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Growth hormone stimulates collagen type I synthesis. Collagen type I is a common matrix compound in a large number of connective tissues. The aim of our study was to prove whether a stimulation of collagen type I synthesis might be accompanied by a deposition of collagen type I in the skin (cutis). Twenty growth hormone-deficient hypopituitary patients were included in a randomised, double-blind, placebo controlled, prospective, twelve-month study (eighteen patients assessable at the end of the study). The patients were treated with recombinant human growth hormone 0.25 U/kg/week subdivided in daily subcutaneous injections beginning with half the dosage during the first four weeks. During the first six months half of the patients were treated with placebo. PICP, the indicator of collagen type I synthesis, was increased after six months of therapy when compared to placebo. Skin thickness measured by ultrasound at the forearm and mechanically at the dorsum of the hand with strong compression of the skin both increased significantly following growth hormone substitution. Our data indicate that the stimulation of collagen type I synthesis by growth hormone substitution is followed by a deposition of collagen type I in the skin.

Recently, major advances have been accomplished in the diagnosis of active tuberculosis. A comprehensive diagnostic approach for a patient with possible tuberculosis includes a detailed medical history and clinical examination as well as the results of radiological, microbiological, immunological, molecular-biological and histological methods. In concert, these results enable the clinician to rapidly develop a decision with a high probability for the diagnosis or exclusion of active tuberculosis. Therapeutic intervention can thus be made early, even though corrections in these decisions need to be considered depending on the results of Mycobacterium tuberculosis culture and sensitivity testing.

Background Intra-myocardial transplantation of bone marrow derived cells is currently under clinical evaluation as a therapy for heart failure. A major limitation of all clinical studies for myocardial restoration through cell transfer is the inability to track the fate of the transplanted cells. We present a clinically applicable technique using advanced ultra high-field 7-Tesla (7T) magnetic resonance imaging (MRI) of nanoparticle-labeled transplanted human EPCs in porcine ischemic hearts. Methods CD133 positive cells were isolated from bone marrow by magnetic bead selection. Positive cells (5 - 8 x 10 (6) cells) were transplanted into porcine ischemic myocardium (n = 8). Control animals (n = 3) received a medium injection. MRI on a 7T scanner was performed to demonstrate the distribution of the EPCs. Results CD133+ cells were identified on gradient echo images (T(1)-weighted) within the myocardium 4 weeks after transplantation. Conclusions Magnetically labeled EPCs transplanted for therapeutic neovascularization or reduction of infarct size in myocardial ischemia can be visualized by MRI at high-field strengths.

Zur Konstruktion des Mainz-Pouch-I werden zwischen 24 und 36 cm des terminalen Ileums sowie ca. 12 cm Colon ascendens inkl. der Ileozökalklappe verwendet. Hierdurch entfällt ein Teil der Resorptionsfläche für Vitamine, Gallensäuren und Spurenlemente. Bei 137 Patienten mit einem Mainz-Pouch-I erfolgte die Bestimmung der Gallensäuren, der fett- und wasserlöslichen Vitamine (A, D, E, K, B1, B2, B6, B12), der Folsäure, des Ammoniaks und des Base excess, der Spurenelemente (Zink, Kupfer, Eisen), des Ferritins sowie eines Differentialblutbildes. Das Vitamin B12 und die Folsäure wurde zusätzlich intrakorpuskulär bestimmt. Kinder und Erwachsene wurden unterschieden und die Patienten in 3 Gruppen eingeteilt (0

Ziele: The challenge facing cancer chemotherapy is the low selectivity to tumor cells versus normal cells. ADEPT (antibody-directed enzyme-prodrug therapy), in which a tumor specific antibody is used to carry a drug-activating enzyme to the tumor tissue, offers an attractive possibility to overcome this problem. Subsequent enzyme-mediated activation of nontoxic prodrugs to toxic drugs only within the tumor increases the specificity of treatment and decreases the drug toxicity in healthy tissues. Methode: The EGFR-targeting antibody Cetuximab was labeled with a near-infrared (NIR) fluorophore (Cetux-Alexa) and binding and internalization of the conjugate to mammary carcinoma cell lines with distinct EGFR expression patterns was analyzed in vitro. Distribution and binding-kinetics of Cetux-Alexa in nude mice bearing orthotopic mammary carcinomas were studied by NIR fluorescence imaging. Localization of the fluorescent probe within the tumor was analyzed ex vivo in tumor sections. To study the feasibility of Cetuximab for ADEPT, the antibody was conjugated with a drug activating enzyme, Galactosidase (Cetux-Gal). Ergebnis: Cetux-Alexa binds to EGFR-expressing cells in vitro and is localized to the cell membrane. In vivo, Cetux-Alexa targets EGFR-expressing tumors, resulting in a high tumor to background contrast. No unspecific accumulation of the fluorescence conjugate could be observed. Localization of Cetux-Alexa within the tumor was confirmed in tumor sections. Cetux-Gal was found to bind to EGFR-expressing cells in vitro specifically, proving a Galactosidase activity according to the distinct EGFR expression pattern. Subsequent addition of the prodrug showed toxicity proportional to the EGFR expression. Schlussfolgerung: A novel ADEPT treatment, in which tumor-bearing mice will be treated with Cetux-Gal in combination with a highly potent prodrug, was designed. In future experiments, the efficacy of the therapy will be assessed by monitoring tumor reduction with CT and SPECT using Tc-99 m labelled Cetuximab. Korrespondierender Autor: Kruwel T Universitatsmedizin Gottingen, Institut fur Diagnostische und Interventionelle Radiologie, Robert-Koch-Str. 40, 37075 Gottingen E-Mail: thomas.kruewel@med.uni-goettingen.de