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H Thieme

Publications and source records attributed to H Thieme.

At least 19 recordsLinked to original sources
PubMed1995

Comparative analysis of vascular endothelial growth factor receptors on retinal and aortic vascular endothelial cells.

Ischemic eye disease often results in ocular neovascularization, presumably due to the elaboration of growth factors. Diabetic retinopathy is a classic example in which dramatic retinal neovascularization arises after ischemic retinal damage. The characterization of vascular endothelial growth factor (VEGF) as an angiogenic molecule whose expression is markedly induced by hypoxia makes it a promising candidate for mediating ischemic retinal neovascularization. Thus, we have characterized the structure, binding, and regulation of VEGF receptors in bovine retinal (BREC) and aortic endothelial cells (BAEC). VEGF stimulated a 2.1-fold increase in BREC number and DNA content at 0.6 nmol/l VEGF (P < 1 x 10(-7)). Scatchard binding analysis demonstrated specific high-affinity VEGF receptors on BREC with a Kd of 4.9 +/- 0.6 x 10(-11) mmol/l, similar to that observed for BAEC at 5.1 +/- 0.4 x 10(-11) mmol/l. BREC, however, possess 1.5 x 10(5) high-affinity receptors/cell, threefold more than BAEC (P < 0.003) and more than any cell type reported previously. 125I-VEGF affinity cross-linking revealed complexes at 220 and 170 kDa in BREC, but only a 220-kDa band of lesser intensity in BAEC. Cross-linking was displaceable in a dose-dependent manner by VEGF (P < 0.01) but not by other hormones. Hypoxia increased VEGF receptor number 50% in BREC without altering affinity. Antiphosphotyrosine immunoblotting showed VEGF-stimulated tyrosine autophosphorylation of VEGF receptor bands at 225 and 220 kDa and another band at 80 kDa within 1 min.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Vascular endothelial growth factor in ocular fluid of patients with diabetic retinopathy and other retinal disorders.

BACKGROUND: Retinal ischemia induces intraocular neovascularization, which often leads to glaucoma, vitreous hemorrhage, and retinal detachment, presumably by stimulating the release of angiogenic molecules. Vascular endothelial growth factor (VEGF) is an endothelial-cell-specific angiogenic factor whose production is increased by hypoxia. METHODS: We measured the concentration of VEGF in 210 specimens of ocular fluid obtained from 164 patients undergoing intraocular surgery, using both radioimmuno-assays and radioreceptor assays. Vitreous proliferative potential was measured with in vitro assays of the growth of retinal endothelial cells and with VEGF-neutralizing antibody. RESULTS: VEGF was detected in 69 of 136 ocular-fluid samples from patients with diabetic retinopathy, 29 of 38 samples from patients with neovascularization of the iris, and 3 of 4 samples from patients with ischemic occlusion of the central retinal vein, as compared with 2 of 31 samples from patients with no neovascular disorders (P < 0.001, P < 0.001, and P = 0.006, respectively). The mean (+/- SD) VEGF concentration in 70 samples of ocular fluid from patients with active proliferative diabetic retinopathy (3.6 +/- 6.3 ng per milliliter) was higher than that in 25 samples from patients with nonproliferative diabetic retinopathy (0.1 +/- 0.1 ng per milliliter, P = 0.008), 41 samples from patients with quiescent proliferative diabetic retinopathy (0.2 +/- 0.6 ng per milliliter, P < 0.001), or 31 samples from nondiabetic patients (0.1 +/- 0.2 ng per milliliter, P = 0.003). Concentrations of VEGF in vitreous fluid (8.8 +/- 9.9 ng per milliliter) were higher than those in aqueous fluid (5.6 +/- 8.6 ng per milliliter, P = 0.033) in all 10 pairs of samples obtained simultaneously from the same patient; VEGF concentrations in vitreous fluid declined after successful laser photocoagulation. VEGF stimulated the growth of retinal endothelial cells in vitro, as did vitreous fluid containing measurable VEGF. Stimulation was inhibited by VEGF-neutralizing antibodies. CONCLUSIONS: Our data suggest that VEGF plays a major part in mediating active intraocular neovascularization in patients with ischemic retinal diseases, such as diabetic retinopathy and retinal-vein occlusion.

Adolescent↗
PubMed1993

Effect of elevated glucose concentration on membrane voltage regulation in retinal capillary pericytes.

The influence of elevated glucose concentration on resting membrane voltage, electrogenic Na(+)-K(+)-ATPase, and ATP-sensitive potassium channels (KATP channels) was studied in cultured bovine retinal capillary pericytes using conventional microelectrodes. The resting membrane voltage in cells grown in medium containing 5 mM glucose (control) averaged -27 +/- 1.2 mV (mean +/- SE, n = 26) and was not different from cells grown in medium containing 22.5 mM glucose (-26 1.2 mV, n = 26). Addition of ouabain (10(-4) M), a specific inhibitor of the Na(+)-K(+)-ATPase, depolarized the membrane potential by 3.6 +/- 0.4 mV (n = 10) in cells grown under control conditions and 0.7 +/- 0.2 mV (n = 6) in cells grown under elevated glucose conditions. Thus, electrogenic activity of the Na(+)-K(+)-ATPase was significantly (P < 0.0001) reduced to 19% compared with control conditions. Electrogenic Na(+)-K(+)-ATPase activity could be partially restored (ouabain-induced depolarization delta V = 2.0 +/- 0.2 mV, n = 6) in cells grown with high glucose in the presence of the aldose reductase inhibitor tolrestat (10(-5) M). The potassium channel opener Hoe 234 (10(-6) M) induced membrane potential hyperpolarization in control cells (delta V = 7.3 +/- 1.2 mV, n = 13), which could be completely inhibited by the KATP channel blocker glibenclamide (10(-7) M, n = 5). This indicates that pericytes possess KATP channels. The effect of KATP channels on membrane voltage was not significantly changed (P = 0.16) in cells cultured under high-glucose conditions (delta V = 9.6 +/- 2.0 mV, n = 6).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Insulin-induced hyperpolarization in retinal capillary pericytes.

PURPOSE: This study investigated the mechanism of insulin-induced membrane voltage hyperpolarization in retinal capillary pericytes, which possess electrical membrane properties typical for smooth muscle cells and are supposed to regulate retinal microcirculation by a contractile mechanism. METHODS: The mechanism of insulin-induced hyperpolarization was studied in cultured bovine retinal capillary pericytes using conventional microelectrodes. RESULTS: Resting voltage averaged -28 +/- 0.9 mV (mean +/- SEM, n = 45). Insulin (10(-9) to 10(-7) mol/l) induced a slow hyperpolarization in a dose-dependent fashion. Voltage change (delta V) was -3.1 +/- 0.4 mV (n = 14, P < 0.0001, = control) with an insulin concentration of 10(-8) mol/l. Blockade of potassium channels with Ba2+ (5 mmol/l) completely abolished the hyperpolarizing effect of insulin (n = 5). Apamin (10(-9) mol/l), a blocker of low-conductance Ca(2+)-activated potassium channels, also completely inhibited the insulin-induced hyperpolarization (n = 4). Blocking ATP-sensitive potassium channels with glibenclamide (10(-7) mol/l) did not reduce the hyperpolarizing action of insulin (delta V = -2.2 +/- 0.4 mV, n = 5, P = 0.29). Equivalent hyperpolarizations were recorded when insulin was added in the presence of ouabain (10(-4) mol/l) to inhibit the electrogenic Na+/-/K+/-ATPase (delta V = -3.5 +/- 1.0 mV, n = 4, P = 0.68). When pericytes were grown for 3 days in culture medium with elevated glucose concentrations (22.5 mmol/l), the resting membrane voltage and the insulin-induced hyperpolarization were not significantly altered. CONCLUSION: Insulin hyperpolarizes the membrane voltage of retinal pericytes probably mediated by activation of apamin-sensitive Ca(2+)-activated potassium channels. Therefore, hormonal modulation of membrane voltage by insulin might be an important factor in the regulation of pericyte contractility and retinal microcirculation under physiological conditions and in diabetes mellitus.

Adenosine Triphosphate↗
PubMed1986

[Residues of organochlorine compounds in plant drugs. 1. Gas chromatographic determination of residues of organochlorine insecticides].

A method for the identification and determination of HCH-and DDT-isomers and their respective metabolites in vegetable drugs is presented. The plant material is extracted with hexane in a Soxhlet apparatus in the presence of silicagel and sodium sulfate. For removing interfering endogenous plant constituents a Celite oleum column cleanup and usually and acetonitrile partitioning to follow are necessary. A mixed stationary phase OV-17/QF-1 has proved effective for the gc separation on packed columns. 3H-ECD is used for detection. For the quantitative determination by using an external standard the peak height measurement is recommended. Recoveries of all insecticides were in the order of 70-105% with coefficients of variation between 6 and 20%. To ensure the results the alkaline treatment and oxidation of extracts are proposed.

Chromatography, Gas↗
PubMed1982

Sepsis associated with urinary tract infection. Antibiotic treatment with piperacillin.

Urosepsis is mostly induced by nosocomial gram-negative organisms. It is an infection that is difficult to treat and has high mortality, especially when associated with septic shock. For obstructive urosepsis, which occurs mostly after an acute stone occlusion of the upper urinary tract in pyelonephritis, intensive systemic medical therapy and drainage (and sometimes removal) of the septic kidney are necessary. For non-obstructive urosepsis, which is mostly an iatrogenic complication of diagnostic or therapeutic procedures on the genito-urinary tract, the same intensive medical care and urinary drainage are adequate. Systemic therapy in the treatment of urosepsis encompasses several disorders. Specific pathogenic mechanisms of shock, including failure of the microcirculation, hemostatic disorders, and microbiological problems, have to be considered in the systemic treatment of urosepsis. Appropriate antibiotic therapy may triple chances of survival. In this connection, piperacillin was successfully used in 30 patients with urosepsis treated at our institution.

Adult↗
PubMed1982

[On the determination of chlorpropham, metobromuron and chlorbromuron residues in drugs of the 2. AB-DDR (author's transl)].

A method for analyzing drugs of the 2. AB-DDR for residues of chlorpropham, metobromuron and chlorbromuron is proposed. It is based on the detection of aniline derivatives resulting from alkaline hydrolysis. Herbicide concentrations greater than 0.25 mg/kg drug may be detected and semiquantitatively estimated by thin-layer chromatography. Smaller amounts of herbicide residues are detected gas chromatographically (using an electron attachment detector) after bromination of the hydrolysis products. The limits of detection are: chlorpropham, 0.006 mg/kg drug; chlorbromuron, 0.008 mg/kg drug; and metobromuron, 0.04 mg/kg drug. For impregnated drugs, the recovery rates lie between 82 and 102%. The herbicide residues are released to infusions at a varying extent, depending on the kinds of drugs used.

Chlorpropham↗
PubMed1978

[In vitro ultrasound pictures of kidney tumors].

In 5 patients with malignant renal tumours apart from in-vivo-sonogrammes ultrasound pictures of the operatively removed perfused preparations of renal tumours were additionally performed. The nephrosonogramme intracorporally showed the typical ultrasound picture of a tumour with coarsely disseminated echostructure in acoustically homogenous normal renal parenchyma. In the extracorporal sonogramme the tumour imposed as relatively echo-poor zone compared with the normal renal parenchyma with strong echos. The loss of the extracorporal turgor is discussed as cause of the reversion of the intensity of the echo pattern. In 3 other tumour-free renal preparations the acoustic reversion phenomenon of the normal renal parenchyma was confirmed in the extra-corporal renal preparation.

Adenocarcinoma↗