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Biomedical subjects

S T Yang

Publications and source records attributed to S T Yang.

At least 37 records · Page 2Linked to original sources
PubMed1999

Performance of fibrous bed bioreactor for treating odorous gas. Scientific note.

A fibrous bed bioreactor was used for treatment of odorous volatile fatty acid (VFA). The effect of gaseous VFA (acetic, propionic, and butyric acids) mass loading on the bioreactor performance was investigated. The VFA degrading microbial culture was selected from activated sludge by the three VFAs using a shake-flask culture. The selected microorganisms were then immobilized in a biofilter using cotton fabric as packing material. In the biofiltration experiment, the inlet gas flow rates ranged from 1 to 4 L/min, the total VFA concentrations ranged from 0.10 to 0.43 g/m3, and the resulting total mass loadings of VFA studied ranged from 9.7 to 104.3 g/m3/h. At total mass loading of 104.3 g/m3/h, the VFA removal efficiency was 87.7%. Higher removal efficiencies (>90%) were achieved at mass loadings below 50.3 g/m3/h.

Journal Article↗
PubMed1999

99mTc-MIBI single-photon emission-computed tomography in diagnosis of lung cancer and mediastinal metastasis lymph nodes.

AIM: To evaluate the value of technetium-99m-methoxyisobutyl isonitrile (99mTc-MIBI) single-photon emission-computed tomography (SPECT) in diagnosis of lung cancer and in preoperative prediction of mediastinal metastasis lymph nodes. METHODS: After the chest image of 99mTc-MIBI SPECT, fifty patients (40M, 10F; age 56 a +/- 11 a) diagnosed "lung field shadow" underwent the lung focus and mediastinal lymph nodes resection. As the golden standard, pathologic diagnosis was used to evaluate the role of preoperative 99mTc-MIBI SPECT. RESULTS: The sensitivity, specificity, and accuracy of 99mTc-MIBI SPECT were 93%, 50%, and 86%, respectively in lung cancer and 81%, 95%, and 88%, respectively in mediastinal metastasis lymph node. The results were also better than those of chest scan with CT. CONCLUSION: The 99mTc-MIBI SPECT is a useful and noninvasive method for diagnosing lung cancer and predicting mediastinal metastasis lymph nodes, which will guide the surgeon to resect the mediastinal metastasis lymph nodes.

Adult↗
PubMed1998

Acetate production from whey lactose using co-immobilized cells of homolactic and homoacetic bacteria in a fibrous-bed bioreactor.

Acetate was produced from whey lactose in batch and fed-batch fermentations using co-immobilized cells of Clostridium formicoaceticum and Lactococcus lactis. The cells were immobilized in a spirally wound fibrous sheet packed in a 0.45-L column reactor, with liquid circulated through a 5-L stirred-tank fermentor. Industrial-grade nitrogen sources, including corn steep liquor, casein hydrolysate, and yeast hydrolysate, were studied as inexpensive nutrient supplements to whey permeate and acid whey. Supplementation with either 2.5% (v/v) corn steep liquor or 1.5 g/L casein hydrolysate was adequate for the cocultured fermentation. The overall acetic acid yield from lactose was 0.9 g/g, and the productivity was 0.25 g/(L h). Both lactate and acetate at high concentrations inhibited the homoacetic fermentation. To overcome these inhibitions, fed-batch fermentations were used to keep lactate concentration low and to adapt cells to high-concentration acetate. The final acetate concentration obtained in the fed-batch fermentation was 75 g/L, which was the highest acetate concentration ever produced by C. formicoaceticum. Even at this high acetate concentration, the overall productivity was 0.18 g/(L h) based on the total medium volume and 1.23 g/(L h) based on the fibrous-bed reactor volume. The cells isolated from the fibrous-bed bioreactor at the end of this study were more tolerant to acetic acid than the original culture used to seed the bioreactor, indicating that adaptation and natural selection of acetate-tolerant strains occurred. This cocultured fermentation process could be used to produce a low-cost acetate deicer from whey permeate and acid whey.

Acetates↗
PubMed1998

Nitric oxide of neuronal origin mediates NMDA-induced cerebral hyperemia in rats.

The goal of this study was to determine whether neuronally derived nitric oxide mediates responses of cerebral blood flow (CBF) to N-methyl-D-aspartate (NMDA). In anesthetized Sprague-Dawley rats, regional CBF of the parietal cortex was monitored by laser-Doppler flowmetry. Topical application of either NMDA or acetylcholine produced concentration-related increases in CBF. Responses of CBF to NMDA (10(-5) M) but not to acetylcholine were inhibited (0+/-3% vs 21+/-5%, p < 0.05) by 7-nitroindazole (50 mg/kg, i.p.). MK-801 (0.5 mg/kg, i.v.) and tetrodotoxin (10(-6) M, topical application) also inhibited NMDA-induced responses. These results suggest that nitric oxide of neuronal origin mediates NMDA-induced increases in CBF.

Acetylcholine↗
PubMed1997

Role of prostaglandins in regulation of cerebral blood flow during acute hypertension.

Endothelium-derived prostaglandins appear to play an important role in myogenic contraction of the cerebral arteries in response to increased transmural pressure. The goal of this study was to determine whether prostaglandins contribute to the autoregulatory response of cerebral blood flow (CBF) during acute hypertension in normotensive and chronically hypertensive animals. In 4-5 months old Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR) anesthetized with pentobarbital sodium (45 mg/kg, i.p.), regional CBF of the right parietal cortex was monitored by laser-Doppler flowmetry. Acute hypertension was induced by intravenous infusion of phenylephrine and the elevated arterial pressure was maintained for 50 seconds for the measurement of CBF. In the control group of WKY rats, CBF increased by 5.6% per 10-mmHg increase in arterial pressure. Changes in CBF were similar between the initial state (0-10 seconds) and the steady state (30-40 seconds) of acute hypertension. In WKY rats pretreated with indomethacin (10 mg/kg, i.v.), increases in CBF in the initial state were slightly but significantly greater than that in the steady state. Indomethacin also tended to enhance the increases in CBF in both the initial state and the steady state; however, the effect was not significant. In the control group and indomethacin-pretreated group of SHR, acute hypertension produced similar increases in CBF. In both groups, no significant difference between changes in CBF in the initial state and the steady state was observed. Thus our findings suggest that 1) in normotensive animals, the early autoregulatory response of CBF during acute hypertension is partially mediated by prostaglandins and 2) the role of prostaglandins in the regulation of CBF during acute hypertension is altered in chronically hypertensive animals.

Acute Disease↗
PubMed1996

Kinetics of continuous GM-CSF production by recombinant Saccharomyces cerevisiae in an airlift bioreactor.

Continuous production of murine GM-CSF by recombinant Saccharomyces cerevisiae in an airlift bioreactor was studied at three different dilution rates. The reactor was initially fed with a selective medium to increase cell concentration, and then was fed with a rich, nonselective medium for GM-CSF production. Ethanol was used as the main carbon source to provoke GM-CSF expression. In continuous culture, GM-CSF production was maintained for over 150 h, even though the fraction of plasmid-carrying cells continuously dropped to lower than 20%. The stable GM-CSF production during the later phase of the continuous culture was attributed to increased specific cell productivity possibly resulting from an increase in the plasmid copy number in plasmid-carrying cells. This also indicated the possibility of natural selection of high-copy number cells in continuous culture. Plasmid stability was found to be growth rate (dilution rate) dependent; it increased with the dilution rate. Reactor productivity and specific productivity also increased with the dilution rate. A two-parameter kinetic equation was used to model the plasmid stability kinetics. The growth rate ratio between plasmid-carrying and plasmid-free cells increased from 0.996 to 0.998 while the segregational instability or the probability of plasmid loss from each cell division increased from 1.1% to 16% as the dilution rate decreased from 0.11 h-1 to 0.05 h-1. Oscillation of the dilution rate between 0.05 h-1 and 0.11 h-1 stabilized the plasmids and gave a higher productivity than that achieved without oscillation.

Animals↗
PubMed1996

Role of nitric oxide in the maintenance of resting cerebral blood flow during chronic hypertension.

The influence of nitric oxide (NO) on basal vascular tone varies with different hypertensive models or vascular beds. The goal of the present study was to examine the role of NO in the maintenance of resting cerebral blood flow (CBF) during chronic hypertension. In 9-10 months old Wistar-Kyoto (WKY) rats (n=47) and spontaneously hypertensive rats (SHR;n=47) anesthetized with pentobarbital sodium (60 mg/kg i.p.), regional CBF of the right parietal cortex was monitored by laser-Doppler flowmetry. Reductions in CBF in response to intravenous infusion of the NO synthase inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME; 1, 3, 10, and 30 mg/kg) were similar between WKY rats (17 +/- 6 approximately 43 +/- 6%; means +/- SE) and SHR (15 +/- 6 approximately 48 +/- 6%) while arterial blood pressure was maintained on the baseline level by controlled hemorrhage. Effects of L-NAME (3 mg/kg i.v.) on arterial blood pressure and CBF were almost completely inhibited by L-arginine (300 mg/kg i.v.), but not by D-arginine (300 mg/kg i.v.). In addition, intravenous infusion of L-arginine (300 mg/kg) alone did not affect resting CBF in both WKY rats and SHR. Thus, these findings suggest that 1) NO plays an important role in the maintenance of resting CBF in both normotensive and chronically hypertensive rats and 2) the contribution of NO to the maintenance of resting CBF is not altered during chronic hypertension.

Animals↗
PubMed1995

Ketamine antagonizes hypoxia-induced dopamine release in rat striatum.

The purpose of this study is to investigate the hypothesis that ketamine, a non-competitive antagonist of the N-methyl-D-aspartate (NMDA) receptor, attenuates hypoxia-induced striatal dopamine release in vivo. High-speed chronoamperometric recording techniques, using Nafion-coated carbon fiber electrodes, were used to evaluate extracellular dopamine (DA) concentration in the striatum. KCl and DA were locally applied directly to the striatum of urethane-anesthetized Sprague-Dawley rats, in order to measure release and clearance, respectively, of DA. These anesthetized animals were paralyzed with D-tubocurarine and connected to a respirator to allow controlled respiration. Systemic concentrations of oxygen and carbon dioxide were altered by changing the partial pressure of O2, CO2, N2 of inspired air and the rate of the respirator. Our data indicate that lowering the respiratory rate from 90 to 20 times/min for 5 min, in room air, caused a decrease in blood O2 while increasing the CO2 concentration. These changes in blood gas concentration were reversible and reproducible. We also found that lowering the respiratory rates potentiated K(+)-induced DA release but not DA clearance in the striatum. In an attempt to induce hypercapnia, the room air was replaced with high CO2-containing air (15% CO2 + 20% O2 + 65% N2), and this change resulted in increased blood CO2 levels without lowering O2 concentration. The hypercapnia did not alter K(+)-induced DA release in the striatum. Next, we attempted to simulate anoxic hypoxia in the absence of hypercapnia. Respiration with pure N2 for 30 s resulted in lowering blood O2 without increasing CO2 levels. Both basal and K(+)-evoked DA releases were increased during N2-induced anoxic hypoxia. These data suggested that transient hypoxia facilitates DA release in the striatum. It has been suggested that NMDA is involved in many hypoxia-mediated responses. We also found that systemic application of ketamine, which itself did not affect blood O2 or CO2 levels, antagonized hypoxia-induced electrochemical responses. These data suggest that the increase in DA release in vivo during short-term hypoxia may probably be mediated through NMDA receptors.

Animals↗
PubMed1995

Novel products and new technologies for use of a familiar carbohydrate, milk lactose.

The cheese industry produces large amounts of lactose in the form of cheese whey and whey permeate, generating approximately 27 million tonnes/yr in the US alone. Many uses have been found for whey and lactose, including uses in infant formula; bakery, dairy, and confectionery products; animal feed; and feedstocks for lactose derivatives and several industrial fermentations. Lactose use in food products, however, is somewhat limited because of its low solubility and indigestibility in many individuals. For this reason, lactose is often hydrolyzed before use. Still, demand is insufficient to use all available whey lactose. The result is a low market value for lactose; almost half of the whey produced each year remains unused and is a significant waste disposal problem. Several approaches are possible for transforming lactose into value-added products. For example, galactooligosaccharides can be produce through enzymatic treatments of lactose and may be used as a probiotic food ingredient. Organic acids or xanthan gum may be produced via whey fermentation, and the fermented whey product can be used as a food ingredient with special functionality. This paper reviews the physical characteristics, production techniques, and current uses of lactose, whey, and lactose derivatives. Also examined are novel fermentation and separation technologies developed in our laboratory for the production of lactate, propionate, acetate, and xanthan gum from whey.

Animal Feed↗
PubMed1994

Fiber optic sensor for Ca2+ based on an induced change in the conformation of the protein calmodulin.

A fiber optic sensor that exploits the natural selectivity of the Ca(2+)-binding protein calmodulin (CaM) is described. In this sensor, a dialysis membrane is used to entrap a fluorescein-labeled CaM (F-CaM) solution at the common end of a bifurcated fiber optic bundle. Ca2+ ions in a sample solution can diffuse through the membrane and bind to the F-CaM. Upon binding with Ca2+, CaM undergoes a conformational change that induces a change in the fluorescence of the attached fluorescein tag. This change in fluorescence can be related to the concentration of Ca2+ in the sample solution. The detection limit for the sensor is 5 x 10(-8) M Ca2+. The sensor has no interference by Mg2+ at concentrations as high as 10(-2) M.

Animals↗
PubMed1993

Effects of cilazapril on cerebral vasodilatation in hypertensive rats.

Endothelium-dependent dilatation of cerebral arterioles is impaired during chronic hypertension. The goal of this study was to determine the effects of an angiotensin converting enzyme inhibitor, cilazapril, on endothelium-dependent dilatation in pial arterioles. Four-month-old Wistar-Kyoto (WKY) rats and stroke-prone spontaneously hypertensive rats (SHRSP) received cilazapril in their drinking water (500 mg/L) for 3 to 6 months. Treatment with cilazapril reduced mean arterial pressure in both WKY rats and SHRSP and had no significant effect on baseline diameter of pial arterioles measured with a cranial window. Responses to bradykinin and A23187, but not to nitroglycerin and adenosine, were impaired in SHRSP. Cilazapril did not affect responses to bradykinin (3 x 10(-7) M) and A23187 (10(-5) M) in WKY rats but significantly increased cerebral vasodilatation in response to bradykinin (52 +/- 4% vs 27 +/- 5%) and A23187 (19 +/- 3% vs 8 +/- 3%) in SHRSP. Cilazapril also tended to increase dilator responses to nitroglycerin and adenosine in SHRSP. In another group of SHRSP, treatment with cilazapril for 4 days produced a moderate reduction in blood pressure and increased cerebral vasodilatation in response to bradykinin, A23187, and adenosine. Topical application of the active form of cilazapril (cilazaprilat) for 40 minutes also increased cerebral vasodilatation in response to bradykinin, A23187, and nitroglycerin in SHRSP. The data indicate that an angiotensin converting enzyme inhibitor enhances cerebral vasodilatation in response to endothelium-dependent agonists in SHRSP and may also increase responses to endothelium-independent agonists.

Animals↗
PubMed1991

Endothelium-dependent responses of cerebral blood vessels during chronic hypertension.

Acetylcholine produces less dilatation of pial arterioles in stroke-prone spontaneously hypertensive rats (SHRSP) than in normotensive (WKY) rats. Responses of cerebral vessels to acetylcholine and bradykinin appear to involve different mechanisms. Our first goal was to determine whether responses of pial arterioles to bradykinin are impaired in SHRSP. Diameter of pial arterioles (20-60 microns) was measured using intravital microscopy in WKY rats and SHRSP (9-12 months old). Superfusion of bradykinin (3 x 10(-7) M) dilated pial arterioles by 35 +/- 6% (mean +/- SEM) in WKY rats, but only 21 +/- 3% in SHRSP (p less than 0.05 versus WKY rats). Both nitric oxide (5 x 10(-7) M) and nitroglycerin (10(-5) M) produced similar vasodilatation in WKY rats and SHRSP. Our second goal was to determine whether alteration of postreceptor mechanisms contributes to impairment of endothelium-dependent cerebral vasodilatation in SHRSP. Calcium ionophore A23187 (10(-5) M) produced more vasodilatation in WKY rats than in SHRSP (32 +/- 8% versus 9 +/- 4%, p less than 0.05). Responses to A23187 (10(-5) M) were inhibited by indomethacin (46 +/- 13% versus 15 +/- 5%, p less than 0.05) in WKY rats, whereas responses to A23187 (10(-6) M) were potentiated modestly by indomethacin (-3 +/- 2% versus 4 +/- 2%, p less than 0.05) in SHRSP.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Mechanisms of impaired endothelium-dependent cerebral vasodilatation in response to bradykinin in hypertensive rats.

Bradykinin produces less dilatation of pial arterioles in stroke-prone spontaneously hypertensive rats than in normotensive Wistar-Kyoto rats. The goals of this study were to determine the mediator of bradykinin-induced dilatation in cerebral arterioles of rats and to determine whether responses to this mediator are altered in hypertensive rats. Diameter of pial arterioles (20-65 microns) was measured using intravital microscopy in 18 normotensive and 17 hypertensive rats. Superfusion of 3 x 10(-7) M bradykinin dilated pial arterioles by 53 +/- 4% (mean +/- SEM) in normotensive rats but only 33 +/- 6% in hypertensive rats (p less than 0.05 versus normotensive rats). Vasodilatation in response to bradykinin was almost completely inhibited by 280 units/ml catalase in both normotensive and hypertensive rats (n = 7 and n = 7, respectively) whereas 150 units/ml superoxide dismutase (n = 6 and n = 5, respectively) and 1 mM deferoxamine (n = 5 and n = 5, respectively) did not attenuate bradykinin-induced vasodilatation. These findings suggest that hydrogen peroxide is the mediator of bradykinin-induced dilatation in cerebral arterioles of rats. We also examined responses of cerebral arterioles to hydrogen peroxide in five normotensive and six hypertensive rats. Dilator responses of cerebral arterioles to 3.2 x 10(-5) M to 1.6 x 10(-4) M hydrogen peroxide did not differ in normotensive and hypertensive rats, which suggests that impaired dilatation of cerebral arterioles in response to bradykinin is not related to altered responsiveness of smooth muscle to an endothelium-derived relaxing factor.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Liquid chromatographic determination of the pH-dependent degradation of eseroline--hydrolysis product of physostigmine.

The stability of eseroline, the hydrolysis product of physostigmine under aerobic conditions, was studied by liquid chromatography. A reversed-phase, ion-pair technique was used to separate eseroline from its degradation products. The degradation of eseroline in phosphate buffer solutions of pH 6.91, 7.40, 7.98, 8.41 and 8.94 appears to follow first-order kinetics; the rate constant increased with an increase in pH. The degradation appears to follow specific base catalysis.

Journal Article↗
PubMed1987

Kinetics of Homoacetic Fermentation of Lactate by Clostridium formicoaceticum.

Clostridium formicoaceticum homofermentatively converted lactate to acetate at mesophilic temperatures (30 to 42 degrees C) and at pHs between 6.6 and 9.6. The production of acetate was found to be growth associated. Approximately 0.96 g of acetic acid and 0.066 g of cells were formed from each gram of lactic acid consumed at 37 degrees C. The concentration of the substrate (lactate) had little or no effect on the growth rate; however, the fermentation was inhibited by acetic acid. The bacterium grew at an optimal pH of 7.6 and an optimal temperature of 37 degrees C. Small amounts of bicarbonate were stimulatory to bacterial growth. Bacterial growth was enhanced, however, by the use of higher concentrations of bicarbonate in the media, only because higher buffer capacities were obtained and proper medium pH could be maintained for growth. Based on its ability to convert lactate to acetate, this homoacetic bacterium may be important in the anaerobic methanogenic process when lactate is a major intermediary metabolite.

Journal Article↗
PubMed1984

Effects of gentamicin solution and cream on the healing of open wounds.

When 0.1% gentamicin solution was applied to full-thickness skin wounds of dogs, the wounds became smaller by contraction during the first 7 days and continued to contract over the next 14 days. Wounds treated with 0.1% gentamicin cream enlarged during the first 7 days, followed by wound contraction over the next 14 days. The wounds treated with gentamicin solution also had more epithelialization at 7 days than did the cream-treated wounds; however, epithelialization of the 2 types of wounds was similar at 14 and at 21 days. Gentamicin solution and cream were effective in controlling bacterial growth on wounds when compared with the bacterial growth on the control wounds (not treated with antibiotics).

Administration, Topical↗
PubMed1978

Macrophage stimulation by bacterial lipopolysaccharides. II. Evidence for differentiation signals delivered by lipid A and by a protein rich fraction of lipopolysaccharides.

Stimulation of macrophages to lyse tumor cells is a property common to lipopolysaccharide (LPS) extracted from a variety of smooth and rough bacterial strains by several different preparative procedures. The relationship between macrophage stimulation and the structural characteristics of LPS is defined. In protein-free LPS, lipid A bears the stimulatory signal which results in the differentiation of elicited macrophages into killer cells. The polysaccharide moiety is neither stimulatory itself nor does it block the activity of complete LPS on macrophages. Extraction of LPS by the butanol or Boivin procedures produces preparations in which LPS is complexed through its lipid A moiety to a protein rich component, LAP. Isolated LAP delivers a macrophage differentiation signal which is independent of lipid A. The presence of these two structurally distinct constituents in the cell walls of gram-negative bacteria broadens the biological environments in which they can stimulate macrophages in vivo.

Cell Differentiation↗