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Keratography as a guide to selective suture removal for the reduction of astigmatism after penetrating keratoplasty 总被引:2,自引:0,他引:2
After penetrating keratoplasty in 52 eyes, keratography refraction and keratometry were used to select appropriate interrupted sutures for removal in order to reduce astigmatism. All eyes had one continuous and either 12 or 16 interrupted nylon sutures. The keratographs were examined retrospectively and separated into six groups on the basis of similar mire patterns. The removal of single sutures associated with three of these patterns reduced astigmatism by the following average amounts: symmetrical oval pattern, 0.44 diopters (D); D-shaped oval pattern, 2.07 D; and focal indentation pattern, 6.60 D. The other three patterns--mildly disrupted mires, incomplete mires, and uninterpretable mires--did not allow quantification of results. Examples of these keratographic patterns are presented and recommendations are made for their use in the management of astigmatism following penetrating keratoplasty. 相似文献
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Perfluorochemicals as US contrast agents for tumor imaging and hepatosplenography: preliminary clinical results 总被引:3,自引:0,他引:3
Mattrey RF; Strich G; Shelton RE; Gosink BB; Leopold GR; Lee T; Forsythe J 《Radiology》1987,163(2):339-343
In animals, perfluorochemicals (PFCs) are effective ultrasound (US) contrast agents that produce hepatic, splenic, and tumor enhancement. The use of Fluosol-DA 20%, an emulsion of perfluorodecalin and perfluorotripropylamine, was studied in nine non-critically ill patients with cancer who had liver lesions. US studies without Fluosol were compared with studies obtained 24, 48, and 72 hours after Fluosol infusion. Vital signs and extensive laboratory analyses are performed before and after Fluosol infusion. Liver metastases from colonic, pancreatic, and gastric carcinoma exhibited rim or diffuse enhancement after a Fluosol dose of 1.6 g/kg or greater. Fluosol produced echogenic enhancement of the liver and spleen relative to kidney at a dose of 2.4 g/kg, allowing the detection of nonenhancing lesions. In addition, Fluosol at a dose of 1.6 g/kg or greater allowed detection of lesions not seen before contrast medium was administered in three of the seven patients studied. There was a mild increase in the level of serum glutamic oxaloacetic transaminase in two patients, one given 2.4 and the other 3.2 g/kg of Fluosol. Mild and transient allergic reactions without change in vital signs were experienced by two patients. 相似文献
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Screening for proteins with polyglutamine expansions in autosomal dominant cerebellar ataxias 总被引:2,自引:8,他引:2
Stevanin G; Trottier Y; Cancel G; Durr A; David G; Didierjean O; Burk K; Imbert G; Saudou F; Abada-Bendib M; Gourfinkel-An I; Benomar A; Abbas N; Klockgether T; Grid D; Agid Y; Mandel JL; Brice A 《Human molecular genetics》1996,5(12):1887-1892
Expansion of trinucleotide CAG repeats coding for polyglutamine has been
implicated in five neurodegenerative disorders, including spinocerebellar
ataxia (SCA) 1 and SCA3 or Machado-Joseph disease (SCA3/MJD), two forms of
type I autosomal dominant cerebellar ataxias (ADCA). Using the 1C2 antibody
which specifically recognizes large polyglutamine tracts, particularly
those that are expanded, we recently reported the detection of proteins
with pathological glutamine expansions in lymphoblasts from another form of
ADCA type I, SCA2, as well as from patients presenting with the distinct
phenotype of ADCA type II. We now have screened a large series of patients
with ADCA or isolated cases with cerebellar ataxia, for the presence of
proteins with polyglutamine expansions. A 150 kDa SCA2 protein was detected
in 16 out of 40 families with ADCA type I. This corresponds to 24% of all
ADCA type I families, which is much more frequent than SCA1 in this series
of patients (13%). The signal intensity of the SCA2 protein was negatively
correlated to age at onset, as expected for an expanded and unstable
trinucleotide repeat mutation. The disease segregated with markers closely
linked to the SCA2 locus in all identified SCA2 families. In addition, a
specific 130 kDa protein, which segregated with the disease, was detected
in lymphoblasts of patients from nine families with ADCA type II. It was
also visualized in the cerebral cortex of one of the patients,
demonstrating its translation in the nervous system. Finally, no new
disease-related proteins containing expanded polyglutamine tracts could be
detected in lymphoblasts from the remaining patients with ADCA or isolated
cases with cerebellar ataxia.
相似文献