Seven cosmid-derived canine microsatellites.
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Animals↗
Biomedical subjects
B Fu
Publications and source records attributed to B Fu.
Effects of ICAM-1 antisense oligonucleotide on the tubulointerstitium in mice with unilateral ureteral obstruction.
UNLABELLED: Effects of ICAM-1 antisense oligonucleotide on the renal tubulointerstitium in mice with unilateral ureteral obstruction. BACKGROUND: To extend our previous study of the therapy of the renal lesions of unilateral ureteral obstruction (UUO) in mice by an inhibitor of intercellular adhesion molecule-1 (ICAM-1), we investigated the blocking effects of ICAM-1 antisense oligonucleotides (ASONs) on the ICAM-1 expression in mouse kidney. METHODS: First, ICAM-1 ASON was transducted into mouse renal tubular epithelial cells to investigate the effects of ICAM-1 ASON in vitro. Second, fluorescein isothiocyanate (FITC)-labeled ICAM-1 ASON was injected intravenously to determine the distribution of the ASON in vivo. Third, the expression of ICAM-1 in kidney and the changes of renal morphology were observed to investigate the therapeutic effects of ICAM-1 ASON on the UUO mice in vivo. RESULTS: The expressions of ICAM-1 in the epithelial cells induced by interleukin-1beta were inhibited by ICAM-1 ASON at the dosages of 100 and 200 nmol/L. Twenty-four hours after an introvenous injection with FITC-labeled ICAM-1 ASON, the highest level of fluorescein was detected within the proximal tubules in mouse kidney. Results of immunohistology and Northern blot showed that the ICAM-1 expression was markedly reduced in the obstructed kidney after treatment with ICAM-1 ASON. The ASON also alleviated the infiltration of inflammatory cells and accumulation of the extracellular matrix in the tubulointerstitium of UUO mice without apparent side effects. CONCLUSION: Our data demonstrate that ICAM-1 ASON is taken up primarily by the proximal tubular cells of mouse kidney. ICAM-1 ASON can selectively inhibit the ICAM-1 expression of the renal tubular cells both in vitro and in vivo.
Animals↗
Identification of monozygotic twins that are concordant for preeclampsia.
Preeclampsia is thought to be discordant in monozygotic twins. While recruiting for a genetic study into preeclampsia, we identified 4 sets of twins and a triplet gestation; all were monozygous on deoxyribonucleic acid "fingerprinting." Two twins were concordant for preeclampsia, and 2 of the triplets had pregnancy-induced hypertension, although only 1 of them had proteinuria. Hence we confirm the existence of monozygotic twins that are concordant for preeclampsia.
Diseases in Twins↗
New bisabolane sesquiterpenes from Ligularia songarica.
Phytochemical investigation of Ligularia songarica (Compositae) afforded seven new bisabolane-type sesquiterpenes. Their structures were confirmed on the basis of spectroscopic methods, especially 2D-NMR techniques, and compound 7 showed stronger antibacterial activity against Escherichia coli, Pseudomonas acruginosa and Salmonella pullorum.
Anti-Bacterial Agents↗
Abnormalities of tumor suppressor genes P16 and P15 in primary maxillofacial squamous cell carcinomas.
As members of the same gene family, tumor suppressor genes P16/CDKN2/INK4A and P15/INK4B have a high degree of structural and functional homology with both P16 and P15 proteins involved directly in the regulation of cell cycles. However, the status of P16 and P15 genes in primary maxillofacial squamous cell carcinomas (MSCC) has not been reported. Studies on abnormalities of these genes including homozygous deletion, methylation of the 5'CpG islands, and mutations were carried out in 65 primary MSCC with polymerase chain reaction (PCR), methylation-specific PCR (MSP), PCR-SSCP (single-strand conformation polymorphism), and DNA sequencing techniques. Of the 65 tumors, 22 (34%) were methylated; 7 (11%) displayed point mutations. The total frequency of alteration of the P16 gene was 43% (28/65). The methylation rate of P15 was 12% (8/65). No homozygous deletion was found in either the P16 gene or P15 gene. In all MSCC samples, almost half (49%) harbored an alteration of the P16 or P15 gene. The P16 gene was altered more frequently than P15, and therefore is inactivated by methylation or mutation in a significant proportion of MSCC. The P15 gene appeared to play a lesser role in tumorigenesis of these tumors.
Adult↗
Frequency of the fragile X syndrome in Chinese mentally retarded populations is similar to that in Caucasians.
Fragile X syndrome is recognized as the most common inherited cause of mental retardation in western countries. The prevalence of the fragile X syndrome in Asian populations is uncertain. We report a multi-institutional collaborative study of molecular screening for the fragile X syndrome from 1,127 Chinese mentally retarded (MR) individuals. We found that 2.8% of the Chinese MR population screened by DNA analysis had the fragile X full mutation. Our screening indicated that the fragile X syndrome prevalence was very close to that of Caucasian subjects. In addition, we found that 62.5% of fragile X chromosomes had a single haplotype for DXS548-FRAXAC1 (21-18 repeats) which was present in only 9.7% of controls. This unique distribution of microsatellite markers flanking the FMR1 CGG repeats suggests that the fragile X syndrome in Chinese populations, as in the Caucasian, may also be derived from founder chromosomes.
Alleles↗
Length bounded molecular computing.
The length of DNA strands is an important resource in DNA computing. We show how to decrease strand lengths in known molecular algorithms for some NP-complete problems, such as like 3-SAT and Independent Set, without substantially increasing their running time or volume.
Algorithms↗
An O(2n) volume molecular algorithm for Hamiltonian path.
We design volume-efficient molecular algorithms for all problems in #P, using only reasonable biological operations. In particular, we give a polynomial-time 0(2(n)n2log2n)-volume algorithm to compute the number of Hamiltonian paths in an n-node graph. This improves Adleman's celebrated n!-volume algorithm for finding a single Hamiltonian path.
Algorithms↗
Integrin alphavbeta3-RGDS interaction mediates fibrin-induced morphological changes of glomerular endothelial cells.
BACKGROUND: In our previous studies, we found that intraglomerular deposition of fibrin and its metabolites was related to glomerular sclerosis and reduced renal function. It has been reported that both overlying and underlying fibrin may induce specific morphological changes of cultured endothelial cells from large blood vessels. The dependency of these morphological changes on the integrin alphavbeta3-arginyl-glycyl-aspartyl-serine (RGDS) interaction is still controversial. We hypothesized that glomerular endothelial cells (GECs) stimulated by fibrin might undergo morphological changes through an integrin alphavbeta3-RGDS interaction. Methods. In vitro studies were performed to examine the growing status of GECs stimulated by overlying and underlying fibrin gels in the presence or absence of the following: 50 microg/ml anti-alphavbeta3 integrin monoclonal antibody 23C6 or nonimmune mouse IgG, 1 mg/ml synthetic RGDS or arginyl-glycyl-glycyl-serine (RGGS) peptide, 10 mg/ml sodium heparin, 100 microg/ml cycloheximide, and 10 microM actinomycin D. Fast protein liquid chromatography (FPLC)-purified fibrinogen and the third to fifth passages of human GECs were also used in this study. RESULTS: GECs developed capillary tube structure after 60 hours of culturing on fibrin gels, and GECs cultured on gelatin-coated plates displayed a monolayer of cobblestone-like cells in the presence or absence of 23C6 and synthetic RGDS peptide. Fibrin-induced capillary tube formation was promoted by 23C6 and inhibited by RGDS peptide, cycloheximide, and actinomycin D. Disorganization of the GEC monolayer was induced by overlying fibrin, but was not induced by overlying agarose gels and glass cover slips or culturing in fibrinogen, 0.05 NIH U/ml thrombin, fibrin supernatants, as well as in fibrin degradation products. Disorganization of GEC monolayer can be induced by both des-AA-fibrin and des-AABB-fibrin and was unaffected by heparin. Furthermore, both 23C6 and synthetic RGDS peptide prevented disorganization of GECs induced by overlying fibrin, whereas nonimmune mouse IgG, synthetic RGGS peptide, cycloheximide, and actinomycin D had no similar effect. CONCLUSIONS: GECs cultured on fibrin gels may develop capillary structure spontaneously, and GECs covered by fibrin gels may undergo disorganization. Our data suggest that these GEC morphological changes are mediated by an integrin alphavbeta3-RGDS interaction.
Antibodies, Monoclonal↗
Effects of air abrasion and acid etching on the microleakage of preventive Class I resin restorations: an in vitro study.
PURPOSE: To evaluate the effects of air abrasion, acid etching, and the combination of both procedures on the microleakage of preventive Class I resin restorations. MATERIALS AND METHODS: Eighty-four extracted human molar teeth were randomly assigned to seven groups with 12 teeth each. Occlusal fissures were opened with a diamond bur and etched with phosphoric acid (groups I and VI); prepared with a diamond bur without etching (group VII); air abraded with the KCP 1000, using 50-micron aluminum oxide particles without etching (group II), and with phosphoric acid etching (group III); or air abraded with 27-micron aluminum oxide particles without etching (group IV), and with phosphoric acid etching (group V). Preparations were filled with a low-viscosity resin composite (Liquicoat, groups I to V) or with a low-viscosity polyacid-modified resin composite (PrimaFlow, groups VI and VII). Six teeth in each group were thermocycled (5 degrees-55 degrees C, 2500 cycles). Dye penetration (methylene blue) was evaluated in ordinal scale. RESULTS: The number of non-thermocycled and thermocycled specimens revealing no microleakage was as follows: group I, 6 and 1; group II, 2 and 2; group III, 4 and 3; group IV, 0 and 0; group V, 1 and 0; group VI, 3 and 2; and group VII, 0 and 0, respectively. No significant differences existed between the thermocycled specimens and non-thermocycled specimens, except within group I. CLINICAL SIGNIFICANCE: Results indicated that (1) air-abrasion treatment with 27-micron particles is less effective in preventing microleakage compared to 50-micron particles, (2) air abrasion should be combined with acid etching to reduce microleakage of preventive Class I resin restorations, and (3) acid etching significantly reduces microleakage of the low-viscosity polyacid-modified resin composite in preventive Class I restorations.
Acid Etching, Dental↗
Factor V Leiden and thermolabile methylenetetrahydrofolate reductase gene variants in an East Anglian preeclampsia cohort.
Preeclampsia is a heritable condition that develops as a result of widespread vascular endothelial dysfunction. The thrombotic tendency in this condition has suggested a number of candidate genes, and there have been recent reports of positive association with the Leiden variant of factor V and the thermolabile variant of methylenetetrahydrofolate reductase. We attempted to reproduce these results in a large cohort of well-characterized women with preeclampsia, recruited prospectively within the East Anglian region of the United Kingdom. Women in the preeclampsia cohort (n=283) were genotyped for both the Leiden variant (G1691A) of factor V and the thermolabile variant (C677T) of methylenetetrahydrofolate reductase. Genotype and allele frequencies were compared with those of 2 control groups, one consisting of women recruited prospectively (n=100) from the same maternity hospital as the subjects and another consisting of normotensive women (n=100) from East Anglia. No significant differences were detected. Specifically, the carrier rate for the Leiden variant was 5.3% in the preeclampsia group and 5. 5% in the combined control group. T677 homozygotes for methylenetetrahydrofolate reductase were 11% and 11.5% in the 2 groups, respectively. We conclude that there is no evidence of association of preeclampsia with either of these 2 polymorphisms in our study population.
Base Sequence↗
Genetic deletion of AT2 receptor antagonizes angiotensin II-induced apoptosis in fibroblasts of the mouse embryo.
To examine whether angiotensin II (Ang II) can trigger apoptosis via Ang II type 2 (AT2) receptor, two genotypes of skin fibroblasts cultured from the AT2 receptor gene targeting homozygous (AT2-/-) and wild-type (AT2+/+) mouse embryos, respectively, were studied when exposed to Ang II. In the AT2+/+ fibroblasts, mRNA expression of the AT2 receptor was modulated by Ang II in a dose-dependent manner and apoptosis appeared with the convincing features of internucleosomal DNA fragmentation and DNA content decrease after stimulation with Ang II, whereas Ang II had no significant impact on the AT2-/- fibroblasts due to the AT2 receptor gene deletion. This is the first report using a gene targeting study to demonstrate that Ang II induces apoptosis through the AT2 receptor in the fibroblasts of the mouse embryo.
Angiotensin II↗
Linkage of Gordon's syndrome to the long arm of chromosome 17 in a region recently linked to familial essential hypertension.
Gordon's syndrome (GS) is a salt-sensitive, hyperkalaemic, familial hypertension syndrome which may masquerade in milder forms as essential hypertension. The response of hyperakalaemia to dietary salt restriction and to mineralocorticoids is heterogeneous, suggesting genetic heterogeneity. In a recently published study using small pedigrees, possible linkage of GS to chromosomes 1 and 17 was described. Studying the largest pedigree so far reported with GS, and using fluorescent-labelled microsatellite markers, we sought evidence of linkage to chromosomes 1 and 17. In this family there was no segregation of GS with any of the markers for chromosome 1. On chromosome 17, however, evidence of linkage was found with a maximum multipoint LOD score of 2.4 (the maximum LOD possible from the pedigree) over markers D17S250 and D17S934. This represents strong evidence in this pedigree for a responsible gene mutation on the long arm of chromosome 17. Recent reports of linkage for essential hypertension and, especially, familial essential hypertension within the same area of chromosome 17 containing the D17S934 marker raise the possibility that the same gene may be responsible for familial essential hypertension and for Gordon's syndrome.
Chromosomes, Human, Pair 1↗
[Effects of Arg-Gly-Asp-Ser (RGDS) tetrapeptide on apoptosis-related genes in glomerular mesangial cells].
OBJECTIVE: To investigate the effects of Arg-Gly-Asp-Ser (RGDS) tetrapeptide on the expressions of apoptosis-related genes interleukin-1 beta-converting enzyme (ICE) and bcl-2 in human glomerular mesangial cells, so as to provide experimental evidence for regulating proliferation and apoptosis of mesangial cells with RGD-containing polypeptide. METHODS: Propidium iodide staining was used to observe the condensation and fragmentation of apoptotic nuclei. The internucleosomal DNA fragmentation was detected by DNA electrophoresis on agarose gel. The expressions of ICE and Bcl-2 were determined by reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: After ten hours of incubation, the glomerular mesangial cells treated with RGDS peptide displayed features consistent with apoptosis, such as nuclear condensation and fragmentation, and a regularly spaced "ladder" shape of genomic DNA electrophoresed. And RT-PCR showed that expressions of both ICE and Bcl-2 mRNAs were apparently increased in RGDS treated group, compared with that of the control group. CONCLUSION: These results demonstrated for the first time that RGDS peptide was able to induce apoptosis in human glomerular mesangial cells, during the process ICE and bcl-2 genes may have an important regulating role.
Apoptosis↗
Detection of filarial larvae in mosquitoes with oligonucleotide probe.
OBJECTIVE: To investigate a new way to detect filarial larvae in mosquitoes and apply it to the surveillance of filariasis. METHODS: An oligonucleotide probe that was species-specific to W. malayi was synthesized and marked with 32P using molecular biological technique. Then the probe was tested with dot hybridization in detection of W. malayi filarial larvae from mosquitoes. RESULTS: The minimal detectable limit was found to be 2 ng DNA of filarial larvae or microfilaria (Mf.), with no cross reaction with other animal filariae. A single larva can be detected when infected mosquitoes were tested one by one. One infected mosquito can be detected from a group of 20 mosquitoes tested together. CONCLUSIONS: Our probe is sensitive and specific. It is practical to apply our probe to mosquito surveillance in Brug's filariasis endemic areas.
Animals↗
RGD-containing peptides trigger apoptosis in glomerular mesangial cells of adult human kidneys.
Substantial evidence was given that different Arg-Gly-Asp (RGD)-containing peptides, linear Arg-Gly-Asp-Ser (RGDS) and cyclic Arg-Gly-Asp-Phe (RGDF), which are sequences present in fibronectin and vitronectin and which can bind alpha5beta1 and alpha(v)beta3 integrins, respectively, both induced apoptosis and expression of interleukin-1beta-converting enzyme (ICE) in cultured glomerular mesangial cells from adult human kidneys, with consistent apoptosis features appearing as nuclei condensation and fragmentation, internucleosomal DNA fragmentation, and DNA content decrease. These results indicated that both fibronectin and vitronectin may be important in the survival of human glomerular mesangial cells and that stable cyclic RGD(D)FV peptide may be a candidate to be used for regulating apoptosis in vivo.
Adult↗
[Mechanisms of thrombin induced proliferation and detachment of glomerular endothelial cells].
To clarify the mechanisms of thrombin contributing to the progression of glomerular diseases by injuring glomerular endothelial cells (GECs), we studied the effects of thrombin on GECs in vitro. Cell proliferation was detected with MTT incorporation, total plasminogen activator (PA) and tissue type PA (t-PA) activities were detected with fibrin plate and chromatogenic substrate methods and fibronectin was detected with ELISA as well as indirect immunofluore scence. 0.4-3.2 NIH U/ml thrombin promoted GEC proliferation significantly (P < 0.05). Thrombin promoted cell detachment, which can be inhibited by hirudin or aprotinin. Thrombin enhanced total PA and t-PA activities of GECs significantly (P < 0.01). Fibronectin in the supernatants of thrombin-stimulated GECs decreased significantly (P < 0.01) and in the extracellular compartment also decreased. The decrease was inhibited by hirudin and aprotinin. In conclusion, thrombin can induce GEC proliferation and GEC detachment. The latter is probably related to PA-mediated over-degradation of extracellular matrices such as fibronectin, which are needed for cell attachment.
Cell Division↗
[Hyperosmotic glucose and antibiotics induce production of plasminogen activator inhibitor and expression of TGF beta mRNA by rat peritoneal mesothelial cells].
To investigate the mechanism of fibrosis in peritoneal dialysis, we observed the effects of the hyperosmotic glucose and antibiotics such as gentamicin and cefazolin on rat peritoneal mesothelial cells with cell culture, fibrin-plate lyzing and Northern blotting analysis method. The peritoneal mesothelial cells may express PAI-1 mRNA. The expression of PAI-1 mRNA in peritoneal mesothelial cells and activities of PAI in the supernatants were enhanced by 11.2 mmol/L glucose, gentamicin and cefazolin at 12 hr. By 24 hr, the activity of PAI-1 also increased in the supernatants with 11.2 mmol/L glucose. The expression of PAI-1 mRNA and production of PAI activities by the peritoneal mesothelial cells were increased by gentamicin, and the TGF-beta mRNA increased in the peritoneal mesothelial cells was induced by 11.2 mmol/L glucose, gentamicin and cefazolin. The results suggested that 11.2 mmol/L glucose, gentamicin and cefazolin may increase the expressions or productions of PAI and TGF-beta in peritoneal mesothelial cells. So by perosmotic glucose, cefazolin and gentamicin promote the peritoneal fibrosis in patients with CAPD.
Animals↗