Direct observation of transfer of angular momentum to absorptive particles from a laser beam with a phase singularity.
Explore the source record for details and available documents.
Journal Article↗
Biomedical subjects
H He
Publications and source records attributed to H He.
[Self-care guide for acute leukemia during complete remission].
Explore the source record for details and available documents.
Acute Disease↗
Effects of a synthetic rat adrenomedullin on regional hemodynamics in rats.
The effects of rat adrenomedullin, a novel vasorelaxant peptide, on systemic and regional hemodynamics were examined in conscious Sprague Dawley (SD) rats and spontaneously hypertensive rats (SHR). The intravenous infusion of adrenomedullin at rates of 1.67 and 5 micrograms/kg per min decreased the mean arterial pressure in a dose-dependent fashion in both types of rats. Adrenomedullin at a rate of 5 micrograms/kg per min increased the heart rate and cardiac output. As a result, the total peripheral resistance significantly decreased. With regards to the regional hemodynamics, adrenomedullin significantly increased the flow rates in the lungs, heart, spleen, kidneys, adrenal glands and small intestine of SHR. The flow rates in the brain and skin did not change and the flow rates in the skeletal muscle and testis were decreased. These regional hemodynamic changes were also observed in SD rats and there was no qualitative difference in the regional responses to adrenomedullin between SHR and SD rats. Thus, adrenomedullin predominantly increased the flow rates in organs in which adrenomedullin gene was highly expressed. It therefore seems that adrenomedullin may act as a local vasodilatory hormone rather than as a circulatory hormone.
Adrenomedullin↗
Polymorphic SINEs in chironomids with DNA derived from the R2 insertion site.
A short interspersed repeat (SINE) in the two sibling species Chironomus pallidivittatus and Chironomus tentans is described. It is present at many sites in the genome and is surrounded by 10 to 14 bp target site duplications. It consists of two sequence modules in different numbers and variable order relative to each other and often has large inversions of different sizes at one end. One of the modules contains pol III promoter consensus sequences. This SINE, nevertheless, is likely to have been dependent on an outside promoter for its formation. It is therefore interesting that both modules start with a 22 bp region with striking similarity to the R2 insertion site in the preribosomal gene of insects. We suggest that this type of SINE, termed Cp1, was formed after a series of events among which the first step was the retroposition of a tRNA gene into the R2 site in the preribosomal gene by the R2 coded protein. The final step is likely to have been due to retroposition from this site.
Animals↗
Development and application of a specific and sensitive radioimmunoassay for trihexyphenidyl to a pharmacokinetic study in humans.
A radioimmunoassay (RIA) for trihexyphenidyl was developed through the use of a bovine thyroglobulin conjugate of trihexyphenidyl hemisuccinate. Immunization of New Zealand white rabbits with this drug-protein conjugate yielded antisera, for which the antibody titer and specificity were evaluated. An antiserum that had the highest titer and minimal cross-reactivities to major metabolites of trihexyphenidyl, such as trihexyphenidyl N-oxide (2%), hydroxytrihexyphenidyl (1%), and the antipsychotic drugs fluphenazine (< 1%), flupenthixol (< 1%), chlorpromazine (< 1%), and haloperidol (< 1%), was selected for development of a RIA. The described RIA enables the quantitation of 7.8 pg of trihexyphenidyl in 200 microL of human plasma with a mean coefficient of variation of < 6% across the range of the standard curve. Assay specificity was further demonstrated by comparison of results obtained directly and after selective extraction of trihexyphenidyl from replicate samples. This RIA procedure was applied to the analysis of steady state plasma samples obtained from patients undergoing treatment with trihexyphenidyl (2-8 mg) and plasma samples obtained from eight healthy male volunteers after administration of a single 4 mg oral dose of the drug. The results of the latter single dose studies demonstrated that the mean +/- SD for the peak concentration (Cmax), the time to Cmax (Tmax), the rate of absorption (Ka), and the area under the curve from 0 to 72 h (AUC0-72) were found to be 7.15 +/- 2.58 ng/mL, 1.32 +/- 0.58 h, 2.07 +/- 0.93 1/h, and 201 +/- 71 ng h/mL, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Dietary sodium intake modulates systemic but not forearm norepinephrine release.
INTRODUCTION: Sodium intake has profound effects on systemic and renal sympathetic activity, but its effects on sympathetic activity in skeletal muscle vascular beds, a site at which local regulatory mechanisms could alter vascular tone directly, are unclear. METHODS: To determine the effect of dietary sodium intake on basal and isoproterenol-stimulated systemic and forearm norepinephrine kinetics, we studied seven healthy male volunteers twice, 4 weeks apart, while they were receiving a low-sodium (10 mmol sodium/24 hours) diet and a high-sodium diet (250 mmol sodium/24 hours). Forearm blood flow, measured by plethysmography, and systemic and forearm norepinephrine spillover, measured by radioisotope dilution, were determined before and after intra-arterial infusion of 60 and 400 ng/min isoproterenol. RESULTS: Baseline (before isoproterenol) systemic norepinephrine spillover was higher when subjects received the low-sodium diet (448.1 +/- 55.7 ng/min) compared with the high-sodium diet (269.7 +/- 42.7 ng/min; p < 0.05). In contrast, sodium intake did not affect local forearm norepinephrine spillover, either at baseline (low-sodium diet, 2.05 +/- 0.48 ng/min versus high-sodium diet, 2.63 +/- 0.79 ng/min; p = 0.50) or after stimulation with isoproterenol in doses of 60 ng/min (low-sodium diet, 8.84 +/- 2.2 ng/min versus high-sodium diet, 6.1 +/- 1.9 ng/min; p = 0.38) or 400 ng/min (low-sodium diet, 16.4 +/- 4.5 ng/min versus high-sodium diet, 16.7 +/- 2.5 ng/min; p = 0.93). CONCLUSIONS: Under conditions of low sodium intake, systemic norepinephrine spillover was increased but forearm norepinephrine spillover was not, suggesting that alteration in sodium intake may produce a differential effect on norepinephrine spillover in different tissues but that decreased local sympathetic activity in skeletal muscle is not the likely mechanism by which a low-sodium diet may lower blood pressure or attenuate stress-induced pressor responses.
Adrenergic beta-Agonists↗
Effect of protein kinase C modulation on gonadotrophin-induced granulosa cell steroidogenesis.
The effect of protein kinase C (PKC) modulation on gonadotrophin-induced ovarian granulosa cell differentiation was investigated by using an activator of PKC, phorbol 12-myristate 13-acetate (PMA) and inhibitors of PKC, sphingosine (SPH) and staurosporine (ST). The effects of PMA (at doses which activate PKC (10 ng mL-1), and down-regulate PKC (1000 ng mL-1)), sphingosine (25 microM) and staurosporine (10(-10)-10(-7) M) on gonadotrophin-induced granulosa cell differentiation were studied by the determination of steroidogenesis and cAMP accumulation in immature rat ovarian granulosa cells treated with or without pregnant mare serum gonadotrophin (100 mU mL-1). PMA (10 ng mL-1) inhibited gonadotrophin-induced granulosa cell steroidogenesis and cAMP accumulation. PMA (1000 ng mL-1)-induced down-regulation of PKC did not affect gonadotrophin-induced steroidogenesis. The inhibitory effect of PMA (10 ng mL-1) on gonadotrophin-induced granulosa cell steroidogenesis was not present in PKC-down-regulated cells. These data indicate that PKC activation by PMA inhibits gonadotrophin-induced steroidogenesis. SPH also inhibited gonadotrophin-induced steroidogenesis and cAMP accumulation. This effect of SPH was not affected by PMA-induced PKC down-regulation, indicating that this action of SPH does not require PKC or is mediated via a phorbol ester-insensitive PKC isoform. ST induced steroidogenesis in the absence of gonadotrophin, but was not synergistic with gonadotrophin. PMA-induced down-regulation of PKC abolished the effect of ST, suggesting that the action of ST requires PKC. The data suggest that ST and PMA, which antagonize each other in gonadotrophin-induced steroidogenesis, act via a PKC-mediated mechanism whereas the cAMP-associated actions of gonadotrophins and SPH are not dependent on PKC.
Alkaloids↗
A pharmacological, pharmacokinetic and clinical overview of risperidone, a new antipsychotic that blocks serotonin 5-HT2 and dopamine D2 receptors.
Risperidone is a benzisoxazole derivative with antipsychotic activity that is chemically unrelated to other currently available antipsychotic agents. Its neuropharmacological properties, characterized by potent central antagonism of both serotonin 5-HT2 and dopamine D2 receptors, also differ from those of most other antipsychotic drugs. The pharmacokinetics of risperidone are well understood, having been studied in healthy subjects as well as in psychotic patients. The absolute oral bioavailability of risperidone is nearly 70%, and after oral administration, it is rapidly absorbed with the plasma level reaching a peak at about 1 h. 9-Hydroxyrisperidone, one of the metabolites of risperidone, is equally active with the parent compound and so the clinical activity of a dose of risperidone is due to the combined actions of both moieties. The plasma concentrations of risperidone and its active metabolite remain dose proportional even at doses exceeding the therapeutic range. In clinical trials with chronic schizophrenia patients, risperidone has an overall therapeutic activity comparable with that of haloperidol, but at doses that produce similar improvements in the positive symptoms of schizophrenia, risperidone has a greater effect on the negative symptoms and produces less extrapyramidal side effects than does haloperidol. However, additional controlled clinical studies are needed before the claims that risperidone is therapeutically superior to haloperidol can be considered to be established firmly. Although risperidone is effective in acute schizophrenia and in non-treatment-resistant schizophrenics, studies adequately comparing risperidone with clozapine in treatment-resistant schizophrenic patients remain to be published. In addition, risperidone has been reported to be of value in patients with schizodepressive disorders. The clinical success of risperidone suggests that the development of compounds with selective affinity for 5-HT2 or other serotonin receptors may result in even further improvements in the pharmacotherapy of psychiatric disorders.
Animals↗
T cell proliferative responses to five human cytomegalovirus proteins in healthy seropositive individuals: implications for vaccine development.
Cell-mediated immunity plays an important role in the host response against human cytomegalovirus (HCMV) infection. For the development of HCMV subunit vaccines it is essential to identify which HCMV proteins can induce protective immune responses in humans. We have studied the T cell proliferative responses to five HCMV proteins (IE1, IE2, pp71, gpUL18 and gB). These five proteins were produced using the maltose-binding protein (MBP) fusion protein system. T cell proliferative responses in 23 seropositive and six seronegative individuals were evaluated. None of the six seronegative individuals showed significant responses to any of the proteins. Of the 23 seropositive individuals, five responded to all five proteins, 14 responded to between one and four proteins and four responded to none of the proteins. The most commonly recognized proteins were gB (17/23, 74%) and IE2 (16/23, 70%). pp71 and IE1 were recognized by 10 of 23 (43%) individuals. Nine of 22 (41%) individuals tested responded to gpUL18, providing evidence that this protein is produced during infection. Our data indicate that a subunit vaccine composed of gB alone may not be sufficient to induce protective immunity in all individuals. The combination of two or three proteins may be more efficient as a potential vaccine.
Capsid↗
Tachyphylaxis of human forearm vascular responses does not occur rapidly after exposure to isoproterenol.
In vitro and limited in vivo data suggest that rapid desensitization of beta-adrenoceptor responses occurs after exposure to agonist. Tachyphylaxis to a beta-adrenoceptor agonist would represent a potentially important mechanism for the short-term regulation of vascular tone. The effects of a 4-hour infusion of 400 ng/min intra-arterial isoproterenol on forearm blood flow and presynaptic beta-adrenoceptor-mediated norepinephrine release were determined in eight healthy volunteers. Intra-arterial isoproterenol at 400 ng/min resulted in a significant increase in forearm blood flow in all eight subjects at all time points, with no evidence of tachyphylaxis. In fact, forearm blood flow after 4 hours of the isoproterenol infusion (22.8 +/- 3.3 mL/100 mL per minute) was significantly greater than after 7 minutes (14.6 +/- 2.8 mL/100 mL per minute), 15 minutes (15.4 +/- 2.4 mL/100 mL per minute), and 30 minutes (17.4 +/- 3.0 mL/100 mL per minute) of the infusion (P < .05). Similarly, presynaptic beta-adrenoceptor responses showed no evidence of tachyphylaxis, so forearm norepinephrine spillover values after 7 minutes (6.6 +/- 0.94 ng/min), 15 minutes (7.6 +/- 1.5 ng/min), and 4 hours (8.8 +/- 1.1 ng/min) of isoproterenol infusion were increased and similar. Minimal systemic effects were observed, and there was no evidence of tolerance, there being no difference in heart rate after 7 minutes (70.7 +/- 2.7 beats per minute) and 4 hours (72.2 +/- 3.6 beats per minute) of isoproterenol infusion.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Cyclosporine impairs vasodilation without increased sympathetic activity in humans.
Hypertension and nephrotoxicity frequently complicate treatment with cyclosporine; two suggested mechanisms are increased sympathetic activity and altered vascular reactivity. It is difficult to assess these mechanisms in patients receiving cyclosporine after transplantation because of the accompanying major physiological alterations. Therefore, we studied 12 patients with rheumatoid arthritis twice--while they were taking and not taking cyclosporine. We measured vascular response in the dorsal hand vein using the linear variable differential transformer technique. Cyclosporine treatment significantly attenuated vasodilation induced by 60 ng/min isoproterenol (no cyclosporine, 19.8 +/- 3.5% versus cyclosporine, 7.9 +/- 2.2%; P = .02) and prostaglandin E1 at 1000 pg/min (no cyclosporine, 72.6 +/- 10.2% versus cyclosporine 45.6 +/- 9.0%) and 2000 pg/min (no cyclosporine, 100.8 +/- 14.7% versus cyclosporine, 68.6 +/- 8.0%; F = 5.47, P = .047). However, neither vascular response to phenylephrine or nitroglycerin nor sympathetic activity assessed by measurement of norepinephrine spillover with a radioisotope dilution technique was affected by cyclosporine (no cyclosporine, 516.1 +/- 47.9 ng/min versus cyclosporine, 476.6 +/- 51.8 ng/min; P = .42). Cyclosporine impaired venodilation in response to two agonists that act through adenylate cyclase without altering alpha-agonist-induced venoconstriction or sympathetic activity. Therefore, in humans impaired vasodilation rather than sympathetic activation or enhanced vasoconstriction may be an important mechanism for the alterations of vascular tone that occur after long-term cyclosporine administration.
Adult↗
Forearm beta adrenergic receptor-mediated vasodilation is impaired, without alteration of forearm norepinephrine spillover, in borderline hypertension.
Impaired beta adrenoceptor-mediated vasodilation associated with enhanced sympathetic activity has been reported in established hypertension. We examined whether altered beta adrenoceptor-mediated vasodilation occurs early in the disease process, when structural vascular changes are likely to be less marked, by measurement of forearm blood flow by strain gauge plethysmography after the intraarterial administration of increasing doses of a beta receptor agonist, isoproterenol, in eight subjects with borderline hypertension (BHT) and 13 normotensive (NT) controls. To determine the role of sympathetic activation in the regulation of responsiveness, we measured local sympathetic activity in the forearm by a radioisotope dilution technique. Vasodilation in response to isoproterenol, measured either as changes in forearm blood flow or forearm vascular resistance, was impaired in the BHT group so that flow at the highest dose of isoproterenol (400 ng/min) increased less (15.2 +/- 1.5 ml/100 ml per min) than in the NT group (24.4 +/- 2.4 ml/100 ml per minute) (P < 0.001). Although, systemic norepinephrine spillover was significantly greater in BHT, the difference in blood flow response to isoproterenol was not accounted for by increased local sympathetic activity since forearm norepinephrine spillover at baseline (BHT 1.0 +/- 0.4 ng/min vs. NT 0.64 +/- 0.13 ng/min) and after the administration of isoproterenol 60 ng/min (BHT 5.2 +/- 1.4 ng/min vs. NT 6.0 +/- 1.5 ng/min) and 400 ng/min (BHT 13.5 +/- 2.9 ng/min vs. NT 16.5 +/- 2.7 ng/min) did not differ between the two groups. We therefore conclude that vasodilation in response to isoproterenol is impaired in subjects with BHT and that this impairment is not explained by locally increased basal, or stimulated, sympathetic activity.
Adult↗
Phase I and II metabolites of benztropine in rat urine and bile.
Following oral administration of benztropine (IO mg/kg, body weight), the phase I metabolites, benztropine N-oxide, N-desmethylbenztropine, tropine, 4'-hydroxybenz- tropine, N-desmethyl-4'-hydroxybenztropine, 4'-hydroxvbenztropine N-oxide and methoxy-4'-hydroxybenztropine, together with unmetabolized benztropine, were isolated and identified in rat urine and bile by GC-electron impact mass spectrometry (EI GC/MS), microcolumn LC-electrospray mass spectrometry (ES LC/MS) and hplc followed by MS analysis. The mass spectra and chromatographic properties of isolated N-desmethylbenztropine, benztropine N-oxide and tropine were confirmed by comparison with authentic reference standards. Sufficient quantities of 4'-hydroxybenztropine and N-desmethyl-4'-hydroxybenztropine were isolated from the urine by tlc and examined by 1H-nmr, ES/MS and EI/MS. The structure of the methoxy-4'-hydroxybenztropine metabolite was determined by EI/MS. 4'-Hydroxybenztropine N-oxide was identified by reacting it with a reducing agent, titanous chloride, to form 4'-hydroxybenztropine, which was then confirmed by comparing its EI/MS and ES/MS behaviour with a previously isolated and 1H-nmr-authenticated sample. In addition, four intact glucuronide conjugates of benztropine were also characterized in bile and urine as phase II metabolites, including 4'-O-glucuronylbenzotropine, N-desmethyl-4'-O-glucuronylbenztropine, methoxy-4'-O-glucuronylbenztropine and 4'- O-glucuronylbenztropine N-oxide by hplc followed by ES/MS analysis. These results provide the first direct evidence of the presence of these metabolites of benztropine in rat.
Animals↗
[Preliminary clinical study of endodontic antiseptic in monotithic type chlorhexidine controlled release delivery system]
The purpose of clinical study was to assess the bacteriological status of the root canal after disinfection with the monotithic type chlorhexidine enrolled release delivery system (CCROS).In experiments the monotithic type CCRDS was found to be more effective than the reservoir type CCRDS.The root canals of 24 teeth with apical periodontitis were completely instrumented and irrigated with sodium hypochloride.After the instrumentations,12 teeth were treated with the monotitihic type CCRDS,12 teeth were treated with formocresol.Bacterological samples from the root canals were taken after 5 days using an anaerobic technique.The results indicated that monotithic type CCRDS was more effective than formocresol in obtaining bacteria-free root canals(Chi-square test P<0.05).The advantages of an antiseptic with along lasting effect for the elimination of bacteria form the root canal and for the prevention of reinfection were emphasized.
Journal Article↗
[Clinical studies of a caries-defense varnish containing sialin-like material].
Explore the source record for details and available documents.
Acetates↗
Determination of low plasma timolol concentrations following topical application of timolol eye drops in humans by high-performance liquid chromatography with electrochemical detection.
A simple and sensitive high-performance liquid chromatographic assay was developed for determination of timolol in human plasma following administration of two drops of a 5% timolol ophthalmic solution. A 4% butyl alcohol-hexane extract of an alkalized sample of plasma was chromatographed on a reversed-phase column and the components in the column effluent were monitored by coulometric detection. The extraction efficiency of timolol was 69.02 +/- 4.16% (mean +/- S.D.) and its detection limit was 107.2 pg/ml. The effect of mobile phase pH, buffer concentration and the working potential of the detector on column performance and the electrochemical response are described.
Chromatography, High Pressure Liquid↗
Effect of velocity gradients on x-ray line transfer in laser-produced plasmas.
Explore the source record for details and available documents.
Journal Article↗