Biomedical subjects

Yan Cheng

Publications and source records attributed to Yan Cheng.

22 records · Page 2Linked to original sources

PubMed2003

A novel amphiphilic adsorbent for the removal of low-density lipoprotein.

Dextran adsorbent with amphiphilic ligands for adsorption of low-density lipoprotein (LDL) was prepared by the following procedures. Cholesterol group was linked to Dextran G 75 by reacting with cholesterol N-(6-isocyanatohexyl) carbamate in the presence of pyridine in DMSO at 80. In order to introduce the hydrophilic moiety, it was then reacted with chlorosulfonic acid in formamide which introduced the sulfonic group. Adsorption capacity of the adsorbent was studied which showed the removal of LDL-cholesterol (LDL-C), total cholesterol (TC) and TG to be 1.916, 2.132 and 1.349 mg/ml, respectively without significantly affecting total protein levels in the plasma. Moreover, the adsorbent has a better selectivity in removing LDL-C, TC, TG compared to dextran which has only hydrophobic or hydrophilic ligand.

Adsorption↗

PubMed2003

Inhibition of nitrobenzene-induced DNA and hemoglobin adductions by dietary constituents.

Nitrobenzene (NB), a widely used industrial chemical, is a likely human carcinogen. Many dietary constituents can suppress the DNA-adduction, acting as the inhibitors of cancer. In this study, we investigated the inhibitory effects of vitamin C (VC), vitamin E (VE), tea polyphenols (TP), garlic squeeze, curcumin, and grapestone extract on NB-DNA and NB-hemoglobin (Hb) adductions in mice using an ultrasensitive method of accelerator mass spectrometry (AMS) with 14C-labelled nitrobenzene. All of these dietary constituents showed their inhibitory effects on DNA or Hb adduction. VC, VE, TP and grapestone extract could efficaciously inhibit the adductions by 33-50%, and all of these six agents could inhibit Hb adduction by 30-64%. We also investigated resveratrol, curcumin, VC and VE as inhibitors of NB-DNA adduction in vitro using liquid scintillation counting technique. These agents in the presence of NADPH and S9 components also pronouncedly blocked DNA adduction in a dose-dependent profile. Our study suggests that these seven constituents may interrupt the process of NB-induced chemical carcinogenesis.

Animals↗

PubMed2003

[Effects of terrestrial input on the harmful algal bloom area--with aluminum as an example].

In recent years, eutrophication and frequently occurred harmful algal blooms (HAB) become serious in the coastal area near Changjiang River estuary, and the nutrients came from Changjiang River may be the main sources for them. Aluminum could be used as a useful tracer for the terrestrial input and the movement of different water mass, since it enters into the natural water with the erosion products of soil and rock, and its residence time in the ocean is short and uneasy to be disturbed by the activities of human being. Based on our results, the concentration of dissolved Al was higher in Autumn than in Summer, and showed some relationships with the salinity and suspended particulate matter (SPM). The concentration of Al in the HAB area was higher than 0.04 mumol.L-1, which showed the significant influence from the terrestrial input. The concentration of dissolved Al decreased nearly 40% after the occurrence of HAB, and the flocculation of dissolved Al and its absorption onto the surfaces of biogenic particles might be the main reasons. There still need further study about the variation of Al forms and its mechanism during the occurrence of HAB.

Aluminum↗

PubMed2002

Role of prostacyclin in the cardiovascular response to thromboxane A2.

Thromboxane (Tx) A2 is a vasoconstrictor and platelet agonist. Aspirin affords cardioprotection through inhibition of TxA2 formation by platelet cyclooxygenase (COX-1). Prostacyclin (PGI2) is a vasodilator that inhibits platelet function. Here we show that injury-induced vascular proliferation and platelet activation are enhanced in mice that are genetically deficient in the PGI2 receptor (IP) but are depressed in mice genetically deficient in the TxA2 receptor (TP) or treated with a TP antagonist. The augmented response to vascular injury was abolished in mice deficient in both receptors. Thus, PGI2 modulates platelet-vascular interactions in vivo and specifically limits the response to TxA2. This interplay may help explain the adverse cardiovascular effects associated with selective COX-2 inhibitors, which, unlike aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs), inhibit PGI2 but not TxA2.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗