perform the Xrroid we are only measuring the inital reacton and thus we can catalog the priority of the inital reacton. To measure the residual resonance would take over one second per item and thus the Xrroid test would take over 6 hours. Afer the Xrroid test is done, we can use the individual test buton to measure any of the single items in the matrix. This will bring up a yellow panel that will display the inital reacton or Reactvity, the Allergic reactvity, and the residual Resonance. The Coherence measurement is the percentage of how close the signal returns to the signal that is sent. The Fourier number is the mathematcal relatonship number of the resultng 7 part harmonic dissecton. This is a complicated mathematcal concept which does not seem to have any meaning yet. Biological speeds are defned as those approaching the ionic exchange speed of a persons’ electrical reacton to the items in their immediate environment. The Xrroid is the process of measuring a patents’ reacton to such items as vitamins, homeopathics, enzymes, hormones, allersodes, isodes, nosodes, etc. The Xrroid has been used on millions of patents around the world for over a decade. The process has been clinically tested with results being published in medical journals and artcles being presented in several worldwide medical conferences. The users of the systems have sent in thousands of testmonials and reports of dramatc success come in daily. The users use the device as directed, which means seeing a patent once a week at best. For over a decade occasionally someone with an overly suspicious mind will try to use the device not as directed but on someone repeatedly in the same day. They will report back to us with dismay as that even though the frst results are always accurate the second or third results seem to not be. Ofen these reports come from persons who cling to older technology or have ulterior motves.
Papillary infoldings of epithelium (ii) Failure to oxidise iodide to iodine prior to incorporaton into tyrosine d discount alfuzosin 10mg with visa prostate cancer years to live. Diminished colloid (iii) Failure to couple mono- and diiodotyrosine to form T3 and T4 e order alfuzosin 10 mg without a prescription prostate 7 pill. Focal lymphocytc infltraton (iv) Failure to de-iodinate iodine-containing by-products of T3/T4 synthesis resultng from a lack of iodotyrosine dehalogenase 454 455 (v) An abnormal iodoprotein is produced instead of synthesis of thyroid hormones (i) Mental deterioraton Efects (ii) Psychosis 1 buy 10mg alfuzosin overnight delivery androgen hormone quiz. Hürthle cell adenoma (ii) Hypoplasia (ii) Teratoma (very rare) (iii) Inborn error of hormone synthesis 2. Other forms of thyroidits (ii) Carcinoma arising from calcitonin-producing cells Medullary carcinoma (with amyloid in stroma) c. Hyperparathyroidism Infltraton of the skin and other tssues by mucoid oedema Aetology 3. Metastatc calcifcaton in Haemoglobin is a conjugated protein composed of four haem groups atached to globin. Haem (i) Kidneys consists of a tetrapyrrole (porphyrin) ring with a ferrous ion at its centre. Nephrocalcinosis Haemoglobin from efete red cells is normally broken down in retculoendothelial cells of the spleen, bone marrow, and liver. It (iii) Lung can be stored in this form, or as a more concentrated iron-protein complex haemosiderin. Iron is transported in the plasma as ferric ion bound to the b globulin transferrin. Pseudo-hypoparathyroidism (Albright) (i) Inherited as autosomal dominants Efects a. Ectodermal changes haem formaton operatng at diferent points in its synthesis for each disease (i) Dry skin/britle nails Results (ii) Eczema a. Calcifcaton of the basal ganglia (ii) Sporadic - symptomatc cutaneous hepatc porphyria. This is usually a consequence of chronic liver disease, especially chronic alcoholism Results a. Hypermelanosis (iii) Siderotc nodules (Gamna-Gandy bodies) in splenomegaly with hepatc cirrhosis c. Excreton of large quanttes of red-coloured uroporphyrin in the urine (i) Excessive absorpton of iron from the diet due to 2. An inborn error of metabolism (i) Congenital erythropoietc porphyria (recessive) Results b. In thalassaemia, sideroblastc anaemia, and spherocytosis (in the absence of transfusions) b. Accumulatons of uro- and coproporphyrins in the bone marrow, red blood cells and teeth Prolonged increased absorpton leads to complete saturaton of circulatng transferrin and thereafer absorbed iron is present in portal blood in the unbound form. Excess excreton of uro- and coproporphyrins in the urine and faeces produces chronic cell injury in vascular shunts in the cirrhosis liver, free iron enters the liver resultng (ii) Erythropoietc protoporphyria (dominant) in cirrhosis. With the development of systemic circulaton and afects other organs, notably the a. Photosensitvity of the skin but no bullae in response to trauma heart and pancreas. A variety of functonal disturbances may ensue and this parenchymatous iron storage disease is haemochromatosis. Increased amounts of protoporphyrin in red cells and faeces but not in the urine (ii) Excessive administraton of iron by multple transfusions or parenteral injectons c. Cirrhosis of the liver This usually results in iron depositon in macrophages of the bone marrow, liver, and spleen d. If administraton is prolonged or massive amounts are given, (iii) Erythropoietc coproporphyria then saturaton followed by parenchymatous depositon and fbrosis may result in a picture indistnguishable from haemochromatosis. Liver - producing cirrhosis which in turn is associated with an increased incidence of B. Carboxyhaemoglobin resultng from combinaton with carbon monoxide and producing a b. Pancreas - interacinar fbrosis with Pigmentaton and atrophy of islets leading to diabetes characteristc cherry-red colour in the blood mellitus 2. Methaemoglobin results from the conversion of the ferrous to a ferric ion, and in this form c. Heart - pigmentaton and atrophy of myocardial fbres resultng in arrhythmias and cardiac failure (ii) Acquired - drug induced, e. Stomach - rare cases show depositon of haemosiderin in efect on pepsin secreton chief cells of the gastric mucosa but the pigment has litle 3. There may be pigmentaton and atrophy in testes, thyroid, adrenals and pituitary Iron is normally stored as ferritn or as haemosiderin, which consists of partly denatured ferritn. Anaemia can be defned as a reducton below normal limits of the total circulatng red cell mass. Localised deposits are found in: The major causes of anaemia are blood loss, haemolysis and diminished producton. Hereditary (i) Folic acid defciency and folic acid antagonists (i) Enzyme defciency a. Antconvulsant drugs (iii) Abnormal haemoglobin synthesis (ii) Vitamin B12 defciency a. Autoimmune reactons which may be idiopathic (primary) or associated with mycoplasma e. Iso-immune reactons such as drug (hapten) induced haemolysis, transfusion reactons, 5. Mechanical injury produced by prosthetc heart valves rapidly replaced by a Populaton of immature cells which leads to the acute efects of marrow C. Diminished red cell producton failure - anaemia, bleeding and susceptbility to infecton. Replacement of the bone marrow gradually replaced by a neoplastc clone which results in inefectve haemopoiesis with release of abnormal cells into the circulaton, inadequate producton (pancytopenia), and a variable rate of (i) Malignancy evoluton towards acute leukaemia. Erythroid stem cell failure distnctons are blurred by the tendency for both myelodysplasia and chronic myeloproliferatve (i) Aplastc anaemia - idiopathic or drug-related disorders to undergo transformaton to leukaemias. These are subdivided according to T or B or common diferentaton and by some aspects of cellular morphology. Dysplastc changes can be found as a secondary phenomenon in a large number of conditons such as marrow replacement by carcinoma and following drug treatment. The primary (ii) Genital infecton form, however, is characterised by several chromosomal abnormalites including monosomy 7 (iii) Dermatopathic reactons which points to its essentally neoplastc nature. Systemic infectons involving lymph nodes myeloblasts exceeds 30% the diagnosis becomes acute leukaemia. Foreign material (v) Hyperviscosity (i) Silicosis (vi) Progression to acute leukaemia (ii) Anthracosis (vii) Presence of the Philadelphia chromosome, a translocaton between chromosomes 9 and (iii) Lipid deposits - lipogranulomas 22 which results in the transcripton of a hybrid gene composed of c-abl - bcr.