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S J Lou

Publications and source records attributed to S J Lou.

6 recordsLinked to original sources
PubMed2006

Fluorescence-based monitoring of tracer and substrate distribution in an UASB reactor.

In this work, rhodamine-related fluorescence was measured on-line at four reactor heights in order to study hydrodynamics within an upflow anaerobic sludge bed reactor. A linear dependence of the dispersion coefficient (D) on the upflow velocity was observed, while the influence of the organic loading rate (OLR) was insignificant. Furthermore, the Bodenstein number of the reactor loaded with granulated sludge was found to be position-dependent with the largest values measured at the bottom of the sludge bed. This trend was not observed in the reactor without sludge. Chemical oxygen demand (COD) and volatile fatty acid (VFA) concentrations were measured at the same reactor heights as in rhodamine tests using conventional off-line analytical methods and on-line multiwavelength fluorometry. Significant spatial COD and VFA gradients were observed at organic loading rates above 6g COD l(R)(-1)d(-1) and linear upflow velocities below 0.8m h(-1).

Bioreactors↗
PubMed1998

The rapid inhibitory effect of glucocorticoid on cytosolic free Ca2+ increment induced by high extracellular K+ and its underlying mechanism in PC12 cells.

The effect of glucocorticoid(GC) on peak cytosolic free calcium net increment (delta[Ca2+]i) induced by high-K+ was detected with MiraCal Image System. The main results were as follows: (1) Corticosterone(B) could inhibit delta[Ca2+]i in a time-dependent and concentration-dependent manner. (2) The inhibitory effect of B could be mimicked by bovine-serum albumin conjugated corticosterone (B-BSA) also in a dose-dependent manner. (3) G-protein inhibitor, either PTX or GDP beta S significantly reduced the inhibitory effect of B and B-BSA on delta[Ca2+]i (4) PMA, a stimulator for protein kinase C(PKC), could inhibit delta[Ca2+]i. (5) Although the inhibitors of PKC, chelerythrine chloride and bisindolylamide I per se had no influence on delta[Ca2+]i, but they significantly antagonized the inhibitory effect of B and B-BSA on delta[Ca2+]i. It is postulated that GC inhibit delta[Ca2+]i induced by high-K+ through a membrane mechanism and by a pathway involving G-protein and PKC.

Animals↗
PubMed1998

Nongenomic mechanisms of glucocorticoid inhibition of nicotine-induced calcium influx in PC12 cells: involvement of protein kinase C.

Nongenomic mechanisms of corticosterone (B) inhibition of nicotine (Nic)-induced calcium influx were investigated in PC12 cells. Corticosterone could rapidly inhibit the Ca2+ influx induced by Nic, and BSA-conjugated B had a similar inhibitory effect. The inhibition of Nic-induced Ca2+ influx by B could be mimicked by protein kinase C (PKC) activator (phorbol 12-myristate 13-acetate) and reversed by PKC inhibitors, chelerythrine chloride and Gö6976. When PC12 cells were pretreated with pertussis toxin, the inhibitory effect of B on Nic-induced Ca2+ influx was blocked. Both B and BSA-conjugated B could activate PKC activity, with the maximal responses at 10(-9) and 10(-7) M at 37 C, respectively. The dose-response curve was bell shaped. At 25 C, however, the dose-response curve considerably shifted to the right, and B was most potent at 10(-5) M. The time course showed that PKC activity was highest at 5 min of B's action. The results suggest that B might act via putative membrane receptors and inhibit the Ca2+ influx induced by Nic through the pertussis toxin-sensitive G protein-PKC pathway and that PKC plays an important role in the mechanisms of glucocorticoid nongenomic action.

Animals↗
PubMed1998

[Effects of glutamic acid and acetylcholine on induction of heat shock proteins 70 mRNA in PC12 cells].

The heat shock response has been found in many strains of bacteria to human beings. Besides heat stimuli, many kinds of factors could also induce the synthesis of heat shock proteins (hsp). It is still unknown whether neurotransmitter could induce the increase of hsp expression in mammalian cells. In the present study, the effects of glutamic acid and acetylcholine (ACh) on the induction of hsp70 mRNA in PC12 cells were studied by Northern blot method. The probe used is specific for inducible hsp70 mRNA. Our results showed that the glutamic acid under limited conditions (such as at 50-500 mumol/L and action time 5-30 min) could induce the expression of hsp70 mRNA, which was partly mediated by NMDA receptors. On the other hand, ACh (0.1-1,000 mumol/L) could not induce the expression of hsp 70 mRNA.

Acetylcholine↗
PubMed1998

[Effect of glucocorticoid on [Ca2+]i induced by high-K+ in single PC12 cells and its characteristics].

The effect of glucocorticoid on the increase of cytosolic free calcium [Ca2+]i) induced by high-K+ was investigated in pheochomocytoma PC12 cells. The main result was as follows: (1) When the cells were preincubated at 37 degrees C for various time intervals in the presence of 10(-5) mol/L of corticosterone and stimulated with 55 mmol/L KCl, an inhibitory effect of corticosterone on delta [Ca2+]i was observed in a time-dependent manner with maximal effect at 5th min and no effect at 25th min. (2) When PC12 cells were preincubated with various concentration of corticosterone at 37 degrees C for 5 min, the inhibitory effect of corticosterone on delta [Ca2+]i induced by 55 mmol/L KCl was concentration-dependent. The effect was found to be maximal at 10(-5) mol/L of corticosterone and disappeared at 10(-9) mol/L of corticosterone. (3) Other steroids such as cortisol, dexamethasone, progesterone, testosterone, 17 beta-estradiol and aldosterone also inhibited the rise of [Ca2+]i evoked by 55 mmol/L KCl in PC12 cells to different extents, i.e., in the rank of P = F > Dex > T > Ald = E2. Cholesterol was ineffective at the concentration up to 10(-5) mol/L for inhibiting [Ca2+]i evoked by 55 mmol/L KCl. (4) Corticosterone could not inhibit the [Ca2+]i rise induced by changing the concentration of extracellular calcium from Ca(2+)-free to 3 mmol/L.

Animals↗