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By M. Pyran. Antioch College.

Increased activity of the rectus muscle seems to be a response of the limited motor control available generic zoloft 25mg line anxiety disorder symptoms. With limited motor control purchase zoloft 100 mg amex mood disorder bipolar 1, a system that is stiffer and has fewer degrees of freedom is easier to control. In children with severe motor impairments, such that they can only stand, the whole quadriceps muscle may be activated. As more motor control is available, only the rectus muscle is kept activated continuously, and with still better control, the rectus is only overactive to keep the knee too stiff, causing toe 11. The activity of the rectus is assessed primarily by the amount of knee flexion in initial swing and the EMG activity. Sometimes the EMG will have increased activity, but there is adequate knee flexion de- fined as 60° of knee flexion peaking between 25% and 30% of swing phase. The increased EMG means that the electrical activity is increased, but the force generated is not abnormal for the mechanical milieu of the limb. If the peak knee flexion is less than 50° or 60°, or the peak flexion is later than 30% of swing, then the rectus is overactive, causing a dynamic contracture limiting knee motion. The symptoms created are toe drag during swing phase and very rapid shoe wear with the front of the shoes wearing through, some- times in as short a time as 4 to 6 weeks, secondary to the toe dragging. Knee Extension Contractures For a few children with significant and prolonged extensor posturing, muscle contractures of the vastus and rectus muscles may develop. These contrac- tures are almost always combined with hip extension contractures and equi- nus ankle contractures. In the most advanced form, this contracture develop- ment includes the type 1 anterior hip dislocation, in which the hip and knee are extended and the hip is adducted and severely externally rotated. A few children develop this pattern without an anterior hip dislocation (Case 11. Knee extension contractures are functionally disabling because it is very dif- ficult to seat these children with the knees fully extended, especially as they reach adult size. It is important to note that back-kneeing in stance phase is seldom di- rectly or even indirectly secondary to the vastus or rectus muscles. These quadriceps muscles usually are not even contracting in midstance phase in children who are back-kneeing. The cause of stance phase back-kneeing is related to the foot and ankle force couple, with a secondary contribution of the hamstrings. Very weak vasti will be accommodated by full knee exten- sion at foot contact so as to avoid the need for the stabilizing effect of the vastus muscles during weight acceptance. Therefore, back-kneeing is not the result of overactivity of a quadriceps muscle, but may be primarily due to weakness of the quadriceps muscle in which the motor control system is protecting the muscle by back-kneeing (Table 11. Secondary Pathology Children with crouched gait pattern of increased knee flexion in midstance may start to depend on the vastus muscles as the main muscle power to pre- vent the knee from collapsing into more flexion. These patterns of crouch will often demonstrate EMG activity in the vastus muscles throughout all of stance phase, combined with a consistent and increased knee extension mo- ment. This constant force on the vastus muscles, which are often somewhat spastic as well, causes decreased muscle fiber growth. The constant force also causes the patellar tendon and patellar ligament to grow, with the net effect of the patella gradually moving more proximal than its normal position. This proximal patellar movement is called patella alta. Because the patella alta moves the patella out of the femoral groove, the moment arm over the ful- crum of the patella decreases, requiring even more muscle force for the quadri- ceps to prevent collapse of the knee. As the force increases, there is usually more patella alta, and as the patella alta increases, more force is required (Case 11. This process occurs especially during the rapid weight gain of adolescent growth and when untreated may cause adolescents to stop walk- ing. This increasing crouch is a purely mechanical set of problems that can be treated and should not be the cause of adolescents discontinuing ambulation. To improve the knee plegia, presented with her mother whose main concern flexion, she had Z-lengthening of the quadriceps tendon was that she had increased difficulty when she sat in her and was splinted in 90° of knee flexion for 3 months (Fig- wheelchair because of the extended knees. Starting on postoperative day 3, the splint had been present for many years, and her mother could not was removed every day and the knee was ranged from full remember how long it had been since she could flex her extension to maximum flexion. The physical examination demonstrated hip flex- she had maintained 90° of knee flexion and could be seated ion to 90°, abduction to 30° bilaterally, knee extension to much more easily in her wheelchair.

Nonphosphorylated BAD acts like Bid in promoting apoptosis (see Fig buy 25mg zoloft free shipping bipolar depression 5htp. The mitochondrial integrity path- Binding of the platelet-derived growth factor to its receptor activates PI-3 kinase purchase zoloft 100 mg mastercard depression definition larousse, way releases cytochrome c, which binds to which phosphorylates and activates the serine/threonine kinase Akt (protein kinase Apaf and forms a multimeric complex called B, see Chapter 11, section III. Activation of Akt results in the phosphorylation the apoptosome. The apoptosome converts of the pro-apoptotic BH3-only protein BAD, which inactivates it. The procaspase 9 to active caspase, which it PDGF/Akt/BAD pathway illustrates the requirement of normal cells for growth fac- releases into the cytosol. One of the features of neoplastic transforma- tion is the loss of growth factor dependence for survival. The MAP kinase pathway is also involved in regulating apoptosis and sends cell survival signals. MAP kinase kinase phosphorylates and activates another protein kinase known as RSK. Like Akt, RSK phosphorylates BAD and inhibits its activity. Thus, BAD acts as a site of convergence for the PI-3 kinase/Akt and MAP kinase pathways in signaling cell survival. Gain-of-function mutations in the genes con- trolling these pathways, such as ras, creates apoptosis- resistant cells. Stimulus Growth factor deprivation Steroids Irradiation Chemotherapeutic drugs Anti-apoptosis Apaf/Bcl-XL (inactive) Bcl-2 Bcl-XL BH3-only Apaf Caspase 9 (Bid) Mitochondrion Apoptosome cyclochrome C Bax Pro-apoptosis Fig. Roles of the Bcl-2 family members in regulating apoptosis. Bcl-2, which is anti- apoptotic, binds Bid (or tBid) and blocks formation of channels that allow cytochrome c release from the mitochondria. Death signals result in activation of a BH3-only protein such as Bid, which can lead to mitochondrial pore formation, swelling, and release of cytochrome c. Bid binds to and activates the membrane ion-channel protein Bax, activating cytochrome c release, which binds to Apaf and leads to formation of the apoptosome. CANCER REQUIRES MULTIPLE MUTATIONS Normal Cancer takes a long time to develop in humans because multiple genetic alter- epithelium ations are required to transform normal cells into malignant cells (see Fig. Loss of APC A single change in one oncogene or tumor suppressor gene in an individual cell is not adequate for transformation. For example, if cells derived from biopsy speci- Hyperproliferative epithelium mens of normal cells are not already “immortalized,” that is, able to grow in cul- ture indefinitely, addition of the ras oncogene to the cells is not sufficient for trans- formation. However, additional mutations in a combination of oncogenes, for Early example ras and myc, can result in transformation (Fig. Epidemiologists adenoma have estimated that four to seven mutations are required for normal cells to be Activation of Ras transformed. Cells accumulate multiple mutations through clonal expansion. When DNA Intermediate adenoma damage occurs in a normally proliferative cell, a population of cells with that muta- Loss of a tumor tion is produced. Expansion of the mutated population enormously increases the suppressor gene probability of a second mutation in a cell containing the first mutation. After one or Late more mutations in proto-oncogenes or tumor suppressor genes, a cell may prolifer- adenoma ate more rapidly in the presence of growth stimuli and with further mutations grow Loss of p53 activity autonomously, that is, independent of normal growth controls. Enhanced growth increases the probability of further mutations. Some families have a strong predis- Carcinoma position to cancer. Individuals in these families have inherited a mutation or dele- Other alterations tion of one allele of a tumor suppressor gene, and as progeny of that cell prolifer- Metastasis ate, mutations can occur in the second allele, leading to a loss of control of cellular proliferation.

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