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This situation leaves a two-fragment fracture with the blade plate and its osteotomy fixation intact purchase 500mg erythromycin visa, but with a fracture just below the plate cheap erythromycin 500mg. Most of these fractures should be treated by open reduction using either anterior plates or interfragmentary screws (Case 10. Occasionally, flexible nails, which are passed in the intermedullary region around the screws, may be used (Figure 10. Later fractures that occur as stress risers from the plate site with the blade plate in place should be treated with removal of the blade plate and repeat open reduction with a device most appropriate for the fracture pattern. Like- wise, fractures immediately after plate removal should be treated as de nova fractures and usually require an open reduction or internal fixation with Case 10. Be- fore this time, he was a full community ambulator, al- though she noticed that he had slowed down over the past year. On physical exami- nation he had full range of motion of the right hip; how- ever, there seemed to be some discomfort. When he tried to stand, he would put no weight on the leg. A radiograph demonstrated a subluxated hip, which was reconstructed with a femoral osteotomy and peri-ilial pelvic osteotomy (Figure C10. He was discharged home with instruc- tions for physical therapy to start gait training. Two weeks later, his mother returned him to the clinic and said she found him in bed with the leg hung through the bedside rails. He did not express much discomfort but his mother felt the leg looked different after she got him out of the side rail. On physical examination his leg was short and externally rotated. A radiograph demonstrated a fracture through the proximal screw holes in a long oblique pat- tern (Figure C10. He was returned to the operating room for an open reduction with intrafragmentary screws and then placed in a cast for 8 weeks. By 6 months after surgery, he was again an independent community ambu- lator, and by the second-year follow-up, his hip had re- Figure C10. This case demonstrates the difficulty in assessing pain level in some individuals with mental retardation and the care that has to be taken to address deformity concerns. It is crucial to ensure that the proximal fragment is not allowed to fall into too much varus or lose the derotation that had been obtained. Recurrent Contracture and Dislocation The incidence of recurrent dislocation varies greatly based on the specific procedure. Failure rates with the recommended peri-ilial osteotomy, varus derotation, and soft-tissue lengthenings vary from 0% to 4% on long-term follow-up. It is very important to continue following the children, and if they start to develop recurrent fixed contractures, these need to be addressed with repeat soft-tissue lengthenings. Also, the redislocation rate is much higher for hypotonic hips, and a different level of skepticism toward the results needs to be communicated to the parents (Case 10. If the recurrent dislocation occurs early, in the first 4 weeks postopera- tively, a very careful assessment of the surgery and why the dislocation oc- curred is required. If the redislocation results from such severe acetabular deficiency that the reconstruction could not adequately recreate a stable ac- etabulum, then further attempts to provide a stable reduction should be post- poned until these children are rehabilitated. If the hip then becomes painful, it would be treated with a palliative approach. However, if children with spastic hip dislocation had a successful reconstruction and years later devel- oped a recurrent adduction and hip flexion contracture followed by a hip 10. Hip 645 subluxation or dislocation, the treatment regimen should be quite different. In general, as these patients are followed, as soon as their maximum ab- duction is less than 0°, a repeat adductor lengthening should be performed.
Furthermore cheap erythromycin 500mg otc, operons are not present in eukaryotes discount 250mg erythromycin with amex, and the genes encod- ing proteins that function together are usually located on different chromosomes. In addition, the processes of transcription and translation are separated in eukaryotes by intracellular compartmentation Hemocytoblast (nucleus and cytosol, or endoplasmic reticulum [ER]) and by time (eukaryotic Heterochromatin Euchromatin hnRNA must be processed and translocated out of the nucleus before it is trans- lated). Thus, regulation of eukaryotic gene expression occurs at multiple levels: • DNA and the chromosome, including chromosome remodeling and gene rearrangement • Transcription, primarily through transcription factors affecting binding of RNA polymerase • Processing of transcripts • Initiation of translation and stability of mRNA Orthochromatic erythroblast Once a gene is activated through chromatin remodeling, the major mechanism of regulating expression affects initiation of transcription at the promoter. Regulation of Availability of Genes for Transcription Once a haploid sperm and egg combine to form a diploid cell, the number of genes in human cells remains approximately the same. As cells differentiate, different genes are available for transcription. A typical nucleus contains chromatin that is condensed (heterochromatin) and chromatin that is diffuse (euchromatin)(Fig. The genes in heterochromatin are inactive, whereas those in Reticulocyte euchromatin produce mRNA. Long-term changes in the activity of genes occur dur- Fig. Inactivation of genes during devel- ing development as chromatin goes from a diffuse to a condensed state or vice opment of red blood cells. The cellular genome is packaged together with histones into nucleosomes, and Condensed chromatin (heterochromatin) is initiation of transcription is prevented if the promoter region is part of a nucleo- inactive. Thus, activation of a gene for transcription requires changes in the state of the their chromatin becomes more condensed. The availability of genes for transcription Eventually, the nucleus is extruded. For example, during lymphocyte matu- + Lys NH3 ration, genes are rearranged to produce a variety of different antibodies. CHROMATIN REMODELING 3 Acetate Acetyl CoA The remodeling of chromatin generally refers to displacement of the nucleosome from HAC HDAC specific DNA sequences so that transcription of the genes in that sequence can be ini- tiated. The first mechanism is by an Histone adenosine triphosphate (ATP)-driven chromatin remodeling complex, which uses O energy from ATP hydrolysis to unwind certain sections of DNA from the nucleosome Lys NH C CH3 core. The second mechanism is by covalent modification of the histone tails through acetylation (Fig. Histone acetyltransferases (HAT) transfer an acetyl group Acetylated histone from acetyl CoA to lysine residues in the tail (the amino terminal ends of histones H2A, H2B, H3, and H4). This reaction removes a positive charge from the -amino Fig. Abbrevia- group of the lysine, thereby reducing the electrostatic interactions between the histones tions: HAC, histone acetylase; HDAC, histone and the negatively charged DNA, making it easier for DNA to unwind from the his- deacetylase. The acetyl groups can be removed by histone deacetylases (HDAC). Each his- tone has a number of lysine residues that may be acetylated and, through a complex mixing of acetylated and nonacetylated sites, different segments of DNA can be freed from the nucleosome. A number of transcription factors and co-activators also contain histone acetylase activity, which facilitates the binding of these factors to the DNA and simultaneous activation of the gene and initiation of its transcription. METHYLATION OF DNA Cytosine residues in DNA can be methylated to produce 5-methylcytosine. The methy- lated cytosines are located in GC-rich sequences (called GC-islands), which are often near or in the promoter region of a gene. In certain instances, genes that are methylated are less readily transcribed than those that are not methylated. For example, globin genes are more extensively methylated in nonerythroid cells (cells which are not a part of the erythroid, or red blood cell, lineage) than in the cells in which these genes are expressed (such as the erythroblast and reticulocyte). Methylation is a mechanism for regulating gene expression during differentiation, particularly in fetal development. Methylation has been implicated in genomic imprinting, a process occurring during the formation of the eggs or sperm that blocks the expression of the gene in the fertilized egg. Males methylate a different set of genes than females. This sex-depen- dant differential methylation has been most extensively studied in two human disorders, Prader-Willi syndrome and Angelman syndrome. Both syndromes, which have very different symptoms, result from deletions of the same region of chromosome 15 (a microdeletion of less than 5 megabases in size). If the deletion is inherited from the father, Prader-Willi syndrome is seen in the child; if the deletion is inherited from the mother, Angelman’s syndrome is observed.
One in 28 Ashkenazi Jews carries this defective gene buy erythromycin 500mg visa. Its presence can be discov- ered by measuring the tissue level of the protein produced by the gene (hex- osaminidase A) or by recombinant DNA techniques buy erythromycin 500 mg on-line. Skin fibroblasts of concerned couples planning a family are frequently used for these tests. Carriers of the affected gene have a reduced but functional level of this enzyme that normally hydrolyzes a specific bond between an N-acetyl-D-galactosamine and a D-galactose residue in the polar head of the ganglioside. Enzyme replacement has met with little success because of the difficulties in getting the enzyme across the blood-brain barrier. BIOCHEMICAL COMMENTS Hexosaminidase A, the enzyme defective in Tay-Sachs disease, is actually composed of two subunits, an and a chain. The exact stoichiometry of the active enzyme is unknown, but it may be 2 2. The subunit is coded for by the HexA gene, whereas the subunit is coded for by the HexB gene. In Tay- Sachs disease, the subunit is defective, and hexosaminidase A activity is lost. However, the subunit can form active tetramers in the absence of the subunit, and this activity, named hexosaminidase B, which cleaves the glycolipid globoside, retains activity in children with Tay-Sachs disease. Thus, children with Tay-Sachs disease accumulate the ganglioside GM2, but not globoside (Fig. Mutation of the HexB gene, and production of a defective subunit, leads to inactivation of both hexosaminidase A and B activity. Both activities are lost because both activities require a functional subunit. The clinical course of this disease is similar to Tay-Sachs but with an accelerated timetable because of the initial accumulation of both GM2 and globo- side in the lysosomes. Sandhoff activator protein + hexosaminidase A (α2β2) Block in Sandhoff disease Block in Tay-Sachs disease GM2 ceramide glc gal NAcGal Sialic acid hexosaminidase A or B (β4) Block in Sandhoff disease Globoside ceramide glc gal gal NAcGal Fig. Substrate specificities of hexosaminidase A, B, and the function of the activator protein. Glc glucose; gal galactose; NAcGal N-acetylgalactosamine. Children were identified with Tay-Sachs symptoms, but when both hexosaminidase A and B activities were measured in a test tube, they were nor- mal. This disease, ultimately named Sandhoff activator disease, is caused by a mutation in a protein that is needed to activate hexosaminidase A activity. In the absence of the activator, hexosaminidase A activity is minimal, and GM2 initially accumulates in lysosomes. This mutation has no effect on hexosaminidase B activity. When a glycolipid cannot be degraded because of an enzymatic mutation, it accumulates in residual bodies (vacuoles that contain material that lysosomal enzymes cannot digest). Normal cells contain a small number of residual bodies, but in diseases of lysosomal enzymes, large numbers of residual bodies accumulate within the cell, eventually interfering with normal cell function. In 70% of the cases of Tay-Sachs disease in persons of Ashkenazai Jewish back- ground, exon 11 of the gene for the chain of hexosaminidase A contains a muta- tion. Suggested References Gravel RA, Kaback MM, Proia RL, Sandhoff K, et al. In: Scriver CR, Beaudet AL, Valle D, Sly WS, et al eds. The Metabolic and Molecular Bases of Inherited Disease. I-cell disease and pseudohurler polydystrophy: disorders of lysosomal enzyme phosphorylation and localization.
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