Hartree-Fock method posed as a density-functional theory: Application to the Be atom.
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Journal Article↗
Biomedical subjects
C Zhang
Publications and source records attributed to C Zhang.
Regulation of glycolytically fueled Ca2+ uptake in smooth muscle plasmalemmal vesicles by phosphorylation.
A highly purified plasma membrane vesicular preparation from porcine antrum had an endogenous protein kinase activity with substrates of molecular weights of 11, 15, 20.5, 25, 35, 44, 155, and 230 x 10(3). Phosphorylation of the plasma membranes by the endogenous protein kinase activity resulted in a stimulation of initial rates of Ca2+ uptake into inside-out vesicles, which was associated with an increase in the maximum velocity of the Ca2+ pump with no apparent changes in the half-maximal effective concentration for calcium. Because we have previously reported that a membrane-associated glycolytic system may preferentially provide ATP to fuel the Ca2+ pump (9), we examined the effects of phosphorylation on Ca2+ uptake when glycolysis was the sole source of ATP for the pump. We found that the stimulation of Ca2+ uptake by phosphorylation was more pronounced when Ca2+ uptake was supported by glycolysis rather than 2 mM ATP. When ATP was added at a level similar to that produced by endogenous glycolysis, the stimulation of Ca2+ uptake by phosphorylation was comparable to when glycolysis supported the Ca2+ pump. Our observations suggest that the dynamic range (up to threefold) for regulation of the plasmalemmal Ca2+ pump by phosphorylation is considerably larger than previously reported and thus likely to be of physiological significance.
Adenosine Triphosphate↗
Chiroinositol deficiency and insulin resistance. III. Acute glycogenic and hypoglycemic effects of two inositol phosphoglycan insulin mediators in normal and streptozotocin-diabetic rats in vivo.
Two insulin mediators, inositol phosphoglycans, were isolated from bovine liver by methods previously developed for rat liver, i.e. chromatography on an AG 1 x 8 ion exchange column and selective elution with HCl at pH 2.0 and 1.3. The pH 2.0 mediator containing D-chiroinositol stimulated pyruvate dehydrogenase phosphatase, whereas the pH 1.3 mediator containing myo-inositol inhibited cAMP-dependent protein kinase. Each mediator was further purified by thin layer and Bio-Gel P4 column chromatography and injected ip into normal fed rats together with [U-14C]glucose. After 2.5 h, diaphragms were removed, and glycogen isolated. Insulin mediators, like insulin, stimulated [U-14C]glucose incorporation into glycogen by 150-160% in a dose-dependent manner in the nanomolar range. Mediators injected iv in the nanomolar range into low dose streptozotocin-diabetic rats decreased plasma glucose 30-45% in 30-60 min, with a return to basal concentrations after 150-180 min. These in vivo insulin-like effects of mediator were observed without changes in serum insulin concentrations. The pH 2.0 mediator was 50-100 times more active (per nmol organic phosphate) than the pH 1.3 mediator in the ip diaphragm glycogenesis assay. Mediator effects on diaphragm were completely blocked by preincubation with an immunopurified inositol phosphoglycan antibody. Both mediators were equally active iv in lowering plasma glucose (per nmol inositol) at concentrations comparable to those of insulin.
Animals↗
[The influence of changing the Ca2+ concentration of the point quze (PC3) on the curative effect of puncturing neiguan (PC6) in experimental arrhythmic rabbits].
The experimental arrhythmic model was made with Aconitin in rabbits. The Neiguan (PC6) point was punctured to observe the influence on recovering time of arrhythmia. After the curative effect of puncturing Neiguan(P6) was confirmed, Ca2+ in the Quze (PC3) point of the Pericardium is chelated by EDTA solution to observe the influence on curative effect of arrhythmia by puncturing Neiguan. The result shows that the curative effect doesn't exist after the Ca2+ in Quze is chelated. It is probable that Ca2+ is one of the most important factors producing acupuncture effect. As a result, Ca2+ probably involves in the activities of channels and collaterals.
Aconitine↗
[Experimental study on bone formation induced by porous HA-beta-TCP bioceramics].
Three types of HA-beta-TCP active bioceramics which have various porosity and porous diameters were implanted into femurs and muscles of dogs. Histological and biomechanical tests proved that the porous HA-beta-TCP could make the active stage of bone formation moved up in bones and induce new bone formation in muscles. The pores were easily filled with new bones in samples which had smaller porous diameter than samples having larger porous diameter. The final strength after accomplishment of repair process was closely related with porosity. In samples with lower porosity, the proportion of organic bone and the strength were also lower, but in samples with higher porosity the proportion of organic bone and the strength were also higher. Up to the fourth month postoperatively, the strength of HA-beta-TCP with proper porous diameter and porosity which had been implanted into bones was as high as that of organic bone.
Animals↗
Suppression of C-1300 murine neuroblastoma cell proliferation in tissue culture and tumor growth in vivo by (Z)5'-fluoro-4',5'-didehydro-5'-deoxyadenosine (MDL 28,842), an irreversible inhibitor of S-adenosyl-L-homocysteine hydrolase.
The effect of the irreversible S-adenosyl-L-homocysteine hydrolase inhibitor, (Z)-5'-fluoro-4',5'-didehydro-5'-deoxyadenosine (MDL 28,842), on C-1300 murine neuroblastoma (MNB) cell proliferation in tissue culture and MNB tumor growth in vivo were investigated. MNB cells were incubated with MDL 28,842 at concentrations ranging from 8 x 10(-9) M to 1.6 x 10(-5) M for 3 days, and cell proliferation was determined by use of a CellTiter 96-well Proliferation Assay Kit. In tissue culture, MDL 28,842 inhibited MNB cell proliferation in a concentration-dependent manner, and the IC50 of MDL 28,842 against MNB in tissue culture was 1.8 x 10(-7) M. The response of in vivo tumor growth and host survival to MDL 28,842d was evaluated in a syngeneic mouse tumor model prepared by s.c. implantation of 1 x 10(6) MNB cells into A/J mice. Following palpation of a tumor mass, osmotic minipumps were implanted into each mouse. MDL 28,842 was infused at rates of 1.0 or 1.5 mg/kg/day over a 10-day period and 1.25 mg/kg/day over a 30-day period. The mean survival time of tumor-bearing mice significantly increased from 28.75 +/- 1.06 days (mean +/- 2 SEM) in the control group (diluent infusion) to 39.33 +/- 1.58 days, 44.11 +/- 1.74 days, and 41.0 +/- 1.30 days in the MDL 28,842-treated groups receiving 10-day infusions of 1.0 and 1.5 mg/kg/day or 30-day infusions of 1.25 mg/kg/day, respectively. No significant differences in survival rate were noted between groups receiving 10 vs 30 days of drug treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
Adenosine↗
Treatment of 121 patients with malignant effusion due to advanced lung cancer by intrapleural transfer of autologous or allogeneic LAK cells combined with rIL-2.
Lymphocytes isolated from malignant pleural effusion in patients with advanced lung cancer or from allogeneic peripheral blood of healthy donors were induced to become LAK cells after in vitro culture with rIL-2. One hundred and twenty-one patients with malignant effusions were treated by intrapleural transfer of autologous or allogeneic LAK cells combined with rIL-2. The effusion disappeared in 71 patients (58.6%) and was significantly decreased in 45 patients (36.2%). Five patients did not respond to treatment. Tumor cells in pleural effusions disappeared or were significantly decreased in number, whereas the lymphocytes were significantly increased in number in all responders. Except for transient fever in 10 patients, no serious side effect was observed.
Adenocarcinoma↗
[Determination of acyclovir in human plasma by RP-HPLC].
A RP-HPLC method was developed for the determination of acyclovir (ACV) in human plasma. ACV was extracted from plasma using ODS, obtained from Sep-Pak C18 cartridge (Waters associates) and reinstalled in a self-made glass tube suitable for extraction of solutes from small volume plasma samples. After extraction, and rinsing the ODS extract with water to remove hydrophilic impurities, ACV was recovered with methanol and chromatographed on YWG C18H37 column, and detected at 254 nm. The mobile phase was 5.0% (v/v) methanol/water. The average recovery of ACV was 73.5%; the minimum detection concentration of ACV in plasma was 20 ng/ml with a plasma volume of 0.2 ml and S/N value of 2. A good linear relationship between the peak area ratios and ACV concentrations was found at the ACV concentrations ranging from 0.2 to 1.0 microgram/ml, CACV = 0.840 AACV/Ais + 0.002, r = 0.9969.
Acyclovir↗
[Capillary blood viscosimeter of the microcomputer].
On the basis of specific property of non-Newtonian fluid (blood) we have worked out the formula of capillary blood viscosimeter:sheat stress tau alpha = alpha rho gh/2L shear rate f (tau alpha) = 1/pi alpha 3 [3q + h(dq/dh)] and designed and produced the prototype. Repetition experiments have indicated that the property of the instrument is stable, and a comparison of the prototype with the cone and plate viscosimeter has demonstrated the reliability of the measurements.
Blood Viscosity↗
Acadesine prevents oxidant-induced damage in the isolated guinea pig heart.
Acadesine is a cardioprotective nucleoside that can attenuate postischemic contractile dysfunction in the isolated heart even if administered at reperfusion, thereby implying an effect on a reperfusion-induced component of injury. Consequently, the effects of acadesine on the maintenance of cardiac function were evaluated in isolated guinea pig hearts in which the perfusion buffer was subjected to electrolysis to produce a mixture of free radicals and oxidants that have been implicated in reperfusion injury. A reduction of left ventricular developed pressure to 38 +/- 3% at 10 min after electrolysis was prevented by acadesine in a concentration-dependent manner (EC50 1 microM). Hypochlorous acid (HOCl) is a principal oxidizing species implicated in electrolysis-induced myocardial damage, and it is a major oxidant produced by neutrophils. Isolated hearts, perfused with HOCl to induce damage, were also protected by acadesine (EC50 1-3 microM). In addition, acadesine protected alpha 1-antiproteinase (alpha 1-AP) against inactivation by 30 microM HOCl with an EC50 of approximately 10 microM, demonstrating that acadesine reacts rapidly enough with HOCl to protect important biological targets. Additionally, acadesine scavenged the hydroxyl radical with a second-order rate constant of 5.0 x 10(9) M-1 s-1. In contrast, acadesine had no effect on superoxide anions generated from either xanthine-xanthine oxidase or hydrogen peroxide-mediated peroxidation. The free base of acadesine 5-amino-4-imidazole carboxamide (AICA) also reduced HOCl and attenuated the electrolysis-induced cardiac injury. However, unlike the parent molecule acadesine, AICA was not protective in the isolated heart subjected to ischemia and reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)
Aminoimidazole Carboxamide↗
Photosensitization with anticancer agents. 18. Perylenequinonoid pigments as potential photodynamic therapeutic agents: preparation and photodynamic properties of amino-substituted hypocrellin derivatives.
Perylenequinonoid pigments have demonstrated several photodynamic therapeutic advantages over the commonly used hematoporphyrin derivatives. Certain new amino-substituted hypocrellin B derivatives have been prepared, and both direct and reductive aminations of hypocrellin B are described. The photophysical and photochemical properties of the amino-substituted hypocrellin B derivatives were investigated, and their significantly enhanced red absorptivities and strong 1O2-generating functions qualify them as promising photodynamic therapeutic agents. In addition, the superoxide anion radical was also determined to be implicated in the photosensitization of the amino-substituted hypocrellin B derivatives.
Amination↗
Mitochondrial DNA mutation associated with aging and degenerative disease.
Previous theories of aging based on somatic mutation neglected mtDNA, which has a high propensity for mutational error. Knowledge of yeast mtDNA mutations and their functional effects, and of human mtDNA mutations identified in the mitochondrial cytopathies, provides for a concept of aging based on the cumulative effect of mutations affecting human mtDNA. An essential feature of this concept is heteroplasmy, representing mixtures of normal and mutant mtDNA at the cellular and mitochondrial level, resulting in a "tissue mosaic" of focal bioenergetic deficits. Direct evidence for the concept is provided by (i) focal loss of staining for mitochondrially encoded enzymes, such as cytochrome c oxidase, in tissues of aged individuals (humans and rats) and (ii) an age-related increase in deletional mutations in mtDNA demonstrable by application of the polymerase chain reaction to DNA templates from individuals of different ages.
Aging↗
Selective IgM deficiency and abnormal B-cell response in a foal.
Selective IgM deficiency was diagnosed in a 3-month-old Standardbred colt that was referred for chronic respiratory tract disease. Immunoglobulin quantification revealed normal IgG and IgA concentrations, but undetectable IgM concentration. Stimulation of blood lymphocytes with the T-cell mitogens concanavalin A and phytohemagglutinin yielded results within the normal range. However, stimulation with the B-cell mitogen lipopolysaccharide produced no response. A B-cell defect similar to that associated with several immunodeficiency disorders in people was suggested as the cause of the IgM deficiency in this colt.
Animals↗
Energy-loss rate of a particle in a marginal Fermi liquid.
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Journal Article↗
An apparently allosteric effect involving N2O with the nitrous oxide reductase from Wolinella succinogenes.
It was shown that kcat for the benzyl viologen cation (BV+)-N2O oxidoreductase activity of nitrous oxide reductase from Wolinella succinogenes was 2-3 times greater at high N2O concentrations than at low. This effect of N2O on kcat exhibited a titration curve implicating a single secondary binding site for N2O with a Kd of 130-200 microM (Km with respect to N2O is about 2.5 microM). This work represents the first evidence of an apparently allosteric kinetic effect among nitrous oxide reductases. Its possible cause is discussed. BV+ was generated in these kinetic studies by addition of sub-stoichiometric amounts of dithionite. This means of reduction proved to be superior to the photochemical generation of BV+ that had been used previously with the enzyme. Mass spectrometric measurements suggested that the M(r) of the subunit of the enzyme is about 95,500 rather than 88,000.
Allosteric Regulation↗
Multiple mitochondrial DNA deletions in an elderly human individual.
We have used the polymerase chain reaction (PCR) to study deletions in the mitochondrial DNA (mtDNA) of an elderly human individual. An extended set of PCR primers has been utilised to identify 10 mitochondrial DNA deletions in a 69-year-old female subject with no known mitochondrial disease. The particular deletions visualised as PCR products depended on the primer pairs used, such that the more distantly separated PCR primers enabled visualisation of larger deletions. Some deletions were common to the heart, brain and skeletal muscle, whereas others were apparently specific to individual tissues. DNA sequencing analysis of PCR products showed that short direct repeat sequences (5 to 13 bp) flanked all deletion breakpoints; in most cases one copy of the repeat was deleted. It is proposed that the accumulation of such multiple deletions is a general phenomenon during the ageing process.
Aged↗
Instabilities of metabolic regulations in aging.
1) That non-invasive NMR and optical methods can a) quantify the work stress on mitochondria for ATP production, and b) indicate the tissue O2 tension in the capillary bed that is responsible for the rate of radical generation. 2) That free radical damage to mitochondrial function can be quantified by reciprocal plots of inverse slope giving the extrapolated Vm of mitochondria. 3) That a particular genetically deficient individual requiring high dosages of menadione has survived over 9 years. 4) That mitochondrial deficiency leads to an exercise hyperoxia.
Adenosine Diphosphate↗
Insulin mediator stimulation of pyruvate dehydrogenase phosphatases.
A two stage assay for detecting insulin mediator based upon its stimulation of soluble pyruvate dehydrogenase (PDH) phosphatase to activate soluble pyruvate dehydrogenase complex (PDC) has been developed. This coupled assay determines the activation of PDC by monitoring production of [14C]CO2 from [1-14C]pyruvic acid. In addition to being more sensitive than the rat liver mitoplast assay previously used, it allows for the separation and investigation of the effects of mediator on the PDH phosphatases individually. It has been previously shown that the insulin mediator stimulates the most abundant PDH phosphatase, the divalent cation dependent PDH phosphatase, by decreasing the phosphatase's metal requirement (1). A metal independent PDH phosphatase has been found in bovine heart mitochondria. This phosphatase is not immunoprecipitated by antiphosphatase 2A antibody, it is not inhibited by okadaic acid, and it is not stimulated by spermine. However, it is stimulated (more than threefold) by insulin mediator prepared from isolated rat liver membranes. It is inhibited by Mg-ATP, with half-maximal inhibition at 0.3 mM; however, this inhibition is overcome by the insulin mediator.
Adenosine Triphosphate↗