Zusammenfassung
Bei Karzinompatienten können Störungen des Glukosestoffwechsels wesentliche Auswirkungen auf das Körpergewicht und die Relationen zwischen den Körperkompartimenten haben. Das sollte beim Entwurf von Ernährungskonzepten beachtet werden. Zusätzlich sind dabei Einflüsse einzelner Nährstoffe auf das Tumorwachstum von Interesse. Wir stellen hier 2 Ernährungskonzepte vor: ein prozentuales Kohlenhydrat / Fett-Energie-Verhältnis von 50 / 50 und die ketogene Kost. Für unsere Vorschläge war u. a. der bei Tumorpatienten gemessene Nettoaustausch von Substraten seitens der peripheren Gewebe, des Splanchnikusgebiets und der Karzinome wegweisend. Postabsorptiv wird bei Tumorkranken vom Ganzkörper und der Muskulatur Glukose vermindert aufgenommen und vermindert oxidiert. Die Insulinresistenz geht den ersten Zeichen der Mangelernährung voraus. Offenbar im Gefolge der reduzierten Glukoseverfügbarkeit nimmt die Fettoxidation zu. Nach oraler Glukosebelastung und bei parenteraler Ernährung ist die Glukoseverwertung vor allem wegen einer verringerten Glykogensynthesekapazität der Leber und der Muskulatur erheblich gestört. Die Fettverwertung, beurteilt nach der Fett-Clearance, ist dagegen gesteigert. Maligne Tumoren behalten Glukose in großer Menge ein und metabolisieren sie vorzugsweise glykolytisch, da es in Tumorzellen oft Blockaden der oxidativen Phosphorylierung gibt. Unter dem Einfluss einer parenteralen Ernährung setzten menschliche Karzinome Fettsäuren netto frei. Vor diesem metabolischen Hintergrund empfehlen sich Ernährungsformen mit viel Fett. Eine fettreiche Kost war in einer randomisierten klinischen Studie bezüglich des Körpergewichts und der Körperzellmasse einer isokalorischen Normalkost überlegen. Die ketogene Diät umgeht das Hindernis der gestörten Glukoseverwertung noch ausgiebiger. Zusätzlich beeinträchtigen fettreiche Kostformen die Glykolyse und das Wachstum der Tumoren.
Abstract
In cancer patients, abnormalities in glucose metabolism have substantial effects on both body weight and composition. Such effects as well as the influence of specific nutrients on tumor growth should be taken into account in forming nutritional strategies. We therefore propose 2 nutritional concepts: (I) a high-fat diet (fat / carbohy-drate caloric ratio 50 / 50) and (II) a ketogenic diet. Our proposals are partly based on the net balances of substrates measured across the peripheral tissues, the splanchnic area and carcinomas in tumor patients. Postabsorptively, whole body and muscle glucose uptake and oxidation are reduced in cancer patients. Insulin resistance occurs before the onset of malnutrition. An increase in lipid oxidation appears to be a consequence of the decline in glucose availability. After an oral glucose load as well as during parenteral nutrition, glucose utilization is severely impaired mainly due to a decrease in both hepatic and muscular glycogen synthesis capacity. By contrast, lipid utilization as judged from lipid clearance is enhanced. Malignant tumors retain glucose avidly and use it via enhanced glycolysis, since oxidative phosphorylation is often inhibited. Parenteral nutrition resulted in a net release of free fatty acids from human carcinomas. This metabolic background favors nutritional regimens high in fat. In a randomized clinical trial such a regimen was superior to isocaloric normal feeding with regard to body weight and cell mass. By using a ketogenic diet the blockade of glucose utilization can be bypassed even more. Additionally, diets high in fat interfere with both tumor glycolysis and tumor growth.
Schlüsselwörter
Tumorpatienten - Stoffwechsel - Ernährungskonzepte - Fette - Kohlenhydrate
Keywords
tumor patients - metabolism - nutritional concepts - lipids - carbohydrates
Literatur
-
1
Rohdenburg G L, Bernhard A, Krehbiel A.
Sugar tolerance in cancer.
J Am Med Ass.
1919;
72
1528-1534
-
2
Marks P A, Bishop J S.
The glucose metabolism of patients with malignant disease and normal subjects as studied by means of an intravenous glucose tolerance test.
J Clin Invest.
1957;
36
254-264
-
3
Rothkopf M.
Fuel utilization in neoplastic disease: Implications for the use of nutritional support in cancer patients.
Nutrition.
1990;
6
14S-16S
-
4
Grosvenor M, Bulcavage L, Chlebowski R T.
Symptoms potentially influencing weight loss in a cancer population.
Cancer.
1989;
63
330-334
-
5
Holm E, Staedt U, Leweling H et al.
Metabolism and artificial nutrition of patients with malignancy.
SA J Clin Nutr.
1993;
6
10-21
-
6
Heymsfield S A, McManus C B.
Tissue components of weight loss in cancer patients. A new method of study and preliminary observations.
Cancer.
1985;
55
238-249
-
7
Fearon K C, Preston T.
Body composition in cancer cachexia.
Infusionstherapie.
1990;
17
(S 03)
63-66
-
8
Evans W K, Nixon D W, Daly J M et al.
A randomized study of oral nutritional support versus ad lib nutritional intake during chemotherapy for advanced colorectal and non-small-cell lung cancer.
J Clin Oncol.
1987;
5
113-124
-
9
Bozzetti F, Gavazzi C, Mariani L et al.
Artificial nutrition in cancer patients: Which route, what composition?.
World J Surg.
1999;
23
577-583
-
10
Makino T, Noguchi Y, Yoshikawa T.
Circulating interleukin 6 concentrations and insulin resistance in patients with cancer.
Br J Surg.
1998;
85
1658-1662
-
11
Toso S, Piccoli A, Gusella M et al.
Altered tissue electric properties in lung cancer patients as detected by bioelectric impedance vector analysis.
Nutrition.
2000;
16
120-124
-
12 Holm E. Stoffwechsel und Ernährung bei Tumorkrankheiten.. Stuttgart, New York: Thieme; 2007
-
13
Cersosimo E, Pisters P WT, Pesola G et al.
The effect of graded doses of insulin on peripheral glucose uptake and lactate release in cancer cachexia.
Surgery.
1991;
109
459-467
-
14
Permert J, Adrian T E, Jacobsson P et al.
Is profound peripheral insulin resistance in patients with pancreatic cancer caused by a tumor-associated factor?.
Am J Surg.
1993;
165
61-66
-
15
Yoshikawa T, Noguchi Y, Matsumoto A.
Effects of tumor removal and body weight loss on insulin resistance in patients with cancer.
Surgery.
1994;
116
62-66
-
16
Marat D, Noguchi Y, Yoshikawa T et al.
Insulin resistance and tissue glycogen content in the tumor-bearing state.
Hepato-Gastroenterology.
1999;
46
3159-3165
-
17
McCall J L, Tuckey J A, Parry B R.
Serum tumour necrosis factor alpha and insulin resistance in gastrointestinal cancer.
Br J Surg.
1992;
79
1361-1363
-
18
Norton J A, Maher M, Wesley R et al.
Glucose intolerance in sarcoma patients.
Cancer.
1984;
54
3022-3027
-
19
Tayek J A, Manglik S, Abemayor E.
Insulin secretion, glucose production, and insulin sensitivity in underweight and normal-weight volunteers, and in underweight and normal-weight cancer patients: A clinical research center study.
Metabolism.
1997;
46
140-145
-
20
Gambardella A, Tortoriello R, Tagliamonte M R et al.
Metabolic changes in elderly cancer patients after glucose ingestion. The role of tumor necrosis factor-α.
Cancer.
1997;
79
177-184
-
21
Wolfe R R.
Metabolic interactions between glucose and fatty acids in humans.
Am J Clin Nutr.
1998;
67
(S 03)
519S-526S
-
22
Körber J, Pricelius S, Heidrich M et al.
Increased lipid utilization in weight losing and weight stable cancer patients with normal body weight.
Eur J Clin Nutr.
1999;
53
740-745
-
23
Hansell D T, Davies J WL, Burns H JG et al.
The oxidation of body fuel stores in cancer patients.
Ann Surg.
1986;
204
637-642
-
24
Richards E W, Long C L, Nelson K M et al.
Glucose metabolism in advanced lung cancer patients.
Nutrition.
1992;
8
245-251
-
25
Selberg O, Weimann A, Meyer H J et al.
Lipolyse und Lipidoxidation bei gewichtsstabilen Patienten mit malignen Tumoren des Verdauungstraktes.
Infusionstherapie.
1991;
18
80-84
-
26
Zuijdgeest-van Leeuwen S D, van den Berg J WO, Darcos Wattimena J L et al.
Lipolysis and lipid oxidation in weight-losing cancer patients and healthy subjects.
Metabolism.
2000;
49
931-936
-
27 Frayn K N. Metabolic Regulation. A Human Perspective.. 3rd ed. Oxford: Wiley-Blackwell; 2010
-
28
Shaw J HF, Wolfe F F.
Fatty acid and glycerol kinetics in septic patients and in patients with gastrointestinal cancer. The response to glucose infusion and parenteral feeding.
Ann Surg.
1987;
205
368-376
-
29
Jeevanandam M, Horowitz G D, Lowry S F et al.
Cancer cachexia and the rate of whole body lipolysis in man.
Metabolism.
1986;
35
304-310
-
30
Beck S A, Mulligan H D, Tisdale M J.
Lipolytic factors associated with murine and human cancer cachexia.
J Natl Cancer Inst.
1990;
82
1922-1926
-
31
Barber M D, McMillan D C, Preston T et al.
Metabolic response to feeding in weight-losing pancreatic cancer patients and its modulation by a fish-oil-enriched nutritional supplement.
Clin Sci.
2000;
98
398-399
-
32 Stütz O. Metabolische Untersuchungen an Karzinompatienten: Substrataustausch der peripheren Gewebe und Hypernephrom-tragender Nieren.. Med Diss. Heidelberg, Mannheim; 1995
-
33
Holm E, Hildebrandt W, Kinscherf R et al.
Low postabsorptive net protein degradation in male cancer patients: Lack of sensitivity to regulatory amino acids?.
Oncol Rep.
2007;
17
695-700
-
34 Ast M, Debatin D. Splanchnischer und peripherer Substrataustausch bei metabolisch Gesunden und Karzinompatienten postabsorptiv und während parenteraler Ernährung.. Med Diss. Heidelberg, Mannheim; 2004
-
35
Tayek J A, Katz J.
Glucose production, recycling, Cori cycle, and gluconeogenesis in humans: relationship to serum cortisol.
Am J Physiol Endocrinol Metab.
1997;
272
E476-E484
-
36
Holroyde C P, Reichard G A.
Carbohydrate metabolism in cancer cachexia.
Cancer Treat Rep.
1981;
65
(S 05)
55-59
-
37
Leij-Halfwerk S, Dagnelie P C, van den Berg J WO et al.
Weight loss and elevated gluconeogenesis from alanine in lung cancer patients.
Am J Clin Nutr.
2000;
71
583-589
-
38
Waterhouse C, Jeanpretre N, Keilson J.
Gluconeogenesis from alanine in patients with progressive malignant disease.
Cancer Res.
1979;
39
1968-1972
-
39
Shaw J HF, Wolfe R R.
Glucose and urea kinetics in patients with early and advanced gastrointestinal cancer: The response to glucose infusion, parenteral feeding, and surgical resection.
Surgery.
1987;
101
181-191
-
40
Edén E, Edström S, Bennegard K et al.
Glucose flux in relation to energy expenditure in malnourished patients with and without cancer during periods of fasting and feeding.
Cancer Res.
1984;
44
1718-1724
-
41
Noguchi Y, Vydelingum N A, Brennan M F.
The reversal in increased gluconeogenesis in the tumor-bearing rat by tumor removal and food intake.
Surgery.
1989;
106
423-431
-
42
Debatin D, Ast M, Tokus M et al.
Hepatic gluconeogenesis (GNG) and splanchnic protein balance (SPB) in early cancer disease.
Clin Nutr.
2001;
20
(S 03)
19
(Abstract)
-
43
Preston T, Slater C, McMillan D C et al.
Fibrinogen synthesis is elevated in fasting cancer patients with an acute phase response.
J Nutr.
1998;
128
1355-1360
-
44
Sauer L A, Dauchy R T.
Ketone body, glucose, lactic acid, and amino acid utilization by tumors in vivo in fasted rats.
Cancer Res.
1983;
43
3497-3503
-
45
Kallinowski F, Vaupel P, Runkel S et al.
Glucose uptake, lactate release, ketone body turnover, metabolic micromilieu, and pH distributions in human breast cancer xenografts in nude rats.
Cancer Res.
1988;
48
7264-7272
-
46
Hagmüller E, Kollmar H B, Günther H-J et al.
Protein metabolism in human colon carcinomas: In vivo investigations using a modified tracer technique with L [1–13C]leucine.
Cancer Res.
1995;
55
1160-1167
-
47
Holm E, Hagmüller E, Staedt U et al.
Substrate balances across colonic carcinomas in humans.
Cancer Res.
1995;
55
1373-1378
-
48
Seyfried T N, Shelton L M.
Cancer as a metabolic disease.
BMC Nutr Metab.
2010;
7
7
-
49
Mazurek S, Boschek C B, Hugo F et al.
Pyruvate kinase type M2 and its role in tumor growth and spreading.
Semin Cancer Biol.
2005;
15
300-308
-
50
Völker A, Tokus M, Breitkreutz R et al.
Die transtumoralen Bilanzen von Glutamin, Alanin und Serin bei parenteral ernährten Patienten richten sich nach der Tumorgröße.
Aktuel Ernahrungsmed.
2002;
27
117
(Abstract)
-
51
Eigenbrodt E, Kallinowski F, Ott M et al.
Pyruvate kinase and the interaction of amino acid and carbohydrate metabolism in solid tumors.
Anticancer Res.
1998;
18
3267-3274
-
52 Eigenbrodt E, Gerbracht U, Mazurek S et al. Carbohydrate metabolism and neoplasia: New perspectives for diagnosis and therapy.. In: Pretlow T G, Pretlow T P, eds Biochemical and Molecular Aspects of Selected Cancers.. San Diego, CA: Academic Press Inc; 1994: 311-385
-
53
Eigenbrodt E, Reinacher M, Scheefers-Borchel U et al.
Double role for pyruvate kinase type M2 in the expansion of phosphometabolite pools found in tumor cells.
Clin Rev Oncogen.
1992;
3
91-115
-
54
Kroemer G, Pouyssegur J.
Tumor cell metabolism: Cancer’s Achilles’ heel.
Cancer cell.
2008;
13
472-482
-
55
Warburg O.
On the origin of cancer cells.
Science.
1956;
123
309-314
-
56
Sonveaux P, Végran F, Schroeder T et al.
Targeting lactate-fueled respiration seletively kills hypoxic tumor cells in mice.
J Clin Invest.
2008;
118
3930-3942
-
57
Walenta S, Mueller-Klieser W F.
Lactate: mirror and motor of tumor malignancy.
Semin Radiat Oncol.
2004;
14
267-274
-
58 Schnurr B. Metabolische Untersuchungen an Karzinompatienten. Peripherer und tumoraler Substrataustausch postabsorptiv und während Nährstoffzufuhr.. Naturwiss Diss. Wien; 1998
-
59
Sauer L A, Blask D E, Dauchy R T.
Dietary factors and growth and metabolism in experimental tumors.
J Nutr Biochem.
2007;
18
637-649
-
60
Owen O E, Felig P, Morgan A P et al.
Liver and kidney metabolism during prolonged starvation.
J Clin Invest.
1969;
48
574-583
-
61
Bozzetti F, Gavazzi C, Mariani L et al.
Glucose-based total parenteral nutrition does not stimulate glucose uptake by human tumours.
Clin Nutr.
2004;
23
417-421
-
62 Köhl M. Konzentrationen und peripherer Austausch energieliefernder Substrate und der Aminosäuren bei Malignompatienten unter dem Einfluss zweier bilanzierter Diäten mit unterschiedlichem Fettgehalt.. Med Diss. Heidelberg, Mannheim; 1994
-
63
Coleman M D, Nickols-Richardson S M.
Urinary ketones reflect serum ketone concentration but do not relate to weight loss in overweight premenopausal women following a low-carbohydrate / high-protein diet.
J Am Diet Assoc.
2005;
105
608-611
-
64
Rofe A M, Bais R, Conyers R AJ.
Ketone-body metabolism in tumour-bearing rats.
Biochem J.
1986;
233
485-491
-
65
Marchut E, Guminska M, Kedryna T.
The inhibitory effect of various fatty acids on aerobic glycolysis in Ehrlich ascites tumour cells.
Acta Biochim Pol.
1986;
33
7-16
-
66
Fine E J, Miller A, Quadros E V et al.
Acetoacetate reduces growth and ATP concentration in cancer cell lines which over-express uncoupling protein 2.
Cancer Cell Int.
2009;
9
14
-
67
Thompson J R, Wu G.
The effect of ketone bodies on nitrogen metabolism in skeletal muscle.
Comp Biochem Physiol B.
1991;
100
209-216
-
68
Tisdale M J, Brennan R A, Fearon K C.
Reduction of weight loss and tumour size in a cachexia model by a high fat diet.
Br J Cancer.
1987;
56
39-43
-
69
Breitkreutz R, Tesdal K, Jentschura D et al.
Effects of a high-fat diet on body composition in cancer patients receiving chemotherapy. A randomized controlled study.
Wien Klin Wochenschr.
2005;
117
685-692
-
70
Keller U, Lustenberger M, Müller-Brand J et al.
Human ketone body production and utilization studied using tracer techniques: regulation by free fatty acids, insulin, catecholamines, and thyroid hormones.
Diabetes Metab Rev.
1989;
5
285-298
-
71
Veech R L.
The therapeutic implications of ketone bodies: the effects of ketone bodies in pathological conditions: ketosis, ketogenic diet, redox states, insulin resistance, and mitochondrial metabolism.
Prostaglandins Leukot Essent Fatty Acids.
2004;
70
309-319
-
72
LeRoith D, Roberts Jr C T.
The insulin-like growth factor system and cancer.
Cancer Lett.
2003;
195
127-137
-
73
Gallagher E J, LeRoith D.
The proliferating role of insulin and insulin-like growth factors in cancer.
Trends Endocrinol Metab.
2010;
21
610-618
-
74
Freedland S J, Mavropoulos J, Wang A et al.
Carbohydrate restriction, prostate cancer growth, and the insulin-like growth factor axis.
Prostate.
2008;
68
11-19
-
75
Ardawi M S, Newsholme E A.
Metabolism of ketone bodies, oleate and glucose in lymphocytes of the rat.
Biochem J.
1984;
221
255-260
-
76
Garland P B, Randle P J.
Control of pyruvate dehydrogenase in the perfused rat heart by the intracellular concentration of acetyl-coenzyme A.
Biochem J.
1964;
91
6C-7C
-
77
van Ness van Alstyne E, Beebe S P.
Diet studies in transplantable tumors. I. The effect of non-carbohydrate diet upon the growth of transplantable sarcoma in rats.
J Med Res.
1913;
29
217-232
-
78
Caspari W.
Über den Einfluss der Kost auf das Wachstum von Impfgeschwülsten. VI. Mitteilung. Über den Einfluss des Palmitins auf das Geschwulstwachstum.
Z Krebs-forsch.
1932;
38
356-360
-
79
Otto C, Kaemmerer U, Illert B et al.
Growth of human gastric cancer cells in nude mice is delayed by a ketogenic diet supplemented with omega-3 fatty acids and medium-chain triglycerides.
BMC Cancer.
2008;
8
122
-
80
Bravata D M, Sanders L, Huang J et al.
Efficacy and safety of low-carbohydrate diets: a systematic review.
J Am Med Ass.
2003;
289
1837-1850
-
81
Brosnan J T.
Comments on metabolic needs for glucose and the role of gluconeogenesis.
Eur J Clin Nutr.
1999;
53
(S 01)
S107-S111
-
82
Dressler A, Stöcklin B, Reithofer E et al.
Long-term outcome and tolerability of the ketogenic diet in drug-resistant childhood epilepsy – the Austrian experience.
Seizure.
2010;
19
404-408
-
83
Patel A, Pyzik P L, Turner Z et al.
Long-term outcomes of children treated with the ketogenic diet in the past.
Epilepsia.
2010;
51
1277-1282
-
84
Dashti H M, Mathew T C, Khadada M et al.
Beneficial effects of ketogenic diet in obese diabetic subjects.
Mol Cell Biochem.
2007;
302
249-256
-
85
Laffel L.
Ketone bodies: a review of physiology, pathophysiology and application of monitoring to diabetes.
Diabetes Metab Res Rev.
1999;
15
412-426
-
86
Umpierrez G E, Kitabchi A E.
Diabetic ketoacidosis: risk factors and management strategies.
Treat Endocrinol.
2003;
2
95-108
-
87
Chen T Y, Smith W, Rosenstock J L et al.
A life-threatening complication of Atkins diet.
Lancet.
2006;
367
958
-
88
Liu Y M, Williams S, Basualdo-Hammond C et al.
A prospective study: growth and nutritional status of children treated with the ketogenic diet.
J Am Diet Ass.
2003;
103
707-712
-
89
Brown J K, Byers T, Doyle C American Cancer Society et al.,.
Nutrition and physical activity during and after cancer treatment: an American Cancer Society guide for informed choices.
CA Cancer J Clin.
2003;
53
268-291
-
90
Norman H A, Butrum R R, Feldman E et al.
The role of dietary supplements during cancer therapy.
J Nutr.
2003;
133
(S 01)
3794S-3799S
-
91
Biesalski H K.
Mikronährstoffsupplemente bei onkologischen Patienten.
Onkologe.
2008;
14
45-57
-
92
Fletcher R H, Fairfield K M.
Vitamins for chronic disease prevention in adults: clinical applications.
J Am Med Ass.
2002;
287
3127-3129
-
93
Willett W C, Stampfer M J.
Clinical practice. What vitamins should I be taking, doctor?.
New Engl J Med.
2001;
345
1819-1824
-
94
Cantor I.
Shedding light on vitamin D and integrative oncology.
Integr Cancer Ther.
2008;
7
81-89
-
95
Zhang R, Naughton D P.
Vitamin D in health and disease: current perspectives.
Nutr J.
2010;
9
65
-
96
Sharman M J, Kraemer W J, Love D M et al.
A ketogenic diet favorably affects serum biomarkers for cardiovascular disease in normal-weight men.
J Nutr.
2002;
132
1879-1885
-
97
Shai I, Schwarzfuchs D, Henkin Y Dietary Intervention Randomized Controlled Trial (DIRECT) Group et al.
Weight loss with a low-carbohydrate, Mediterranean, or low-fat diet.
New Engl J Med.
2008;
359
229-241
-
98
Gardner C D, Kiazand A, Alhassan S et al.
Comparison of the Atkins, Zone, Ornish, and LEARN diets for change in weight and related risk factors among overweight premenopausal women: the ATOZ Weight Loss Study: a randomized trial.
J Am Med Ass.
2007;
297
969-977
-
99
Pérez-Guisado J, Muñoz-Serrano A et al.
Spanish Ketogenic Mediterranean Diet: a healthy cardiovascular diet for weight loss.
Nutr J.
2008;
7
30
-
100
Foster G D, Wyatt H R, Hill J O et al.
Weight and metabolic outcomes after 2 years on a low-carbohydrate versus low-fat diet: a randomized trial.
Ann Intern Med.
2010;
153
147-157
-
101
Schmidt M, Pfetzer N, Schwab M et al.
Effects of a ketogenic diet on the quality of life in 16 patients with advanced cancer: A pilot trial.
Nutr Metab.
2011;
8
54
-
102
McNally M A, Pyzik P L, Rubenstein J E et al.
Empiric use of potassium citrate reduces kidney-stone incidence with the ketogenic diet.
Pediatrics.
2009;
124
e300-304
-
103
Sampath A, Kossoff E H, Furth S L et al.
Kidney stones and the ketogenic diet: risk factors and prevention.
J Child Neurol.
2007;
22
375-378
-
104
Bier D M, Brosnan J T, Flatt J P et al.
Report of the IDECG Working Group on lower and upper limits of carbohydrate and fat intake. International Dietary Energy Consultative Group.
Eur J Clin Nutr.
1999;
53
(S 01)
S177-S178
-
105
Holm E, Schade I.
Einflüsse kurzkettiger und gesättigter langkettiger Fettsäuren auf das Tumorwachstum – In-vitro- und experimentelle In-vivo-Effekte.
Aktuel Ernahrungsmed.
2008;
33
1-6
Prof. Dr. med. Eggert Holm
Universitätsklinikum Mannheim
Bergstraße 161
69121 Heidelberg
Email: eggert.holm@urz.uni-heidelberg.de
Prof. Dr. rer. hum. biol. Ulrike Kämmerer
Frauenklinik des Universitätsklinikums Würzburg
Josef-Schneider-Straße 4
97080 Würzburg
Email: u.kaemmerer@mail.uni-wuerzburg.de
