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Biomedical subjects

Frank Bergmann

Publications and source records attributed to Frank Bergmann.

16 recordsLinked to original sources
PubMed2006

The neurotrophic factor artemin influences the extent of neural damage and growth in chronic pancreatitis.

BACKGROUND AND AIMS: Chronic pancreatitis is characterised by severe abdominal neuropathic pain, perineural inflammatory cell infiltrations and intrapancreatic neural growth. Artemin was recently shown to eliminate neuropathic pain and reverse neurochemical damage after nerve injury. The role of artemin and its receptor GFRalpha3 was investigated in patients with chronic pancreatitis. METHODS: Expression of artemin and its receptor GFRalpha3 was studied in chronic pancreatitis (n = 66) and normal (n = 22) pancreatic tissues by quantitative reverse transcription-polymerase chain reaction (QRT-PCR) and western blot analysis. Artemin expression was correlated with pain and pathomorphological changes (inflammation, perineural inflammatory cell infiltration, neural alterations and fibrosis). Immunohistochemistry was used to localise artemin and GFRalpha3 in the tissues. To detect sources of artemin, primary human pancreatic stellate cells (hPSCs) were isolated and analysed by QRT-PCR and immunocytology analysis. RESULTS: In chronic pancreatitis, artemin and GFRalpha3 were significantly overexpressed and located in smooth muscle cells of arteries, Schwann cells and neural ganglia. Increased levels of artemin mRNA correlated with pain severity, inflammation, perineural inflammatory cell infiltration, neural density and hypertrophy. Furthermore, the severity of fibrosis was positively related with artemin expression and neural alterations. Activated hPSCs expressed low basal levels of artemin mRNA which were upregulated by exposure to transforming growth factor (TGF)beta1. CONCLUSIONS: Overexpression of artemin in chronic pancreatitis might function as a compensatory upregulation in order to repair neural damage incurred by ongoing pancreatic inflammation. Upregulation of TGFbeta1 seems not only to increase pancreatic fibrosis but also to contribute to neural alteration by stimulating artemin expression in hPSCs. However, overexpression of endogenous artemin does not seem to be sufficient to prevent pain in chronic pancreatitis.

Abdominal Pain↗
PubMed2006

Overexpression of cellular inhibitor of apoptosis protein 2 is an early event in the progression of pancreatic cancer.

AIM: To determine the role of two antiapoptotic proteins of the inhibitor of apoptosis protein family, cellular inhibitor of apoptosis protein 1 (cIAP1) and cellular inhibitor of apoptosis protein 2 (cIAP2), in human pancreatic carcinogenesis. METHODS: mRNA levels were measured in pancreatic tissues and pancreatic cancer cell lines by quantitative reverse transcriptase PCR. Protein expression was assessed in pancreatic cancer cell lines by immunoblotting and in pancreatic tissues by immunohistochemistry, and correlated with pathological and survival data. RESULTS: cIAP1 expression was constantly high in non-neoplastic pancreatic tissues, in pancreatic intraepithelial neoplasia (PanIN) lesions, as well as in a subset of primary and metastatic pancreatic ductal adenocarcinomas (PDAC), and a preferential cytoplasmatic localisation was observed in the tumour tissues. cIAP1 expression was rare in a cohort of cystic tumours. cIAP2 mRNA levels were significantly higher (2.4 fold) in PDAC than in normal tissues. cIAP2 protein was overexpressed in PDAC, and was detectable in low- and high-grade PanIN lesions. Moreover, cIAP2 was often expressed in pancreatic cystic tumours. cIAP1 and cIAP2 mRNA and protein were detected in all the examined cell lines. Survival analysis revealed a shorter survival in patients with cIAP1/cIAP2-positive tumours. CONCLUSIONS: cIAP1 might contribute to the regulation of the apoptotic process in the normal and in the neoplastic pancreas, depending on its subcellular localisation. Overexpression of cIAP2 is a common and early event in the progression of pancreatic cancer, and could therefore potentially influence the important pathophysiological aspects of PDAC, such as anoikis or chemoresistance.

Adenocarcinoma↗
PubMed2005

Pancreatic metastasis of Merkel cell carcinoma and concomitant insulinoma: case report and literature review.

BACKGROUND: Merkel cell carcinomas are rare neoplasm of neuroendocrine origin, usually observed in elderly people in areas with abundant sunlight, and predominantly located on the head and neck, extremities, and trunk. In many patients, a local recurrence after resection of the primary tumour and even distant metastases can be found. CASE PRESENTATION: We report an unusual occurrence of pancreatic metastases from a previously diagnosed Merkel cell carcinoma with the discovery of a concomitant insulinoma. An 82-year old lady suffered from recurrent attacks of hypoglycemia and presented with an abdominal mass, 2 years prior she had an excision done on her eyebrow that was reported as Merkel cell carcinoma. An extended distal pancreatectomy and splenectomy along with resection of the left flexure of the colon for her abdominal mass was carried out. Final histopathology of the mass was a poorly differentiated endocrine carcinoma in the pancreatic tail, in the peripancreatic tissue and in the surrounding soft tissue consistent with metastatic Merkel cell carcinoma in addition to an insulinoma of the pancreatic body. CONCLUSION: This is the first documented case of a metastatic Merkel cell carcinoma and a concomitant insulinoma, suggesting either a mere coincidence or an unknown neuroendocrine tumor syndrome.

Journal Article↗
PubMed2005

Bifurcation discovery tool.

MOTIVATION: Biochemical networks often yield interesting behavior such as switching, oscillation and chaotic dynamics. This article describes a tool that is capable of searching for bifurcation points in arbitrary ODE-based reaction networks by directing the user to regions in the parameter space, where such interesting dynamical behavior can be observed. RESULTS: We have implemented a genetic algorithm that searches for Hopf bifurcations, turning points and bistable switches. The software is implemented as a Systems Biology Workbench (SBW) enabled module and accepts the standard SBML model format. The interface permits a user to choose the parameters to be searched, admissible parameter ranges, and the nature of the bifurcation to be sought. The tool will return the parameter values for the model for which the particular behavior is observed. AVAILABILITY: The software, tutorial manual and test models are available for download at the following website: http:/www.sys-bio.org/ under the bifurcation link. The software is an open source and licensed under BSD.

Algorithms↗
PubMed2005

Respiratory disease caused by a species B2 adenovirus in a military camp in Turkey.

In April 2004, two patients were admitted to hospital in Berlin, Germany, with clinical signs of acute respiratory infection after returning from a military exercise in their home country of Turkey. They were admitted to a high security infectious disease unit as epidemiological data pointed to an outbreak of unknown etiology. Samples taken at the time of admission proved to be strongly positive for Adenovirus by PCR, but negative for Influenza A/H1N1 virus, Influenza A/H3N2 virus, Influenza B virus, Respiratory syncytial virus, and SARS coronavirus. No evidence for bacterial infection was obtained by serological tests and blood cultures. The adenovirus detected was characterized further by genotyping and was identified as a species B2 virus with the highest similarity to adenovirus type 11a.

Adenovirus Infections, Human↗
PubMed2004

Pancreatic metastasis from gastric carcinoma: a case report.

BACKGROUND: The pancreas is a rare but occasionally favored target for metastasis. Metastatic lesions in the pancreas have been described for various primary cancers, such as carcinomas of the lung, the breast, renal cell carcinoma and sarcomas. CASE PRESENTATION: We report the case of a 60-year old female with a mass in the pancreatic head four years after partial gastrectomy for gastric adenocarcinoma. The patient underwent a pancreatoduodenectomy. Pathological examination revealed metastases of the primary gastric carcinoma within the pancreatic head and in regional lymph nodes. CONCLUSIONS: Pancreatic tumors in patients with a history of non-pancreatic malignancy should always be considered to be a putative metastatic lesion at an unusual site. If the pancreas can be identified as the only site of spread, radical resection may prolong survival.

Journal Article↗
PubMed2004

Microcystic tubulopapillary carcinoma of the pancreas: a new tumor entity?

An unusual pancreatic tumor with microcystic and tubulopapillary features was observed in a 53-year-old woman. The tumor presented as a large, focally cystic mass in the head of the pancreas, which compressed the surrounding structures. The histological and immunohistochemical analysis revealed a neoplasm that could not be assigned to any of the known pancreatic tumor types. At the molecular level, the tumor showed inactivation of the DPC4/SMAD4 gene, deletion of exon 1 of the p16(INK4A) gene and a point mutation at codon 34 (GGA>AGA) of beta-catenin. Transcriptional profiling analyses and subsequent correspondence cluster analysis demonstrated that the transcriptional profile of the tumor differed distinctly from that of ductal adenocarcinomas, pancreatic cystic tumors and normal pancreatic tissues. These data suggest that the neoplasm most likely represents a new pancreatic tumor entity, which we would like to refer to as microcystic tubulopapillary tumor.

Adenocarcinoma↗
PubMed2004

Oligoclonal T-cell populations in an inflammatory pseudotumor of the pancreas possibly related to autoimmune pancreatitis: an immunohistochemical and molecular analysis.

Inflammatory pseudotumors (IPT), also known as inflammatory myofibroblastic tumors (IMT), are benign inflammatory processes that may have an infectious etiology and are very rare in the pancreatico-biliary region. Recent studies suggest a biological distinction between IPT and IMT, the latter being a true neoplastic process. We describe a case of pancreatic IPT, originally diagnosed as malignancy, which presumably recurred 4 months after the operation. Histologically, the tumor consisted of a smooth muscle actin and CD68-positive spindle cell population and a more abundant mononuclear inflammatory cell population, primarily composed of macrophages and T-lymphocytes. Inflammatory cells were the source of connective tissue growth factor and transforming growth factor-beta1 and tended to accumulate around nerves and blood vessels, as well as around residual pancreatic parenchymal elements, where an intense angiogenetic response was detected. Comparative genomic hybridization analysis of the tumor showed no chromosomal imbalances. Polymerase chain reaction-based analysis of T-cell receptor gamma gene rearrangement revealed an oligoclonal pattern. These findings suggest that the pathogenesis of aggressive cases of IPT could be related to the development of an intense and self-maintaining immune response, with the emergence of clonal populations of T-lymphocytes. The relation of the pancreatic IPT to autoimmune pancreatitis is emphasized.

Adenocarcinoma↗
PubMed2004

Differential diagnosis of non-epithelial tumors of the pancreas: malignant non-epithelial pancreatic tumor with focal pigmentation.

Non-epithelial tumors only rarely affect the pancreas. In this report, we describe a malignant non-epithelial tumor with combined characteristics of malignant peripheral nerve sheath tumor (MPNST) and malignant melanoma. To more closely define the differential diagnosis of MPNST with focal pigmentation versus metastatic melanoma resembling MPNST, the tumor was investigated using histomorphology, immunohistochemistry, electron microscopy, and comparative genomic hybridization. As a result, from these analyses and from clinical findings, the diagnosis of a pancreatic MPNST with focal pigmentation was favored. However, the diagnosis of a malignant melanoma or a composite tumor could not be definitely ruled out, due to the considerable morphological and genotypical overlap between both entities, which can be explained by the close histogenetic relationship between both tumor entities.

Brain Neoplasms↗
PubMed2004

[Cost of care for depressive disorders in primary and specialized care in Germany].

Service utilization and total direct cost of care was assessed in 270 patients suffering from depressive disorder. Patients were recruited from primary care physicians or family doctors (n = 43) or psychiatrists (n = 23) in office practice, from three different regions in Germany (county of Düren and city of Aachen, Lörrach-county, city of Munich). A detailed catalogue of unit costs (including inpatient, outpatient and rehabilitative services) was used for calculating total cost of care on an individual basis. Service utilization and costs referred to 2001. Mean cost of total medical care of the study patients was euro 3849 (excluding cost of drugs for physical illness). The cost for treating depressive disorders and additional psychiatric co-morbidity (which is included into the total cost of care) was euro 2073 per patient and year. When cross-checking with ICD-10 criteria for depressive disorders, the original diagnosis by family doctors or psychiatrists could be confirmed in 186 patients of the total sample (n = 270), suggesting that there is a high amount of falsely diagnosed patients in primary and specialized care of depressive patients in Germany. Direct cost of the 186 confirmed patients was higher (total care cost: euro 4715, cost for treatment of depression and psychiatric co-morbidity: euro 2541) than in the total group and should be considered as reference cost, when discussing cost of care in depressive patients in Germany. Results suggest to analyse cost of care in depressive patients further and to discuss a more efficient allocation of health budgets in the field.

Adult↗
PubMed2004

A new type of thermoluminometer: a highly sensitive tool in applied photosynthesis research and plant stress physiology.

Here we describe a newly developed thermoluminescence measuring device that employs flash excitation, peltier heating, and light detection by channel photomultipliers (CPM). The new thermoluminometer is equipped with four sample holders for simultaneous measurements of thermoinduced light emission in the temperature range from -20 degrees C to +180 degrees C. It allows one to measure leaf samples, chloroplasts, thylakoids, algae, or even bioorganic material lacking chlorophyll by means of naturally induced or artificially applied chemilumigenic probes. The temperature range of the thermoluminometer allows one to analyse the thermoinduced radical pair recombination of photosystem II in the lower temperature region as well as chemiluminescence from lipid peroxidation in the higher temperature region. Hence, plant material can be assessed concerning both its photosynthetic and its oxidative stress status. Since the device is equipped with four sample holders and four CPM channels for simultaneous detection of thermoinduced light emission, it facilitates a high throughput. Therefore, the new device is interesting, not only in ecophysiology, but also in the field of plant breeding, as it can be used to study the stress tolerance of various cultivars of cultural crop plants.

Equipment Design↗
PubMed2003

Origin and development of the precursor lesions in experimental pancreatic cancer in rats.

Notwithstanding the importance of understanding how pancreatic ductal adenocarcinoma develops, the process remains controversial. A key question is whether the cells of origin of the tubular complexes that constitute precursor lesions are derived from a single cell type or from multiple types. Suggestions that they arise solely from centroacinar cells or ductal cells have been based on inference due to their morphologic appearance in tissue from patients or investigation of limited numbers of tubular complexes in animal models later in the carcinogenic process. The present study establishes clearly that two steps are involved; rapid transdifferentiation to produce tubular complexes followed later by transformation of the component cells. Animals were killed at intervals beginning 1 day after implantation of the carcinogen dimethylbenzanthracene. Transdifferentiation of acinar cells to ductal cells does not require cell division. Transition of lobules to tubular complexes begins by 2 days after implantation of carcinogen. Within 4 days after implantation well-developed tubular complexes are present. Islets participate in the process. Ductal adenocarcinoma is observed by 1 month after implantation of carcinogen. Chymotrypsin and cytokeratin localized by immunocytochemistry indicate acinar and ductal cell characteristics. Acino-ductal transdifferentiation persists in carcinogen-implanted animals, but not in controls implanted with sodium chloride crystals or subjected to sham implantation. The precursor lesions (tubular complexes) are formed by the transdifferentiation of acinar cells and to a lesser extent islet cells, with the incorporation of the duct cells pre-existing in the lobules. Therefore, cells that at one time were acinar cells, islet cells, and duct cells, provide the precursor cells for the ductal adenocarcinoma that develops from tubular complexes. The results raise the question whether the transdifferentiated cells in the tubular complexes of patients with chronic pancreatitis are more susceptible to carcinogenic influences, resulting in the increased rate of pancreatic cancer.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed2002

Biological and clinical significance of cytogenetic abnormalities in low-risk and high-risk gastrointestinal stromal tumors.

We report cytogenetic findings in 19 c-Kit-positive gastrointestinal stromal tumors (GISTs) that represent a heterogenous group of mesenchymal neoplasms with respect to site, histology, and biologic behavior. All of the GISTs (5 low-risk, 11 high-risk, 3 recurrences) displayed clonal chromosomal aberrations; 15 were hypo- to near-diploid, and 4 were near-triploid and hypotetraploid. The most common abnormalities were loss of chromosomes 14 and/or 22, demonstrated in 14 GISTs irrespective of site or predominant phenotype. Ten cases (2 low-risk, 5 high-risk, 3 recurrences) were characterized by loss of both chromosomes 14 and 22, 2 cases (1 low-risk, 1 high- risk), by loss of chromosome 14; and 2 high-risk cases, by loss of chromosome 22. Additional chromosomal aberrations occurred preferentially in high-risk and recurrent GISTs, including loss of 9p and 1p in 8 cases each, loss of 15 in 6 cases, loss of 3p in 5 cases, loss of 13q and 10q in 4 cases each, loss of 19 in 3 cases, and complete or partial gains of chromosomes 5 and 4 in 2 cases each. More significantly, 5 of 6 patients with clinically aggressive GISTs, including 2 recurrences and 3 metastasing GISTs, were additionally characterized by loss of 9p; four of these had additional loss of chromosomes 1p and 15. The presented results herein indicate that loss of chromosome 14 and/or 22 is an early change in GIST tumorigenesis irrespective of site or differentiation, whereas malignant transformation and progression of GISTs appear to be associated with an increasing incidence of additional secondary aberrations.

Adult↗