Helmut Friess

Technische Universität München, München, Bavaria, Germany

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Publications (688)3417.41 Total impact

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    ABSTRACT: Purpose: With improved chemotherapeutic regimens, metastasized gastric cancer may show a good response rendering an initially unresectable tumor resectable. We performed a retrospective analysis on the outcome of stage IV gastric cancer patients treated by chemotherapy followed by oncologic resection in a western institution. Methods: From August 1988 to December 2010, a total number of 1,817 patients underwent surgery for gastric cancer at the Department of Surgery, Technical University of Munich. A retrospective analysis of our prospective gastric cancer database identified 58 patients with stage IV gastric cancer having undergone induction chemotherapy followed by surgery in an individualized treatment concept. After induction chemotherapy usually consisting of 2 cycles of PLF (cisplatin, 5-fluorouracil, leucovorin), resection was performed with or without removal of metastases in patients without disease progression. Patients were followed up until death or loss to follow up. Results: The three most common metastatic locations were liver (27.6 %), distant lymph nodes (22.4 %), and peritoneum (19.0 %). Of patients, 13.8 % had metastases in more than one location. Thirty-day mortality was 5.2 %, 90-day mortality was 13.8 %, while overall postoperative morbidity accounted for 24 %. In 19 (32.8 %) patients, a complete resection without any macroscopic tumor residues was achieved. In 39 (67.2 %) patients, tumors could not be completely removed with either local residual disease or residual disease at distant sites. Overall median survival was 20 months, while patients without residual tumor survived significantly longer (72 months) than patients with residual disease (12 months, p = 0.001). Conclusion: Secondary surgery of metastasized gastric cancer may be justified in selected cases without progression under induction chemotherapy. An achievable complete removal of the primary tumor and metastases appears the main selection criterion for patients benefitting from this approach.
    Langenbeck s Archives of Surgery 06/2014; 399(6). DOI:10.1007/s00423-014-1217-3 · 2.19 Impact Factor

  • Pancreatology 06/2014; 14(3):S17. DOI:10.1016/j.pan.2014.05.431 · 2.84 Impact Factor

  • Pancreatology 06/2014; 14(3):S73. DOI:10.1016/j.pan.2014.05.624 · 2.84 Impact Factor

  • Pancreatology 06/2014; 14(3):S20. DOI:10.1016/j.pan.2014.05.441 · 2.84 Impact Factor
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    ABSTRACT: Background This position statement was developed in order to expedite a consensus on definition and treatment for borderline resectable pancreatic ductal adenocarcinoma (BRPC) that would have worldwide acceptability. Methods An international panel of pancreatic surgeons from well-established high-volume centers collaborated on a literature review and development of consensus on issues related to borderline resectable pancreatic cancer. Results The International Study Group for Pancreatic Surgery (ISGPS) supports the National Comprehensive Cancer Network (NCCN) criteria for the definition of BRPC. Current evidence supports operative exploration and resection in the case of involvement of the mesenterico-portal venous axis; in addition, a new classification of extrahepatic mesenterico-portal venous resections is proposed by the ISGPS. Suspicion of arterial involvement should lead to exploration to confirm the imaging-based findings. Formal arterial resections are not recommended; however, in exceptional circumstances, individual therapeutic approaches may be evaluated under experimental protocols. The ISGPS endorses the recommendations for specimen examination and the definition of an R1 resection (tumor within 1mm from the margin) used by the British Royal College of Pathologists (RCPath). Standard preoperative diagnostics for BRPC may include: 1) serum levels of CA19-9, because CA19-9 levels predict survival in large retrospective series, and also 2) the modified Glasgow Prognostic Score (mGPS) and the neutrophil/lymphocyte ratio (NLR), because of the prognostic relevance of the systemic inflammatory response. Various regimens of neoadjuvant therapy are recommended only in the setting of prospective trials at high-volume centers. Conclusion Current evidence justifies porto-mesenteric venous resection in patients with BRPC. Basic definitions were identified, that are currently lacking but that are needed to obtain further evidence and improvement for this important patient subgroup. A consensus for each topic is given.
    Surgery 06/2014; 155(6). DOI:10.1016/j.surg.2014.02.001 · 3.38 Impact Factor

  • Pancreatology 06/2014; 14(3):S54-S55. DOI:10.1016/j.pan.2014.05.564 · 2.84 Impact Factor

  • Pancreatology 06/2014; 14(3):S14. DOI:10.1016/j.pan.2014.05.424 · 2.84 Impact Factor
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    ABSTRACT: Aim: To systematically characterize specific pain patterns in the most frequent pancreatic diseases. Methods: Pain in patients with chronic pancreatitis (n = 314), pancreatic cancer (n = 469), and other pancreatic tumors (n = 249) including mucinous (n = 20) and serous cystadenoma (n = 31), invasive (n = 37) and non-invasive intraductal papillary mucinous neoplasia (IPMN; n = 48), low stage (n = 18) and high stage neuroendocrine neoplasia (n = 44), and ampullary cancer (n = 51) was registered and correlated with clinicopathological data. Survival times were estimated by the Kaplan-Meier method. Patients alive at the follow-up time were censored. Survival curves were compared statistically using the log-rank test. Results: Forty-nine point one percent of pancreatic cancer patients revealed no pain, whereas in chronic pancreatitis only 18.3% were pain free. In contrary, moderate/severe pain was registered in 15.1% in pancreatic cancer patients that was increased in chronic pancreatitis with up to 34.2%. Serous cystadenoma was asymptomatic in most cases (58.1%), whereas 78.9% of all mucinous cystadenoma patients suffered pain. In neuroendocrine neoplasia pain was not a key clinical symptom since 64% of low stage neuroendocrine neoplasia and 59% of high stage neuroendocrine neoplasia patients were pain free. Cancer localization in the pancreatic body and patients with malignant pancreatic neoplasms were associated with more severe pain. Tumor grading and stage did not show any impact on pain. Only in pancreatic cancer, pain was directly associated with impaired survival. Conclusion: Pancreatic pain depicts different patterns of abdominal pain sensation according to the respective pancreatic disorder and does not allow a unification of the term pancreatic pain.
    Pancreatology 06/2014; 14(3):S13. DOI:10.3748/wjg.v20.i27.9154 · 2.84 Impact Factor

  • Pancreatology 06/2014; 14(3):S120. DOI:10.1016/j.pan.2014.05.787 · 2.84 Impact Factor
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    Simone Hausmann · Bo Kong · Christoph Michalski · Mert Erkan · Helmut Friess ·
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    ABSTRACT: Pancreatic ductal adenocarcinoma (PDAC) is a devastating disease with an extremely poor prognosis. Inflammatory processes have emerged as key mediators of pancreatic cancer development and progression. In genetically engineered mouse models, induction of pancreatitis accelerates PDAC development, and patients with chronic pancreatitis are known to have a higher risk of developing pancreatic cancer. In recent years, much effort has been given to identify the underlying mechanisms that contribute to inflammation-induced tumorigenesis. Many inflammatory pathways have been identified and inhibitors have been developed in order to prevent cancer development and progression. In this chapter, we discuss the role of inflammatory pathways in the initiation and progression of pancreatic cancer as well as the role of inhibitors used in treatment and prevention of pancreatic cancer.
    Advances in Experimental Medicine and Biology 05/2014; 816:129-51. DOI:10.1007/978-3-0348-0837-8_6 · 1.96 Impact Factor
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    ABSTRACT: Neuroplasticity is an inherent feature of the enteric nervous system and gastrointestinal (GI) innervation under pathological conditions. However, the pathophysiological role of neuroplasticity in GI disorders remains unknown. Novel experimental models which allow simulation and modulation of GI neuroplasticity may enable enhanced appreciation of the contribution of neuroplasticity in particular GI diseases such as pancreatic cancer (PCa) and chronic pancreatitis (CP). Here, we present a protocol for simulation of pancreatic neuroplasticity under in vitro conditions using newborn rat dorsal root ganglia (DRG) and myenteric plexus (MP) neurons. This dual-neuron approach not only permits monitoring of both organ-intrinsic and -extrinsic neuroplasticity, but also represents a valuable tool to assess neuronal and glial morphology and electrophysiology. Moreover, it allows functional modulation of supplied microenvironmental contents for studying their impact on neuroplasticity. Once established, the present neuroplasticity assay bears the potential of being applicable to the study of neuroplasticity in any GI organ.
    Journal of Visualized Experiments 05/2014; DOI:10.3791/51049 · 1.33 Impact Factor
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    ABSTRACT: Background Pancreatoduodenectomy (PD) provides the best chance for cure in the treatment of patients with localized pancreatic head cancer. In patients with a suspected, clinically resectable pancreatic head malignancy, the need for histologic confirmation prior to proceeding with PD has not historically been required, but still remains controversial. Methods An international panel of pancreatic surgeons working in well-known, high-volume centers reviewed the literature and worked together to establish a consensus on when to perform a pancreatoduodenectomy in the absence of positive histology. Results The incidence of benign disease after PD for a presumed malignancy is 5-13%. Diagnosis by ERCP brushings and percutaneous fine needle aspiration (FNA) are highly specific but poorly sensitive. Aspiration biopsy guided by endoscopic ultrasonography (EUS) has greater sensitivity, but it is highly operator-dependent and increases expense. The incidence of autoimmune pancreatitis (AIP) in the benign resected specimens is 30-43%. EUS-guided trucut biopsy, serum levels of IgG4, and HISORt (Histology, Imaging, Serology, Other organ involvement, and Response to therapy) are used for diagnosis. If AIP is suspected but not confirmed, the response to short course of steroids is helpful for diagnosis. Conclusions In the presence of a solid mass suspicious for malignancy, consensus was reached that biopsy proof is not required before proceeding with resection. Confirmation of malignancy, however, is mandatory for patients with borderline resectable disease to be treated with neo-adjuvant therapy prior to exploration for resection.. When a diagnosis of AIP is highly suspected, a biopsy is recommended, and a short course of steroid treatment should be considered if the biopsy does not reveal features suspicious for malignancy
    Surgery 05/2014; 155(5). DOI:10.1016/j.surg.2013.12.032 · 3.38 Impact Factor
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    ABSTRACT: Exocrine pancreatic insufficiency (EPI) is frequent in patients with chronic pancreatitis (CP). This 1-year, prospective, multicenter, observational, disease management study aimed to assess symptom improvement and quality of life in patients with CP with EPI who were receiving pancreatic enzyme replacement. Patients with CP and chronic EPI were either assigned to cohort 1 that consisted of patients already taking pancreatin (Kreon; Abbott Arzneimittel GmbH, Hannover, Germany) or cohort 2 that consisted of patients with newly diagnosed EPI without prior pancreatic enzyme treatment. Symptoms were documented, and quality of life was assessed using the gastrointestinal quality of life index (GIQLI) at baseline, 6 months, and 1 year. A total of 294 patients were evaluated (cohort 1, n = 206; cohort 2, n = 88). The proportion of patients experiencing gastrointestinal symptoms and recurrent pain after 1 year was significantly reduced in both cohorts (P < 0.001). The alleviation of symptoms was reflected in GIQLI score improvements at 1 year in both cohorts (P < 0.001), independent of CP severity and etiology. Improvements in GIQLI score were more pronounced in cohort 2 (P < 0.001). Pancreatin demonstrated symptom relief and improvement in quality of life in patients with CP-related EPI in this disease management study.
    Pancreas 04/2014; 43(6). DOI:10.1097/MPA.0000000000000131 · 2.96 Impact Factor
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    ABSTRACT: Patients with chronic liver diseases frequently exhibit decreased bone mineral densities (BMD), which is defined as hepatic osteodystrophy (HOD). HOD is a multifactorial disease whose regulatory mechanisms are barely understood. Thus, an early diagnosis and therapy is hardly possible. Therefore, the aim of our study consisted in characterizing a mouse model reflecting the human pathomechanism. Serum samples were collected from patients with chronic liver diseases and 12-week old C57Bl6/N mice after 6-week treatment with carbon tetrachloride (CCl4). Repetitive injections of CCl4 induced liver damage in mice, resembling liver fibrosis in patients, as assessed by serum analysis and histological staining. Although CCl4 did not affect primary osteoblast cultures, μCT analysis revealed significantly decreased BMD, bone volume, trabecular number and thickness in CCl4-treated mice. In both HOD patients and CCl4-treated mice, an altered vitamin D metabolism with decreased CYP27A1, CYP2R1, vitamin D-binding protein GC and increased 7-dehydrocholesterol reductase hepatic gene expression, results in decreased 25-OH vitamin D serum levels. Moreover, both groups exhibit excessively high active transforming growth factor-beta (TGF-β) serum levels, inhibiting osteoblast function in vitro. Summarizing, our mouse model presents possible mediators of HOD, e.g. altered vitamin D metabolism and increased active TGF-β. Liver damage and significant changes in bone structure and mineralization are already visible by μCT analysis after 6 weeks of CCl4 treatment. This fast response and easy transferability makes it an ideal model to investigate specific gene functions in HOD.
    Archives of Toxicology 04/2014; 88(4). DOI:10.1007/s00204-013-1191-5 · 5.98 Impact Factor
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    ABSTRACT: Background Heparin, the standard perioperative anticoagulant for prevention of graft vessel thrombosis in patients undergoing liver transplantation (LT), binds to the chemokine platelet factor 4 (PF4). Antibodies which are formed against the resulting PF4/heparin complexes can induce heparin-induced thrombocytopenia (HIT). LT is a clinical situation, which allows to study T-cell-dependency of immune responses as T-cell function are largely suppressed pharmacologically in these patients to prevent graft rejection.Objectives To investigate the immune response against PF4/heparin complexes in patients undergoing LT.Patients/Methods In this prospective cohort study, 38 consecutive patients undergoing LT were systematically screened for anti-PF4/heparin antibodies (enzyme immunoassay [EIA] and functional assay [HIPA]), platelet count, liver function, and engraftment.ResultsAt baseline, 5/38 (13%) patients tested positive for anti-PF4/heparin IgG (non-platelet-activating) antibodies. By day 20, additional 5/33 patients (15%) seroconverted for IgG (two platelet-activating) antibodies. No patient developed clinical HIT. Two of six patients with graft function failure had anti-PF4/heparin IgG antibodies at the time of graft function failure. Graft liver biopsies in these patients showed thrombotic occlusions of the microcirculation.Conclusions As anti-PF4/heparin IgG antibodies are generated despite strong pharmacologic suppression of T-cells indicating that T-cells have likely a limited role in the immune response to PF4/heparin complexes in humans.This article is protected by copyright. All rights reserved.
    Journal of Thrombosis and Haemostasis 03/2014; 12(6). DOI:10.1111/jth.12569 · 5.72 Impact Factor
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    ABSTRACT: Urinary tract complications are relevant sources of morbidity and mortality after kidney transplantation. Incidence is reported within 3-14% in recent studies. Secondary ureteropyelostomy using the native ureter is a surgical option to treat severe urinary tract complications after kidney transplantation.The aim of this study was to evaluate the outcome after ureteropyelostomy using the native ureter in the management of urinary tract complications after kidney transplantation. A single centre, retrospective clinical review of prospectively collected data of all patients who received kidney transplantation or combined kidney-pancreas transplantation between January 2001 and June 2009 was performed. All patients who underwent surgical therapy for urinary tract complications were identified and followed up to evaluate graft function and survival. Six hundred forty-six patients received kidney transplantation or combined kidney/pancreas transplantation. Twenty-six patients (4%) had to undergo re-operation due to severe urinary tract complications after kidney transplantation. Sixteen of the 26 patients (62%) received ureteropyelostomy using the ipsilateral native ureter. This reconstructive operation was successful in 14 of 16 patients (87.5%). Two patients needed to be re-operated for surgical complications. Ureteropyelostomy using the native ureter to treat ureter-related urinary tract complications after kidney transplantation can be performed safely and result in good graft and patient survival.
    ANZ Journal of Surgery 01/2014; 84(9). DOI:10.1111/ans.12526 · 1.12 Impact Factor
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    ABSTRACT: Increased neural density and neural hypertrophy are characteristic features of pancreatic neuropathy in chronic pancreatitis. Here, we present the extraordinary case of prominent pancreatic neuropathy in a 21-year-old female patient with hereditary chronic pancreatitis and intractable pain who underwent total pancreatectomy. The histopathological analysis demonstrated remnant pancreatic tissue which was only composed of prominent intrapancreatic nerves and fibrosis, without any visible remaining functional pancreatic parenchyma. These histological alterations, including nerve hypertrophy and increased neural density, are known for different aetiologies of chronic pancreatitis, e.g. alcoholic, idiopathic and tropic pancreatitis. However, this is the first report of a patient with hereditary chronic pancreatitis demonstrating the characteristic features of pancreatic neuropathy and neuropathic pain.
    Pancreatology 11/2013; 13(6):629–630. DOI:10.1016/j.pan.2013.05.009 · 2.84 Impact Factor
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    ABSTRACT: In addition to a preoperative antibiotic single-shot prophylaxis, we tested the impact of a one-time preoperative water-filtered infrared A irradiation (wIRA) on postoperative wound healing of patients. wIRA improves wound healing in postoperative settings. A total of 400 consecutive patients undergoing gastrointestinal surgery were randomly assigned to the treatment group (A) or placebo group (B). We applied wIRA for 20 minutes while patients were prepared for surgery. Patients and observer were blinded to group assignment. Primary endpoints were surgical site infections (SSIs), wound healing, and rate and level of pain within 30 days after surgery. Primary efficacy analysis was carried out on the basis of an intention-to-treat (ITT) population and a full-analysis set (FAS). Missing values of primary outcome variables were considered as SSIs and maximum pain levels in the ITT analysis, respectively. The incidence of SSI was 9 of 178 patients (5.1%) within group A compared with 22 of 182 (12.1%) within group B [P = 0.018; relative risk (RR) = 0.42; 95% CI: 0.18-0.93]. ITT: 32 of 200 (16%) SSIs occurred within group A and 39 of 200 (20%) within group B (P = 0.248) with an RR of 0.74 (95% CI: 0.43-1.28). The wIRA group showed lower postoperative pain at both the ITT (P = 0.092) and the FAS analysis (P = 0.045). This trial indicates a clinically relevant benefit of one-time application of preoperative wIRA as a supportive addition to prophylactic antibiotics. wIRA contributes to both reduced SSI rates and postoperative pain but also effectively decreases morbidity and related expenses in the health care system.
    Annals of surgery 10/2013; 258(6). DOI:10.1097/SLA.0000000000000235 · 8.33 Impact Factor
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    ABSTRACT: Unlabelled: Neurotrophic factors possess an emerging role in the pathophysiology of several gastrointestinal disorders, regulating innervation, pain sensation and disease-associated neuroplasticity. Here, we aimed at characterizing the role of the neurotrophic factor neurturin (NRTN) and its receptor glial-cell-line-derived neurotrophic factor receptor alpha-2 (GFRα-2) in pancreatic cancer (PCa) and pancreatic neuropathy. For this purpose, NRTN and GFRα-2 were studied in normal human pancreas and PCa tissues via immunohistochemistry, quantitative reverse transcription-polymerase chain reaction, immunoblotting and correlated to abdominal pain. The impact of NRTN/GFRα-2 on PCa cell (PCC) biology was investigated via exposure to hypoxia, 3-(4,5-dimethylthiazole-2-yl)-2,5-diphenyl tetrazolium bromide viability and matrigel invasion assays in native and specific small interfering RNA-silenced PCCs. To assess the influence of NRTN on pancreatic neuroplasticity and neural invasion (NI), its impact was explored via an in vitro 'neuroplasticity assay' and a 3D neural migration assay. NRTN and GFRα-2 demonstrated a site-specific upregulation in PCa, predominantly in nerves, PCCs and extracellular matrix. Patients with severe pain demonstrated higher intraneural GFRα-2 immunoreactivity than patients with no pain. PCa tissue and PCCs contained increased amounts of NRTN, which was suppressed under hypoxia. NRTN promoted PCC invasiveness, and silencing of NRTN limited both PCC proliferation and invasion. Depletion of NRTN from PCa tissue extracts and PCC supernatants decreased axonal sprouting in neuronal cultures but did not influence glial density. Silencing of NRTN in PCCs boosted NI. We conclude that increased NRTN/GFRα-2 in PCa seems to promote an aggressive PCC phenotype and neuroplasticity in PCa. Accelerated NI following NRTN suppression constitutes a novel explanation for the attraction of PCC to nerves in the hypoxic PCa tumor microenvironment. Summary: PCa is characterized by intrapancreatic neuroplasticity and NI. Here, we show that PCC produce the neurotrophic factor NRTN, which reinforces their biological properties, triggers neuroplastic alterations, NI and influences pain sensation via the GFRα-2 receptor.
    Carcinogenesis 09/2013; 35(1). DOI:10.1093/carcin/bgt312 · 5.33 Impact Factor
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    ABSTRACT: Longlasting and unbearable pain is the most common and striking symptom of chronic pancreatitis. Accordingly, pain relief and improvement in patients' quality of life are the primary goals in the treatment of this disease. This systematic review aims to summarize the available data on treatment options. A systematic search of MEDLINE/PubMed and the Cochrane Library was performed according to the PRISMA statement for reporting systematic reviews and meta-analysis. The search was limited to randomized controlled trials and meta-analyses. Reference lists were then hand-searched for additional relevant titles. The results obtained were examined individually by two independent investigators for further selection and data extraction. A total of 416 abstracts were reviewed, of which 367 were excluded because they were obviously irrelevant or represented overlapping studies. Consequently, 49 full-text articles were systematically reviewed. First-line medical options include the provision of pain medication, adjunctive agents and pancreatic enzymes, and abstinence from alcohol and tobacco. If medical treatment fails, endoscopic treatment offers pain relief in the majority of patients in the short term. However, current data suggest that surgical treatment seems to be superior to endoscopic intervention because it is significantly more effective and, especially, lasts longer.
    HPB 08/2013; 16(6). DOI:10.1111/hpb.12173 · 2.68 Impact Factor

Publication Stats

22k Citations
3,417.41 Total Impact Points


  • 2007-2015
    • Technische Universität München
      • Clinic and Polyclinic for Surgery
      München, Bavaria, Germany
  • 2010-2014
    • Deutsches Herzzentrum München
      München, Bavaria, Germany
  • 2013
    • Technische Universität Dresden
      Dresden, Saxony, Germany
  • 2002-2013
    • Universität Heidelberg
      • • Institute of Immunology and Serology
      • • Institute of Papyrology
      • • Institute of Pathology (Mannheim)
      Heidelburg, Baden-Württemberg, Germany
  • 2011
    • Heinrich-Heine-Universität Düsseldorf
      Düsseldorf, North Rhine-Westphalia, Germany
    • Southeast University (China)
      Nan-ching-hsü, Jiangxi Sheng, China
  • 2006
    • German Cancer Research Center
      Heidelburg, Baden-Württemberg, Germany
  • 2003
    • Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center
      Torrance, California, United States
    • Peking Union Medical College Hospital
      • Department of General Surgery
      Beijing, Beijing Shi, China
    • University of California, Los Angeles
      • Department of Surgery
      Los Angeles, CA, United States
  • 1995-2002
    • Universität Bern
      • • Visceral and Transplantation Surgery Research Group
      • • Institute of Pathology
      Berna, Bern, Switzerland
  • 1993-2002
    • University of California, Irvine
      • • Division of Endocrinology
      • • Department of Biological Chemistry
      • • Department of Medicine
      Irvine, California, United States
  • 2001
    • Freie Universität Berlin
      Berlín, Berlin, Germany
    • University of Nebraska at Omaha
      • Department of Pathology and Microbiology
      Omaha, Nebraska, United States
  • 2000-2001
    • Inselspital, Universitätsspital Bern
      • Department of Visceral Surgery and Medicine
      Berna, Bern, Switzerland
    • Lower Saxony Institute for Historical Coastal Research
      Wilhelmshaven, Lower Saxony, Germany
    • Charité Universitätsmedizin Berlin
      • Medical Department, Division of Nephrology and Internal Intensive Care Medicine
      Berlín, Berlin, Germany
  • 1999
    • Università degli Studi G. d'Annunzio Chieti e Pescara
      Chieta, Abruzzo, Italy
    • CSU Mentor
      • Department of Medicine
      Long Beach, California, United States
  • 1991-1999
    • Universität Ulm
      • Institute of General Medicine
      Ulm, Baden-Württemberg, Germany
    • Johannes Gutenberg-Universität Mainz
      Mayence, Rheinland-Pfalz, Germany