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Biomedical subjects

Q L Cheng

Publications and source records attributed to Q L Cheng.

13 recordsLinked to original sources
PubMed2000

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↗
PubMed2000

[Expression of citrate transporter mRNA in the kidneys of rats with metabolic acidosis].

The purpose of the present study was to examine whether metabolic acidosis affects the expression of rat renal Na(+)/citrate cotransporter. Female Wistar rats were pair-fed with normal rat chow and drinking water (control) or water with 0.28 mol/L NH4Cl (metabolic acidosis). The mRNA of two renal Na(+)/citrate cotransporters, which were respectively expressed on apical and basolateral membrane, were measured by Northern blot with two probes, SDCT1 and SDCT2. Animals were sacrificed on day 1,3 and 7. On the 1st day, the blood plasma HCO(-)3 of acidosis group decreased significantly (P<0.01), but the mRNA abundance did not change. On the 3rd day in the acidosis group, the blood plasma HCO(-)3 increased slightly more than that on the 1st day, but was still significantly lower than that of the control group (P<0.01). Both the probes detected some increase in mRNA of brush border and basolateral Na(+)/citrate cotransporter. On the 7th day, the blood plasma HCO(-)3 of the acidosis group continuously increased and there was no significant difference between the two groups. The abundance of brush border and basolateral Na(+)/citrate cotransporter mRNA increased, but there was no difference between those of the 3rd day and the 7th day. It is concluded that metabolic acidosis can induce increase of Na(+)/citrate cotransporter mRNA, which may be responsible for hypocitraturia.

Acidosis↗
PubMed1997

Characterization of the receptor binding determinants of granulocyte colony stimulating factor.

We performed a series of experiments using alanine-scanning mutagenesis to locate side chains within human granulocyte colony-stimulating factor (G-CSF) that are involved in human G-CSF receptor binding. We constructed a panel of 28 alanine mutants that examined all surface exposed residues on helices A and D, as well as all charged residues on the surface of G-CSF. The G-CSF mutants were expressed in a transiently transfected mammalian cell line and quantitated by a sensitive biosensor method. We measured the activity of mutant proteins using an in vitro proliferation assay and an ELISA binding competition assay. These studies show that there is a region of five charged residues on helices A and C employed by G-CSF in binding its receptor, with the most important residue in this binding patch being Glu 19. Both wild-type G-CSF and the E19A mutant were expressed in E. coli. The re-folded proteins were found to have proliferative activities similar to the analogous proteins from mammalian cells: furthermore, biophysical analysis indicated that the E19A mutation does not cause gross structural perturbations in G-CSF. Although G-CSF is likely to signal through receptor homo-dimerization, we found no compelling evidence for a second receptor binding region. We also found no evidence of self-antagonism at high G-CSF concentrations, suggesting that, in contrast to human growth hormone (hGH) and erythropoietin (EPO), G-CSF probably does not signal via a pure 2:1 receptor ligand complex. Thus, G-CSF, while having a similar tertiary structure to hGH and EPO, uses different areas of the four helix bundle for high-affinity interaction with its receptor.

Alanine↗
PubMed1995

Progressive renal lesions induced by administration of monoclonal antibody 1-22-3 to unilaterally nephrectomized rats.

A new animal model of progressive glomerulosclerosis was developed by administering a single i.v., injection of MoAb 1-22-3 to unilaterally nephrectomized rats. Renal morphological analysis revealed that glomerular lesions characterized by mesangial cell proliferation and mesangial matrix expansion were induced in about 95% of the glomeruli. Approximately 20% of the glomeruli of the unilaterally nephrectomized rats showed sclerosis or segmental sclerosis by week 6 after MoAb injection and crescent formation was observed in some glomeruli (ca 4%). Cellular infiltration was also noted in some parts of the interstitium. Increased expression of transforming growth factor-beta (TGF-beta) was observed in the unilaterally nephrectomized rats treated with MoAb 1-22-3, but we could not demonstrate pathological involvement of platelet-derived growth factor (PDGF), even though early-stage mesangial cell proliferation was observed. The mechanism of mesangial cell proliferation in this model remains to be elucidated. The relatively short period of time needed to induce the sclerotic changes in considered to be a great advantage of this model for clarifying the mechanisms involved in the chronic progression of mesangial proliferative glomerulonephritis.

Animals↗
PubMed1994

[Effects of Epimedium sagittatum on immunopathology and extracellular matrices in rats with chronic renal insufficiency].

Chinese herb medicine, Epimedium sagittatum (EP), was used to treat animal models of chronic renal insufficiency induced in Wistar rats with 7/8 nephrectomy. The results showed: 1. EP decreased significantly the level of BUN and serum creatinine in the rats. 2. EP inhibited the hypertrophy of glomeruli in the rats. 3. EP inhibited deposition of IgG, C3, Fib and FN along the glomerular capillary walls in these rats.

Animals↗
PubMed1993

[Treatment of rapid progressive glomerulonephritis (RPGN) with pulse methylprednisolone (MP) and urokinase (UK): a renal rebiopsy study].

We have performed a case controlled study on the morphological and immunopathological alterations which can be induced by pulse MP combined with UK in RPGN by means of before and post therapy renal biopsies. The results showed renal function and histologic patterns improved. The histopathological (endothelium and mesangial cell proliferation, crescent and interstitial infiltration) and immunopathological (deposition of IgG, C3, Collegen type III, IV, Laminin and FN.) changes improved in all the patients after treatment with pulse MP and UK. The results indicated that pulse MP and UK therapy seems to be useful in treatment of RPGN in early stage and renal rebiopsy could lead to a better understanding of RPGN outcome.

Adolescent↗
PubMed1992

Mouse ornithine decarboxylase is stable in Trypanosoma brucei.

The cDNA encoding mouse ornithine decarboxylase (ODC) was incorporated into a transforming vector pTSA-NEO2 carrying a procyclic acidic repetitive protein promoter and a neomycin phosphotransferase gene. The plasmid thus constructed, pMOD300, was introduced into the procyclic forms of Trypanosoma brucei via electroporation, and the transformants, selected under G418, expressed an ODC activity 100 times above the background level. Contrary to the commonly observed short half-life of mouse ODC in mammalian cells, however, the mouse ODC activity expressed in T. brucei remained stable for at least 6 h when protein synthesis was inhibited by cycloheximide. Pulse labelings and chase experiments with the irreversible ODC inhibitor [3,4-3H]difluoromethylornithine followed by gel electrophoresis, or with L-[35S] methionine followed by immunoprecipitation and gel electrophoresis indicated that the stable mouse ODC expressed in T. brucei has the same subunit molecular weight as the native enzyme. By an in vitro assay of protein stability in rabbit reticulocyte lysates (Loetscher, P., Pratt, G., and Rechsteiner, M. (1991) J. Biol. Chem. 266, 11213-11220), the native mouse ODC and the enzyme expressed in T. brucei had the same degree of instability. Thus, the mouse ODC expressed in T. brucei is probably identical to the native mouse ODC. Its remarkable stability in T. brucei must be due to the absence in trypanosomes of the proteolytic machinery present in mammalian cells responsible for rapid degradation of mouse ODC.

Animals↗
PubMed1992

In vivo import of firefly luciferase into the glycosomes of Trypanosoma brucei and mutational analysis of the C-terminal targeting signal.

The compartmentalization of glycolytic enzymes into specialized organelles, the glycosomes, allows the bloodstream form of Trypanosoma brucei to rely solely on glycolysis for its energy production. The biogenesis of glycosomes in these parasites has been studied intensively as a potential target for chemotherapy. We have adapted the recently developed methods for stable transformation of T. brucei to the in vivo analysis of glycosomal protein import. Firefly luciferase, a peroxisomal protein in the lantern of the insect, was expressed in stable transformants of the procyclic form of T. brucei, where it was found to accumulate inside the glycosomes. Mutational analysis of the peroxisomal targeting signal serine-lysine-leucine (SKL) located at the C-terminus of luciferase showed that replacement of the serine residue (Serine548) with a small neutral amino acid (A, C, G, H, N, P, T) still resulted in an import efficiency of 50-100% of the wild-type luciferase. Lysine549 could be substituted with an amino acid capable of hydrogen bonding (H, M, N, Q, R, S), whereas the C-terminal leucine550 could be replaced with a subset of hydrophobic amino acids (I, M, Y). Thus, a peroxisome-like C-terminal SKL-dependent targeting mechanism may function in T. brucei to import luciferase into the glycosomes. However, a few significant differences exist between the glycosomal targeting signals identified here and the tripeptide sequences that direct proteins to mammalian or yeast peroxisomes.

Animals↗
PubMed1992

[Effect of serum from IgA nephropathy patients on IL-1 production from P388 D1 cell lines].

The study was designed to investigate IL-1 production from P388D1 cell using serum from 40 cases with IgA nephropathy (IgAN) as stimulative factor. It was found that there was a relationship between IL-1 and renal morphological change. The result indicated that IL-1 production by P388D1 cell was much higher in the presence of the serum than that in the absence (CPM: 47597 +/- 26213 vs 36567 +/- 14377 P less than 0.05). The level of IL-1 correlated obviously to the renal morphologic changes (r = 0.406, P less than 0.05). It is suggested that in the serum of IgAN patients there are certain factors stimulating P388D1 cell to produce IL-1, which may contribute to the pathogenesis of IgAN.

Adolescent↗
PubMed1991

[Analysis of lymphocyte subpopulation in chronic dialyzed end stage renal failure by flow cytometry].

To investigate the change of immune function in patients with ESRF, peripheral blood lymphocytes of 15 maintenance hemodialysis patients were analyzed using FITC labelled monoclonal antibodies and laser flow cytometry (FACS 440). Lymphocytes of phenotype CD 3 (Pan T cell), CD 4 (helper/inducer), CD 8 (suppressor/cytotoxic), CD 16 (NK cell), CD 25 (IL-2 Receptor) and HLA-DR were enumerated. The results were summarized as follows: (1) CD 3, CD 8 and CD 16 were decreased markedly in ESRF patients. (2) CD 4 and CD 25 showed a tendency of decrement also yet statistically insignificant, (3) Value for HLA-DR was higher than normal, probably related with the hemodialysis. (4) CD 4, CD 8 and CD 4/CD 8 in a transfused group were not different from those in a non-transfused group. (5) CD 4/CD 8 was negatively correlated with the serum creatinine level (r = -0.524). In conclusion, there is a marked suppression of immune function in ESRF patients as evidenced from the change of T cell subpopulation.

Adolescent↗
PubMed1987

ECG waveform analysis by significant point extraction. I. Data reduction.

We present a new technique for automatic data reduction and pattern recognition of time-domain signals such as electrocardiogram (ECG) waveforms. Data reduction is important because only a few significant features of each heart beat are of interest in pattern analysis, while the patient data collection system acquires an enormous number of data samples. We present a significant point extraction algorithm, based on the analysis of curvature, that identifies data samples that represent clinically significant information in the ECG waveform. Data reduction rates of up to 1:10 are possible without significantly distorting the appearance of the waveform. This method is unique in that common procedures help in both data reduction as well as pattern recognition. Part II of this work deals specifically with pattern analysis of normal and abnormal heart beats.

Algorithms↗
PubMed1987

ECG waveform analysis by significant point extraction. II. Pattern matching.

From a set of significant points which characterizes the ECG waveform, the pattern matching algorithm detects and classifies QRS complexes. R waves are detected from the analysis of global curvature. Next, the morphology of the QRS complex is determined. QRS complexes with different morphologies are classified by a correlation algorithm. This method is sensitive to changes in shape, such as that of abnormal QRS complexes. The algorithm should be useful in automated analysis of waveforms, such as ECG signals recorded in clinical environments.

Algorithms↗