By J. Xardas. Georgia Southern University. 2018.
This is because influenza displays a structural plasticity as it can tolerate many amino acid substitutions in its structural proteins without losing its infectivity generic 100mg zenegra overnight delivery causes of erectile dysfunction in 50s. These changes are the reason for the annual epidemic spread of influenza and require new vaccines to be formulated before each annual epidemic cheap zenegra 100mg with visa erectile dysfunction labs. In contrast, antigenic shift is a major change in the surface protein of a virion, as genes encoding completely new surface proteins arise after recombination or reassortment of genomes or genome segments. In contrast, antigenic shift can only occur under certain circumstances, is relatively rare and the likely reason for pandemics. The cellular immune response Dendritic cells have been shown to play a central role in initiating and driving T lymphocyte responses. They are a sparsely distributed, migratory group of bone- marrow derived leukocytes that are specialized for the uptake, transport, processing and presentation of antigens to T cells (Figure 3). The basic paradigm is that lung- resident dendritic cells acquire antigen from the invading pathogen, become acti- vated, and subsequently travel to the local draining lymph nodes (Legge & Braciale 2003). The newly activated T cells acquire effector cell functions and migrate 104 Pathogenesis and Immunology to the site of infection in the lung where they mediate their antiviral activities (Fig- ure 3). Following recovery from an infection, a state of immunological memory ensues in which the individual is better able to control a subsequent infection with the same pathogen (Ahmed & Gray 1996). Memory is maintained by antigen-specific T cells that persist at increased frequencies, have reduced requirements for co-stimulatory signals in comparison to naïve T cells, and respond quickly to antigenic re- stimulation (Woodland & Scott 2005). Th cells can be further sub- divided into at least Th1 and Th2 cells, based on the type of cytokines they produce. Recent studies in ani- mals suggest that the recall response in lungs is comprised of several distinct phases that are temporally and anatomically separated. The first phase is mediated by memory T cells that are resident in the lung airways (Woodland & Radall 2004). Importantly, these cells are able to respond to the first signs of infection when the viral load is still very low. While unable to proliferate in response to infection due to the constraints of the airway environment, they can produce cytokines that may limit viral replication and spread in the epithelium. The second phase of the re- sponse is mediated by memory T cells that are rapidly recruited to the airways in the first few days of the response. The third stage is the antigen-driven expansion of memory T cells that occurs in the secondary lymphoid organs. These memory cells proliferate for several days in the lymphoid organs and are only recruited to the lung airways after about 5 days of infection (Woodland & Randall 2004). Whether these complex models generated from animal experiments apply to the situation in Conclusion 105 humans is unclear. It will be essential, however, to better understand the types of immune response and the generation and maintenance of an effective memory T cell response during influenza infection in order to improve future vaccine strate- gies. Conclusion We have seen how influenza virus infection leads to the acute development of a febrile respiratory illness. The pathogenesis is characterized by the rapid replication and distribution of the virus within the lungs, causing local and systemic inflamma- tion and cytokine release. These events, together with the adaptive immune re- sponse, help to reduce the viral burden, to eliminate the virus, and to trigger disease recovery. The humoral and cellular immune responses, provoked by infection or vaccination, provide individuals and populations with long-lasting protective im- munity against related viral strains. Influenza, however, can undermine this infec- tion- or vaccine-derived immunity by means of antigenic shift and drift, resulting in epidemic and pandemic outbreaks. Technical improvements, including genetic and functional studies, will help to gain a deeper insight into the pathogenesis of historic and currently circulating virulent influenza strains. This knowledge and an ad- vanced understanding about the viral immune defense mechanisms in the human lung will hopefully facilitate the development of better treatment options and more effective vaccines to be distributed worldwide against present and future influenza virus variants. Influenza type A in humans, mammals and birds: determinants of virus virulence, host-range and interspecies transmission. Risk of influenza A (H5N1) infection among health care workers exposed to patients with influenza A (H5N1), Hong Kong. Proinflammatory cytokine responses induced by influenza A (H5N1) viruses in primary human alveolar and bronchial epithelial cells. Induction of proinflammatory cytokines in human macrophages by influenza A (H5N1) viruses: a mechanism for the unusual severity of human disease? Antigenic analyses of influenza virus haemag- glutinins with different receptor-binding specificities.
Physiologic Characteristics of muscle tissue Muscle tissue has four principal characteristics that enable it to carry out its functions and thus contribute to homeostasis buy 100 mg zenegra overnight delivery erectile dysfunction relationship. Excitability (irritability) purchase zenegra 100mg line erectile dysfunction ed treatment, a property of both muscle and nerve cells (neurons), is the ability to respond to certain stimuli by producing electrical signal called action potentials (impulses). For example, the stimuli that trigger action potentials are chemicals-neurotransmitters, released by neurons, hormones distributed by the blood. Contractility is the ability of muscle tissue to shorten and thicken (contract), thus generating force to do work. Elasticity means that muscle tissue tends to return to its original shape after contraction or extension. Connective Tissue Component A skeletal muscle is an organ composed mainly of striated muscle cells and connective tissue. Each skeletal muscle has two parts; the connective tissue sheath that extend to form specialized structures that aid in attaching the muscle to bone and the fleshy part the belly or gaster. The extended specialized structure may take the form of a cord, called a tendon; alternatively, a broad sheet called an aponeurosis may attach muscles to bones or to other muscles, as in the abdomen or across the top of the skull. Connective tissue also extends into the muscle and divides it into numerous muscle bundles (fascicles). Microscopic structures The muscle bundles are composed of many elongated muscle cells called muscle fibres. Each muscle fibre is a cylindrical cell containing several nuclei located immediately beneath the cell membrane (sarcolemma). Myofibrils consist of two major kinds of protein fibres: actins or thin myofilaments, and myosin or thick myofilaments. The actins and myosin myofilaments form highly ordered units called sarcomers, which are joined end-to-end to form the myofibrils (see Figure 6-1). The ends of a sarcomere are a network of protein fibres, which form the Z-lines when the sarcomere is viewed from side. The arrangement of the actin and myosin myofilaments in a sarcomere gives the myofibril a banded appearance because the myofibril appears darker where the actin and myosin myofilaments overlap. The alternating light (I-band) and dark (A-band) areas of the sarcomers are responsible for striation (banding pattern) seen in skeletal muscle cells observed through the microscope. Within the sarcoplasm of the muscle fibre there is an extensive network of branching and anastomosing channels, which forms the sarcoplasmic reticulum (this structure is a modified endoplasmic reticulum). The channels of the sarcoplasmic reticulum lay in close contact around the ends of T-tubules, and contain stores of calcium. The thin myofilaments are composed of a complex protein called actin, arranged in a double stranded coil. Structure of a skeletal muscle (From Memmler, Ruth Lundeen et al: The human body in Health and disease,ed. When a nerve impulse reaches a muscle fibre it is conducted over the sarcolemma and in to the T-tubules, then to the sarcoplasmic reticulum. The liberated calcium ions combine with troponin causing it to push tropomysin away from the receptor sites on the actins filaments. The myosin crossbridges interact 114 Human Anatomy and Physiology with the actin receptor sites and pull the actins myofilaments toward the centre (H-zone) of each sarcomere. The bond between the myosin crossbridges and actin breaks down under the influence of enzymes and the crossbridges are then free to rejoin with other actin receptor sites. The actin filaments do not shorten but slide past the myosin filaments overlapping them so that the Z lines are drawn toward each other, shortening the sarcomere. Relaxation of the muscle fibres occurs when the calcium ions are actively reabsorbed by the sarcoplasmic reticulum thus allowing troponin and tropomysin to again inhibit the interaction of the actins and myosin filaments (see Table 6-1 for summary of events in the contraction of a muscle fibre). Although some glucose is used as an energy source, fatty acids are a more important energy source during sustained exercise as well as during resting conditions. Summary of events in the contraction of a muscle fibre Nerve impulse is transmitted via a motor nerve to the motor end plate Nerve impulse crosses neuromuscular junction by causing release of acetylcholine which depolarizes sarcolemma. Myosin cross-bridges interact with actin receptor sites and thin myofilaments are drawn towards the centre of each sarcomere.
It might take a fraction of a millisecond for the channel to open + + once that voltage has been reached 100mg zenegra for sale impotence type 1 diabetes. The timing of this coincides exactly with when the Na flow peaks order zenegra 100 mg fast delivery erectile dysfunction treatment in jamshedpur, so voltage-gated K + channels open just as the voltage-gated Na channels are being inactivated. As the membrane potential repolarizes and the voltage passes -50 mV again, the channel closes—again, with a little delay. Potassium continues to leave the cell for a short while and the membrane potential becomes more negative, resulting in the hyperpolarizing overshoot. Then the channel closes again and the membrane can return to the resting potential because of the ongoing activity of the non-gated channels + + and the Na /K pump. There are two phases of the refractory period: the absolute refractory period and the relative refractory period. Once that channel is back to its resting conformation (less than -55 mV), a new action potential could be started, but only by a stronger stimulus than the one that + initiated the current action potential. Because that ion is rushing out, any + Na that tries to enter will not depolarize the cell, but will only keep the cell from hyperpolarizing. Propagation of the Action Potential The action potential is initiated at the beginning of the axon, at what is called the initial segment. There is a high density of + voltage-gated Na channels so that rapid depolarization can take place here. Going down the length of the axon, the action + potential is propagated because more voltage-gated Na channels are opened as the depolarization spreads. This spreading + + occurs because Na enters through the channel and moves along the inside of the cell membrane. As the Na moves, or flows, a short distance along the cell membrane, its positive charge depolarizes a little more of the cell membrane. As that + depolarization spreads, new voltage-gated Na channels open and more ions rush into the cell, spreading the depolarization a little farther. The action potential must propagate toward the axon terminals; as a result, the polarity of the neuron is maintained, as mentioned above. Sodium ions that enter the cell at the initial segment start to spread along the length of the axon + segment, but there are no voltage-gated Na channels until the first node of Ranvier. Because there is not constant opening of these channels along the axon segment, the depolarization spreads at an optimal speed. The distance between nodes is + the optimal distance to keep the membrane still depolarized above threshold at the next node. If the node were any farther down the axon, that + depolarization would have fallen off too much for voltage-gated Na channels to be activated at the next node of Ranvier. Propagation along an unmyelinated axon is referred to as continuous conduction; along the length of a myelinated axon, + it is saltatory conduction. Continuous conduction is slow because there are always voltage-gated Na channels opening, + and more and more Na is rushing into the cell. Saltatory conduction is faster because the action potential basically jumps + from one node to the next (saltare = “to leap”), and the new influx of Na renews the depolarized membrane. Along with the myelination of the axon, the diameter of the axon can influence the speed of conduction. Much as water runs faster in a + wide river than in a narrow creek, Na -based depolarization spreads faster down a wide axon than down a narrow one. This concept is known as resistance and is generally true for electrical wires or plumbing, just as it is true for axons, although the specific conditions are different at the scales of electrons or ions versus water in a river. The concentrations of ions in the extracellular fluid are the basis for how the membrane potential is established and changes in electrochemical signaling. After the repolarizing phase of the action + + + potential, K leakage channels and the Na /K pump ensure that the ions return to their original locations. Astrocytes can become reactive in cases such as these, which impairs their ability to maintain the local chemical + environment. This sodium/potassium imbalance negatively affects the internal chemistry of cells, preventing them from functioning normally. Often, the action potentials occur so rapidly that watching a screen to see them occur is not helpful.
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