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Oligo- dendrocytes purchase 30gm v-gel with mastercard, along with the astrocytes v-gel 30 gm on-line, form a supporting matrix for the neurons v-gel 30 gm. Oligodendrocytes have a limited capacity for mitosis purchase v-gel 30 gm with mastercard, and if damaged v-gel 30 gm line, do not repli- cate. If this occurs, demyelination of the axons may occur, resulting in abnormali- ties in signal conduction along that axon (see Biochemical Comments). SCHWANN CELLS Peripheral axons can regenerate if Schwann cells are the supporting cells of the PNS. Like oligodendrocytes, Schwann Schwann cells are available to cells form myelin sheaths around the axons, but unlike the oligodendrocytes, guide the growth of the axon. Schwann cells also clean up cellular debris There is a synergistic interaction between in the PNS. These are the smallest type of glial cells in the nervous system. They serve as immunologically responsive cells similar to the action of macrophages in the circu- lation. Microglial cells destroy invading microorganisms and phagocytose cellular debris. EPENDYMAL CELLS For many years, it had been The ependymal cells are ciliated cells that line the cavities (ventricles) of the CNS believed that damaged neurons in and the spinal cord. In some areas of the brain, the ependymal cells are function- the CNS could not regenerate, for it ally specialized to elaborate and secrete cerebrospinal fluid (CSF) into the ven- was thought that there were no pluripotent tricular system. The beating of the ependymal cilia allow for efficient circulation stem cells (cells that could differentiate into of the CSF throughout the CNS. The CSF acts as both a shock absorber protect- various cell types found in the CNS) in the ing the CNS from mechanical trauma and a system for the removal of metabolic CNS. The CSF can be aspirated from the spinal canal and analyzed to determine found within the ependymal layer can act as whether disorders of CNS function, with their characteristic CSF changes, are neural stem cells, which under appropriate stimulation can regenerate neurons. Capillary Structure In the capillary beds of most organs, a rapid passage of molecules occurs from the blood through the endothelial wall of the capillaries into the interstitial fluid. Thus, the composition of interstitial fluid resembles that of blood, and specific receptors or transporters in the plasma membrane of the cells being bathed by the interstitial fluid may directly interact with amino acids, hormones, or other compounds from the blood. In the brain, transcapillary movement of substrates in the peripheral cir- culation into the brain is highly restricted by the blood-brain barrier. This barrier limits the accessibility of blood-borne toxins and other potentially harmful com- pounds to the neurons of the CNS. CHAPTER 48 / METABOLISM OF THE NERVOUS SYSTEM 885 The blood-brain barrier begins with the endothelial cells that form the inner lin- Inside of capillary ing of the vessels supplying blood to the CNS (Fig. Unlike the endothelial cells of other organs, these cells are joined by tight junctions that do not permit the movement of polar molecules from the blood into the interstitial fluid bathing the neurons. They also lack mechanisms for transendothelial transport that are present in other capillaries of the body. These mechanisms include fenestrations (“win- 4 dows” or pores that span the endothelial lining and permit the rapid movement of 5 molecules across membranes) or transpinocytosis (vesicular transport from one side of the endothelial cell to another). Because they contain a variety of drug-metabolizing enzyme systems similar to the 2 Narrow intercellular spaces drug-metabolizing enzymes found in the liver, the endothelial cells can metabolize 3 Lack of pinocytosis neurotransmitters and toxic chemicals and, therefore, form an enzymatic barrier to entry of these potentially harmful substances into the brain. They actively pump 4 Continuous basement membrane hydrophobic molecules that diffuse into endothelial cells back into the blood (espe- cially xenobiotics) with P-glycoproteins, which act as transmembranous, ATP- 5 Astrocyte extension dependent efflux pumps. Although lipophilic substances, water, oxygen, and carbon dioxide can readily cross the blood-brain barrier by passive diffusion, other mole- Fig. Differential transporters on the luminal pounds in the blood cannot freely pass into the and abluminal endothelial membranes can transport compounds into, as well as out brain; they must traverse the endothelial cells, basement membrane, and astrocytes, by use of of, the brain. Further protection against the free entry of blood-borne compounds into the CNS Very lipophilic molecules may pass through all is provided by a continuous collagen-containing basement membrane that com- of these membranes in the absence of a carrier. The basement membrane appears to be surrounded by the foot processes of astrocytes. Thus, compounds must pass through endothe- lial cell membranes, the enzymatic barrier in the endothelial cells, the basement membrane, and possibly additional cellular barriers formed by the astrocytes to reach the neurons in the brain. Transport through the Blood-Brain Barrier Many nonpolar substances, such as drugs and inert gases, probably diffuse through the endothelial cell membranes. A large number of other compounds are transported through the endothelial capillaries by facilitative transport, whereas others, such as nonessential fatty acids, cannot cross the blood-brain barrier. Essential fatty acids, A number of disorders of glucose however, are transported across the barrier. The most com- mon of these is facilitated glucose trans- 1.

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The strap is placed immediately inferior to the breasts discount 30 gm v-gel. Another very important aspect of controlling the anterior fall of the trunk is to have a lap tray and armrest placed in an elevated position discount 30gm v-gel visa. By using the upper extremity on the arm rest or lap tray buy cheap v-gel 30gm on-line, children are encouraged to sit upright order 30 gm v-gel overnight delivery. In some children 30gm v-gel with amex, the tray may be placed as high as the nipple line, which will greatly encourage sitting upright. Headrests Headrests provide two functions, first, to provide support for individuals with poor head control, and second, as a safety feature when riding in a ve- hicle. For children who have good head control but sit in a wheelchair while riding in a van or school bus, the headrest may be needed only during vehi- cle transportation. This headrest can be a simple flat extension of the back that can flip down or be removed easily when not needed. For individuals who need head control, a more elaborate system may be needed. If the only head control needed is to prevent hyperextension, a simple flat or mildly contoured headrest only may be required. If a lateral support is needed, a lateral extension, usually coming inferiorly and anteriorly, is preferred. These anterior extensions should be inferior far enough to avoid causing irritation to the ears (Figure 6. Proper anterior trunk control is important for the best function of these head restraints. To restrain the severe anterior drop of the head, a mobile forehead strap may be used. This system only works if the forehead has a shape with some ledge or protrusion, which will allows the strap to stay in place. A forehead shape with a posterior slope does not allow Figure 6. Another approach to preventing anterior drop of the tems available, and often trial and error is re- head is to use cervical collars that place the support under the mandible. Many Some of these are attached to the chair posteriorly and some are free float- headrest systems have modular posterior ing on the children. The free-floating collars, either anterior opening or pos- and lateral sections (A). The lateral sections terior opening, are safer and are more comfortable for children. These free- can be adjusted separately, which is helpful floating collars are excellent options for use in vehicles for individuals with in children with significant asymmetry (B). The lateral parts provide good side-bending control (C), whereas the posterior element prevents hyperextension. A 222 Cerebral Palsy Management Back-to-Seat Position The best position for the back-to-seat angle has been extensively debated, with many therapists feeling that individuals do better with the back inclined forward slightly, up to 20°, or the seat raised anteriorly 10° to 20°. All studies that have evaluated these different constructs have found that there is no consistent functional benefit from either position. Some indi- viduals seem more comfortable with a seat that has anterior elevation of 5° to 10°, but these factors are variable and require individual evaluation. The seat-to-back angle should almost always be close to 90° or greater. Tray For individuals who spend most of their time in a wheelchair, the availability of a good stable lap tray is very important for sitting in an optimal upright posture and having a work surface that is always at the right height. Clear, plastic material is best because it is easy to clean, lightweight, and the child’s position in the wheelchair can be monitored more easily while the tray is in place. Attachments It is very important for the seating clinic to do a good medical and social his- tory to understand all the needs of caretakers and families for the use of the wheelchair. The wheelchair has to be adapted to carry all the things care- takers need when these children are taken out in the community because the caretakers cannot push a wheelchair and also carry a large bag of other things. This careful history should make sure that these things are not over- looked because commonly, when something is overlooked, it takes 6 to 12 months from the time the item is found to be missing until it is ordered, approved by the insurance company, and placed on the wheelchair. Crutch holders are often overlooked and should be added on the wheelchairs of all individuals who use crutches.

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O H H C O C R1 O HC O C R2 O + HC P CH2CH2N(CH3)3 H O– Lecithin (PC) HO Cholesterol LCAT O R2 C O Cholesterol ester O H HC O C R1 HC OH O + HC P CH2CH2N(CH3)3 H O– Lysolecithin Fig purchase 30 gm v-gel amex. Nascent HDL is synthesized in liver and intestinal cells cheap v-gel 30gm on-line. This cholesterol is converted to cholesterol ester (CE) by the LCAT reaction buy generic v-gel 30gm on line. HDL transfers CE to VLDL in exchange for triacylglycerol (TG) quality v-gel 30gm. The cholesterol ester transfer protein (CETP) mediates this exchange v-gel 30 gm otc. When depleted of cholesterol and its esters, the HDL particle dissociates from the SR-B1 receptor and re-enters the circulation. SR-B1 receptors can be upregu- lated in certain cell types that require cholesterol for biosynthetic purposes, such as the cells that produce the steroid hormones. The SR-B1 receptors are not downreg- ulated when cholesterol levels are high. HDL INTERACTIONS WITH OTHER PARTICLES CE In addition to its ability to pick up cholesterol from cell membranes, HDL also TG exchanges apoproteins and lipids with other lipoproteins in the blood. For exam- ple, HDL transfers apolipoprotein E (apoE) and apolipoprotein CII (apoCII) to chy- lomicrons and to VLDL. The apoCII stimulates the degradation of the triacylglyc- erols of chylomicrons and VLDL by activating LPL (Fig. After digestion Cholesterol ester of the chylomicrons and the VLDL triacylglycerols, apoE and apoCII are trans- transfer protein ferred back to HDL. When HDL obtains free cholesterol from cell membranes, the (CETP) free cholesterol is esterified at the third carbon of the A ring via the LCAT reaction (see Fig. From this point, HDL either transports the free cholesterol and cholesterol esters directly to the liver, as described above, or by CETP to circulat- CE ing triacylglycerol-rich lipoproteins such as VLDL and VLDL remnants (see Fig. In exchange, triacylglycerols from the latter lipoproteins are transferred to HDL (Fig. The greater the concentration of triacylglycerol-rich lipopro- teins in the blood, the greater the rate of these exchanges. Thus, the CETP HDL exchange pathway may explain the observation that whenever triacylglycerol-rich Fig. Function of cholesterol ester trans- lipoproteins are present in the blood in high concentrations, the amount of choles- fer protein (CETP). CETP transfers cholesterol terol reaching the liver via cholesterol-enriched VLDL and VLDL remnants esters (CE) from HDL to VLDL in exchange increases, and a proportional reduction in the total amount of cholesterol and cho- for triacylglycerol (TG). Mature CHAPTER 34 / CHOLESTEROL ABSORPTION, SYNTHESIS, METABOLISM, AND FATE 637 HDL particles are designated as HDL3; after the CETP reaction and loss of cho- lesterol and gain of triacylglycerol, the particles become larger and are designated as HDL2 particles (see Table 34. LIPOPROTEINS ENTER CELLS BY RECEPTOR- MEDIATED ENDOCYTOSIS As stated earlier, each lipoprotein particle contains specific apoproteins on its surface that act as ligands for specific plasma membrane receptors on target tis- sues such as the liver, the adrenal cortex, the gonads, and other cells that require one or more of the components of the lipoproteins. With the exception of the scavenger receptor SR-B1, the interaction of ligand and receptor initiates the process of endocytosis depicted for LDL in Figure 34. The receptors for LDL, for example, are found in specific areas of the plasma membrane of the target cell for circulating lipoproteins. These are known as coated pits, and they con- tain a unique protein called clathrin. The plasma membrane in the vicinity of the receptor–LDL complex invaginates and fuses to form an endocytic vesicle. These vesicles then fuse with lysosomes, acidic subcellular vesicles that contain a number of degradative enzymes. The cholesterol esters of LDL are hydrolyzed to form free cholesterol, which is rapidly reesterified through the action of ACAT. This rapid reesterification is necessary to avoid the damaging effect of high levels of free cholesterol on cellular membranes. The newly esterified cho- lesterol contains primarily oleate or palmitoleate (monounsaturated fatty acids), unlike those of the cholesterol esters in LDL, which are rich in linoleate, a polyunsaturated fatty acid.

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