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Biomedical subjects

J Peng

Publications and source records attributed to J Peng.

At least 145 records · Page 8Linked to original sources
PubMed1998

Newly developed initial-flow cell filtrometer and the comparison with viscometry and ektacytometry on erythrocyte deformability.

According to Hanss's initial-flow rate method, F. Liao designed a new cell filtrometer in the early 1990s. The parameters, cell initial transit time (Tc) and membrane clogging rate (CR), can be determined by a single measurement with timing accuracy of 1 ms. The new cell filtrometer has two valuable features: a button-pushing operation to control electromagnetic valves; and an autocirculation of fluid in the cell filtrometer resulting in the same volume of leading fluid. A series of comparisons of the new filtrometry with viscometry or ektacytometry shows that the instrument seems to be more sensitive in detecting subpopulations of glutaraldehyde-hardened cells and the shift of deformability for all the cells. The reproducibility of the filtrometer for different membranes made in China and the USA is reasonable (CV < 5% for Tc). Preliminary application of the filtrometer indicates that it might be useful for trial study and routine clinical application.

Animals↗
PubMed1997

The Arabidopsis GAI gene defines a signaling pathway that negatively regulates gibberellin responses.

The Arabidopsis gai mutant allele confers a reduction in gibberellin (GA) responsiveness. Here we report the molecular cloning of GAI and a closely related gene GRS. The predicted GAI (wild-type) and gai (mutant) proteins differ only by the deletion of a 17-amino-acid segment from within the amino-terminal region. GAI and GRS contain nuclear localization signals, a region of homology to a putative transcription factor, and motifs characteristic of transcriptional coactivators. Genetic analysis indicates that GAI is a repressor of GA responses, that GA can release this repression, and that gai is a mutant repressor that is relatively resistant to the effects of GA. Mutations at SPY and GAR2 suppress the gai phenotype, indicating the involvement of GAI, SPY, and GAR2 in a signaling pathway that regulates GA responses negatively. The existence of this pathway suggests that GA modulates plant growth through derepression rather than through simple stimulation.

Alleles↗
PubMed1997

Transcription elongation factor P-TEFb is required for HIV-1 tat transactivation in vitro.

P-TEFb is a key regulator of the process controlling the processivity of RNA polymerase II and possesses a kinase activity that can phosphorylate the carboxy-terminal domain of the largest subunit of RNA polymerase II. Here we report the cloning of the small subunit of Drosophila P-TEFb and the finding that it encodes a Cdc2-related protein kinase. Sequence comparison suggests that a protein with 72% identity, PITALRE, could be the human homolog of the Drosophila protein. Functional homology was suggested by transcriptional analysis of an RNA polymerase II promoter with HeLa nuclear extract depleted of PITALRE. Because the depleted extract lost the ability to produce long DRB-sensitive transcripts and this loss was reversed by the addition of purified Drosophila P-TEFb, we propose that PITALRE is a component of human P-TEFb. In addition, we found that PITALRE associated with the activation domain of HIV-1 Tat, indicating that P-TEFb is a Tat-associated kinase (TAK). An in vitro transcription assay demonstrates that the effect of Tat on transcription elongation requires P-TEFb and suggests that the enhancement of transcriptional processivity by Tat is attributable to enhanced function of P-TEFb on the HIV-1 LTR.

Amino Acid Sequence↗
PubMed1997

P-TEFb kinase is required for HIV Tat transcriptional activation in vivo and in vitro.

To identify novel inhibitors of transcriptional activation by the HIV Tat protein, we used a combination of in vitro and in vivo Tat-dependent transcription assays to screen >100,000 compounds. All compounds identified blocked Tat-dependent stimulation of transcriptional elongation. Analysis of a panel of structurally diverse inhibitors indicated that their target is the human homolog of Drosophila positive transcription elongation factor b (P-TEFb). Loss of Tat transactivation in extracts depleted of the kinase subunit of human P-TEFb, PITALRE, was reversed by addition of partially purified human P-TEFb. Transfection experiments with wild-type or kinase knockout PITALRE demonstrated that P-TEFb is required for Tat function. Our results suggest that P-TEFb represents an attractive target for the development of novel HIV therapeutics.

Animals↗
PubMed1997

Polychlorinated biphenyl congener 153-induced ultrastructural alterations in rat liver: a quantitative study.

Alterations in the liver of male and female Sprague-Dawley rats fed PCB congener 153 (2,2',4,4',5,5'-hexachlorobiphenyl) at 0.5, 5, or 50 ppm concentrations in diets for 13 weeks were determined morphometrically. A dose-dependent increase in hepatocyte volume was detected; the cytoplasmic compartment contributed to the increase in cell volume in an overwhelming fashion. Eighty percent and 250% increase in smooth endoplasmic reticulum volume and its surface area in hepatocytes were estimated in animals of both genders from 5- and 50-ppm groups, respectively; the organelle played the largest part in the increase in cytoplasmic volume. Rough endoplasmic reticulum alteration was shown to depend on gender, where the volume per hepatocyte was augmented by 40% and 45% in females of 5- and 50-ppm groups, respectively, however, 30% and 20% decreases in volume of this organelle were noted in males at those congener concentrations. A decrease of 13% in normal mitochondria volume at 50 ppm concentration was observed, which may have been a consequence of a transformation of these mitochondria to abnormal types. Two types of abnormal mitochondria, named Type I and Type II, were defined: the former comprised mitochondria that had cristae which laying parallel to the long axis of the organelle and the latter showed C- or ring-shaped profiles. Data analysis revealed a trend toward an increase in abnormal mitochondria volume in the cells as the congener concentration elevated. In addition, a threefold increase in the volume of lysosomal elements per hepatocyte was noted in 50 ppm PCB-fed rats of both genders. Also, a significant increase in peroxisome volume per cell in female rats was detected at a lower concentration than it was in the male. This study, which is a first ultrastructural quantitative investigation on the effects of a PCB that included many parameters. The methodology, and the data may prove useful to provide better understanding of pathology in the evaluation and regulation of toxic chemicals.

Animals↗
PubMed1997

Activation of AP-1 by okadaic acid in mouse keratinocytes associated with hyperphosphorylation of c-jun.

Okadaic acid (OA), a specific inhibitor of protein phosphatases 1 and 2A, is also a potent mouse skin tumor promoter. The effects of OA on regulation of c-jun/activator protein-1 (AP-1) transcriptional activation were investigated in mouse keratinocytes. AP-1 DNA binding to the jun 12-O-tetradecanoylphorbol-13-acetate-response element (TGACATCA) as determined by gel shift analysis was strongly induced by OA (100 ng/mL) at 6 and 12 h. Preincubation of nuclear extracts with anti-c-jun antibody demonstrated that c-jun was a major component of the DNA-bound AP-1 complex induced by OA in 308 cells. Transfection of a c-jun promoter-reporter construct demonstrated that AP-1 transactivation was induced by OA. The mRNA level of the c-jun proto-oncogene was dramatically increased by 6 and 12 h of OA treatment. Furthermore, a significant induction of c-jun protein was stimulated by 6 and 12 h of OA treatment. Upon further analysis, it was found that OA induced a significant accumulation of Ser 73-phosphorylated c-jun protein in 308 cells. In summary, our data suggest that skin tumor promotion by OA is due at least in part to increased AP-1 DNA binding and transactivation mediated by c-jun hyperphosphorylation.

Animals↗
PubMed1997

Transcriptional inhibition of manganese superoxide dismutase (SOD2) gene expression by DNA methylation of the 5' CpG island.

Manganese superoxide dismutase (MnSOD) enzyme activity and SOD2 gene expression have often been reported to decrease during the development of cancer. SOD2 has also been implicated as a candidate tumor suppressor gene for human malignant melanoma. Genomic DNA methylation patterns are also known to change during carcinogenesis and serve as a mechanism for tumor suppressor gene inactivation. We hypothesized that decreased SOD2 gene expression in some malignant cell populations may be due, at least in part, to methylation of upstream transcriptional regulatory sequences in the SOD2 gene. To test this hypothesis we transfected methylated and unmethylated SOD/2-CAT promoter-reporter constructs in cells known to express the SOD2 gene. Our results indicate that methylation of specific cytokines in the SOD2 5' flanking region is sufficient to repress transcriptional activity of the SOD2 promoter by at least 50%. Moreover, we show that this transcriptional repression was likely mediated by inhibition of AP-2 DNA binding and transactivation from a methylated AP-2 binding site in the SOD2 promoter. DNA methylation may provide a mechanism for transcriptional inactivation of the SOD2 gene during the development of some cancers.

Animals↗
PubMed1997

Gibberellin deficiency and response mutations suppress the stem elongation phenotype of phytochrome-deficient mutants of Arabidopsis.

Plant growth and development are regulated by numerous internal and external factors. Among these, gibberellin (GA) (an endogenous plant growth regulator) and phytochrome (a photoreceptor) often influence the same processes. For example, in plants grown in the light Arabidopsis thaliana hypocotyl elongation is reduced by GA deficiency and increased by phytochrome deficiency. Here we describe experiments in which the phenotypes of Arabidopsis plants doubly homozygous for GA-related and phytochrome-related mutations were examined. The double mutants were studied at various stages in the plant life cycle, including the seed germination, young seedling, adult, and reproductive phases of development. The results of these experiments are complex, but indicate that a fully functional GA system is necessary for full expression of the elongated phenotypes conferred by phytochrome deficiency.

Arabidopsis↗
PubMed1997

[Significance of p16 and C-myc expression in the laryngeal squamous cell carcinoma].

OBJECTIVE: To study the clinical significance of p16 and C-myc expression in the laryngeal squamous cell carcinoma (LSCC). METHOD: Immunohisto-chemical detection of p16 proteins and C-myc proteins, in 47 cases of LSCC and 6 cases of normal tissues from the larynx, were conducted in paraffin-embeded sections. RESULTS: No staining was found in 6 cases of normal tissue; The positive expression of p16 and C-myc proteins expression rates did not correlate with sex, age and position of the tumors (P > 0.05); but related to the staging and grade of LSCC (P < 0.05). The expression of C-myc proteins were higher in the case with lymph nodal metastasis than that without lymph nodal metastasis (P < 0.05). CONCLUSION: The expression of p16 and C-myc protein may play an important role in the development of LSCC, and may be a new indicator to assess the prognosis of LSCC.

Adult↗
PubMed1997

[Epidemiology of breast cancers in the Somme department (1990-1993)].

Breast cancer is the commonest female cancer in the Somme region and represents the leading cause of cancer mortality in women. It therefore constitutes an important public health problem. From 1990 to 1993, 1,106 new cases of breast cancer were recorded by the Somme Cancer Registry. The incidence continued to increase over this period in the Somme region. The mortality rate for this period was 35.1/100,000 women, while the standardized mortality rate for the world population was 20.9/100,000 women. The most frequent histological types were invasive ductal carcinoma (64.3%) and invasive lobular carcinoma (5%). Carcinoma in situ represented 2.9% cases; 4% of patients presented metastases at the time of diagnosis. For the period 1990-1993, 44.3% cases were classified as T1, 37.9% as T2 and 11.5% as T3-T4. The lymph node extension rate was less than 15% for tumours less than 10 mm (on the resection specimen). The 5-year survival rate was 73%. It is important to increase the rate of early diagnosis in order to improve the overall survival of this disease.

Adult↗
PubMed1997

[Determination of Cu, Pb, Sn, Fe and Zn in the ancient Chinese bronzes by X-ray fluorescence filter paper method].

The determination of Cu, Pb, Sn, Fe and Zn in the ancient chinese bronzes has been performed using X-ray fluorescence filter paper method. The result is satisfactory. The samples are dissolved in the HCl-H2O2 system, ard then the solution is dropped on the filter paper. It is convenient for detection by XRF. In addition this method is efficient to reduce the matrix effect of sample. The correlative coefficients of calibration curves between element concentration and X-ray intensity are over 0.99. The rate of recovery is 97-104%, and the relative standard deviation for each element is less than 2.00%. The copper's result measured by this method agrees well with that of chemical method. This method is simple, rapid and accurate. It is also applied to determine the elements in the other ancient objects.

English Abstract↗
PubMed1997

Erythropoietin administration increases production and reactivity of platelets in dogs.

Administration of erythropoietin (EPO) to adult dogs resulted in a dramatic increase in the number of thiazole orange-positive (TO+) platelets, also referred to as reticulated platelets. Pre-treatment level of TO+ platelets was 6.2 +/- 0.5% (mean +/- 1 SE: n = 5); following day 5 of treatment with 500 U EPO/kg/day, the percentage of TO+ platelets peaked at 16.8 +/- 2.3% (n = 5; p <0.02). After cessation of the hormone, the number of TO+ platelets fell rapidly to below starting levels. Unexpectedly, there was a significant decline in total platelet count during EPO administration despite an increased level of TO+ platelets. To assess platelet reactivity, total platelets and TO+ platelets from EPO-treated dogs were analyzed for thrombin-responsiveness as quantitated by P-selectin expression on the cell surface; reactivity was expressed as a thrombin EC50, the thrombin concentration required to activate 50% of platelets. Both total and TO+ platelets were hyperreactive during EPO treatment when compared either to pre-treatment values or to control animals. Thrombin EC50 values for total and TO+ platelets on day 5 fell to 66.5 +/- 5.4% (mean +/- 1 SE; n = 5; p <0.02) and 62.2 +/- 8.7% (n = 5; p <0.025), respectively, of pre-treatment levels. These data indicate that EPO not only promotes the synthesis of increased numbers of TO+ platelets in the dog but that these newly produced platelets are hyperreactive when compared to TO+ platelets from control animals.

Animals↗
PubMed1996

Control of RNA polymerase II elongation potential by a novel carboxyl-terminal domain kinase.

The entry of RNA polymerase II into a productive mode of elongation is controlled, in part, by the postinitiation activity of positive transcription elongation factor b (P-TEFb) (Marshall, N. F., and Price, D. H. (1995) J. Biol. Chem. 270, 12335-12338). We report here that removal of the carboxyl-terminal domain (CTD) of the large subunit of RNA polymerase II abolishes productive elongation. Correspondingly, we found that P-TEFb can phosphorylate the CTD of pure RNA polymerase II. Furthermore, P-TEFb can phosphorylate the CTD of RNA polymerase II when the polymerase is in an early elongation complex. Both the function and kinase activity of P-TEFb are blocked by the drugs 5, 6-dichloro-1-beta-D-ribofuranosylbenzimidazole (DRB) and H-8. P-TEFb is distinct from transcription factor IIH (TFIIH) because the two factors have no subunits in common, P-TEFb is more sensitive to DRB than is TFIIH, and most importantly, TFIIH cannot substitute functionally for P-TEFb. We propose that phosphorylation of the CTD by P-TEFb controls the transition from abortive into productive elongation mode.

Hydrolysis↗
PubMed1996

Low levels of erythroid and myeloid progenitors in thrombopoietin-and c-mpl-deficient mice.

Thrombopoietin (TPO), the ligand for the c-mpl receptor, has been shown to be the major regulator of platelet production. Mice deficient in either c-mpl or TPO generated by homologous recombination show a dramatic decrease in platelet counts, but other blood cell counts are normal. Because TPO treatment of myelosuppressed mice not only enhances the recovery of platelets but also accelerates erythroid recovery, we investigated the levels of myeloid and erythroid progenitor cells in TPO-or c-mpl-deficient mice. Our results show that the number of megakaryocyte, granulocyte-macrophage, erythroid, and multilineage progenitors are significantly reduced in the bone marrow, spleen, and peripheral blood of either TPO-or c-mpl-deficient mice. Administration of recombinant murine TPO to TPO-deficient mice and control littermate mice significantly increased the absolute number of myeloid, erythroid, and mixed progenitors in bone marrow and spleen. This increase was especially apparent in TPO-deficient mice where numbers were increased to a level greater than in diluent-treated control mice and approached or equaled that in the TPO-treated control mice. Moreover, TPO-administration greatly increased the number of circulating progenitors as well as platelets in both TPO-deficient and control mice. Furthermore, the megakaryocytopoietic activity of other cytokines in the absence of a functional TPO or c-mpl gene was shown both in vitro and in vivo.

Animals↗
PubMed1996

Relative reactivity of platelets from thrombopoietin- and interleukin-6-treated dogs.

Previous reports have shown that interleukin-6 (IL-6) enhances the responsiveness of platelets to thrombin stimulation and has modest thrombocytopoietic effects in vivo. Thrombopoietin (TPO; mpl ligand) has been shown to have dramatic thrombocytopoietic effect in vivo, but little is known of its capacity to alter platelet function. In this study, a direct comparison of the effects of IL-6 and TPO on platelet function in dogs has been performed, with modest doses of TPO (1 microgram/kg/d) chosen to match or moderately exceed the platelet counts achieved with IL-6 (40 micrograms/kg/d) for 10 days. Platelet responsiveness to thrombin stimulation was assessed in TPO-treated, IL-6-treated, and control dogs by flow cytometric measurement of P-selectin expression. On day 5, the dose of thrombin promoting half maximal stimulation (EC50) of platelets was not significantly changed in TPO-treated dogs, whereas in IL-6-treated dogs the EC50 decreased to 73.1% +/- 6.1% (mean +/- 1 SD; n = 5) of control values (P < 0.01). These experiments were performed on both gel-filtered platelets and washed whole blood, indicating that the observed changes in EC50 were caused by cytokine-mediated alteration of platelets rather than plasma components. Because it has been shown that thiazole orange specifically labels a subpopulation of dog platelets that is less than 24 hours old, the thrombin responsiveness of these young, newly synthesized platelets was determined. The EC50 of thiazole orange-positive platelets from IL-6-treated dogs decreased dramatically by day 5 to 46.5% +/- 13.1% (n = 4) of control values (P < 0.001), whereas TPO-treated dogs did not significantly change. When TPO was directly incubated with platelets ex vivo, no effects on either thrombin-mediated P-selectin expression or adenosine diphosphate-induced fibrinogen binding were observed. These data show that IL-6 alters platelet function, as measured by reactivity to thrombin, whereas TPO does not. This divergence in function is observed even though TPO is equally, or more, effective at promoting platelet production under these experimental conditions.

Adenosine Diphosphate↗