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Bleeding may be minimal or severe, depending on the location and nature of the injury. When a person has experienced a traumatic amputation, call 9-1-1 or the designated emergency number. If the body part is completely detached from the body, try to locate it because surgeons may be able to reattach it. Keep the bag containing the body part cool by placing it in a larger bag or container filled with a mixture of ice and water. Burns A burn is a traumatic injury to the skin (and sometimes the underlying tissues as well) caused by contact with extreme heat, chemicals, radiation or electricity (Figure 6-3). Causes of burns include extreme heat (A), chemicals (B), radiation (C) and electricity (D). A critical burn is one that is life threatening or potentially disfiguring or disabling, and it requires immediate medical attention. When evaluating whether a burn is critical or not, consider the following factors: the depth of the burn. Burns can be classified a large percentage of the person’s total body according to depth (Figure 6-4). Partial-thickness burns involve the hands, feet or groin; those that involve the head, epidermis and the dermis (the layer of skin neck, nose, or mouth or affect the person’s ability underneath the epidermis that contains blood to breathe; and circumferential burns. Full that go all the way around a limb) are considered thickness burns involve both layers of skin and critical burns. Burns caused by more than one part of the body or covers a electricity, exposure to chemicals, exposure to large percentage of the person’s total body nuclear radiation or an explosion are considered surface area requires medical attention. Hair Superficial Epidermis burn Partial-thickness burn Dermis Hair follicle Full-thickness Vein Subcutaneous burn Artery tissue Nerve Sensory receptor Sweat gland Figure 6-4. The burned area may be extremely painful or almost painless (if the burn is deep enough to destroy the nerve endings). Burns involving blistering or broken skin should be evaluated by a healthcare provider. Putting butter, mayonnaise, petroleum jelly or any other greasy substance on a burn is not effective for relieving pain or promoting healing. In fact, applying a greasy substance to the burn can seal in the heat and make the burn worse. First, after sizing up the scene, stop the burning by removing the source of the injury if it is safe for you to do so. Depending on the cause of the burn, this may involve removing the person from the source or removing the source from the person. Next, cool the burn and relieve pain using clean, cool or cold water for at least 10 minutes. Never use ice or ice water to cool a burn because doing so can cause more damage to the skin. If clean cool or cold water is not available, you can apply a cool or cold (but not freezing) compress instead. Cooling a burn over a large area of the body can bring on hypothermia (a body temperature below normal), so be alert to signs and symptoms of this condition (see Chapter 7). Make sure that whatever you use to cover the wound is sterile or at least clean, because burns leave the person highly susceptible to infection. Burns of all types, especially if they cover a large percentage of the body, can cause a person to go into shock, so monitor the person closely. When caring for a burn, do not remove pieces of clothing that are stuck to the burned area, do not attempt to clean a severe burn and do not break any blisters. Chemical Burns the general care for a chemical burn is the same as for any other type of burn: stop, cool, cover. Because the chemical will continue to burn as long as it is on the skin, you must remove the chemical from the skin as quickly as possible. If the burn was caused by a dry chemical, such as lime, brush off the powder or granules with gloved hands or a cloth, being careful not to get any of the chemical on your skin or on a different area of the person’s skin. Carefully remove, or help the person to remove, any clothing that was contaminated with the chemical.

Cortes Lacassie syndrome

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Several of these, including Rosa26 on 118 chromosome 6, were made susceptible for gene targeting (Soriano, 1999; Srinivas, 2001). Inserting the driver transgene into the Rosa26 locus should overcome the uncertainty of position effects, and allow more appropriate conditional transgene expression patterns to be generated. In certain cases, this will not lead to Sox9 expression, but instead another LacZ cassette. This is a rather rare event, but if this occurs it can lead to deletion of the genes situated between the transgene insertion loci. This is another rare event, which can affect not only transgene expression patter, but also intrinsic gene expression. The only transgenic female obtained from the founder bred normally, however her offspring of either sex did not display (3-galactosidase activity. Also, strong expressors of the transgene might have died during embryogenesis, as the 119 number of transgenic embryos obtained declined as the stage of harvest progressed. This also explained why only one transgenic pup was obtained out of 70 bom and genotyped. However, during backcrossing, it was impossible to maintain Z/Sox9 lines on this background, perhaps with the exception of Line B. It will require further characterization during outbreeding to monitor the influence of different genetic backgrounds. Testicular expression of Sox9 then persists throughout life, specifically in Sertoli cells. The upregulation of Sox9 was found to coincide with the onset of Sry expression in supporting cell precursors and the protein products of the two genes can be seen to co-localise within a subset of these cells prior to Sry switching off (Sekido et al. In mice harbouring heterozygous loss of function mutations in Sox9, the testes develop normally despite perinatal lethality (Bi et al. Taken together, Sox9 is not only essential for initiating testis differentiation, but also able to do so in the absence of Sry. Male and female offspring were then intercrossed until animals homozygous for the flox allele (,Sox9Flox/Flax) were obtained. However, as Sox9 displays widespread expression pattern in numerous tissues, phenotypic observation in some of these tissues would also be briefly described in this section. Embryos positive for both Cre and the Z/Sox9 transgene from Line J were not fluorescent (data not shown) indicating insufficient transgene expression. The small litter sizes and failure to obtain double transgenic embryos/pups indicated possible embryonic lethality. To investigate this assumption, analyses were carried out at earlier embryonic stages. We also observed that the number of transgenic embryos obtained decreased as the stage of harvest progressed, supporting the hypothesis that overexpression of Sox9 causes embryonic lethality. The inserts on the bottom left corner show a magnified > icw of the indicated i area of the gonad show n in each panel. Mutants displayed various levels of craniofacial defects, ranging from gaps around the oral area (Figure 6. This includes reduction in size of the lungs, and incomplete formation of the heart, especially the auricles. The limbs were shorter compared to those of wildtype littermates, and in some cases were still at limb-bud stages, and had failed to start forming digits (Figure 6. These observations suggested that Sox9 overexpression might have led to developmental retardation in several organs, although the primordial of these organs did form. It is highly likely that embryonic lethality was caused by heart defects, but further investigation is required to confirm this assumption. Further investigation will be required to confirm the fate of these ectopic cords. Cells w ere cultured either in the presence o f 2pM O H T or ethanol for 48 hours.

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The childhood (juvenile) type is manifested in infancy or early childhood as a myopathy. Weakness is more proximal than distal, and there may be calf enlargement simulating muscular dystrophy. The adult type is manifested between the second and seventh decades of life either as slowly progressive limb muscle weakness that mimics limb-girdle dystrophy or in a scapuloperoneal pattern. These patients often experience insidious ventilatory muscle weakness leading to respiratory failure. Muscle biopsy demonstrates a vacuolar myopathy with high glycogen content and acid phosphatase reactivity in the vacuoles. The diagnosis is confirmed by demonstrating -glucosidase deficiency in either muscle, skin fibroblasts, or lymphocytes. Treatment and Prognosis Enzyme replacement therapy with intravenous recombinant -glucosidase (Myozyme) can be life-saving and was recently approved by the Food and Drug Administration for the infantile, childhood, and adult forms of the disease. Debranching Enzyme Deficiency Debranching enzyme deficiency is a rare disease that can affect the liver, heart, or skeletal muscle. The disease is most 27 commonly manifested in childhood as hepatomegaly with fasting hypoglycemia that spontaneously resolves by adulthood. Patients less frequently have a disabling myopathy that affects both proximal and distal muscles and can appear in childhood or (more commonly) in adult life. There may be a depressed lactate response on forearm testing, but myoglobinuria is rare. Branching Enzyme Deficiency Deficiency of the branching enzyme is manifested in infancy as progressive liver and cardiac dysfunction, which leads to death in the first years of life. Muscle weakness is variable; if weakness is present, the tongue is severely affected. Disorders of Fatty Acid Metabolism Lipids are essential for the aerobic energy needs of muscle during sustained exercise. Serum long-chain fatty acids, which are the primary lipid fuel for muscle metabolism, are transported into the mitochondria as carnitine esters and are metabolized via -oxidation. As with glycogen pathway defects, the myopathic manifestations of fatty acid metabolism can consist of dynamic exercise intolerance with myoglobinuria or static weakness with a lipid storage myopathy. A lipid storage myopathy can be caused by primary carnitine deficiency or by another defect in fatty acid oxidation with secondary carnitine deficiency. Most lipid disorders occur sporadically; they are believed to be autosomal recessive. It causes a Reye syndrome–like illness with hypoketotic hypoglycemia, encephalopathy, hyperammonemia, and liver dysfunction. These attacks are distinct from those associated with glycolytic defects in that they occur after prolonged exercise, fasting, febrile illness, or other provocations that may increase muscle dependence on free fatty acids. Findings on muscle biopsy are usually normal except for evidence of muscle myopathic injury after rhabdomyolysis. Although there is no specific treatment, increasing intake of carbohydrates and the frequency of meals prevents episodes of rhabdomyolysis. In the systemic form, the impaired transport of carnitine into multiple tissues results from nonfunctional high-affinity carnitine receptors. Patients have a myopathy with cardiac involvement, as well as episodes of hepatic dysfunction with hypoketotic hypoglycemia and altered mental status. There is no urinary excretion of organic acids to suggest a secondary metabolic illness. When the disease is limited to muscle, patients are usually seen in childhood with limb girdle myopathy. Patients have diminished muscle uptake of carnitine and a fixed lipid storage myopathy but a normal serum carnitine level. Secondary Carnitine Deficiency Most carnitine deficiencies are secondary to enzyme defects in -oxidation. Defects in lipid metabolism lead to accumulation of acyl-CoA molecules, which are converted to acylcarnitines, forms that are more readily excreted in urine. This process leads to negative carnitine balance and, ultimately, to carnitine deficiency. Impaired metabolism of valproic acid may similarly lead to excretion of valproylcarnitine and secondary carnitine deficiency. Most of these illnesses occur in early childhood or infancy and lead to Reye syndrome–like episodes.

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