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  • 1
    ISSN: 1520-4995
    Source: ACS Legacy Archives
    Topics: Biology , Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    The @journal of organic chemistry 27 (1962), S. 850-854 
    ISSN: 1520-6904
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Analytical chemistry 36 (1964), S. 1023-1024 
    ISSN: 1520-6882
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Analytical chemistry 36 (1964), S. 1574-1576 
    ISSN: 1520-6882
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Analytical chemistry 37 (1965), S. 167-167 
    ISSN: 1520-6882
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-0428
    Keywords: Diabetes mellitus ; experimental neuropathy ; taurine ; osmoregulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Diabetic neuropathy results from progressive nerve fibre damage with blunted nerve regeneration and repair and may be complicated by nerve hyperexcitability resulting in pain. The naturally occurring amino acid taurine functions as an osmolyte, inhibitory neurotransmitter, and modulator of pain perception. It is also known to have neurotrophic actions. The compatible osmolyte hypothesis proposes that levels of intracellular organic osmolytes including taurine and myo-inositol, respond co-ordinately in response to changes in intracellular sorbitol or external osmolality to maintain the intracellular milieu. We hypothesize that glucose-induced sorbitol accumulation in diabetes mellitus will result in taurine depletion in peripheral nerve which may potentially impair nerve regeneration and precipitate neuronal hyperexcitability and pain. This study explored the relationships of taurine, myo-inositol and sorbitol in the rat nerve and their effects on nerve conduction velocity. Osmolyte levels and nerve conduction velocity were determined in sciatic nerve from non-diabetic and streptozotocin-induced diabetic rats, with or without dietary taurine or myo-inositol supplementation. Taurine levels decreased by 31% (p〈 0.01) and myo-inositol decreased by 37% (p〈0.05) in diabetic nerve as sorbitol accumulated. Taurine supplementation of diabetic animals did not affect nerve conduction velocity but further reduced nerve myo-inositol levels. Prevention of sorbitol accumulation with the aldose reductase inhibitor sorbinil increased nerve taurine levels by 22% (p〈0.05) when compared with untreated diabetic animals. Thus, we have demonstrated an interdependence of organic osmolytes within the nerve. Abnormal accumulation of one osmolyte results in reciprocal depletion of others. Diabetic neuropathy may be an example of maladaptive osmoregulation, nerve damage and instability being aggravated by taurine depletion.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1432-0428
    Keywords: Keywords Lens ; streptozotocin-diabetic rat ; dl-α-lipoic acid ; sorbitol pathway ; redox and energy status
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The study was aimed at evaluating changes in lens antioxidant status, glucose utilization, redox state of free cytosolic NAD(P)-couples and adenine nucleotides in rats with 6-week streptozotocin-induced diabetes, and to assess a possibility of preventing them by dl-α-lipoic acid. Rats were divided into control and diabetic groups treated with and without dl-α-lipoic acid (100 mg · kg body weight–1· day–1, i. p.). The concentrations of glucose, sorbitol, fructose, myo-inositol, oxidized glutathione, glycolytic intermediates, malate, α-glycerophosphate, and adenine nucleotides were assayed in individual lenses spectrofluorometrically by enzymatic methods, reduced glutathione and ascorbate – colorimetrically, and taurine by HPLC. Free cytosolic NAD+:NADH and NADP+:NADPH ratios were calculated from the lactate dehydrogenase and malic enzyme systems. Sorbitol pathway metabolites were found to increase, and antioxidant concentrations were reduced in diabetic rats compared with controls. The profile of glycolytic intermediates (increase in glucose 6-phosphate and fructose 6-phosphate, decrease in fructose1,6-diphosphate, increase in dihydroxyacetone phosphate, 3-phosphoglycerate, phosphoenolpyruvate, pyruvate, and no change in lactate), and 5.9-fold increase in α-glycerophosphate suggest diabetes-induced inhibition of glycolysis. Free cytosolic NAD+:NADH ratios, ATP levels, ATP/ADP × inorganic phosphate (Pi), and adenylate charge were reduced in diabetic rats while free cytosolic NADP+:NADPH ratios were elevated. Diabetes-induced changes in the concentrations of antioxidants, key glycolytic intermediates, free cytosolic NAD+:NADH ratios, and energy status were partially prevented by dl-α-lipoic acid, while sorbitol pathway metabolites and free cytosolic NADP+:NADPH ratios remained unaffected. In conclusion, diabetes-induced impairment of lens antioxidative defense, glucose intermediary metabolism via glycolysis, energy status and redox changes are partially prevented by dl-α-lipoic acid. The findings support the important role of oxidative stress in lens metabolic imbalances in diabetes. [Diabetologia (1998) 41: 1442–1450]
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1432-0428
    Keywords: Charcot arthropathy ; selective neuropathy ; blood flow
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Charcot arthropathy is a disabling complication of diabetic neuropathy. It is however, unclear why it occurs in only a small number of neuropathic patients. We have studied 12 diabetic patients (10 insulin-dependent) with an acute Charcot arthropathy, and compared their neuropathy and vascular responsiveness with 12 diabetic patients (10 insulin-dependent) with recurrent neuropathic foot ulceration, 12 diabetic control subjects (9 insulin-dependent) and 10 normal non-diabetic subjects. The Charcot arthropathy patients demonstrated a preservation of warm perception, 6 (5.5) °C, but complete loss of peripheral cold perception, 10 (0) °C, p〈0.001 (median (interquartile range)). This contrasted with the ulcerated neuropathy patients, who had equally severe impairment of both warm and cold sensory thresholds, 10 (0.5) °C vs 10 (1) °C, respectively, the diabetic control subjects who were able to detect a 2 (1.3) °C warm stimulus and 3 (3.5) °C cold stimulus and the normal subjects, whose warm threshold was 2 (1) °C and cold was 2 (1) °C. Light touch perception at the foot was preserved in the Charcot patients 4 (4) g vs 100 (50) g, p〈0.0002, in the ulcerated neuropathy patients. Vibration perception at the great toe and cardiovascular autonomic function tests (heart rate variability, Valsalva ratio and postural systolic blood pressure fall) were abnormal in both the Charcot patients and ulcerated neuropathy group, with no differences seen between the two groups. Peak skin blood flow at the great toe in response to local heating was preserved in the Charcot arthropathy patients, 63.36 (28.72) flow units when compared to the diabetic and normal subjects, 62.72 (47) flow units and 76.3 (33.92) flow units, respectively and much greater than in the ulcerated neuropathy patients 28.94 (37.39) flow units, p〈0.0002. The diabetic patients developing Charcot arthropathy thus have a neuropathy and vascular responsiveness which distinguishes them from diabetic subjects developing neuropathic ulceration. This may be important in the pathogenesis of the Charcot foot.
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Springer
    Der Anaesthesist 45 (1996), S. 533-537 
    ISSN: 1432-055X
    Keywords: Schlüsselwörter Leitungsanästhesien ; Lokalanästhetika ; Bupivacain ; frequenzabhängige Blockade ; elektrische Stimulation ; Key words Conduction block ; Anaesthetics ; local ; Bupivacaine ; Frequency-dependent block ; Electrical stimulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Abstract The action of local anaesthetics on isolated nerves is enhanced by high stimulation frequencies. The aim of our study was to investigate whether high-frequency stimulation enhances regional anaesthesia in man. Methods. Seven healthy volunteers underwent three ulnar nerve blocks while non-noxious electrical stimulation with high (10, 50 Hz) or low (0.2 Hz) frequencies was applied via a widespread cutaneous electrode in the area supplied by the ulnar nerve. Perception was monitored continuously by means of a visual analogue scale. Skin temperature (infrared telethermometry) was evaluated every minute as an indicator of vasomotor block. After complete loss of perception or after 45 min, the spread of anaesthesia was determined by sharp-dull discrimination. The nerve block was preceded by a control stimulation of 45 min under otherwise identical conditions. Results. During stimulation with 10 and 50 Hz, perception was lost significantly earlier than with 0.2 Hz. The spread of sensory block at the end of the experiments was also enhanced by stimulation with high frequencies, whereas the onset of vasomotor block (rise in skin tempeature) remained unaltered. Conclusion. Non-oxious electrical stimulation with high frequencies significantly accelerates the onset of anaesthesia and extends the spread of sensory block.
    Notes: Zusammenfassung Die Wirkung von Lokalanästhestika am isolierten Nerven ist abhängig von der Aktionspotentialfrequenz, d.h. die Wirkung des Lokalanästhetikums wird durch hohe Aktionspotentialfrequenzen verstärkt. Ob dieses Prinzip auch bei Leitungsblockaden am Menschen gilt, ist jedoch unbekannt. An sieben gesunden Probanden wurden deshalb drei Ulnarisblockaden durchgeführt, während eine Elektrostimulation mit verschiedenen Frequenzen (0,2; 10 und 50 Hz) über eine Flächenelektrode im Versorgungsgebiet des Nerven an der Hand appliziert wurde. Die Probanden gaben die Empfindungsintensität kontinuierlich auf einer visuellen Analogskala an. Die Hauttemperatur wurde mittels Infrarot-Telethermometrie bestimmt. Nach komplettem Empfindungsverlust, höchstens aber nach 45 min wurde die Ausbreitung der Leitungsblockade mittels Spitz-Stumpf-Diskrimination bestimmt. Zur Kontrolle wurde vor jeder Untersuchung die Empfindungsintensität bei 45minütiger Stimulation ohne Leitungsblockade für jede Stimulationsfrequenzen ermittelt. Bei Leitungsblockaden unter hohen Stimulationsfrequenzen (10 bzw. 50 Hz) trat der Empfindungsverlust signifikant eher ein als bei der niedrigen Frequenz (0,2 Hz). Auch die Ausbreitung der sensiblen Blockade am Ende der Untersuchung wurde durch die hochfrequente Stimulation verbessert, hingegen blieb der Beginn der vasomotorischen Blockade (Anstieg der Hauttemperatur) unverändert. Nicht schmerzhafte, elektrische Stimulation mit hohen Frequenzen beschleunigt also Anschlagzeit und Ausdehnung einer Leitungsblockade des N. ulnaris.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    European journal of clinical pharmacology 8 (1975), S. 241-248 
    ISSN: 1432-1041
    Keywords: pharmacokinetics ; experimental design
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary It is apparent from studying recent articles on pharmacokinetics that a number of misunder-standings exist, both about the design of experiments and the analysis of results. The purpose of this paper is to outline many of the common pitfalls associated with the design of experiments and also the limitations upon the analysis of results. The paper describes mathematical, laboratory and clinical aspects which must be examined in designing a protocol for pharmacokinetic experiments. Simulated data is presented to demonstrate the dangers of using standard computer programs for parameter estimation. Even when convergence is obtained the answers may be dependent on the method employed. A mathematical model is of little use unless a reasonable amount of good, accurate data is obtained.
    Type of Medium: Electronic Resource
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