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Biomedical subjects

C Deng

Publications and source records attributed to C Deng.

At least 109 records · Page 6Linked to original sources

Respective degree of expression of beta 1-, beta 2- and beta 3-adrenoceptors in human brown and white adipose tissues.

1. The possible existence of a beta 3-adrenoceptor in human brown and white adipose tissues was investigated by mRNA expression and binding studies. 2. The relative amounts of beta 1-, beta 2- and beta 3-adrenoceptor mRNA, as determined by total RNA Northern blot analysis in newborn brown adipose tissue, were 28, 63 and 9% respectively of the total beta-adrenoceptor mRNA. 3. The beta 1/beta 2-adrenoceptors of human brown adipose tissue plasma membranes were characterized using [3H]-CGP 12177 as a ligand. Their Kd and Bmax values were 1.9 nM and 156 fmol mg-1 of membrane proteins, respectively. The beta 3-adrenoceptor was characterized by use of the new specific radioligand [3H]-SB 206606. The binding of this ligand was stereospecifically displaced by the active R,R- or the inactive S,S-enantiomer of BRL 37344 up to a concentration of about 10 microM. The Kd and Bmax values of the brown adipose tissue membrane beta 3-adrenoceptors were 87 nM and 167 fmol mg-1 of proteins, respectively. A low affinity [3H]-CGP 12177 binding site population was also detected in these membranes. 4. In human omental white adipose tissue, no beta 3-adrenoceptor mRNA could be detected in total RNA Northern blots and the beta 1-and beta 2-adrenoceptor mRNAs represented 9 and 91%, respectively of the total beta-adrenoceptor mRNA, and no specific binding of [3H]-SB 206606 could be measured.

Adipose Tissue↗

[Pharmacokinetic study of intraperitoneal chemotherapy with high-dose cisplatin for advanced ovarian cancer].

OBJECTIVE: To determine the characteristics of pharmacokinetics with high-dose cisplatin (DDP) instilled intraperitoneally and its toxicity as compared with that by intravenous (i.v.) route of administration (i.p.). METHODS: Sixteen patients with advanced ovarian cancer, not previously treated, were randomly divided into two groups: every patient in group I received intraperitoneal administration of DDP (100mg/m2) and those in group II received the same dose of DDP by intravenous route. The blood, ascitic fluid and urine were collected in different intervals as scheduled for 8 days after administration of these drugs. The total platinum of all samples were measured by a flameless type of atomic absorption spectrometry. RESULTS: The concentration of total platinum in the ascitic fluid was very high in i.p. group. The area under the concentration-time curve (AUC) for total platinum in ascitic fluid after i.p. therapy was 5 folds greater than that after i.v. therapy (P < 0.05). The total platinum concentration in serum after i.p. therapy was about the same as that after i.v. therapy. The half-life time for the elimination phase of total platinum from ascitic fluid and serum after i.p. administration was longer than that after i.v. administration. The toxicity of high-dose DDP given i.p. was not increased as compared with that given i.v.. CONCLUSIONS: This study indicates that high-dose DDP i.p. therapy offers some advantages in the treatment of ovarian cancer. The tumor tissues and peritoneal growths could be bathed in a high concentrations of DDP with a longer duration, so that the tumorcidal effect may be increased. The drug concentration in serum after i.p. therapy was as high as i.v. route. The toxicity of high-dose DDP i.p. therapy was not higher than that of i.v. therapy.

Adult↗

Expression of Brca1 is associated with terminal differentiation of ectodermally and mesodermally derived tissues in mice.

We have isolated genomic and cDNA clones of Brca1, a mouse homolog of the recently cloned breast cancer-associated gene, BRCA1. Brca1 encodes an 1812-amino-acid protein with a conserved zinc finger domain and significant homology to the human protein. Brca1 maps to Chromosome 11 within a region of conserved synteny with human chromosome 17, consistent with the mapping of the human gene to 17q21. Brca1 transcripts are expressed in a variety of cultured cells but reveal a specific and dynamic expression pattern during embryonic development. For example, expression is observed first in the otic vesicle of embryonic day 9.5 (E9.5) embryos. This expression diminishes and is replaced by expression in the neuroectoderm at E10.5. By E11-12.5, higher levels are observed in differentiating keratinocytes and in whisker pad primordia. Transcripts also become evident in epithelial cells of the E14-17 kidney. Brca1 expression occurs in differentiating epithelial cells of several adult organs as well, suggesting a general role in the functional maturation of these tissues. Consistent with this, Brca1 transcripts are expressed in both alveolar and ductal epithelial cells of the mammary gland. During pregnancy, there is a large increase in Brca1 mRNA in mammary epithelial cells, an increase that parallels their functional differentiation. Because high rates of breast cancer are associated with loss of BRCA1 in humans, it is possible that this gene provides an important growth regulatory function in mammary epithelial cells. In addition, increased transcription of mammary Brca1 during pregnancy might contribute, in part, to the reduced cancer risk associated with exposure to pregnancy and lactation.

Amino Acid Sequence↗

Modulation of obese gene expression in rat brown and white adipose tissues.

The ob gene mRNA expression in rat brown adipose tissue (BAT) and epididymal white adipose tissue (WAT) was measured on Northern blots hybridized with a rat ob gene probe. The level of ob gene mRNA in BAT was about 40% of that in WAT. Fasting (36 h) or semi-starvation (10 days) decreased the ob gene mRNA level in both tissues by 62-68%, and cold exposure at 6 degrees C (24 h) decreased it in BAT (-84%) but not in WAT. Acute administration of the beta 3-adrenergic agonist Ro 16-8714 decreased the ob gene mRNA level in BAT (-51%) and WAT (-28%) of lean Zucker rats and only in BAT (-74%) of obese falfa rats. This study demonstrates that, in the rat, the ob gene is not only expressed in WAT but also in BAT, and suggests that in these two tissues, the modulation of the ob gene expression might be more closely associated with known alterations in cell lipid content than with changes in sympathetic activity.

Adipose Tissue↗

Mice lacking p21CIP1/WAF1 undergo normal development, but are defective in G1 checkpoint control.

p21CIP1/WAF1 is a CDK inhibitor regulated by the tumor suppressor p53 and is hypothesized to mediate G1 arrest. p53 has been suggested to derive anti-oncogenic properties from this relationship. To test these notions, we created mice lacking p21CIP1/WAF1. They develop normally and (unlike p53-/- mice) have not developed spontaneous malignancies during 7 months of observation. Nonetheless, p21-/- embryonic fibroblasts are significantly deficient in their ability to arrest in G1 in response to DNA damage and nucleotide pool perturbation. p21-/- cells also exhibit a significant growth alteration in vitro, achieving a saturation density as high as that observed in p53-/- cells. In contrast, other aspects of p53 function, such as thymocytic apoptosis and the mitotic spindle checkpoint, appear normal. These results establish the role of p21CIP1/WAF1 in the G1 checkpoint, but suggest that the anti-apoptotic and the anti-oncogenic effects of p53 are more complex.

Animals↗

The MMTV/c-myc transgene and p53 null alleles collaborate to induce T-cell lymphomas, but not mammary carcinomas in transgenic mice.

A number of properties of the cancer-related genes c-myc and p53 suggest that they might collaborate to induce tumorigenesis. To test this notion, we produced doubly heterozygotic mice bearing disrupted p53 alleles and a fusion transgene consisting of the mouse mammary tumor virus (MMTV) LTR and the oncogene c-myc. Mice bearing both the MMT/c-myc transgene and a single p53- allele develop very aggressive pre-T- and T-cell lymphomas with a significantly shorter latency than mice carrying either the p53- allele or the c-myc transgene alone. Moreover, every lymphoma occurring in these animals has lost or suffers an inactivation of its wild type p53 allele indicating that loss of p53 activity is necessary for this c-myc-accelerated lymphomagenesis. Nonetheless, p53 inactivation and expression of the MMTV/c-myc transgene are not sufficient for lymphoid transformation. Tumors that arise in homozygous p53- mice carrying the c-myc transgene are monoclonal, suggesting that at least one additional event is necessary for their transformation. Moreover, since mice bearing only the MMTV/c-myc transgene predominantly develop mammary carcinomas, it was surprising that the p53- allele failed to accelerate the incidence of mammary carcinomas. Further, in contrast to the lymphomas, only one in four mammary tumors that arose in the double heterozygotic mice had lost its wild type p53 allele. Apparently cell context influences the ability of c-myc and p53- to cooperate in inducing oncogenesis.

Alleles↗

[Radiolabelling and assay of Chinese agkistrodon acutus venom with carrier-free Na 125I].

Chinese agkistroden acutus venom (CAAV) was radiolabelled with carrier-free Na 125I by the method of Iodogen. The specific activity and radiochemical purity for radiolabelled products were 4236.5 x 10(10) Bq/mmol and 98%, respectively. Each CAAV molecule carried 0.52 125I atom. Physical and chemical characterization of radiolabelled CAAV was similar to unradiolabelled CAAV. Binding analysis showed that 125I-CAAV was bound to platelet in a saturable manner. Binding sites per platelet were 13,255 +/- 6292/platelet. The dissociation constant (Kd) was 3.2 +/- 0.69 x 10(-10) mol/L. These results are similar to binding sites of other snake venom on platelet. The investigation showed that radiolabelled CAAV made by our laboratory was useful for radioligand binding assay.

Agkistrodon↗

[Establishment of a human fetal thymocyte cell line and observation of its biological properties].

Thymocytes were isolated from a five month fetus after caesarean section and cultured in vitro. A cell line named human fetal thymocyte 8810 (HFT8810) was established and cultured continuously for 2 years in our lab, and grew well after recovery from the state of being frozen in liquid nitrogen. The HFT 8810 cells retained their ability to secrete thymosin after many generations in vitro culture.

Animals↗

[Clinical significance of detection of plasma fibronectin in respiratory failure].

Plasma fibronectin (PFn) level was measured with immumoelectrophoresis in 40 healthy adults and 174 patients (221 person-times) with respiratory insufficiency (R I). The levels of PFn in 40 healthy adults, 85 person-times of R I, 27 person-times of Type I respiratory failure (RF I), 82 person-times of RF II, and 27 person-times of iatrogenic RF (IRF) were 292.48 +/- 43.11 mg/L, 253.12 +/- 67.00 mg/L 141.97 +/- 70.84 mg/L, 180.48 +/- 49.96 mg/L and 263.49 +/- 70.05 mg/L respectively. The levels of PFn of patients with R I, RF I and RF II were significantly lower than that in healthy adults (P < 0.001). The level of PFn of patients with TRF was significantly lower than that in healthy adults (P < 0.05). There was positive correlation between the levels of PFn and PaO2 in 221 person-times of R I (r = 0.5358, P < 0.001), RF I r = 0.3822, P < 0.05). RF II (r = 0.3050, P < 0.01), and IRF (r = 0.4963, P < 0.02). There was negative correlation between the levels of PFn and PaCO2 in 221 person-times of R I (r = -0.2053, P < 0.005) and RF II (r = -0.2181, P < 0.05). In 34 patients with RF, the PFn before treatment was significantly lower than that two weeks after treatment (147.80 +/0 61.59 mg/L vs 214.56 +/- 56.12 mg/L) (P < 0.001). Among 33 cases of RF whose level of PFn was < 150 mg/L, 18 cases complicated multiple system organ failure and 4 cases complicated adult respiratory distress syndrome. The average level of PFn in 3 death cases was lower than 100 mg/L. It is suggested that PFn level might be used as an index in making early diagnosis, monitoring RF and predicating progosis of RF.

Adolescent↗

Active anaphylaxis in IgE-deficient mice.

The IgE-triggered release of mast cell mediators in response to antigen is thought to be the primary event in immediate hypersensitivity reactions such as systemic anaphylaxis. Although mast cells and basophils can be activated in vitro by non-IgE stimuli, it is not known whether these triggers lead to physiological changes in vivo. To investigate this possibility, we generated mice with a homozygous null mutation of the C epsilon gene. Such mice make no IgE, but produce other immunoglobulin isotypes normally. We report that despite the IgE deficiency, sensitized mutant mice become anaphylactic on antigen challenge and display tachycardia and pulmonary function changes similar to those seen in wild-type animals. These responses are accompanied by vascular leak, sharply elevated plasma histamine and rapid death. IgE-independent anaphylaxis does not depend on complement activation, but, as indicated in studies using genetically immunodeficient RAG-2- and SCID mice, does require a functional immune system. Such results clearly demonstrate that non-IgE pathways for hypersensitivity reactions exist in mice.

Anaphylaxis↗

[Studies on the detection of Legionella pneumophila by the application of polymerase chain reaction (PCR)].

DNA fragment of Legionella pneumophila, the PCR was performed with a pair of artificial synthesized primer. Results of agarose electrophoresis and EB staining showed that there was a 870 bp band shared by serogroups 1-14 of L.pneumophila. The sensitivity of PCR in detecting Legionella from water was 350cfu/ml, however, the specific DNA probe labeled with 32P was .43cfu/ml by blot hybridization. The positive rate of tissue specimens from infected guinea-pigs with Legionella pneumophila was 83.3% by PCR detection, and only 26.6% by bacteriological culture method. An outbeak caused by Lp10 was verified by PCR. The result showed that the PCR could detect the infection of Legionella rapidly, specifically and sensitively.

Animals↗

[Experimental study of Chinese Agkistrodon acutus venom in activation of rabbit platelets in vivo].

Fourteen Albino rabbits, male and female, were allocated randomly into two groups: control group which had intravenous infusion of normal saline, and experimental group which had intravenous infusion of Chinese Agkistrodon Acutus venom (CAAV) 0.075 mg/kg. Platelet was reduced, plasma PF4 activity and 5-HT concentration increased, 5-HT content in platelets was reduced in the experimental group 10, 20, and 50 minutes after the infusion. It had a significant difference (P < 0.01), compared with that in the control group. Platelets were aggregated into masses under electron microscope 10 minutes after the infusion of CAAV. The study has proved that blood platelets in rabbits are activated by Chinese Agkistrodon Acutus venom.

Agkistrodon↗

Convergence of somatic and visual afferent impulses in the Wulst of pigeon.

In 79 pigeons, unit discharges of Wulst neurons responding to bilateral stimulation of N. radialis and N. sciaticus and to bilateral light flashes were recorded. Of 178 such neurons, 55 showed multisensory convergence of various types: 40 of these were somatic convergent neurons, characterized as 3 types; three were binocular convergent cells; and twelve were bimodal (visual-somatosensory) convergent neurons. Of these neurons, the convergent action was either inhibitory or excitatory. These results suggest that the Wulst may function as an important centre for integrating visual and somatic sensory information.

Afferent Pathways↗

Location of crossovers during gene targeting with insertion and replacement vectors.

Gene targeting was used to introduce nonselectable genetic changes into chromosomal loci in mouse embryo-derived stem cells. The nonselectable markers were linked to a selectable marker in both insertion- and replacement-type vectors, and the transfer of the two elements to the Hprt locus was assayed. When insertion vectors were used as substrates, the frequency of transfer was highly dependent upon the distance between the nonselectable marker and the double-strand break in the vector. A marker located close to the vector ends was frequently lost, suggesting that a double-strand gap repair activity is involved in vector integration. When replacement vectors were used, cotransfer of a selectable marker and a nonselectable marker 3 kb apart was over 50%, suggesting that recombination between vector and target often occurs near the ends of the vector. To illustrate the use of replacement vectors to transfer specific mutations to the genome, we describe targeting of the delta F508 mutation to the CFTR gene in mouse embryo-derived stem cells.

Animals↗