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Biomedical subjects

H Cui

Publications and source records attributed to H Cui.

At least 91 records · Page 5Linked to original sources

Identification of predictors for lower extremity vein graft stenosis.

BACKGROUND: The cause of intrinsic vein graft stenosis, which develops in at least 20% of infrainguinal autogenous bypass grafts during the intermediate follow-up interval, is unknown. We performed standard duplex surveillance of all lower extremity bypass grafts and evaluated the potential of comorbid patient risk factors that might predict development of vein graft flow disturbance or high-grade graft stenosis. METHODS: Patients with at least 6 months of postoperative duplex surveillance were identified through our vascular registry. The association of clinical and hemodynamic profiles of graft performance were compared with specific patient risk factors, including demographics, cigarette smoking, antihypertensive medical therapy, type and quality of conduit, degree of ischemia, bypass run-off, and presence of infection, using stepwise logistic regression analysis. RESULTS: Ninety-three patients (55 male, 38 female; mean age 69) underwent 100 infrainguinal bypasses. Twenty-six high-grade graft stenoses (>70%) were identified in 26 patients during follow-up (mean 21 months) by graft-flow peak systolic velocity (PSV) >300 cm/sec on more than one duplex examination, and were electively revised. Graft flow disturbances (180 cm/sec >PSV <300 cm/sec) were identified in an additional 13 grafts (6 regressed, 7 observed). The need for graft revision was associated with an early graft flow disturbance (P = 0.02), or drop in ankle-brachial index >0.15 (P = 0.03), and the use of an alternative conduit in 13 of 100 grafts (P = 0.04). Only smoking was associated with the development of a duplex detected graft flow disturbance during follow up (P = 0.03). CONCLUSION: Grafts with early flow disturbances warrant close duplex surveillance to identify graft-threatening stenosis. Risk factors that may predict future lower extremity bypass graft stenosis are smoking and the use of alternative bypass conduits.

Aged↗

DNA based biosensors.

Compared to advances in enzyme sensors, immunosensors, and microbial biosensors, relatively little work exists on DNA based biosensors. Here we review the DNA based biosensors that rely on nucleic acid hybridization. Major types DNA biosensors--electrochemical, optical, acoustic, and piezoelectric--are introduced and compared. The specificity and response characteristics of DNA biosensors are discussed. Overall, a promising future is foreseen for the DNA based sensor technology.

Journal Article↗

[The comparison of selenium status between the children suffered from pneumonia and the normal children from kindergarten].

In order to investigate the relationship between selenium (Se) status and pneumonia children, the levels of Se and glutathione peroxidase (GSH-Px) in plasma and white blood cells and Se content in urine were determined in 57 cases with pneumonia and 85 control children under 10 years old. The results showed that the levels of Se and GSH-Px in plasma and white blood cell in the group of pneumonia were significantly lower, but the content of Se in urine was higher. Se content and GSH-Px activity in white blood cells of patients during crisis were significantly lower than those of patients during convalescence.

Adolescent↗

Suppression of malignant phenotype of a transformed mouse mammary epithelial cell line (11A1) by tumor suppressor gene RB.

A malignant transformed mammary epithelial cell line (11A1) was transfected with liposome encapsulated eukaryotic expression plasmid pCMV-neo-RB, yielding 4 constant clones which have obvious phenotypic reversion changes, and named 11A1-R1-R4 respectively. Further experiments showed that the 11A1-R1 behaved like normal epithelial cells in both morphological and biological characteristics, with decreased clonogenicity in solid argar medium as well as decreased tumorigenicity. Northern blot hybridization showed increased expression of RB gene and decreased expression of c-myc gene in 11A1-R1, 11A1-R2 cells compared to 11A1 cells. This was an ideal phenotypic reversion model for epithelial transformed cell line and demonstrated that the RB gene can reexpress and suppress malignant phenotype in RB inactive cells.

Animals↗

[Preparation and property investigations of nanosized titanium oxide microcrystals].

A naosized TiO2 powder was successfully prepared by the hydrolysis of titanium isopropoxide through sol-gel process. The microstructure of TiO2 powder was investigated by transmission electron microscopy and X-ray diffraction. Both anatase and rutile phases were found in TiO2 powder annealed for 1 hour at 600 degrees C. The characteristics of X-ray photoelectron spectra and infrared spectra could be affected by the size and aggregation state of the microsrystalc constituting the TiO2 powder.

English Abstract↗

Functional expression of Fas (CD95) protein in autoimmune lpr mice.

Fas (CD95) has been shown in multiple systems to play a critical role in deletion of autoreactive lymphocytes by transducing cell death signals. The role of Fas in clonal deletion may best be exemplified in autoimmune lpr mice, in which a defect in the lpr gene leads to persistence of autoreactive clones in the periphery. Since negative selection in the lpr thymus appears not to be ablated, it has been suggested that Fas is not essential to thymic negative selection. A recent study has shown that lpr thymocytes express low levels of Fas protein. However, it is not determined whether this low level of Fas could transduce the death signal. This is a critical issue for the hypothesis that lpr thymocyte negative selection does not involve a Fas-death pathway. Here, we demonstrate that thymocytes, but not peripheral lymphocytes, from 2- to 4-week-old C3H.MRL-lpr mice are killed by Fas-dependent cytotoxicity at levels commensurate with the low levels of Fas expression. The level of lpr thymocyte killing is approximately 20% of that observed in wild-type controls. Both Fas staining and Th1 cytotoxicity are specifically blocked by a recombinant Fas-hIgG fusion protein. Thymocyte subset analyses indicate that Fas is expressed primarily on CD4+/CD8+ lpr thymocytes and that CD4+/CD8+ lpr thymocytes are the primary targets for Th1 effector cytotoxicity. The data suggest that the lpr mutation is functionally "leaky" and that the demonstration of normal negative selection in lpr thymocytes should not be taken as evidence that Fas is not involved in clonal deletion in the thymus.

Animals↗

Precolumn fluorescence derivatization of the antagonist [Arg6,D-Trp7,9,MePhe8]-substance P[6-11] with benzoin in high-performance liquid chromatography and selective detection of arginine-containing fragments in its degradation products.

Precolumn fluorescence derivatization for the determination of the antagonist [Arg6,D-Trp7,9,MePhe8]-Substance P¿6-11¿ (antagonist G) using benzoin in HPLC was studied. Under the conditions chosen (0.067 M NaOH, heating at 100 degrees C for 10 s), a good yield of fluorescent derivatives was obtained and no methodology-related degradation occurred. The detection limit of antagonist G was 0.21 nmol/ml. The method has been applied to the selective and sensitive detection of arginine-containing fragments in degradation products of antagonist G.

Amino Acid Sequence↗

Regulation of T-cell death genes: selective inhibition of FasL- but not Fas-mediated function.

Activation-induced cell death (AICD) requires coexpression of Fas and FasL. Hybridoma T-cells express detectable FasL mRNA 3 to 5 hr after culture in anti-CD3-coated wells. High and steady expression of FasL mRNA was observed after 8-10 hr of activation. Expression of FasL cytotoxicity and AICD is consistent with the time-course of FasL mRNA induction. Fas-Ig was effective in inhibiting AICD when added no later than 5 hr after activation, but was ineffective when added after 8-10 hr of activation. These observations suggest that FasL gene activation is a critical step for AICD. By contrast, Fas was constitutively expressed and the time-course study did not support the idea that up-regulation of Fas is critical for AICD. The critical role of FasL gene activation for AICD was confirmed by studies using inhibitors of AICD. Dexamethasone (Dex) inhibited FasL induction and Fas up-regulation, but not basal Fas expression of hybridoma T-cells. All-trans retinoic acid (RA) inhibited FasL induction, but had little effect on Fas up-regulation. Both agents inhibited FasL cytotoxicity. The Fas-mediated death pathway distal to Fas/FasL interactions remained intact in the protected hybridoma T-cells. These results demonstrate that FasL gene activation, but not Fas up-regulation, is critical for AICD and that Dex and all-trans RA selectively inhibits FasL but not Fas function. The system may prove useful for the identification of critical factors regulating T-cell death genes. It may also serve as a useful system to study gene regulation in AICD-dependent phenomena.

Animals↗

Characterization of lpr-derived T cell hybridomas: Fas-deficient hybridomas are deathless, growth-arrested, and cytotoxic upon activation.

T cell hybridomas that are deathless upon TCR crosslinking were generated from lpr mice. The deathless hybridomas (1.4 and 5D5) expressed extremely low Fas even after anti-CD3 activation, whereas activation-induced cell death (AICD) was observed for Fas-expressing hybridomas. The deathless hybridomas were activated to produce FasL and IL-2, indicating that the intrinsic defect in Fas expression or up-regulation resulted in AICD blockade. The deathless hybridoma cells expressed longer and stronger FasL cytotoxicity than AICD-sensitive hybridomas. Although deathless, activated 5D5 cells were arrested at the G1/S border. Growth arrest lasted for at least 5 days, but some cells eventually recovered and proliferated. The deathless 5D5 cells were used to demonstrate that AICD includes a fratricidal mechanism that kills AICD-sensitive bystanders. The deathless T cell hybridomas are useful tools for studying T cell activation-dependent functions sensitive to AICD.

Animals↗

Dielectric properties of human fetal organ tissues at radio frequencies.

The in vitro dielectric properties of human fetal organ tissues were measured in the frequency range from 100 kHz to 500 MHz at 24 degrees C. The dielectric measurements were performed by using a network analyzer (HP4195A) and a coaxial line capacitive sensor. The tested samples, including skin, muscle, heart, lung, liver, kidney, spleen, and brain tissues, were obtained from the legal abortion of five women with 14-16 weeks gestation periods.

Abortion, Legal↗

Fluoranthene-induced apoptosis in murine T cell hybridomas is independent of the aromatic hydrocarbon receptor.

Recent studies suggest that environmental chemicals such as polycyclic aromatic hydrocarbons (PAH) compromise the immune system in part through the induction of programmed cell death (apoptosis). Nevertheless, mechanisms through which PAH induce apoptosis remain elusive. In particular, the role of the 8S AhR remains controversial and the nature of intracellular signal transduction in PAH-induced apoptosis remains largely undefined. To extend previous studies to the T cell compartment and to develop a clonal system in which intracellular signals leading to PAH-induced apoptosis can be dissected, the ability of fluoranthene, a ubiquitous, but less well-studied PAH, to induce apoptosis in murine T cell hybridomas was evaluated. Particular emphasis was placed on the role of the 8S AhR. The data indicate that (1) three of four hybridomas studied undergo apoptosis within 8 hr of fluoranthene exposure; (2) fluoranthene induces growth arrest concurrent with apoptosis; (3) at doses sufficient to induce lymphocyte apoptosis, fluoranthene does not induce AhR nuclear translocation in cells expressing high AhR levels; (4) fluoranthene-responsive hybridomas do not express AhR mRNA or protein; (5) the Ca2+ chelating agent EGTA partially inhibits fluoranthene-induced apoptosis. These results (1) indicate the immunosuppressive potential of fluoranthene; (2) support a role for apoptosis in PAH immunotoxicity; (3) demonstrate that fluoranthene-mediated T cell death and growth arrest are AhR independent; and (4) illustrate similarities between PAH- and antigen-specific receptor-mediated apoptosis. These findings encourage consideration of AhR- independent events in PAH risk assessment.

Animals↗

A light and electron microscopic radioautographic study on RNA synthesis in the retina of chick embryo.

The incorporation of 3H-uridine into RNA of chick embryo retina was studied by light and electron microscopic radioautography. The numbers of silver grains were counted over the nucleus, nucleolus and cytoplasm of the cells in three different regions of the same retina of 2, 3, 4, and 7 day chick embryos. The results showed an increase of 3H-uridine incorporation from embryonic day 2 to 7. In every stage of development of the chick embryo retina, the number of silver grains was higher in the anterior than in the other two regions of the retina. In the three cell compartments of every embryo group, the number of silver grains was higher in the nucleus than in the nucleolus and cytoplasm. The results show further that the grains were less in the cytoplasm of the retinal cells of the day 2 embryo group and higher in the other groups especially in the day 7 embryos. Ultrastructural changes were also observed during the studied period of retina development.

Animals↗

Utility of routine carotid duplex screening in patients who have claudication.

PURPOSE: The recently published Asymptomatic Carotid Atherosclerosis Study (ACAS) demonstrated the benefit of performing carotid endarterectomy in selected asymptomatic patients who have > 60% carotid stenoses. It therefore becomes clinically important to identify the subgroups of patients who have a sufficiently high incidence of high-grade carotid stenosis to warrant routine carotid duplex screening. METHODS: To determine the incidence of asymptomatic carotid disease in patients who had a chief complaint of claudication, we evaluated 188 patients who had claudication and no history of cerebrovascular symptoms. After a complete history was taken and a physical examination performed, patients underwent standard lower-extremity noninvasive vascular laboratory studies and carotid duplex scanning. Carotid duplex findings were interpreted by the Strandness criteria. Associated atherosclerotic risk factors were assessed (patient age, male sex, diabetes, hypertension, smoking history, lipid levels, history of coronary artery disease, coronary or vascular surgery, and family history of cerebrovascular disease). Presence of a carotid bruit was also noted. Univariate analysis, logistic regression, and odds ratios were performed to identify subgroups of patients that had an increased incidence of significant carotid disease. RESULTS: Of the 188 patients with claudication who were screened, 8% had an internal carotid artery stenosis of 16% to 49%, 21.8% had a stenosis that exceeded 50%, and 2.7% had an occluded internal carotid artery. The presence of a carotid bruit on physical examination was predictive of a > or = 50% internal carotid artery stenosis (p = 0.027). The ankle-brachial index was highly predictive of the presence of carotid stenoses in an inverse relationship (p = 0.001). Patient age approached significance (p = 0.143). Patients older than 65 years of age who had claudication, an ankle-brachial index less than 0.7, and a carotid bruit had a 45% incidence of significant carotid disease. The atherosclerotic risk factors of male sex, diabetes, hypertension, hyperlipidemia, smoking history, coronary history, previous coronary or vascular surgical history, and family history were not predictive of the presence of a > 50% carotid stenosis. CONCLUSIONS: In patients who seek medical attention with the chief complaint of claudication and who have no cerebrovascular symptoms, there is a 24.5% incidence of a > 50% internal carotid artery stenosis or occlusion on duplex examination. Select subsets of these patients have upwards of a 45% incidence of significant asymptomatic carotid disease. All patients who seek medical attention with claudication should therefore undergo routine carotid duplex screening to detect asymptomatic high-grade stenosis.

Aged↗

Allele-specific in situ hybridization (ASISH) analysis: a novel technique which resolves differential allelic usage of H19 within the same cell lineage during human placental development.

Precursory studies of H19 transcription during human foetal development have demonstrated maternally derived monoallelic expression. Analyses in extra-embryonic tissues, however, have been more equivocal, with discernible levels of expression of the paternal allele of H19 documented in the first trimester placenta. By refining the in situ hybridization technique we have developed an assay to enable the functional imprinting status of H19 to be determined at the cellular level. This assay involves the use of oligonucleotide DNA probes that are able to discriminate between allelic RNA transcripts containing sequence polymorphisms. Biallelic expression of H19 is confined to a subpopulation of cells of the trophoblast lineage, the extravillous cytotrophoblast, while the mesenchymal stroma cells maintain the imprinted pattern of monoallelic expression of H19 throughout placental development. This data demonstrates that the low level of paternal H19 expression previously detected in normal human placenta is not due to a random loss of functional imprinting, but appears to result from a developmentally regulated cell type-specific activation of the paternal allele. In addition, biallelic expression of H19 does not seem to affect the functional imprinting of the insulin-like growth factor II gene, which is monoallelically expressed at relatively high levels in the extra-villous cytotrophoblasts. These results imply that the allelic usage of these two genes in normal human placental development may not be directly analogous to the situation previously documented in the mouse embryo.

Alleles↗

Expression levels of the insulin-like growth factor-II gene (IGF2) in the human liver: developmental relationships of the four promoters.

We have studied the insulin-like growth factor-II gene (IGF2) promoter usage in normal human liver from fetal to late adult life by quantifying the specific transcripts by RNase protection assays using exon-specific probes. While the fetal liver uses only three promoters (P2, P3, P4) for the transcription of IGF2, all four promoters can be used from the age of 2 months after birth. The levels of the individual promoter transcripts vary substantially during development and the P3 promoter, which is a highly active fetal promoter, was not used by all the investigated adult patients but was detected in 30% of the adult group as a whole. The P1 promoter, which has previously been considered as the only one responsible for IGF2 transcription in the postnatal/adult liver, displayed a trend of increasing relative and absolute activity throughout life, but in some adult cases it was found to be less active than the P4 promoter. The P4 promoter displayed an age-related trend of decreasing activity from a very high fetal level, but individual exceptions were apparent. The P2 promoter transcript, peaking at the age of 2 months, showed a relatively even absolute amount from 18 months onwards. Thus, while P2 and P3 were both found to reach their highest activity after birth, the P4 promoter displayed its highest transcription at the fetal stage. The total IGF2 transcription, primarily from P2, P3 and P4, was found to peak shortly after birth. After this age, the P3 promoter transcript declined most rapidly and a low or zero amount was detected in adulthood. From the age of 18 months to old adulthood the total IGF2 mRNA, derived primarily from P1, P2 and P4, displayed a relatively even amount (approximately one tenth) of that seen at the peak at 2 months. This data may be important in relation to translatability of the various IGF2 transcripts.

Adult↗