TY  - JOUR
A1  - Schmidt, Melanie
A1  - Pfetzer, Nadja
A1  - Schwab, Micheal
A1  - Strauss, Ingrid
A1  - Kaemmerer, Ulrike
T1  - Effects of a ketogenic diet on the quality of life in 16 patients with advanced cancer: a pilot train
N2  - Background: Tumor patients exhibit an increased peripheral demand of fatty acids and protein. Contrarily, tumors utilize glucose as their main source of energy supply. Thus, a diet supplying the cancer patient with sufficient fat and protein for his demands while restricting the carbohydrates (CHO) tumors thrive on, could be a helpful strategy in improving the patients’ situation. A ketogenic diet (KD) fulfills these requirements. Therefore, we performed a pilot study to investigate the feasibility of a KD and its influence on the quality of life of patients with advanced metastatic tumors. Methods: Sixteen patients with advanced metastatic tumors and no conventional therapeutic options participated in the study. The patients were instructed to follow a KD (less than 70 g CHO per day) with normal groceries and were provided with a supply of food additives to mix a protein/fat shake to simplify the 3-month intervention period. Quality of life [assessed by EORTC QLQ-C30 (version 2)], serum and general health parameters were determined at baseline, after every two weeks of follow-up, or after drop out. The effect of dietary change on metabolism was monitored daily by measuring urinary ketone bodies. Results: One patient did not tolerate the diet and dropped out within 3 days. Among those who tolerated the diet, two patients died early, one stopped after 2 weeks due to personal reasons, one felt unable to stick to the diet after 4 weeks, one stopped after 6 and two stopped after 7 and 8 weeks due to progress of the disease, one had to discontinue after 6 weeks to resume chemotherapy and five completed the 3 month intervention period. These five and the one who resumed chemotherapy after 6 weeks report an improved emotional functioning and less insomnia, while several other parameters of quality of life remained stable or worsened, reflecting their very advanced disease. Except for temporary constipation and fatigue, we found no severe adverse side effects, especially no changes in cholesterol or blood lipids. Conclusions: These pilot data suggest that a KD is suitable for even advanced cancer patients. It has no severe side effects and might improve aspects of quality of life and blood parameters in some patients with advanced metastatic tumors.
KW  - Lebensqualität
KW  - Krebskranker
KW  - Ketogenic diet
KW  - cancer patients
KW  - pilot study
KW  - quality of life
Y1  - 2011
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-68871
ER  - 
TY  - JOUR
A1  - Kleinschnitz, Christoph
A1  - Grund, Henrike
A1  - Wingler, Kirstin
A1  - Armitage, Melanie E.
A1  - Jones, Emma
A1  - Mittal, Manish
A1  - Barit, David
A1  - Schwarz, Tobias
A1  - Geis, Christian
A1  - Kraft, Peter
A1  - Barthel, Konstanze
A1  - Schuhmann, Michael K.
A1  - Herrmann, Alexander M.
A1  - Meuth, Sven G.
A1  - Stoll, Guido
A1  - Meurer, Sabine
A1  - Schrewe, Anja
A1  - Becker, Lore
A1  - Gailus-Durner, Valerie
A1  - Fuchs, Helmut
A1  - Klopstock, Thomas
A1  - de Angelis, Martin Hrabe
A1  - Jandeleit-Dahm, Karin
A1  - Shah, Ajay M.
A1  - Weissmann, Norbert
A1  - Schmidt, Harald H. H. W.
T1  - Post-Stroke Inhibition of Induced NADPH Oxidase Type 4 Prevents Oxidative Stress and Neurodegeneration
N2  - Ischemic stroke is the second leading cause of death worldwide. Only one moderately effective therapy exists, albeit with contraindications that exclude 90% of the patients. This medical need contrasts with a high failure rate of more than 1,000 pre-clinical drug candidates for stroke therapies. Thus, there is a need for translatable mechanisms of neuroprotection and more rigid thresholds of relevance in pre-clinical stroke models. One such candidate mechanism is oxidative stress. However, antioxidant approaches have failed in clinical trials, and the significant sources of oxidative stress in stroke are unknown. We here identify NADPH oxidase type 4 (NOX4) as a major source of oxidative stress and an effective therapeutic target in acute stroke. Upon ischemia, NOX4 was induced in human and mouse brain. Mice deficient in NOX4 (Nox42/2) of either sex, but not those deficient for NOX1 or NOX2, were largely protected from oxidative stress, blood-brain-barrier leakage, and neuronal apoptosis, after both transient and permanent cerebral ischemia. This effect was independent of age, as elderly mice were equally protected. Restoration of oxidative stress reversed the stroke-protective phenotype in Nox42/2 mice. Application of the only validated low-molecular-weight pharmacological NADPH oxidase inhibitor, VAS2870, several hours after ischemia was as protective as deleting NOX4. The extent of neuroprotection was exceptional, resulting in significantly improved long-term neurological functions and reduced mortality. NOX4 therefore represents a major source of oxidative stress and novel class of drug target for stroke therapy.
KW  - Schlaganfall
Y1  - 2010
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-68416
ER  - 
TY  - JOUR
A1  - Marenholz, Ingo
A1  - Esparza-Gordillo, Jorge
A1  - Rüschendorf, Franz
A1  - Bauerfeind, Anja
A1  - Strachan, David P.
A1  - Spycher, Ben D.
A1  - Baurecht, Hansjörg
A1  - Magaritte-Jeannin, Patricia
A1  - Sääf, Annika
A1  - Kerkhof, Marjan
A1  - Ege, Markus
A1  - Baltic, Svetlana
A1  - Matheson, Melanie C.
A1  - Li, Jin
A1  - Michel, Sven
A1  - Ang, Wei Q.
A1  - McArdle, Wendy
A1  - Arnold, Andreas
A1  - Homuth, Georg
A1  - Demenais, Florence
A1  - Bouzigon, Emmanuelle
A1  - Söderhäll, Cilla
A1  - Pershagen, Göran
A1  - de Jongste, Johan C.
A1  - Postma, Dirkje S.
A1  - Braun-Fahrländer, Charlotte
A1  - Horak, Elisabeth
A1  - Ogorodova, Ludmila M.
A1  - Puzyrev, Valery P.
A1  - Bragina, Elena Yu
A1  - Hudson, Thomas J.
A1  - Morin, Charles
A1  - Duffy, David L.
A1  - Marks, Guy B.
A1  - Robertson, Colin F.
A1  - Montgomery, Grant W.
A1  - Musk, Bill
A1  - Thompson, Philip J.
A1  - Martin, Nicholas G.
A1  - James, Alan
A1  - Sleiman, Patrick
A1  - Toskala, Elina
A1  - Rodriguez, Elke
A1  - Fölster-Holst, Regina
A1  - Franke, Andre
A1  - Lieb, Wolfgang
A1  - Gieger, Christian
A1  - Heinzmann, Andrea
A1  - Rietschel, Ernst
A1  - Keil, Thomas
A1  - Cichon, Sven
A1  - Nöthen, Markus M.
A1  - Pennel, Craig E.
A1  - Sly, Peter D.
A1  - Schmidt, Carsten O.
A1  - Matanovic, Anja
A1  - Schneider, Valentin
A1  - Heinig, Matthias
A1  - Hübner, Norbert
A1  - Holt, Patrick G.
A1  - Lau, Susanne
A1  - Kabesch, Michael
A1  - Weidinger, Stefan
A1  - Hakonarson, Hakon
A1  - Ferreira, Manuel A. R.
A1  - Laprise, Catherine
A1  - Freidin, Maxim B.
A1  - Genuneit, Jon
A1  - Koppelman, Gerard H.
A1  - Melén, Erik
A1  - Dizier, Marie-Hélène
A1  - Henderson, A. John
A1  - Lee, Young Ae
T1  - Meta-analysis identifies seven susceptibility loci involved in the atopic march
JF  - Nature Communications
N2  - Eczema often precedes the development of asthma in a disease course called the 'atopic march'. To unravel the genes underlying this characteristic pattern of allergic disease, we conduct a multi-stage genome-wide association study on infantile eczema followed by childhood asthma in 12 populations including 2,428 cases and 17,034 controls. Here we report two novel loci specific for the combined eczema plus asthma phenotype, which are associated with allergic disease for the first time; rs9357733 located in EFHC1 on chromosome 6p12.3 (OR 1.27; P = 2.1 x 10(-8)) and rs993226 between TMTC2 and SLC6A15 on chromosome 12q21.3 (OR 1.58; P = 5.3 x 10(-9)). Additional susceptibility loci identified at genome-wide significance are FLG (1q21.3), IL4/KIF3A (5q31.1), AP5B1/OVOL1 (11q13.1), C11orf30/LRRC32 (11q13.5) and IKZF3 (17q21). We show that predominantly eczema loci increase the risk for the atopic march. Our findings suggest that eczema may play an important role in the development of asthma after eczema.
KW  - chromosome 11Q13
KW  - risk
KW  - genomewide association
KW  - hay fever
KW  - birth cohort
KW  - filaggrin mutations
KW  - food allergy
KW  - juvenile myoclonic epilepsy
KW  - childhood asthma
KW  - dermatitis
Y1  - 2015
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-139835
VL  - 6
IS  - 8804
ER  -