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Feasibility and Diagnostic Potential of Pulmonary Transit Time Measurement by Contrast Echocardiography: A Pilot Study 下载免费PDF全文
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Maggie L Naguib Iris Schrijver Phyllis Gardner Lynn M Pique Samiha S Doss Mona A Abu Zekry Mona Aziz Samya Z Nasr 《Journal of cystic fibrosis》2007,6(2):111-116
BACKGROUND: Knowledge about Cystic Fibrosis (CF) in Egypt is very limited. The objective of this study was to screen for CF in Egyptian children with suggestive clinical features and to identify causative genetic mutations. METHODS: Sixty-one patients from the Chest Unit, Cairo University Children's Hospital, Egypt, were included. Subjects presented with persistent or recurrent respiratory symptoms, failure to thrive, diarrhea and/or steatorrhea and unexplained persistent jaundice. Patients were screened using the CF Indicatortrade mark sweat test system (PolyChrome Medical, Inc., Brooklyn Center, MN). A quantitative sweat testing was conducted on 10 of the 12 positive patients. Seven probands and one sibling underwent molecular analysis by direct DNA sequencing of the coding region and of the intronic sequences adjacent to the 27 exons of the CFTR gene. RESULTS: Of 61 patients, 12 (20%) had positive sweat chloride screening. Ten of the 12 patients underwent quantitative sweat testing and were positive. Eight CFTR sequence changes were identified in seven affected probands and two were confirmed in one sibling by direct DNA sequencing. CONCLUSION: The study results suggest that CF is more common in Egypt than previously anticipated. Larger studies are warranted to identify the incidence, molecular basis and clinical pattern of CF in the Egyptian population. 相似文献
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Ross BD; Jacobson S; Villamil F; Korula J; Kreis R; Ernst T; Shonk T; Moats RA 《Radiology》1994,193(2):457
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δ-aminolevulinic acid dehydrase (porphobilinogen synthase) in two families with inherited enzyme deficiency 总被引:1,自引:0,他引:1
The inheritance of a deficient delta-aminolevulinic acid dehydrase (ALA-D; synonym: porphobilinogen synthase; EC 4.2.1.24) was studied in blood samples of two families over three generations. The propositus in each family was a young male acute hepatic porphyria patient with an almost complete ALA-D deficiency in the homozygous state (ALA-D activity less than 2% of controls). Heterozygotes are clinically non-affected (mean ALA-D 36% of controls). The mode of transmission could be traced by enzyme activity and electrophoretic polymorphism studies. Heterozygotes are detected by the demonstration of enzyme activity in the gel. The notation D was used for the gene expressing the defective enzyme. The "phenotype" D-1 was observed in six, the "phenotype" D-2 in three of all heterozygotes studied. These results are compatible with a single normal allele in heterozygotes responsible for enzyme activity. Quantitative assays and the segregation pattern in both families suggest a 3-allele-system for the inheritance of ALA-D deficiency. 相似文献
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Summary Porphyria cutanea tarda (PCT) was diagnosed in 27 women aged 23–48 years (mean, 35 years) who had been under oral-hormonal-contraceptive medication for 1–18 years, in 3 women under substitutional estrogen treatment in the menopause, and in 2 men aged 65 and 76 years after estrogen treatment of prostatic carcinoma. In all patients, total urinary porphyrin excretion was elevated, with an average uro-and heptacarboxyporphyrin predominance of 88%, thus proving PCT. On the patients, 84% showed a significant decrease of erythrocyte uroporphyrinogen-decarboxylase (UD; EC 4.1.1.37) activity to 50% of control levels suggesting a hereditary predisposition for the development of a chronic hepatic porphyria. Estrogens and alcohol are capable of reducing hepatic UD activity. Women with hereditary red cell UD deficiency may be regarded as predisposed to PCT when under estrogen intake, especially in combination with the potentiating influence of alcohol and chronic liver disease. Normal erythrocyte UD values in patients with additive alcohol consumption may implicate a stronger inhibitory effect for alcohol on UD, suggesting a merely toxic form of chronic hepatic porphyria. 相似文献
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Suzanne M. Jacques Faisal Qureshi Barbara J. Doss Adnan Munkarah 《Pediatric and developmental pathology》1998,1(5):380-387
Choriocarcinoma arising in the placenta, or intraplacental choriocarcinoma, has seldom been reported, particularly in the
absence of maternal metastases. Reluctance to diagnose choriocarcinoma in the presence of chorionic villi can delay diagnosis;
however, timely diagnosis of choriocarcinoma is prognostically important, both for the mother and infant. We report the clinicopathologic
findings in five mothers and infants in whom choriocarcinoma was identified in the placenta. None of the mothers had a history
of gestational trophoblastic disease in previous pregnancies. Three placentas were similar with a single small lesion grossly
suggesting a small infarct; microscopically these consisted of infarcted areas surrounded by choriocarcinoma. These three
mothers were unusual in that none had metastatic choriocarcinoma; two were treated with chemotherapy and remained disease-free;
the third was lost to follow-up shortly following delivery. The remaining two mothers had known pulmonary metastases at time
of delivery. One of these latter two placentas contained a large marginal lesion microscopically identified as choriocarcinoma.
The fifth placenta had rare microscopic foci of choriocarcinoma, and sheets of necrotic choriocarcinoma were identified in
“blood clot” submitted with the placenta. In four of the five cases the choriocarcinoma appeared to be arising from otherwise
normal chorionic villi, and in no case was there invasion of the villous stroma. All of the infants survived, and none had
evidence of choriocarcinoma. These cases support the concept that choriocarcinoma associated with otherwise normal pregnancy
arises in the placenta and may be more common than reported.
Received August 11, 1997; accepted December 8, 1997. 相似文献