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Fascicles may be further divided into bundles of fibers (or muscle cells) surrounded by a connective tissue sheath called the endomysium cheap levitra extra dosage 40mg online impotence with condoms. In humans cheap 60mg levitra extra dosage with visa erectile dysfunction and diabetes treatment, the pinnation angle ranges from 0 to 25°. Fibers attach at both ends to tendon or other connective tissue. Muscle fibers contain mitochondria, multiple nuclei, ribosomes, soluble proteins, lipids, glycogen, and satellite cells. Fibers are cylindrical, with their diameter ranging from 10 micrometers (µm) to 100 µm (smaller than the size of a human hair). Fibers are subdivided radially into myofibrils having diameters of approximately 1 µm. Myofibrils are divided longitudinally into sarcomeres and radially into myofilaments. A saromere is defined as the region between Z-lines (defined below). Myofila- ments are often classified as either thick or thin filaments. Thick filaments are composed primarily of myosin molecules. Myosin accounts for approximately 55% of the myofibril volume. It is composed of two heavy chains and four light chains. Two light chains are associated with each heavy chain. The two heavy chains are identical, whereas the light chains vary within different fiber types. Each myosin molecule is rod shaped with two adjacent globular heads at one end. The myosin molecule structure has been defined in terms of two general regions: the light meromyosin (LMM), and the heavy meromyosin (HMM). The HMM contains the two heads, and the remaining part of the tail not considered part of the LMM. HMM is further divided into subfragment 1 (S1) and subfragment 2 (S2) (see Fig. Myosin molecules are about 160 nanometers (nm) long (myosin rod is 140 nm and head is 15 nm) and 2 nm in diameter. The number of myosin molecules terminating at each axial repeat location is still controversial. Most of the evidence has been interpreted as suggesting three myosin ends per axial repeat distance. A whole muscle is shown in A, a muscle fiber in B, a myofibril in C, a sarcomere in D, a thin filament in E, a thick filament in F, and a myosin molecule in G. Thin filaments are approximately 1 µm long and 8 nm in diameter. Each thin filament contains about 360 actin monomers. Each actin monomer consists of a single polypeptide chain. Each groove is filled by a series of tropomyosin-troponin complexes, each spanning a length of seven actin monomers (41 nm in length). There is one troponin molecule, approximately 26 nm long, for each tropomyosin molecule. The troponin molecule can be further divided into troponins C, I, and T. The region containing the thick filaments is referred to as the anisotropic or A-band, approximately 1.

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He has no history of retinopathy or neuropa- thy levitra extra dosage 60 mg line erectile dysfunction naturopathic treatment, and he states that he saw his ophthalmologist 6 weeks ago 60 mg levitra extra dosage sale erectile dysfunction age 29. The patient has had protein in his urine, and he takes an angiotensin-converting enzyme (ACE) inhibitor. Later that day, you decide to read further on adaptive immunity. Which of the following statements regarding antigen processing and presentation is false? Class I molecules are expressed on virtually all tissues and are impor- tant in the recognition of virally infected cells 4 BOARD REVIEW B. Class II molecules are expressed on a limited variety of cells known as antigen-presenting cells C. MHC molecules first bind peptide fragments after the MHC molecules reach the cell surface D. Exogenous proteins are taken up by endosomes or lysosomes, where they are catabolized; their peptides are then bound to MHC class II molecules Key Concept/Objective: To understand the processing of foreign proteins and their relationship to the MHC system The breakdown of protein molecules into peptide fragments is an important part of the process by which antigens are presented to T cells and other immune effector cells. MHC molecules come to the cell surface with peptides already bound. Proteins are first degrad- ed internally, and the peptide fragments are bound to MHC class I and MHC class II mol- ecules within the cell. Class I molecules are expressed on virtually all tissues. Virally infect- ed cells are recognized principally by class I-restricted T cells, usually those with a cyto- toxic function. In contrast, class II-directed T cells are restricted to antigen-presenting cells of the immune system (i. Exogenous and endogenous antigens reach the cell surface by different pathways. Exogenous proteins are taken up into endosomes or lysosomes, where they are catabolized. Peptides from exoge- nous proteins are generally bound to MHC class II molecules, and the class II–peptide com- plexes are then brought to the surface for presentation to T cells. A 23-year-old primigravida who is known to be Rh-negative is told by her obstetrician that she needs a medication to prevent complications (i. She wonders why she should be using this medication. Which of the following immunologic responses is prevented by the use of anti–Rh-positive antibodies (RhoGAM)? Secondary immune response (anamnestic or booster response) C. Class switch recombination Key Concept/Objective: To understand the genesis and prevention of the secondary immune response If an antigen is encountered a second time, a secondary response (also called an anamnes- tic or booster response) occurs because of the existence of memory B cells. Administration of RhoGAM to the mother at the time of delivery prevents the fetal red blood cells, which are Rh positive, from generating a primary response in the Rh-negative mother, thus decreasing significantly the possibility of an anamnestic response in future pregnancies. Both IgM and IgG titers rise exponentially, without the lag phase seen in the primary response. Whereas the peak IgM level during the secondary response may be the same as, or slightly higher than, the peak IgM level during the primary response, the IgG peak level during the secondary response is much greater and lasts longer than the peak level during the primary response. This variation in response is an apt illustration of immunologic memory and is caused by a proliferation of antigen-specific B cells and helper T cells dur- ing the primary response. The primary immune response characterizes the first exposure to antigen and is largely IgM mediated; later production of IgG is not as great in magni- tude or duration as that produced during the secondary response. Somatic hypermutation, class switch recombination, and immunoglobulin class switching are all mechanisms involved in producing the appropriate immunoglobulin with the highest antigen speci- ficity. A 48-year-old woman with severe rheumatoid arthritis (RA) is advised by a rheumatologist to consider a novel antibody, because her arthritis is not responding to therapy with methotrexate. Of the following, which is the therapeutic target of approved engineered human monoclonal anti- bodies in the management of RA? IL-1 Key Concept/Objective: To understand the clinical application of engineered monoclonal antibodies Humanized monoclonal antibodies to TNF-α have been used successfully in the treatment of Crohn disease and RA. These monoclonal antibodies are indicated for patients with moderate to severe RA that is not responsive to methotrexate or for patients in whom methotrexate toxicity has occurred.

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