Inhibition of restriction endonucleases by common clinical anticoagulants.
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Biomedical subjects
Publications and source records attributed to J E Coad.
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It has been shown that a 600 bp long cluster of cell lineage specific hypomethylated sites in the major breakpoint cluster region (M-bcr) on chromosome 22 exists in hematopoietic cells. To determine possible relationships between methylation patterns within the M-bcr and the stage of hematopoietic cell development, the M-bcr methylation status of 39 patients with leukemia and lymphoma and two patients with myelodysplastic syndrome with non-rearranged M-bcrs was examined by BgIII-HpaII digestion. In the myeloid malignancies, the presence of a hypermethylated 4.8 kb BgIII-BgIII M-bcr allele was directly proportional to the combined myeloblast and promyelocyte percentage of the specimen, whereas the presence of a 2.5 kb BgIII-HpaII allele was directly proportional to the combined percentage of monocytic cells and neutrophils. All five acute monoblastic leukemias showed a methylation pattern that closely resembled neutrophils. All of thirteen surface immunoglobulin positive B-cell malignancies showed a distinct methylation pattern consisting of three or more BgIII-HpaII restriction fragments of 2.5 kb or less in length. The B-cell precursor leukemias showed heterogeneous M-bcr methylation patterns, with four of seven showing a B-cell pattern and three showing a hypermethylated pattern with 4.8, 3.1/3.0 and/or 2.5 kb BgIII-HpaII M-bcr alleles. It is concluded that the M-bcr methylation status is related to the maturation of the neutrophil series; the surface immunoglobulin positive B-cell malignancies are characterized by a distinct, extreme hypomethylation pattern of the M-bcr; and the B-cell precursor malignancies appear to have a heterogeneous M-bcr methylation pattern.
This report of an 88-year-old woman with familial hemifacial spasm includes the first published postmortem description of hemifacial spasm with cross-compression of the seventh cranial nerve root exit zone by a redundant loop of the anterior inferior cerebellar artery and associated vascular plexus. Histological examination of the seventh and eighth cranial nerve complex suggested nerve degeneration because increased numbers of corpora amylacea were present just distal to the compression concavity. There was no evidence of demyelination or gliosis of the nerve. This case suggests that vascular compression of the nerve root exit zone is an important condition in the etiology of most of these cases. This is the third reported case of familial hemifacial spasm; to date, all such patients have had left facial involvement. The family pedigree in this case suggests a pattern of autosomal-dominant inheritance with partial penetrance. The genetic basis for familial hemifacial spasm may involve anatomical variants or anomalies of the posterior circulation, since both posterior inferior cerebellar arteries were congenitally absent in this case.
A patient with chronic lymphocytic leukemia (CLL) transforming into a small non-cleaved cell lymphoma (SNCL) with the occurrence of a t(8;22) is described. The SNCL and the CLL were both found to have a germline lambda light chain gene configuration and the same heavy chain and kappa light chain gene rearrangements. The SNCL was CD10 (CALLA) negative and appeared to be CD5 negative. It is concluded that the SNCL is derived from the CLL and that activation of the c-myc oncogene may have played a role in this transformation.
A 10-year follow-up study of neuroelectric implant integrity has been completed for 27 subjects who were treated for movement disorders associated with cerebral palsy. Data used for analysis included X-ray material, clinical data, and results from electrophysiological testing. Of the 21 subjects with subcutaneous receivers placed in the thoracic region, 81% experienced wire (67%) or receiver (14%) failure. Of the 6 subjects with subcutaneous receivers placed in the occipital region, there were no wire failures and one (17%) receiver failure. The occipital units lasted a minimum of 5.2 years without complications, whereas the thoracic units failed as early as 6 months after surgery, and lasted an average of 3.8 years. All wire fractures occurred between C1 and T1. Two types of fracture occurred, one consisting of a clean break and the other consisting of a scenario of bending and kinking, then thinning and fraying, and finally progressive multiple fragmentation. With a few exceptions the clean breaks occurred between C1 and C3, while the fraying scenario occurred between C6 and T1. Mechanisms for failure are discussed, as are results from material tests of wire samples.
Seating pressure in 10 subjects using a thoracic suspension orthosis was studied quantitatively. Anterior, posterior, and ischial pressures were measured bilaterally both unsuspended and during a 90 to 120 minute interval while suspended. Significant decreases in seating pressure were noted following suspension, with a mean decrease of 59.8%. Significant changes in lateral support were noted with suspension, as was a reduction in both the absolute pressure and relative distribution of pressure to the ischial areas. Relative redistribution of pressure in the anterior-posterior direction was related to leg support condition. All subjects who presented with pressure sores healed subsequent to thoracic suspension. Those with spinal curvature showed a 10 to 20 degree correction immediately following suspension. This correction generally was not maintained, however, in a temporal analysis. The data indicates that thoracic suspension can effectively reduce seating pressure and alter lateral posture, while leg support condition has a greater effect upon anterior-posterior pressure distribution. The use of a seat cushion to prevent subject swinging while suspended did not adversely affect the overall suspended pressures in this study, although the subjects without seat cushions showed lower overall suspended pressures.
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