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Using a wire or a thin probe cheap nexium 20mg online, document that the drillhole is entirely within bone proven nexium 40mg. Repeat the same procedure on the iliac crest on the opposite side purchase 20 mg nexium. Pack Gelfoam into the drillholes to prevent bone bleeding cheap nexium 40mg otc. Pack the lateral side of the iliac crest with a sponge to prevent bleed- ing purchase nexium 20 mg visa. These sponges have to be inserted completely over the edge of the iliac crest or they will become entangled in the rod or wires. These sponges will be removed just before wound closure. Remove the sponge packs from the prior exposure of the spine, and clean each vertebra so that all the soft tissue is removed from the tips 2. In the thoracic spine, cut vertically approximately 1 cm distal to the superior aspect of the lamina. By proper removal of the spinous processes, the spinal interspace is opened. It is important never to violate the superior bor- der of the posterior elements, as this is where the strength for wire fixation occurs. In the lumbar spine, the spinous processes should be transected transversely at their base (Figure S2. In the lumbar area, the spinous process is cut horizonally; then at the thora- columbar junction they are cut at 45°, and in the thoracic area the process are cut off vertically (Figure S2. Use a rongeur with a serrated end to remove the ligamentum flavum (Figure S2. If more bone removal is indicated, remove the bone from the inferior aspect of the spinous process base and lamina only. Never remove bone from the superior aspect of the lamina be- cause this is the aspect of the lamina that provides strength for the wire (Figure S2. Complete the spinal interspace opening with a curette, making sure that the ligamentum flavum is cut a sufficient distance on either side so wire can be passed (Figure S2. If epidural bleeding occurs during this time, the interspace should be packed gently with Gelfoam and a neural sponge. There may be substantial bleeding from these epidural veins; however, it is almost impossible to cau- terize them without an extremely large exposure that destroys the lamina. The bleeding can be controlled with gentle pressure, and 898 Surgical Techniques Figure S2. Wires are inserted starting at the distal end at L5. Usually, two double wires are inserted at L5 and T1 and only a single double wire at each other level (Figure S2. Spinal Procedures 899 laminae so that the double end of the wire is bent into the midline pointing caudally, and each beaded lateral single wire is brought out laterally and cross-cranially over the laminae. This double cross- ing of the wires provides extra protection to prevent the inadvertent protrusion of the wires into the neural canal (Figure S2. When passing wires it is important to roll the wires under the lam- ina, being especially careful not to roll the wire with the tip caught under the lamina, as this will cause high pressure on the spinal cord (Figure S2. Utilizing gouges or rongeurs, all facet joints are removed from T1 to the sacrum (Figure S2. Bone graft then is packed into this decorticated bone. Bleeding that cannot be con- trolled with electrocautery will occur during this period as the bone is opened, and it should be controlled by packing the wound with bone graft soaked with thrombin and Gelfoam. Pressure from addi- tional sponge packing also will help control the bleeding. If severe bleeding is encountered, this portion of the procedure can be done after insertion of the rod, but it is more difficult, and decortication and facetectomy performed after rod insertion will be much less adequate.

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FUELS FOR THE LIVER The reactions used to modify and inactivate dietary toxins and waste metabolites are energy requiring nexium 40 mg with amex, as are the reactions used by anabolic (biosynthetic) pathways such as gluconeogenesis and fatty acid synthesis quality 20mg nexium. Thus buy generic nexium 40 mg line, the liver has a high energy requirement and consumes approximately 20% of the total oxygen used by the body discount nexium 40 mg visa. The principle forms in which energy is supplied to these reactions is the high- energy phosphate bonds of adenosine triphosphate (ATP) buy nexium 40 mg mastercard, uridine triphosphate (UTP), and guanosine triphosphate (GTP), reduced NADPH, and acyl-CoA thioesters. The energy for the formation of these compounds is obtained directly CHAPTER 46 / LIVER METABOLISM 853 Table 46. Major Fates of Carbohydrates in the Liver • Storage as Glycogen • Glycolysis to pyruvate • Followed by oxidation to carbon dioxide in the TCA cycle • Precursors for the synthesis of glycerol-3-phosphate (the backbone of triacylglycerols and other glyceolipids), sialic acid, and serine • Entry into the TCA cycle and exit as citrate, followed by conversion to acetyl CoA, mal- onyl CoA, and entry into fatty acid synthesis and secretion as VLDL I Synthesis of phospholipids and other lipids from triacylglycerols • Conversion to mannose, sialic acid, and other sugars necessary for the synthesis of oligosaccharides for glycoproteins, including those secreted into blood • Synthesis of acid sugars for proteoglycan synthesis and formation of glucuronides • Oxidation in the pentose phosphate pathway for the formation of NADPH (necessary for biosynthetic reactions such as fatty acid synthesis, glutathione reduction, and other NADPH-utilizing detoxification reactions) from oxidative metabolism, the TCA cycle, or the electron transport chain and oxidative phosphorylation. After a mixed meal containing carbohydrate, the major fuels used by the liver are glucose, galactose, and fructose. If ethanol is consumed, the liver is the major site of ethanol oxidation, yielding principally acetate and then acetyl CoA. During an overnight fast, fatty acids become the major fuel for the liver. They are oxidized to carbon dioxide or ketone bodies. The liver also can use all of the amino acids as fuels, converting many of them to glucose. The urea cycle dis- poses of the ammonia that is generated from amino acid oxidation. Carbohydrate Metabolism in the Liver After a carbohydrate-containing meal, glucose, galactose, and fructose enter the Why would you expect fructose 1- portal circulation and flow to the liver. This organ serves as the major site in the phosphate levels to promote the body for the utilization of dietary galactose and fructose. It metabolizes these com- dissociation of glucokinase from pounds by converting them to glucose and intermediates of glycolysis. Glucose as a Fuel The entry of glucose into the liver is dependent on a high concentration of glucose in the portal vein after a high-carbohydrate meal. Because the Km for both the glu- cose transporter (GLUT2) and glucokinase is so high (approximately 10 mM), glu- cose will enter the liver principally after its concentration rises to 10 to 40 mM in the portal blood and not at the lower 5-mM concentration in the hepatic artery. The increase in insulin secretion that follows a high-carbohydrate meal will promote the conversion of glucose to glycogen. In addition, the rate of glycolysis will be increased (PFK-2 is active; thus, PFK-1 is activated by fructose-2, 6 bisphos- phate) such that acetyl CoA can be produced for fatty acid synthesis (acetyl CoA carboxylase will be activated by citrate; see Chapter 33). Thus, after a high-carbo- hydrate meal, the liver uses glucose as its major fuel, while activating the pathways The role of glucokinase RP is very for glycogen and fatty acid synthesis. Mice that have been The rate of glucose utilization by the liver is determined, in part, by the level of genetically engineered to no activity of glucokinase. Glucokinase activity is regulated by a glucokinase regula- longer express the RP (a knockout mouse) tory protein (RP, Fig. In the absence of glu- display reduced levels of total glucokinase activity in the liver. This is attributable to the cose, glucokinase is partially sequestered within the nucleus, bound to RP, in an finding that RP is important in the post-tran- inactive form. High concentrations of fructose 6-phosphate promote the interaction scriptional processing of the mRNA for glu- of glucokinase with RP, whereas high levels of either glucose or fructose cokinase. In the absence of RP, less glucoki- 1-phosphate block glucokinase from binding to RP and promote the dissociation of nase is produced. Thus, as glucose levels rise in the cytoplasm and nucleus (because of have no glucokinase in the nucleus, a increased blood glucose levels after a meal, for example), there is a significant reduced cytoplasmic glucokinase content, enhancement of glucose phosphorylation as glucokinase is released from the and inefficient glucose phosphorylation in nucleus, travels to the cytoplasm, and phosphorylates glucose. The major dietary source of fructose, the ingestion of which would lead to Nucleus GK increased fructose 1-phosphate levels, is sucrose. Sucrose is a disaccharide of glu- RP RP GK cose and fructose. Thus, an elevation of fruc- tose 1-phosphate usually indicates an eleva- GK GK tion of glucose levels as well. Regulation of glucokinase by regulatory protein (RP). RP is localized to the nucleus, and in the absence of glucose or presence of fructose 6-phosphate, most glucokinase is translocated to the nucleus and binds RP. This leads to the formation of the inactive form of glucokinase. When glucose or fructose-1-phosphate levels rise, glucokinase is released from RP.

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When ice was applied a second time generic 40 mg nexium free shipping, intramuscular temperature continued to fall proven nexium 20 mg. Higher temperatures were recorded in the traumatised limb buy nexium 20 mg fast delivery. In a study of cold applied to the skin of the mouse cheap nexium 20 mg without prescription, increased blood vessel permeability with fluid extravasation and oedema occurred with temperatures below 15ºC purchase 20 mg nexium. In a study of the effect of ice on injured rat muscle, however, cryotherapy did not reduce microvascular diameters or decrease microvascular perfusion. Human studies Animal studies can help us understand the physiological effect of temperature reduction but the key to clinical care is to understand the therapeutic effect in clinical practice. A number of researchers have examined the effect of tissue temperature reduction, but it is difficult to compare the results of the different studies because of variation in research methods and measurements. The temperature reduction at tissue level is illustrated in one study where ice was applied continuously for 85 minutes27 and the temperature dropped by 5ºC, 9ºC and 7ºC at depths of 7 cm, 6 cm and 4 cm. Compression may also enhance temperature reduction28 with the changes at 1 cm below the fat layer and at 2 cm below the fat layer being greater with compression at 12⋅8ºC and 10⋅1ºC. Subcutaneous fat, being an insulating material, inhibits the cooling effect and while significant cooling occurs with 10 minutes of ice application to a depth of 2 cm in those with less than 1 cm of fat,29 athletes with more than 2 cm of fat, required 20–30 minutes. There is an inverse relationship between adipose tissue and temperature decrease so that subcutaneous fat may mean that short duration ice application may be ineffective in cooling deeper tissue levels. The above paragraphs highlight only some of the studies on ice application. The consensus from studies of ice application, for periods varying from five minutes to 85 minutes, is that the temperature is reduced in the first 10 minutes with little further reduction from 10 to 20 minutes. The temperature drop is determined by the area of contact between the ice and the skin, the temperature difference and tissue conductivity but most published studies do not measure the area of ice application, subcutaneous fat, nor use comparable methods of calculating depth, or measuring temperature. Where temperature is 48 The role of ice in soft tissue injury management measured, in human and animal studies, there is wide variation in the temperature recorded at different depths in different studies with wide standard deviations. It is almost impossible to consider the dynamic effect of tissue movement and blood flow on temperature and experimental measurements of tissue temperature cannot be directly compared to the effect on the injured athlete. Summary Subcutaneous fat is an insulator so may impair cold conduction A barrier should be used to prevent ice burns A wet towel is a most effective barrier and conductor Ice therapy may cause temporary neurological impairment Ice may temporarily impair muscle strength Application of different modalities Ice, or cold, is used in different ways. The standard ice application of melting iced water ensures a constant temperature of 0ºC. Ice taken straight from a freezer may be considerably below freezing point and reusable chemical gel packs may be as cold as −5 to −15ºC. Iced water may also be used in different ways, such as frozen in paper cups or in moulded packs, and convenience packs (for example frozen peas) have also been recommended. A temperature of 0ºC is certain with melting iced water, which is important as there is a risk of tissue damage and frostbite with excess cold. The traditional method of cryotherapy is through melting iced water, but there are a number of proprietary preparations available including chemical packs, reusable gels, sprays and applications. There is little research on comparison of the various methods although one animal study gives us particular insight. Ice can cause burns if applied directly to the skin34 so a barrier is usually recommended. This can, of course, act as an insulator and prevent cold conduction but this depends on the nature of the barrier. The effect of different barriers was clear after 30 minutes of ice application. Repeated 10 minute applications through a wet towel are most effective. Ice taken straight from a freezer may be below freezing point. Reusable chemical gel packs, may be as cold as −5 to −15°C. There is little research on comparison of the various methods.

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In quiescent cells cheap 40 mg nexium, Rb is complexed with E2F purchase nexium 40mg, The synthesis of cyclin E allows it to complex resulting in inhibition of these transcription factors 20mg nexium. On growth factor stimulation buy 40 mg nexium amex, with cdk2 discount nexium 20mg with mastercard, forming another active cyclin the cyclin Ds are induced (there are three types of cyclin D; D1, D2, and D3). They complex that retains activity into S phase bind to cdk4 and cdk6, converting them to active protein kinases. Thus, of cyclin/cdk phosphorylation is the Rb protein. Phosphorylation of Rb releases it each phase of the cell cycle activates the next from E2F, and E2F is then free to activate the transcription of genes required for through cyclin synthesis. The Rb protein is a tumor suppressor gene (more below). Progression through the cell cycle is opposed by the CKIs (see Fig. The CKIs regulating cyclin/cdk expression in the G1 phase of the cell cycle fall into two categories: the Cip/Kip family and the INK4 family. The Cip/Kip family members (p21, p27, and p57) have a broad specificity and inhibit all cyclin–CDK complexes. The INK4 family, which consists of p15, p16, p18, and p19, are specific for the Cyclin cyclin D–cdk4/6 family of complexes (inhibitors of cyclin-dependent kinase-4). The regulation of synthesis of different CKIs is complex, but some are induced by CDK DNA damage to the cell and halt cell cycle progression until the damage can be Active complex repaired. For example, the CKI p21 (a protein of 21,000 Daltons) is a key member CKI of this group that responds to specific signals to block cell proliferation. If the dam- age cannot be repaired, an apoptotic pathway is selected, and the cell dies. Cyclin CKI In addition to sunlight and a preexisting nevus, hereditary factors also play a CDK role in the development of malignant melanoma. Ten percent of melanomas Inactive complex tend to run in families. Some of the suspected melanoma-associated genes include the tumor suppressor gene p16 (an inhibitor of cdk 4) and CDK4. CKI inhibition of cyclin/CDK activ- the single child of parents who had died of a car accident in their 50s, and thus, a famil- ity. CHAPTER 18 / THE MOLECULER BIOLOGY OF CANCER 325 Growth factor Receptor Initiates Ras/Raf signal pathway Induction of Activated Inhibited CdK complexes complexes Cyclin D Cyclin D Cyclin D Cyclin D Cyclin D CdK4 CdK6 CdK4 CdK6 CkI CdK4 CdK6 CkI CkI P E2F P P E2F Rb Rb Inhibitory Nucleus complex E2F DNA Increased gene transcription Cell cycle progression Fig. The genes encoding cyclins and CDKs are oncogenes, and the gene encoding the Retinoblastoma protein (Rb) is a tumor suppressor gene. Abbreviations: CDK, cyclin- dependent kinase; CDKI, cyclin-dependent kinase inhibitor. TUMOR SUPPRESSOR GENES Like the oncogenes, the tumor suppressor genes encode molecules involved in the regulation of cell proliferation. The normal function of tumor suppressor proteins is generally to inhibit proliferation in response to certain signals such as DNA damage. The signal is removed when the cell is fully equipped to proliferate; the effect of their elimination of tumor sup- pressor genes is to remove the brakes on cell growth. They affect cell cycle regula- tion, signal transduction, transcription, and cell adhesion. The products of tumor suppressor genes frequently modulate pathways that are activated by the products of proto-oncogenes. This is different from the case of proto-oncogene mutations because only one allele of a proto-oncogene needs to be converted to an oncogene to initiate transformation. Tumor Suppressor Genes That Directly Regulate the Cell Cycle The two best understood cell cycle regulators that are also tumor suppressors are the retinoblastoma (rb) and p53 genes. THE RETINOBLASTOMA (rb) GENE As previously discussed, the retinoblastoma gene product, Rb, functions in the tran- sition from G1 to S phase and regulates the activation of members of the E2F fam- ily of transcription factors (see Fig. If an individual inherits a mutated copy Inheritance of a mutation in p53 of the rb allele, there is a 100% chance of that individual developing retinoblastoma, leads to Li-Fraumeni syndrome, because of high probability that the second allele of rb will gain a mutation which is characterized by multiple (Fig.

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