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Molecular genetic techniques were utilized to examine antithrombin III (ATIII) gene status in 16 independently ascertained kindreds with hereditary ATIII deficiency. In one of these families antithrombin III deficiency is caused by hemizygosity of the ATIII locus. In the remaining 15 kindreds, two copies of the ATIII gene are present and appear to be grossly normal at the level of whole genome Southern blotting, suggesting that small deletions, insertions or limited nucleotide substitution(s) in the antithrombin III gene, or "trans- acting" defects at other loci involved in the processing, modification, and secretion of biologically active ATIII are responsible for the observed anticoagulant disorders. 相似文献
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The uptake of 57Co-cyanocobalamin (CN-Cbl) and its conversion to 5- deoxyadenosylcobalamin (Ado-Cbl), methylcobalamin (Me-Cbl), and hydroxocobalamin (OH-Cbl) has been studied in phytohemagglutinin (PHA)- transformed lymphocytes from normal subjects and patients with patients with pernicious anemia. Uptake and conversion were much greater by PHA- stimulated lymphocytes than by mature non-transformed lymphocytes. In normal cells, uptake of 57Co-CN-Cbl and synthesis of the cobalamin coenzymes were approximately linear between 3 and 48 hr incubation. Ado- Cbl was the major cobalamin formed, and after 72 hr the cells contained about twice as much Ado-Cbl as Me-Cbl. Uptake by lymphocytes from patients with untreated pernicious anemia (PA) was greater than that by normal lymphocytes, but the proportions of Ado-Cbl and Me-Cbl synthesized by each were similar. Folic acid and methyltetrahydrofolate enhanced synthesis of Me-Cbl both in normal and in PA cells, while methotrexate and 5-fluorouracil depressed it. This depression was overcome by 5-formyltetrahydrofolate, suggesting that an uninterrupted folate cycle may play an important role in Me-Cbl synthesis. 相似文献
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Sullivan EV; Lim KO; Mathalon D; Marsh L; Beal DM; Harris D; Hoff AL; Faustman WO; Pfefferbaum A 《Cerebral cortex (New York, N.Y. : 1991)》1998,8(2):117-124
Quantitative magnetic resonance imaging (MRI) studies from our laboratory
have reported that patients with schizophrenia show a widespread cortical
gray matter volume deficit, which is especially pronounced in the
prefrontal and anterior superior temporal cortices. The present study
compared two separate samples of schizophrenic patients -- 71 men from a
Veterans Administration (VA) hospital and a sample of 57 severely ill men
from a state hospital (SH) -- in an effort to test whether the pattern of
brain volume abnormalities previously observed in VA schizophrenic patients
can be generalized to other groups of schizophrenic patients. MRI-derived
brain volumes of gray matter, white matter and sulcal cerebrospinal fluid
(CSF) in six cortical regions, and CSF in the lateral and third ventricles
were computed. All MRI volumes were adjusted for normal variation in head
size and age and were expressed as standardized Z-scores, which also
permitted structures of different sizes to be compared directly. The two
schizophrenic groups displayed similar patterns of volume abnormalities:
cortical gray matter but not white matter volume deficits that were
widespread but especially notable in the prefrontal and temporal regions.
The regional gray matter deficits in the SH group were generally greater
than those in the VA group, particularly in the prefrontal and posterior
superior temporal regions. Both schizophrenic groups had abnormally large
volumes of the cortical sulci and lateral and third ventricles; however,
the SH group showed greater enlargements, the most prominent occurring in
the ventricles and temporal sulci. The overlapping patterns of cortical
gray matter deficits in the two groups provide evidence for generality of
this pattern of regional brain volume abnormalities in schizophrenia.
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