BACKGROUND AND OBJECTIVE: To investigate the cause of hypofluorescent spots detected by indocyanine green (ICG) videoangiography in areas subjected to ICG-enhanced transpupillary thermotherapy in pigmented rabbits. MATERIALS AND METHODS: In 6 eyes, two similar areas were treated with transpupillary thermotherapy. A standard dose of ICG (0.5 mg/kg) was injected intravenously before treatment of the second area. Red-free photographs without further injection of ICG (first ICG videoangiography) were then performed. The first area was re-irradiated using the same parameters. Red-free photographs and a second ICG videoangiography, still without further injection of ICG, were performed. ICG was then re-injected and a third ICG videoangiography was obtained. Finally, fluorescein angiography was performed. RESULTS: The first ICG videoangiography demonstrated hyperfluorescence of the first area and normofluorescence of the second area. The second ICG videoangiography demonstrated hypofluorescence of the first area. The third ICG videoangiography showed hyperfluorescence of both areas. CONCLUSIONS: Hypofluorescence detected after re-irradiation is probably related to ICG photobleaching. 相似文献
Tamoxifen and its analogues 4-hydroxytamoxifen, toremifene, 4-
hydroxytoremifene, clomifene and droloxifene were tested for clastogenic
effects in a human lymphoblastoid cell line (MCL-5) expressing elevated
native CYP1A1 and containing transfected CYP1A2, CYP2A6, CYP2E1 and CYP3A4
and epoxide hydrolase and in a cell line containing only the viral vector
(Ho1). MCL-5 or Ho1 cells were incubated with 4-hydroxytamoxifen,
4-hydroxytoremifene, clomifene or droloxifene and the incidence of
micronuclei estimated. With MCL-5 cells there was an increase in
micronuclei with 4-hydroxytamoxifen, 4- hydroxytoremifene and clomifene but
not with droloxifene. With Ho1 cells only 4-hydroxytamoxifen and
4-hydroxytoremifene caused an increase in micronuclei. MCL-5 cells were
incubated with tamoxifen, 4- hydroxytamoxifen, toremifene, droloxifene,
clomifene or diethylstilbestrol (0.25-10 microg/ml) for 48 h and subjected
to 3 h treatment with vinblastine (0.25 microg/ml) to arrest cells in
metaphase. The incidence of cells with chromosomal numerical aberrations
(aneuploidy) was increased in cells treated with tamoxifen,
4-hydroxytamoxifen, toremifene, clomifene and diethylstilbestrol but not
droloxifene. The frequency of cells with structural abnormalities
(excluding gaps) was increased in cells treated with tamoxifen and
toremifene but not 4-hydroxytamoxifen, clomifene, droloxifene or
diethylstilbestrol. The clastogenic activities of tamoxifen (35 mg/kg),
toremifene (36.3 mg/kg), droloxifene (35.2 mg/kg) and diethylstilbestrol
(25 mg/kg) were compared in groups of four female Wistar rats. Each
chemical was dissolved in glycerol formal, administered as a single dose by
gavage and hepatocytes isolated by collagenase perfusion 24 h later. The
cells were cultured in the presence of epidermal growth factor (40 ng/ml)
for 48 h, colchicine (10 microg/ml) being added for the final 3 h of
incubation. At least 100 chromosomal spreads were examined from each animal
for the presence of numerical and structural abnormalities. The incidences
of aneuploidy following treatment were: tamoxifen 81%, toremifene 46%,
droloxifene 9.6%, diethylstilbestrol 45.7%, vehicle control 5.3%. The
incidences of chromosomal structural abnormalities excluding gaps were:
tamoxifen 4.3%, toremifene 0.8%, droloxifene 0.5%, diethylstilbestrol 0.8%,
control 0.5%. The incidence of chromosomal structural aberrations excluding
gaps in the treated animals was not statistically significantly different
from controls except in the tamoxifen-treated group. Tamoxifen (35 mg/kg
per os) and toremifene (36.3 mg/kg per os) were dosed to rats for 4 weeks
and chromosomal spreads made from hepatocytes. The incidences of aneuploidy
were: tamoxifen 94%, toremifene 57%, control 6.5%. The incidences of
chromosomal aberrations excluding gaps were: tamoxifen 12%, toremifene 1%,
control 0.5%. The incidence of tamoxifen-induced chromosomal structural
abnormalities was significantly elevated compared with control levels. The
results demonstrate that tamoxifen and toremifene are the only two drugs
tested in the study that cause chromosomal structural and numerical
aberrations in vitro and tamoxifen is the only drug that induces both these
effects in rat liver cells stimulated to divide in culture following oral
dosing. Since chromosomal mutations require cell division for their
manifestation and tamoxifen is the only compound of those tested that
causes hyperplasia in the rat liver, chromosomal aberrations and aneuploidy
in the rat liver would only be expected to occur following treatment with
tamoxifen alone, although aneuploidy could be induced by toremifene in
conjunction with a promoter such as phenobarbitone.
相似文献
A previous study from this laboratory demonstrated that treatment of
pregnant mice with 3-methylcholanthrene (MC) caused lung tumors in the
offspring at 1 year after birth, the incidence of which correlated with
fetal inducibility of Cyp1a1. Analysis by PCR amplification and allele-
specific hybridization (ASO) of paraffin-embedded tumors generated from
that study revealed the presence of point mutations in exon 1 of the Ki-
ras gene. This work has now been expanded by PCR amplification and ASO
analysis of 31 additional lesions. Point mutations were found in 37 of the
47 (79%) lesions analyzed in this and the previous study, the majority of
which were G-->T transversions in the first or second base of codon 12.
The mutational spectrum appeared to be dependent on the relative stage of
differentiation of the lesion, as both the incidence of mutation and type
of mutation produced correlated with malignant progression. Mutations
occurred in 60% of the hyperplasias, 80% of the adenomas and 100% of the
adenocarcinomas. In the lesions with mutations, GLY12-->CYS12
transversions occurred in 100% of the hyperplasias, 42% of the adenomas and
14% of the adenocarcinomas. The GLY12-->VAL12 transversions occurred in
none of the hyperplasias, 42% of the adenomas and 57% of the
adenocarcinomas. The remaining mutations, which consisted of ASP12
transitions and ARG13 transversions, occurred only in adenomas (17%) and
adenocarcinomas (29%). Between this study and our previous analyses, the
identity of the mutations obtained by ASO were confirmed by sequence
analysis of eight of the 37 lesions that harbored mutations at the Ki-ras
gene locus. There were no differences in the type or incidence of mutations
relative to the metabolic phenotype or sex of the mice. These data suggest
that mutational activation of the Ki-ras gene locus is an early event in
transplacental lung tumorigenesis, and that the type of mutations produced
by exposure to chemical carcinogens can influence the carcinogenic
potential of the tumor. This may have prognostic significance in
determining the malignant progression of the neoplasm.
相似文献
ABSTRACT An unusual presentation of acute lymphoblastic leukaemia (ALL) in a 6-year-old girl is reported. She presented with unilateral cervical lymphadenopathy, a mixed obstructive/cholestatic jaundice and a progressive pancytopenia. Ultrasound examination revealed an obstructed common bile duct with gross thickening of the wall of the duct and intrahepatic bile duct dilatation. The jaundice resolved with high dose intravenous (i.v.) methylprednisolone. It is postulated that this was due to infiltration of the common bile duct, given the failure to demonstrate any other cause for the bile duct pathology. 相似文献
Background: The purpose of this study was to determine whether combination of 1-5 [mu]g intrathecal neostigmine would enhance analgesia from a fixed intrathecal dose of morphine.
Methods: A total of 60 patients undergoing gynecologic surgery were randomized to one of five groups. Patients received 15 mg bupivacaine plus 2 ml of the test drug intrathecally (saline, 100 [mu]g morphine, or 1-5 [mu]g neostigmine). The control group received spinal saline as the test drug. The morphine group received spinal morphine as test drug. The morphine + 1 [mu]g neostigmine group received spinal morphine and 1 [mu]g neostigmine. The morphine + 2.5 [mu]g neostigmine group received spinal morphine and 2.5 [mu]g neostigmine. Finally, the morphine + 5 [mu]g neostigmine group received spinal morphine and 5 [mu]g neostigmine.
Results: The groups were demographically similar. The time to first rescue analgesic (minutes) was longer for all patients who received intrathecal morphine combined with 1-5 [mu]g neostigmine (median, 6 h) compared with the control group (median, 3 h) (P < 0.02). The morphine group (P < 0.05) and the groups that received the combination of 100 [mu]g intrathecal morphine combined with neostigmine (P < 0.005) required less rescue analgesics in 24 h compared with the control group. The incidence of perioperative adverse effects was similar among groups (P > 0.05). 相似文献
从贝母新种——宁国贝母(Fritillaria ningguoensis S. C. Chen et S. F. Yin)鳞茎中分离出五个生物碱,其中碱V是一种新的生物碱,命名为宁贝新(ningpeisine),根据理化常数和光谱解析以及衍生物制备,测定其结构为N-methyl-3β-hydroxy-5α-veratranine-6-one。其余四种生物碱鉴定为浙贝甲素(peimine,verticine,Ⅰ),浙贝乙素(peiminine,verticinone,Ⅱ),异浙贝甲素(isoverticine,Ⅲ)和贝母辛(peimisine,Ⅳ)。 相似文献