The protozoans are unified by their heterotrophic mode of nutrition, meaning that these organisms acquire carbon in reduced form from their surrounding environment. However, this is not a unique feature of protozoans.
References Abstract Skeletal muscle continuously adapts to changes in its mechanical environment through modifications in gene expression and protein stability that affect its physiological function and mass. However, mechanical stresses commonly exceed the parameters that induce adaptations, producing instead acute injury.
Furthermore, the relatively superficial location of many muscles in the body leaves them further vulnerable to acute injuries by exposure to extreme temperatures, contusions, lacerations or toxins.
In this article, the molecular, cellular, and mechanical factors that underlie muscle injury and the capacity of muscle to repair and regenerate are presented.
Evidence shows that muscle injuries that are caused by eccentric contractions result from direct mechanical damage to myofibrils. However, muscle pathology following other acute injuries is largely attributable to damage to the muscle cell membrane.
Evidence is also presented to show that the myogenic program that is activated by acute muscle injury and the inflammatory process that follows are highly coordinated, with myeloid cells playing a central role in modulating repair and regeneration.
Although this system provides an effective mechanism for muscle repair and regeneration following acute injury, it is dysregulated in chronic injuries.
In this article, the process of muscle injury, repair and regeneration that occurs in muscular dystrophy is used as an example of chronic muscle injury, to highlight similarities and differences between the injury and repair processes that occur Mechanisms and physiology of regeneration in acutely and chronically injured muscle.
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Lecture announcement for a presentation by Professor D. Scanning electron micrograph of two skeletal muscle fibers terminating at their myotendinous junctions MTJswhere they are mechanically coupled to tendon collagen fibers. Bundles of collagen fibers pass from the tendon in the bottom third of the micrograph to bind to the ends of the muscle fibers at the MTJ between brackets.
During muscle strain injuries, lesions occur at or near the MTJ depending on the state of activation of the fiber and the muscle experiencing the strain injury.
Transmission electron micrographs of longitudinal sections through the myotendinous junction MTJ region of frog skeletal muscle that was strained to failure.
A The upper portion of the micrograph shows tendon collagen fibers. This muscle was unstimulated and shows tissue tears occurred within the connective tissue, near the surface of the muscle fiber outlined with arrowheads.
B Complete separations S occurred in the connective tissue near the MTJs in unstimulated muscles strained to failure. Other cells in the same preparations show complete lesions within the muscle fiber near the MTJ.
Rabbit tibialis anterior muscle subjected to a strain injury. A The muscle on the left was photographed immediately after the strain injury and shows a hematoma bracket in the area of the distal, myotendinous junction MTJ. The muscle on the right is an unstrained control.
B A longitudinal section of a strained muscle preserved immediately following injury showing the distal MTJ region of muscle fibers red.
The dark, vertical band on the left of the micrograph is tendon. Note that the morphology of the muscle fibers near the tendon is disrupted. Note the separation tissue separation in the MTJ region of the injured muscle between tendon blue and muscle fibers red panel A and the large number of red cells and leukocytes arrow heads in the injured MTJ region panel B.
Increased numbers of leukocytes have entered the sites of tissue separation in the MTJ region panels C and D and necrotic fibers brown invaded by leukocytes are apparent at the sites of tissue damage panel D. Transmission electron micrograph of human skeletal muscle sampled after injury caused by eccentric contractions.
Simplified schematic representing some of the steps of the complement cascade that have been implicated in skeletal muscle injury.
Current experimental data support a role for the classical pathway, a component of humoral immunity, and the alternative pathway, a component of innate immunity, in causing muscle damage. The potential involvement of the lectin pathway has not been explored.
Each pathway progresses through multiple steps to lead to the proteolysis of C3. The products of C3 cleavage, C3a and C3b, can contribute to muscle inflammation and injury through multiple effects. C3a released into the extracellular space can increase the expression of adhesion molecules on the surface of leukocytes and endothelial cells that enables the more rapid extravasation of leukocytes into injured tissue.Dec 03, · The molecular mechanisms that lead to impairment of wound healing are poorly understood.
The complexity of the wound-healing process, which involves many cell types locally at the site of the wound as well as systemically (Fig. 2), along with comorbidities represent hurdles in identifying therapeutic targets and in clinical trial design.
Discovery. In , August Krogh was awarded the Nobel Prize in Physiology or Medicine for his discovering the mechanism of regulation of capillaries in skeletal muscle. Krogh was the first to describe the adaptation of blood perfusion in muscle and other organs according to demands through the opening and closing of arterioles and .
Dead cardiac muscle tissue is replaced by scar tissue, which cannot contract. As scar tissue accumulates, the heart loses its ability to pump because of the loss of contractile power. However, some minor regeneration may occur due to stem cells found in the blood that occasionally enter cardiac tissue.
Mechanism and Physiology of Regeneration in Urodeles Urodeles or more commonly known as salamanders are any of approximately extant species of amphibians under the Order Caudata.1 Urodeles’ distinctive factor that makes them different from other amphibians like frogs and caecilians is the retention of a full tail.
Ross and Wilson Human Anatomy and Physiology PDF 12th Edition - Free ebook download as PDF File .pdf), Text File .txt) or read book online for free. Taking advantage of animal models they genetically manipulated not to express the REV-ERB receptor and comparing them with animals normally expressing the receptor, the researchers could identify REV-ERB’s role in the muscle cell regeneration mechanism.