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Biomedical subjects

C M Yang

Publications and source records attributed to C M Yang.

At least 127 records · Page 7Linked to original sources
PubMed1991

Ocular fundus examination in premature infants.

In order to better acknowledge the ocular fundus picture in premature infants and to determine the incidence and clinical course of retinopathy of prematurity (ROP), from October 1987 to April 1989, 187 cases with a gestational age of less than 38 weeks or a birth weight of less than 2,500 g were enrolled for examination and follow-up study with indirect ophthalmoscope. One hundred and fifty cases (80.21%) were free from ROP bilaterally. Thirty-seven cases (19.79%) had ROP. Except for one case that showed unilateral regressed ROP, all were bilaterally affected. The mean birth weight and gestational age in the nonROP group were 1,824 +/- 426 g and 33.6 +/- 2.9 weeks, respectively, and in the ROP group were 1,395 +/- 490 g and 30.7 +/- 3.9 weeks, respectively. The difference for both factors between the two groups were statistically significant (p less than 0.05). Several specific fundus features were noticed in a high percentage of the nonROP group, these included a small cup to disc (C/D) ratio, pigmented ring around the disc, hypopigmented fundus and a greenish-gray color in the peripheral vascularized retina. In addition, 8.2% of this group had persistent primary vitreous remnant, and 5.6% had retinal hemorrhage. The macular development was subdivided into three stages. In both the ROP and nonROP groups, the difference of gestational age at each advancing stage was statistically significant by the Student t-test. No delay in macular development was noticed in the ROP group.(ABSTRACT TRUNCATED AT 250 WORDS)

Follow-Up Studies↗
PubMed1990

Temperature sensitivity as a general phenomenon in a collection of chlorophyll-deficient mutants of sweetclover (Melilotus alba).

A collection of chlorophyll (Chl)-deficient mutants of sweetclover (Melilotus alba) with defects in eight nuclear loci were grown at 17 or 26 degrees C. Plants grown at either temperature were examined for Chl content, Chl a/b ratio, expression of the light-harvesting complex II (LHC-II) apoproteins, and protochlorophyllide (Pchlide) biosynthetic capacity. Except for the ch4 mutant, the parental strain and all mutants accumulate more Chl when grown at 26 degrees C than at 17 degrees C. The ch5 mutants, lacking Chl b under any growth condition, and the ch12 mutant showed little temperature-dependent phenotypic plasticity, whereas this was a marked phenomenon in the other mutants. The ch10 and ch11 mutants demonstrated extreme temperature sensitivity with regard to the production of Chl b and the Chl b-binding LHC-II apoproteins. When excised trifoliolates were supplemented with exogenously supplied delta-aminolevulinic acid, only the ch4 mutant was markedly impaired in the ability to produce Pchlide. These data indicate that temperature-sensitive phenotypic plasticity is a common phenomenon of chlorphyll-deficient mutants and substantiate that only a minority of Chl-deficient mutants is impaired in the biosynthesis of Chl.

Animals↗
PubMed1990

Down-regulation of muscarinic receptors in the striatum of organophosphate-treated swine.

Subacute (daily) administration of diisopropylfluorophosphate (DFP) to male swine (Yorkshire white) resulted in a 97% inhibition of cholinesterase and a decrease of [3H]quinuclidinyl benzilate [( 3H]QNB) binding sites in homogenates of striata by approximately 50% after 14 days. The maximal density of receptors (Bmax) decreased from 2.1 +/- 0.3 to 1.0 +/- 0.2 pmole/mg protein. There was no significant change in the dissociation constant (Kd) for [3H]QNB binding (control: 52.6 +/- 10.7 pM; 7-day: 57 +/- 2.8 pM). Carbachol displacement of [3H]QNB binding yielded data best fit by a two-binding site model. The dissociation constants were KiL = 115 +/- 62 microM (55 +/- 3%) and KiH = 1.8 +/- 0.7 microM (45 +/- 3%), respectively, for the low- and high-affinity states. Seven-Day treatment with DFP reduced the percentage of high-affinity receptors to 22 +/- 8.6%, but affected neither the low- nor the high-affinity Kd (100 +/- 20 and 2 +/- 0.6 microM). With the addition of Mg2+, striatal homogenates had low- and high-affinity receptors in the proportion of approximately 1 to 1. In the presence of Gpp(NH)p + Mg2+ the ratio of high- to low-affinity receptors was 3:1 in homogenates of control tissue (to 26 +/- 5%). This treatment had no effect on this ratio in homogenates of tissue from 7-day DFP-treated swine (3:1) since it was already 3:1. Pirenzepine displacement of [3H]QNB binding was best described by a two-binding site model, with Ki values of 38 +/- 14 and 201 +/- 78 nM, which represent 74 and 26% of the binding sites, respectively. The high affinity Kd value was unchanged following 7 days of DFP treatment (24 +/- 5 nM). There appears to be little change in the displacement curves for pirenzepine inhibition of [3H]QNB binding. This suggests that about 75% of the receptors are of the M1 subtype. Thus, subacute administration of DFP causes not only a decrease in the number of receptors, but also a change in the proportion of agonist affinity states which is related to the interaction of the guanine nucleotide binding protein and the muscarinic receptor.

Acetylcholinesterase↗
PubMed1990

Influence of ethanol on glutathione-S-transferase activity and glutathione content in the isolated perfused rabbit lung.

The induction of pulmonary glutathione-S-transferase (GST) by ethanol was investigated using the isolated perfused rabbit lung (IPRL) preparation with particular attention paid to the duration and route of ethanol administration. For perfusion with buffer containing 0.2% ethanol or acute ethanol treatment (4 g/kg by gastric intubation) 4 h before the IPRL preparation, there were no differences in the rate of glutathione (GSH) conjugation with 1-chloro-2,4-dinitrobenzene (CDNB) at low substrate concentrations (100-400 microM) but a decrease was observed in the rate at high substrate concentrations (500-1000 microM). Lungs from rabbits treated acutely showed the lowest maximal rate of GSH conjugation in the IPRL. Prolonged treatment with ethanol (10% in drinking water for 3 weeks) increased GSH conjugation (CDNB concentration of 300-750 microM). None of these ethanol treatments altered GSH conjugation with 1,2-epoxy(p-nitrophenoxy)propane (ENP). Upon termination of perfusion, there were no differences in pulmonary GSH concentration between control and ethanol-treated groups. Therefore, the effect of altered GSH level as a co-substrate on GST activity in lung might be excluded as an explanation for the effects of ethanol. These data suggest that ethanol has differential effects on GST activity depending upon the substrate and duration of ethanol administration.

Animals↗
PubMed1990

Glutathione conjugation in the isolated perfused rabbit lung: the effects of carbon monoxide, buthionine sulfoximine and cibacron blue.

The effect of carbon monoxide (CO) on pulmonary glutathione-S-transferase (GST) activity was investigated using the isolated perfused rabbit lung (IPRL) preparation. CO at a concentration of 7.5% did not alter the conjugation of glutathione (GSH) with 1,2-epoxy-(p-nitrophenoxy)propane (ENP) in the IPRL. The rate of GSH conjugate formation with ENP was not altered when the lung was exposed to a selective inhibitor of gamma-glutamylcysteine synthetase, buthionine sulfoximine (0.1 mM), but was significantly diminished (P less than 0.01) by co-administration of GST inhibitor cibacron blue (1 microM) with ENP. These results indicate that the rabbit lung actively conjugates GSH with ENP and that this reaction may be decreased by specific inhibitors of GST. However, the rate of GSH conjugation is not affected by CO ventilation in the IPRL.

Administration, Inhalation↗
PubMed1990

Muscarinic receptor expression in the primary culture of tracheal smooth muscle cells.

Tracheal smooth muscle cells (TSMCs) were isolated from dog trachea in order to analyze the direct effects of growth factors and hormones on cell proliferation and muscarinic receptor (mAchR) expression. Dissection and dissociation of tracheal smooth muscle tissue with a collagenase I, deoxyribonuclease I and elastase IV mixture resulted in high yield and viability of TSMCs. A screen of growth factors, hormones, and serum concentration for the stimulation of cell growth, revealed that insulin-like growth factor, basic fibroblast growth factor, epidermal growth factor, insulin, transferrin, or hydrocortisone alone at the concentration used was not necessary or sufficient to stimulate growth of TSMCs in the primary culture with DMEM/F-12 containing 1% FBS. The regulation of cell surface mAchR expression in response to serum and cell growth in primary culture of TSMCs has been examined. In the presence of 1% serum, TSMCs withdraw from the cell cycle and express high levels of cell surface mAchRs. Exposure of quiescent TSMCs to 10% serum results in a loss of surface mAchRs. In addition, insulin-like growth factor, insulin or transferrin could stimulate the expression of mAchRs on TSMCs cultured in DMEM/F-12 containing 1% FBS. The results demonstrated that low serum concentration culture system may provide a useful model to elucidate the expression of mAchRs in the culture of TSMCs.

Animals↗
PubMed1989

Effects of sulfhydryl reagents on [3H] inositol trisphosphate binding to dog cerebellar membranes.

Homogenates from dog cerebellum were fractionated using sucrose gradient centrifugation. The [3H]inositol 1,4,5-trisphosphate binding and the glucose 6-phosphatase activities were found to co-purify. The binding was saturable and had high affinity (Bmax = 44 pmol/mg protein, Kd = 116 nM). Selective chemical modification was used to examine amino acid residues of the microsomal receptor that might be critical for the binding of inositol trisphophate. Sulfhydryl reagents, p-chloromercuricphenyl sulfonic acid. eosin 5-maleimide, N-ethyl maleimide and fluorescein 5-maleimide were found to be highly potent inhibitors of the binding with half-maximal inhibition occurring at about 20 microM, 70 microM, 1 mM, and 0.1 mM, respectively. The inhibition was specific since the presence of 10 microM of inositol trisphosphate during the reaction completely protected against the inhibition by these reagents. These results suggest that sulfhydryl group is essential for inositol trisphosphate binding to its receptor.

Animals↗
PubMed1989

Effect of three concentrate feeding frequencies on rumen protozoa, rumen digesta kinetics, and milk yield in dairy cows.

Three rumen-cannulated Holstein cows in mid to late lactation were randomly assigned to a 3 x 3 Latin square with the following concentrate feeding frequencies: one, two, and four times daily. Cows were fed ad libitum a diet containing 55% corn silage and 45% concentrate (DM basis). The forage portion of the diet was fed twice daily to all cows separately from the concentrate. Each experimental period was 20 d in duration. After a 12-d adaptation, daily individual feed consumption and milk production were measured. Rumen digesta were collected prior to (0 h) and at 2, 4, and 8 h after the morning feeding to measure postprandial changes in protozoa numbers, pH, VFA, and NH3 N. Chromium-EDTA and ytterbium chloride were used as liquid and particulate markers to estimate liquid and solid digesta turnover rate in the rumen. Concentrate and forage DM intake, ruminal protozoa numbers, pH, VFA, and NH3 N concentrations, and digesta turnover rate were not affected by concentrate feeding frequency. There was a significant concentrate feeding frequency with sampling time interaction influence on NH3 N in which feeding concentrate four times daily minimized postprandial fluctuation of rumen NH3 N concentration. Feeding concentrate four times daily increased milk fat and protein production.

Animal Feed↗
PubMed1989

Dietary calcium and development of hypertension in spontaneously hypertensive rats.

The purpose of the present study was to attempt to correlate four calcium diets (0.02, 0.1, 0.5 and 2.5%) with changes in the development of hypertension in both spontaneously hypertensive and Wistar-Kyoto rats. Our findings confirm that an inverse relationship exists between dietary calcium content and the development of hypertension. The relationship does not rely upon altered serum ionized sodium, potassium, or calcium or parathyroid hormone levels. In addition, no consistent dietary calcium-dependent changes were noticed in cardiovascular reactivity. In contrast, anesthesia with pentobarbital completely abolished the relationship. These data support the hypothesis that dietary calcium influences autonomic tone through some, as yet, undefined processes.

Animals↗
PubMed1989

An animal study of portal hypertension.

For the purpose of elucidation the mechanism of portal venous resistance and portal venous blood flow in maintaining an elevated portal hypertension. The splanchnic and systemic hemodynamics were evaluated in portal hypertensive rat model, which is induced by partial portal vein ligation (PVL). Organ blood flow and portal-systemic shunting were measured by radio-active microsphere techniques. In this study all the PVL rats had higher mean portal venous pressure (15.2 +/- 1.6 mmHg) when compared to the Sham-operation control rats (5.3 +/- 1.2 mmHg). Furthermore, portal systemic shunting was significantly higher in the 14th day PVL rats (87.2 +/- 3.6%) than control rats (0.3 +/- 0.1%) (p less than 0.05). There was a rapid increase in portal venous inflow from the 4th day (6.1 +/- 0.8 vs 4.2 +/- 0.7 ml/min/100 gm BW, p less than 0.05) in the PVL rats than in control rats. However, the total peripheral resistance and splanchnic arterial resistance were reduced in the 14th PVL rats than control rats. The Cardiac index was much higher in the 14th PVL rats than control rats. Thus our results demonstrate that portal hypertension is maintained by a hyperdynamic portal venous inflow. This model is reproducible for us to study portal hypertension within a short period of time.

Animals↗
PubMed1988

The influence of verapamil and nifedipine on hepatic indocyanine green clearance in patients with HBsAg-positive cirrhosis and ascites.

The influence of verapamil and nifedipine on hepatic indocyanine green kinetics was studied in 12 patients with HBsAg-positive cirrhosis and ascites. Hepatic clearance and its two biologic determinants, hepatic blood flow and metabolic activity (intrinsic clearance [maximum velocity/metabolite elimination rate constant, or Vmax/km]), were determined from hepatic indocyanine green elimination at steady state in patients with cirrhosis. Acute intravenous administration 10 mg verapamil significantly increased the hepatic indocyanine green blood flow (p less than 0.05), but significantly decreased the hepatic clearance (p less than 0.05), extraction ratio (p less than 0.05) and Vmax/km (p less than 0.05). However, acute sublingual administration of 10 mg nifedipine resulted in no significant change in any parameters of hepatic elimination function. These results show that verapamil, but not nifedipine, might impair the transhepatic extraction activity of hepatocytes in patients with HBsAg-positive cirrhosis and ascites.

Aged↗
PubMed1988

Changes in affinity states during down-regulation of muscarinic receptors in tracheal smooth muscle of organophosphate-treated swine.

1. Subacute (daily) treatment of male swine with the organophosphate acetylcholinesterase inhibitor diisopropylfluorophosphate (DFP) resulted in tolerance to the effects of DFP within 5-6 days. 2. Subacute administration of DFP resulted in a 98% inhibition of tissue cholinesterase after 7 days and in a decrease of [3H]quinuclidinyl benzilate [( 3H]QNB) binding sites in homogenates of tracheal smooth muscle by 77%. The maximal density of receptors (Bmax) decreased from 1.8 +/- 0.4 to 0.5 +/- 0.1 pmole mg-1 protein. There was no significant change in the dissociation constant (Kd) for [3H]QNB binding. 3. Pirenzepine displacement of [3H]QNB binding was best described by a single binding site model, with a Ki of 230 +/- 40 nM. This value was unchanged following seven days of DFP treatment (250 +/- 30 nM). The low affinity for this M1 antagonist suggests that there is predominantly a single population of [3H]QNB binding sites of the M2 subtype in tracheal smooth muscle. 4. Carbachol displacement of [3H]QNB binding yielded data best fit by a two-binding site model. The dissociation constants were KiL = 210 +/- 60 microM (61 +/- 1%) and KiH = 1.2 +/- 0.4 microM (39 +/- 1%) respectively (n = 7) for the low and high affinity states. Seven-day treatment with DFP reduced the percent of high affinity receptors to 25 +/- 4%. 5. Addition of Mg++ to the incubation medium prevented this shift in the proportion of low and high affinity receptors. Gpp(NH)p and Mg++ together decreased the proportion of the high affinity receptors when added to the incubation medium in control tissue (to 25%), but not tissue from 7-day DFP-treated swine. NEM increased the proportion of muscarinic receptors in the high affinity state both for controls and for the DFP-treated swine, in both cases yielding receptors with identical binding properties. 6. Thus, subacute administration of DFP causes not only a decrease in the number of receptors, but also a change in the affinity of the receptors for agonists which is related to the interaction of the guanine nucleotide binding protein and the muscarinic receptor.

Animals↗
PubMed1988

Contractile responses of tracheal smooth muscle in organophosphate-treated swine: 1. Agonist changes.

1. Male weanling swine were injected daily for up to 14 days with the organophosphate cholinesterase inhibitors, diisopropylfluorophosphate (DFP) or sarin. The clinical signs of poisoning disappeared or were attenuated by 7 days after starting the DFP treatment, indicating the development of tolerance to DFP toxicity. 2. A significant decrease in acetylcholinesterase activity (85-98%) occurred over the course of this treatment followed by a decrease in the maximal density (Bmax) of [3H] quinuclidinyl benzilate ([3H]QNB) and [3H] N-methylscopolamine ([3H]-NMS) binding sites in isolated cells. The affinity of the muscarinic receptors (KD) for [3H]QNB and [3H]NMS binding, however, remained unaffected. 3. Dose-response curves for ACh-induced increase in isometric tension of tracheal smooth muscle (TSM) showed a leftward shift from control, 2 h after DFP injection. Twenty-four hours after the last DFP treatment, for animals receiving 1 or up to 14 daily injections of DFP, all the dose-response curves were shifted to the left to approximately the same ACh sensitivity when compared with that for control tissue. 4. In vitro treatment of the muscle with 10(-4) M DFP shifted the dose-response curves leftward, in both control and injected animals, and rendered the muscles from control, 1- and 3-day injected animals sensitive to ACh concentrations as low as 10(-10) M. Sensitivity to 10(-10) M ACh was eliminated by carefully cleaning the smooth muscle of adherent connective tissue containing nerves and ganglia and after subacute treatment of swine for 7 days with DFP. DFP-induced spontaneous contractions were also eliminated by careful cleaning. 5. Subacute DFP treatment caused a small leftward shift in the dose-response curve for bethanechol at 2 h and a rightward shift at 1,3 and 7 days, compared to controls. 6. Dose-response curves for K+ were shifted to the right after 1 and 3 days of DFP treatment, but shifted back towards the control after 7 days of treatment. The muscle cells were hyperpolarized by approximately 5 mV after 7 days of DFP or sarin injections. The membrane potential was slightly more sensitive to changes in K+ concentration after 7 days of sarin injection. 7. Subacute treatment of swine with organophosphates modifies the response of neural elements in swine TSM to ACh. Chronic cholinesterase inhibition causes a reduction in the sensitivity of the neural elements to ACh. The decrease in muscarinic receptor density which occurs with chronic cholinesterase inhibition is not sufficient to explain tolerance to organophosphates since TSM maintains an almost normal responsiveness to ACh.

Acetylcholine↗
PubMed1988

Contractile responses of tracheal smooth muscle in organophosphate-treated swine: 2. Effects of antagonists.

1. Swine tracheal smooth muscles (TSM) developed spontaneous contractions following the acute administration of DFP in vivo and/or in vitro which could be blocked pharmacologically using atropine (2 x 10(-7) M), pirenzepine (3 x 10(-7) M), or hemicholinium 3 (HC3, 5 x 10(-6) M). 2. Treatment of TSM in vitro with DFP caused them to become responsive to ACh concentrations as low as 10(-10) M. 3. Atropine and pirenzepine (at 2 and 3 x 10(-7) M respectively) increased the EC50 concentrations for ACh approximately 300- and 8-fold respectively. The shifts caused by atropine and pirenzepine in the dose-response curves for ACh were not parallel after in vitro treatment of the muscle with DFP. By contrast, the shifts in the dose-response curves were parallel when muscles from swine injected for 7 days with DFP were used. 4. HC3 had no effect on the control dose-response curve for ACh, but steepened the dose-response curve after in vitro treatment of the muscle with DFP. The ACh dose-response curve obtained in the presence of HC3 and DFP was identical to that obtained using muscles from swine treated for 7 days with DFP. 5. McN-A-343, a partial agonist at muscarinic receptors, also induced contraction although the maximal tension induced was 56% of the maximal tension obtained using ACh. In vitro treatment of the muscle with DFP caused a leftward shift in the dose-response curve for McN-A-343. The muscles from animals treated for 7 days with DFP did not respond to McN-A-343 at doses up to 10(-3) M. 6. McN-A-343 competition for [3H]QNB binding suggested that the loss of the contractile response can be correlated with the loss of a high affinity site for McN-A-343 from the muscle. 7. We conclude that tolerance to DFP with subacute treatment results in part from the reduction in sensitivity of neural elements associated with swine tracheal smooth muscle to ACh. In addition the response to the partial agonist McN-A-343 is lost after subacute DFP treatment.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗
PubMed1988

Muscarinic stimulation of submucosal glands in swine trachea.

The properties of muscarinic acetylcholine receptors (mAChR) on tracheal explants and isolated submucosal gland cells were determined using [3H]quinuclidinyl benzilate ([3H]QNB) and N-[3H]methylscopolamine ([3H]NMS) as ligands. Analysis of competitive displacement of ([3H]NMS binding by pirenzepine demonstrated the presence of M1- (27 +/- 2%) and M2G- (73 +/- 2%) receptors on isolated tracheal submucosal gland cells (TSGC's) in control. Daily administration of diisopropylfluorophosphate (DFP) inhibited cholinesterase activity by greater than 95%. After 7 days of DFP treatment, [3H]QNB binding to intact TSGC's decreased from 14.2 +/- 0.6 to 6.3 +/- 0.8 fmol/10(6) cells; similarly, [3H]NMS binding fell from 8.1 +/- 1.9 to 2.0 +/- 0.8 fmol/10(6) cells. The loss of mAChR's was predominantly of the M2G subtype with the relative proportion dropping to 33%. In addition, 90% of the receptors assumed the high-affinity state for carbachol displacement of [3H]NMS. Mucus secretion was quantitated by measuring the release of 3H-labeled mucus macromolecules from explants of tracheal submucosal glands and isolated cells. Acetylcholine (ACh), 2 X 10(-5) M, stimulated mucus secretion by 2.5 and 2.3 times the basal rate, respectively. Elimination of acetylcholinesterase (AChe) by DFP increased the ACh sensitivity by 18- and 5-fold. Tracheal explants or TSGC's obtained 2 h after an in vivo DFP treatment showed a 6- and 3-fold ACh stimulation. This ACh sensitivity decreased during the continued daily dosing with DFP such that only a 1.3- and 1.1-fold ACh stimulation was apparent after 7 days of treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Acetylcholine-stimulated chloride flux in tracheal submucosal gland cells.

The Cl content of isolated tracheal submucosal gland cells was studied using 36Cl as a tracer. 36Cl uptake reached a steady state within 10 min, yielding an estimate of intracellular Cl concentration of approximately 40 mM. Intracellular Cl fell rapidly when ouabain or furosemide was added, indicating that isolated tracheal submucosal gland cells concentrate Cl above its electrochemical equilibrium concentration. Acetylcholine (ACh) caused a Ca2+-dependent decline in cell Cl, with an effective concentration for a 50% response (EC50) of 62 nM; this loss of cell Cl was blocked by atropine or pirenzepine. The EC50 was 6 nM in cells when 95% of the acetylcholinesterase activity was abolished by diisopropylfluorophosphate (DFP) treatment. ACh continued to cause a decline in cell Cl even after a 7-day course of DFP treatment, which has been shown to abolish ACh-stimulated mucous glycoprotein secretion (23). After the 7-day course of DFP treatment, the EC50 for ACh increased to 77 nM. Thus the Cl economy of the tracheal submucosal gland cell resembles that of cells in epithelia that secrete fluid; in addition, the transmitter-dependent loss of cell Cl is under long-term metabolic control of the cell.

Acetylcholine↗