Biomedical subjects
A Stern
Publications and source records attributed to A Stern.
The effect of association on the nuclear magnetic resonance spectra of tyrocidine B1.
Explore the source record for details and available documents.
[Myocardial ischemia and experimental revascularization of the myocardium].
Explore the source record for details and available documents.
A conformational analysis of gramicidin S-A by nuclear magnetic resonance.
Explore the source record for details and available documents.
[Arterial embolisms of the extremities: current therapeutic management. Study based on a series of 27 cases surgically treated with use of the Fogarty balloon catheter].
Explore the source record for details and available documents.
Effects of hypokalemia on carbohydrate and lipid metabolism in the rat.
Explore the source record for details and available documents.
Adler and Sartre: comment.
Explore the source record for details and available documents.
The treatment of pollinosis with small doses of emulsions of ironated ragweed extract.
Explore the source record for details and available documents.
[Function tests in rheumatic fever].
Explore the source record for details and available documents.
In vitro cytotoxicities of 1,4-naphthoquinone and hydroxylated 1,4-naphthoquinones to replicating cells.
Using the human hepatoma cell line, HepG2, and the BALB/c mouse fibroblast cell line, 3T3, as the bioindicators in the neutral red cytotoxicity assay, the effect of hydroxyl substitution on the toxicity of 1,4-naphthoquinone was studied. The sequence of potency for the quinones was 5,8-dihydroxy-1,4-naphthoquinone > 5-hydroxy-1,4-naphthoquinone > 1,4-naphthoquinone >> 2-hydroxyl-1,4- naphthoquinone. Pretreatment of the cells with dicoumarol, an inhibitor of DT-diaphorase, enhanced the cytotoxicity of 1,4-naphthoquinone but not of the hydroxylated naphthoquinones. Pretreatment of the BALB/c cells with buthionine sulfoximine, an inhibitor of glutathione synthesis, enhanced the sensitivity of the cells to all the hydroxylated naphthoquinones but not to 1,4-naphthoquinone. A similar pretreatment of the HepG2 cells with buthionine sulfoximine enhanced the toxicity of the 2-hydroxy- and 5,8-dihydroxy-1,4-naphthoquinones but not of 5-hydroxy-1,4-naphthoquinone or of 1,4-naphthoquinone. Some differences were noted in the responses to the hydroxylated 1,4-naphthoquinones between buthionine sulfoximine-treated replicating cells and buthionine sulfoximine-treated isolated rat hepatocytes, a nonreplicating cell in culture. The use of a replicating cell system in studying the mechanisms of the cytotoxicity of quinones may be an important adjunct to studies using the isolated rat hepatocytes, which is the standard model system.
The isoprostanes: novel prostaglandin-like products of the free radical-catalyzed peroxidation of arachidonic acid.
The isoprostanes (IsoPs) are a unique series of prostaglandin-like compounds formed in vivo from the free radical-catalyzed peroxidation of arachidonic acid. This review summarizes our current knowledge regarding these compounds. Novel aspects of the biochemistry and bioactivity of IsoPs are detailed and methods by which these compounds are analyzed are discussed. A considerable portion of this review deals with the utility of measuring IsoPs as markers of oxidant injury in human diseases particularly in association with risk factors that predispose to atherosclerosis, a condition in which excessive oxidative stress has been causally implicated.
The isoprostanes: unique bioactive products of lipid peroxidation. An overview.
The development of a specific, reliable and noninvasive method for measuring oxidative stress in humans is essential for establishing the role of free radicals in human diseases. Currently, accurate techniques to assess oxidant injury in vivo are extremely limited although a number of approaches are being investigated. Of these, the measurement of specific products of nonenzymatic lipid peroxidation, the F2-isoprostanes (F2-IsoPs), appears to be a more accurate marker of oxidative stress in vivo in humans than other available methods. The purpose of this brief review is to acquaint the reader with the IsoPs from a biochemical perspective and to provide information regarding the utility of quantifying these compounds as indicators of oxidant stress.
A photothrombotic model of small early ischemic infarcts in the rat brain with histologic and MRI correlation.
Over the last two decades several studies have suggested the role of photothrombotic occlusion of cerebral microvessels using rose bengal, resulting in small strokes in rodents that resemble those in humans. This paper describes such a photothrombotic method of acute small stroke induction in rats with histopathologic and in vivo magnetic resonance imaging (MRI) observations from 3 to 6 h after irradiation, which is homologous to a human autopsy specimen. Utilizing 30 min of irradiation with minimal beam intensity (0.1 W/cm(2)) cold white light in conjunction with 20 mg of intravenous (iv) rose bengal as a rapid infusion, small infarcts were induced photochemically in the frontal lobes of six rats. The infarcts showed a consistent pattern on histologic and in vivo MR sections when examined within 7 h or less of irradiation. Both MRI and histologic sections were comprised of (a) a superior zone of infarcted neurons, (b) a middle curvilinear transition zone of edema on MRI and histologically vacuolated neuropil, and (c) an inferior zone of normal neurons. Shorter duration water-sensitive (T2)- and postgadolinium longer duration (T1)-weighted signal decay images both showed a curvilinear hyperintense transition zone of edema. The mean infarct and transition zone areas measured from the histologic sections were comparable to those measured on the MRI. The infarct model described above allows in vivo observations using MRI with the potential for use in testing putative neuroprotective agents. As demonstrated by a comparison with the histologic features of such infarcts in surgical and autopsy brain specimens, the model is relevant to acute human ischemic infarcts.
Physiology of the excretory urogram. 3. A densitometric and subjective assessment of changes in contrast medium concentration.
Explore the source record for details and available documents.
Tetrabenazine treatment in movement disorders.
Tetrabenazine (TBZ) is a catecholamine depletor used for the treatment of a variety of movement disorders. The purpose of this study was to assess the efficacy of TBZ in a retrospective chart review in 3 tertiary care movement disorders centers over long-term treatment. Of 150 patients to whom TBZ was prescribed, 118 were followed up and assessed using the Clinical Global Impression of Change (CGIC), (-3 to +3), a composite grade from a patient and caregiver scale over variable periods. The patients had a variety of hyperkinetic movement disorders including dystonia (generalized and focal: axial, Meige syndrome, torticollis, blepharospasm, bruxism), Huntington disease (HD) or other choreas, tardive dyskinesia (TD) or akathisia, and Tourette syndrome. Mean patient age was 48.8 +/- 18.7 years; 48 were men (40.7%) with a mean disease duration of 93 months. The mean follow-up time was 22 months and the mean TBZ dose was 76.2 +/- 22.5 mg/d (median 75 mg, range 25-175 mg/d). The mean CGIC score was +1 (mild improvement). The group of patients who scored +3 on the CGIC (very good improvement) represented 18.6% (n = 22) of all patients. They had HD or other types of chorea 7.6% (n = 9), facial dystonia/dyskinesia (n = 7, 5.9%), 1 with TD, 2 with trunk dystonia, 2 with Tourette syndrome, and 1 with tardive akathisia. This group had the longest treatment duration and received a mean TBZ dose of 70.5 mg/d (median 75 mg/d) for a mean of 25.4 +/- 21.3 months. The report concludes that TBZ is a moderately effective treatment of a large variety of hyperkinetic movement disorders, with excellent effects in a subgroup with chorea and facial dystonia/dyskinesias.
Medial discoid meniscus with cyst formation in a child.
A medial discoid meniscus with cystic formation was found in a 9-year-old girl. The cyst was located in the anterolateral part of the meniscus, mechanically blocking knee extension. The presenting symptom was knee flexion contracture. Total meniscectomy was followed by full recovery.
Vanadium as a modulator of cellular regulatory cascades and oncogene expression.
Vanadium, a trace metal in the environment and in biological systems, influences the behavior of enzymes, mimics and regulates growth factor activity, is a potential mutagenic and carcinogenic agent, and regulates gene expression. The diverse biological actions of vanadium result from its capacity to function as an oxyanion, oxycation, or prooxidant. Vanadium is found in water, rocks, and soils in low concentration and in relatively high concentrations in coal and oil deposits. Vanadium compounds at much higher concentrations than are typically ingested are being considered in the treatment of diabetes mellitus. The actions of insulin and vanadium on the insulin receptor are similar, but the mechanisms are not identical. Vanadium modulates growth-factor-mediated signal transduction pathways. Vanadium promotes cell transformation and diminishes cell adhesion. Consistent with its mitogenic action and its capacity to mimic mitogenic growth factors, vanadium stimulates expression of protooncogenes. In particular, oxygen-derived active species are involved in the expression of the jun protooncogene in the presence of vanadium. The unique cellular activity of vanadium makes it a tool of unparalleled potential for studying mechanisms of cell growth, differentiation, and metabolism.
Among a range of transition metals and ligands vanadium.desferroxamine excels in accelerating reactivity of ferrocytochrome c toward molecular oxygen.
Despite early knowledge of the requirement for metals in the reactions of ferrocytochrome c with oxygen, the relative effectiveness of metals and the factors that modulate effectiveness remain unknown. We have compared the catalytic power of five metals and report the effects of pH and ligand on their effectiveness as catalysts. Catalysis by metal ions was greatest at higher pH, where the rate of aerobic oxidation was lowest. Iron (Fe2+), copper (Cu2+), vanadium(V) (V(V)), manganese (Mn2+), and aluminum (Al3+) were tested in combination with EDTA, ADP, histidine, or desferrioxamine (Des) at pH 2.6, 3.2, and 4.0. At pH 2.6, only vanadium(V) increased the initial rate of the oxidation of ferrocytochrome c (by 6.2-fold). At pH 4.0, however, all the metals markedly stimulated the oxidation of cytochrome c. The order of effectiveness was V(V).Des >> Cu.ADP2+ > Fe.EDTA2+ > Mn.Des2+ > Al.EDTA3+ (where the stated ligand represents the most stimulating one for a given metal). At pH 3.2 the metal complexes had intermediate effects, with vanadium again being the most effective. The preeminence of vanadium among the metals is novel. Where the heme crevice is closed (pH 4), transition metal ions mediated almost all of the reduction of oxygen, while at the lowest pH (2.6) transition metal ions were largely unnecessary. Vanadium(V) was the most active of the metals at all values of pH and the only metal to accelerate the oxidation of ferrocytochrome c at pH 2.6. Understanding of the range of biological actions of vanadium will not be complete without a knowledge of its redox reactivity within the components of biological systems.