Surface soils from the outskirts of Beijing were analyzed for 16 priority polycyclic aromatic hydrocarbons (PAHs) using gas chromatography and mass spectrometry (GC-MS). The distribution map of total PAHs content was obtained as a contour plot. The concentration range of 16 PAHs varied by over two orders of magnitude from 0.016 microg g-1 in rural to 3.884 microg g-1 in suburban soils with the relatively standard deviation of 70.5%, showing large differences in the extent of PAHs pollution at the various sampling sites. It was notable that the concentration of BaP was 0.005-0.270 microg g-1 with a mean of 0.055 microg g-1. In general, the distribution of PAHs centered on the high molecular weight PAHs known to be carcinogenic. The 4-6 ring PAHs represented about 66% in rural samples and 70% in suburban soils of the total PAHs found. There was relatively good relationship among most of the individual PAHs and the compounds of Pyr, BaA, Flu, BbF, BaP, Chr and Ph gave strong correlation (r>0.8) with the sum of PAHs. The selected marked compounds, a principal component analysis (PCA) and special PAHs compound ratios (Ph/An vs Flu/Pyr; summation operator COMB/ summation operator EPA-PAHs) suggest the pyrogenic origins, especially traffic exhausts, are the dominant sources of PAHs in Beijing outskirts soils.

China↗

PubMed2004

Effect of plasticization on heparin release from biodegradable matrices.

Heparin-loaded polymer films of poly-L-lactide (PLLA) and poly-L-lactide-co-glycolide (PLLGA) as well as poly-DL-lactide-co-glycolide (PLGA) were produced. A plasticizer, PEG, was added to the polymers. It was found that the release profile in general consisted of a burst effect, a diffusion-controlled phase and a degradation-controlled phase. The plasticizer accelerated the onset of degradation in all cases, but its effect on the release profile differed significantly depending on the polymer. The plasticizer depressed the burst effect for PLLA, and accelerated the kinetics of the diffusion-controlled phase. For the PLLGA 80/20, however, the plasticizer had no significant effect on the release profile or kinetics. We explain these observations in terms of hydrophilicity and crystallinity effects.

Absorbable Implants↗

PubMed2004

Contamination of priority polycyclic aromatic hydrocarbons in water from Guanting Reservoir and the Yongding River, China.

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China↗

PubMed2004

Determination of trihalomethanes in drinking water from Beijing, People's Republic of China.

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China↗

PubMed2003

Organochlorine pesticide residues in water from Guanting Reservoir and Yongding River, China.

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China↗

PubMed2003

The psychology of the Monty Hall problem: discovering psychological mechanisms for solving a tenacious brain teaser.

The Monty Hall problem (or three-door problem) is a famous example of a "cognitive illusion," often used to demonstrate people's resistance and deficiency in dealing with uncertainty. The authors formulated the problem using manipulations in 4 cognitive aspects, namely, natural frequencies, mental models, perspective change, and the less-is-more effect. These manipulations combined led to a significant increase in the proportion of correct answers given by novice participants, largely because of the synergy of frequency-based formulation and perspective change (Experiments 1, 2). In a raining study (Experiment 3) frequency formulation and mental models, but not Bayes's rule training, showed significant positive transfer in solving related problems.

Adult↗

PubMed2001

Oxidative stress-induced phospholipase C-gamma 1 activation enhances cell survival.

Phospholipase C-gamma1 (PLC-gamma1) is rapidly activated in response to growth factor stimulation and plays an important role in regulating cell proliferation and differentiation through the generation of the second messengers diacylglycerol and inositol 1,4,5-trisphosphate, leading to the activation of protein kinase C (PKC) and increased levels of intracellular calcium, respectively. Given the existing overlap between signaling pathways that are activated in response to oxidant injury and those involved in responding to proliferative stimuli, we investigated the role of PLC-gamma1 during the cellular response to oxidative stress. Treatment of normal mouse embryonic fibroblasts (MEF) with H2O2 resulted in time- and concentration-dependent tyrosine phosphorylation of PLC-gamma1. Phosphorylation could be blocked by pharmacological inhibitors of Src family tyrosine kinases or the epidermal growth factor receptor tyrosine kinase, but not by inhibitors of the platelet-derived growth factor receptor or phosphatidylinositol 3-kinase. To investigate the physiologic relevance of H2O2-induced tyrosine phosphorylation of PLC-gamma1, we compared survival of normal MEF and PLC-gamma1-deficient MEF following exposure to H2O2. Treatment of PLC-gamma1-deficient MEF with H2O2 resulted in rapid cell death, whereas normal MEF were resistant to the stress. Pretreatment of normal MEF with a selective pharmacological inhibitor of PLC-gamma1, or inhibitors of inositol trisphosphate receptors and PKC, increased their sensitivity to H2O2, whereas treatment of PLC-gamma1-deficient MEF with agents capable of directly activating PKC and enhancing calcium mobilization significantly improved their survival. Finally, reconstitution of PLC-gamma1 protein expression in PLC-gamma1-deficient MEF restored cell survival following H2O2 treatment. These findings suggest an important protective function for PLC-gamma1 activation during the cellular response to oxidative stress.

Alleles↗

PubMed2001

Regulation of phospholipase C-gamma(1) by the actin-regulatory protein villin.

The actin-regulatory protein villin is tyrosine phosphorylated and associates with phospholipase C-gamma(1) (PLC-gamma(1)) in the brush border of intestinal epithelial cells. To study the mechanism of villin-associated PLC-gamma(1) activation, we reconstituted in vitro the tyrosine phosphorylation of villin and its association with PLC-gamma(1). Recombinant villin was phosphorylated in vitro by the nonreceptor tyrosine kinase c-src or by expression in the TKX1 competent cells that carry an inducible tyrosine kinase gene. Using in vitro binding assays, we demonstrated that tyrosine-phosphorylated villin associates with the COOH-terminal Src homology 2 (SH2) domain of PLC-gamma(1). The catalytic activity of PLC-gamma(1) was inhibited by villin in a dose-dependent manner with half-maximal inhibition at a concentration of 12.4 microM. Villin inhibited PLC-gamma(1) activity by sequestering the substrate phosphatidylinositol 4,5-bisphosphate (PIP(2)), since increasing concentrations of PIP(2) reversed the inhibitory effects of villin on PLC activity. The inhibition of PLC-gamma(1) activity by villin was reversed by the tyrosine phosphorylation of villin. Further, we demonstrated that tyrosine phosphorylation of villin abolished villin's ability to associate with PIP(2). In conclusion, tyrosine-phosphorylated villin associates with the COOH-terminal SH2 domain of PLC-gamma(1) and activates PLC-gamma(1) catalytic activity. Villin regulates PLC-gamma(1) activity by modifying its own ability to bind PIP(2). This study provides biochemical proof of the functional relevance of tyrosine phosphorylation of villin and identifies the molecular mechanisms involved in the activation of PLC-gamma(1) by villin.

Actins↗

PubMed2001

[Pharmacological study on Tianxiong (tuber of Aconitum carmichaeli Debx.), a Chinese drug for reinforcing the kidney yang retail in Hong Kong market].

OBJECTIVE: To explore the pharmacodynamic mechanism of Tianxiong (Aconitum carmichaeli) in tonifying the kidney and supporting Yang, so as to provide evidences for further development of new drugs treating Yang-eficiency of the kidney. METHOD: Observing parameters such as visceral index, survival time of low-temperature swimming for hydrocortisone-induced Yang-deficiency model mouse and testis-removed kidney-deficiency model rat. RESULT: The decoction of processed Tianxiong could strengthen the antifatigual ability and prolong the survival time of low-temperature swimming for mice, and promote immunization in rats. CONCLUSION: Tianxiong is able to reinforce the kidney Yang, which reconforms the conclusion of "replenishing the fire of vital gate and the Qi of kidney" recorded in Chinese historical literature and proved by overseas clinical practice.

Aconitum↗

PubMed2001

[Roles of Galphaq/11 mediated- and platelet-derived growth factor mediated-signal transduction pathways in rat aorta restenosis].

To observe the roles of Galphaq/11 mediated- and platelet-derived growth factor (PDGF) mediated-signal transduction pathways in proliferation and migration of vascular smooth muscle cells (VSMC) after arterial injury, a vascular cell proliferation model was established by balloon injury in rat aorta and the morphologic changes in injured vascular walls after the injury were studied. Activities of angiotensin converting enzyme (ACE) and aorta phospholipase C (PLC) were tested, and levels of platelet-derived growth factor receptor-beta (PDGFR-beta) and Galphaq/11 protein were measured by Western blot analysis. At l day after operation, injured aortic segments showed denudation in endothelial cells. Medial VSMC proliferation and intimal hyperplasia were not observed. As compared with the sham group, ACE activities were increased by 382.7 percent; (P<0.0l), but the expression of PDGFR-beta and PLC activities did not show significant changes (P>0.05). In addition, the level of Galphaq/11 protein was decreased by 20.0 percent; (P<0. 05). At l4 days after operation, sections of injured aorta showed marked intimal thickening with large numbers of VMSCs proliferating throughout intima and media. In comparison with the sham group, ACE activity, PLC activity and the level of PDGFR-beta were increased by 420.2 percent; (P<0.01), 186.2 percent; (P<0.05) and 85.0 percent; (P<0.05), respectively. While the level of Galphaq/11 protein was decreased by 33.1 percent; (P<0.01). The above data suggest that the PDGF-mediated signal transduction pathway plays an important role in VSMC proliferation.

Angioplasty, Balloon↗

PubMed2000

Mice lacking renal chloride channel, CLC-5, are a model for Dent's disease, a nephrolithiasis disorder associated with defective receptor-mediated endocytosis.

Nephrolithiasis (kidney stones) affects 5-10% of adults and is most commonly associated with hypercalciuria, which may be due to monogenic renal tubular disorders. One such hypercalciuric disorder is Dent's disease, which is characterized by renal proximal tubular defects that include low molecular weight proteinuria, aminoaciduria and glycosuria, together with rickets in some patients. Dent's disease is due to inactivating mutations of the renal-specific voltage-gated chloride channel, CLC-5, which is expressed in the proximal tubule, thick ascending limb and collecting duct. The subcellular localization of CLC-5 to the proximal tubular endosomes has suggested a role in endocytosis, and to facilitate in vivo investigations of CLC-5 in Dent's disease we generated mice lacking CLC-5 by targeted gene disruption. CLC-5-deficient mice developed renal tubular defects which included low molecular weight (<70 kDa) proteinuria, generalized aminoaciduria that was more pronounced for neutral and polar amino acids, and glycosuria. They also developed hypercalciuria and renal calcium deposits and some had deformities of the spine. Furthermore, endocytosis as assessed by horseradish peroxidase uptake in the proximal tubule was severely impaired in CLC-5-deficient mice, thereby demonstrating a role for CLC-5 in endosomal uptake of low molecular weight proteins. Thus, CLC-5-deficient mice provide a model for Dent's disease and this will help in elucidating the function of this chloride channel in endocytosis and renal calcium homeostasis.

Animals↗

PubMed2000

Comparison of tyrosine hydroxylase and preproenkephalin expression in rat adrenal medullary explants in vitro and transplanted into subarachnoid space.

When adrenal medullary cells are cultured in vitro, tyrosine hydroxylase (TH) mRNA, preproenkephalin (PPEnk) mRNA, and methionine enkephalin (Mek) immunoreactivity was markedly increased compared with intact adrenal medullary cells in situ, suggesting an increased biosynthesis of catecholamines and enkephalin-containing peptides. In transplanted adrenal medullary cells in vivo, TH mRNA and TH immunoreactivity are still apparent for at least 1 year after transplantation, indicating continued capacity for catecholamine biosynthesis. PPEnk mRNA levels in surviving adrenal medullary grafted cells increased, particularly in the first week after transplantation, and remained above levels found in the intact adrenal gland for at least 1 year after transplantation. These results support other studies in our laboratory, suggesting that adrenal medullary transplants reduce pain by synthesis and secretion of both catecholamines and enkephalin-containing peptides. The differences in expression of TH mRNA and PPEnk mRNA in the adrenal medulla in situ, in explants in culture and in transplants in the spinal subarachnoid space, indicate that the mechanisms regulating the expression of neurohumoral factors depend upon environmental factors extrinsic to the medullary cells themselves.

Adrenal Medulla↗

PubMed2000

The mRNA of L-type calcium channel elevated in colon cancer: protein distribution in normal and cancerous colon.

Previous reports indicate that the mRNA for the cardiac isoform of the voltage-gated L-type calcium channel (alpha(1C)) is elevated in colon cancer. The aim of these experiments was to verify that the mRNA for alpha(1C) was significantly increased in tumors of two separate populations of patients when compared to normal adjacent mucosa. The second aim was to measure the distribution of alpha(1C) using immunocytochemistry in normal human colon and in colon cancer and to determine what might regulate the channel expression. Biopsies were taken from patients with various stages of colon cancer and nearby normal mucosa were used as control. RNA was prepared and mRNA level measured by semiquantitative reverse transcriptase-polymerase chain reaction. The mRNA of the calcium channel was compared with other markers including beta-actin. The mRNA for alpha(1C) was increased significantly in colon cancers compared to nearby adjacent mucosa. Using confocal microscopy alpha(1C) was localized mainly at the apical membrane in the surface epithelium of normal human colon with less distribution on the lateral and basal membranes. The channel was localized on the lateral and basal membranes in crypt cells. Calcium channel localization appeared to be nearer nuclei in colon cancer samples, in part because of the smaller size of the cells. Likewise, cultured Caco-2 and T84 cells showed a membrane distribution. Western blotting indicated that alpha(1C) protein was increased in nonconfluent cultures of colonic carcinoma cells compared to confluent cells and immunocytochemistry confirms that there is more calcium channel protein in cells that are nonconfluent. We conclude that the increase in mRNA of alpha(1) subunit of the cardiac isoform of the L-type calcium channel may be a useful marker of colon cancer compared to other markers because the increase is large and this increase can be documented on small samples using a simple semiquantitative reverse transcriptase-polymerase chain reaction. We found that alpha(1C) protein is increased when colonic cells are nonconfluent or dividing which may account for the increase in cancer.

Blotting, Western↗

PubMed2000

pH-regulated chloride secretion in fetal lung epithelia.

The fetal lung actively transports chloride across the airway epithelium. ClC-2, a pH-activated chloride channel, is highly expressed in the fetal lung and is located on the apical surface of the developing respiratory epithelium. Our goal was to determine whether acidic pH could stimulate chloride secretion in fetal rat distal lung epithelial cells mounted in Ussing chambers. A series of acidic solutions stimulated equivalent short-circuit current (I(eq)) from a baseline of 28 +/- 4.8 (pH 7.4) to 70 +/- 5 (pH 6.2), 114 +/- 12.8 (pH 5.0), and 164 +/- 19.2 (pH 3.8) microA/cm(2). These changes in I(eq) were inhibited by 1 mM cadmium chloride and did not result in large changes in [(3)H]mannitol paracellular flux. Immunofluorescent detection by confocal microscopy revealed that ClC-2 is expressed along the luminal surface of polarized fetal distal lung epithelial cells. These data suggest that the acidic environment of the fetal lung fluid could activate chloride channels contributing to fetal lung fluid production and that the changes in I(eq) seen in these Ussing studies may be due to stimulation of ClC-2.

Animals↗