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S S Saygi N S Oztekin O Sariba? M Eryilmaz T Zileli 《Clinical neurology and neurosurgery》1991,93(3):231-232
We present a 28-year old patient with left hemidystonia since early childhood after head trauma. This is the first report of a patient who had hemidystonia due to CT proven porencephalic cyst involving the caudate nucleus. 相似文献
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Studies of proteins that inhibit tissue factor activity have generally been conducted using either an extracted tissue homogenate ("thromboplastin") or tissue factor protein reconstituted into phospholipid vesicles rather than with tissue factor expressed in cell membranes (its physiological environment). In the present study, a human fibroblast cell strain was used to evaluate the effects of lipoprotein associated coagulation inhibitor (LACI), placental anticoagulant protein (PAP), and apolipoprotein A-II (apo A-II) on human tissue factor in cell membranes. LACI was tested from 7.8 to 500 pmol/L on fibroblasts cultured at cell densities ranging from 3,500 to 9,925 cells/well, and caused a progressive inhibition of tissue factor activity. PAP was tested from 3.9 nmol/L to 1 mumol/L at cell densities ranging from 4,500 to 15,400 cells/well and caused up to 83% inhibition of tissue factor activity. Inhibition by these proteins appeared to be influenced by cell density as well as whether the cells were intact or disrupted. Apo A-II, up to 1 mumol/L, did not inhibit the tissue factor activity of intact or disrupted fibroblasts at any cell density examined even though it did inhibit the activity of tissue factor in phospholipid vesicles. Of these inhibitors of tissue factor-dependent activation of factor X, LACI was the most effective in suppressing the generation of factor Xa activity. The effects obtained with apo A-II are clearly dependent on the nature of the tissue factor preparation with which it is tested. The disparity between the inhibitory effect of apo A-II on the activity of tissue factor reconstituted into lipid vesicles and the absence of effect on the activity of tissue factor remaining in cell membranes serves to reemphasize the necessity of reexamining results obtained with model systems using as nearly physiological reagents as possible. 相似文献
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Myosin VIIA gene: heterogeneity of the mutations responsible for Usher syndrome type IB 总被引:8,自引:1,他引:8
Levy G; Levi-Acobas F; Blanchard S; Gerber S; Larget-Piet D; Chenal V; Liu XZ; Newton V; Steel KP; Brown SD; Munnich A; Kaplan J; Petit C; Weil D 《Human molecular genetics》1997,6(1):111-116
Usher syndrome is recognized as the most frequent cause of hereditary
deaf-blindness. Usher syndrome type I (USH1), the most severe form of the
disease, is characterized by profound congenital sensorineural deafness,
constant vestibular dysfunction, and retinitis pigmentosa of prepubertal
onset. This form is genetically heterogeneous and five loci (USH1A-E) have
been mapped thusfar. However, only the gene responsible for USH1 B (which
accounts for approximately 75% of USH1 cases) has been characterized. It
encodes a long-tailed unconventional myosin, myosin VIIA, with a predicted
2215 amino acid sequence. Primers covering the complete myosin VIIA coding
sequence as well as the 3' non coding sequence were designed, allowing
direct sequence analysis of each of the 48 coding exons and flanking splice
sites in seven patients affected by USH1. Four novel mutations were thereby
identified. The possibility should now be considered of a sequence-based
prenatal diagnosis in some of the families affected by this very severe
form of Usher syndrome.
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To compare morphological changes in the umbilical cords from chronic hypertensive and preeclamptic patients having normal or pathological umbilical artery Doppler ultrasonographic results. Umbilical cords from 34 normotensive, 31 chronic hypertensive and 70 preeclamptic women with normal and abnormal Doppler flow velocity waveforms (FVW) at 35-40 gestational weeks were studied. Morphological changes in the umbilical cords were examined on formalin-fixed, paraffin-embedded sections. The total umbilical cord area, total vessel area, and wall thickness of umbilical vessels were measured in systematic random samples using unbiased stereology methods. An ANOVA test was used for statistical analysis. In the chronic hypertensive and preeclamptic groups with normal Doppler FVW, the thickness of the umbilical cord vessels remained nearly constant, whereas both the total area and the lumen area were reduced. These changes correlate with the histopathological findings, suggesting a mainly vasoconstrictive effect. By contrast, analysis of the preeclamptic group with pathologic Doppler FVW showed a comparable reduction of all parameters of the umbilical cord. Histopathological findings were related to smaller, contracted smooth muscle cells of the vessel wall, which is suggestive of a predominant hypoplastic mechanism. As a result of reduced uteroplacental perfusion, fetal hypoxia and intrauterine growth retardation become unavoidable in preeclampsia. The histopathological changes in the umbilical cord between the chronic hypertensive and preeclamptic patients depend on the Doppler results. In conclusion, the umbilical artery Doppler FVW indices provide good values for predicting intrauterine growth retardation in preeclamptic patients. 相似文献
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