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J Kriegsmann

Publications and source records attributed to J Kriegsmann.

At least 19 recordsLinked to original sources
PubMed2003

Helicobacter pylori genotyping in gastric adenocarcinoma and MALT lymphoma by multiplex PCR analyses of paraffin wax embedded tissues.

BACKGROUND: Gastric infection with Helicobacter pylori is the major cause of chronic active gastritis and is associated with the pathogenesis of peptic ulcer and gastric carcinoma. Gastric mucosal damage involves both host and H pylori dependent factors, such as the presence of the cag pathogenicity island and allelic variations of the vacA and iceA genes. AIMS: To evaluate the association of these virulence factors with the development of gastric malignancies, a retrospective study was performed on archived tissue routinely obtained for diagnostic histopathology. METHODS: DNA was extracted from formalin fixed, paraffin wax embedded gastric tissue sections of 93 patients with chronic active gastritis (n = 39), adenocarcinoma (n = 28), or mucosa associated lymphoid tissue (MALT) lymphoma (n = 24). The extracted DNA was used to perform a polymerase chain reaction based, simultaneous analysis of the following: (1) cagA status, (2) allelic variation of the iceA genes (iceA1, iceA2), allelic variation of the signal peptide (s1a, s1b, s2) and the midregion (m1, m1a, m2) of the vacA gene. RESULTS: The iceA1 gene showed a 3.6 fold and the vacA s1a variant a 4.2 fold higher prevalence in gastric adenocarcinoma than in gastritis. The combined presence of both the vacA s1a and iceA1 genes had a 5.6 fold higher frequency in adenocarcinoma. The vacA m2 allele was the predominant subtype in MALT lymphoma and the combination of the vacA m2 subtypes with the vacA s1 and the iceA1 variants occurred in MALT lymphoma nearly five times more often than in chronic active gastritis. CONCLUSIONS: Certain H pylori subtype combinations possess a differentiating and predictive value for the development of gastric adenocarcinoma and MALT lymphoma.

Adenocarcinoma↗
PubMed2002

Metastasizing chordoma of the lumbar spine.

Chordoma is a dysontogenetic bone tumour that appears in the region of the axial skeleton. Its malignant transformation has been underestimated in the past, since the incidence of metastasis is disputed. This paper describes a chordoma of the fifth lumbar vertebra, which at first was monolocular, but in the course of the disease led to a diffuse metastasis of the spine. Specific histological findings and the differential diagnosis of the chordoma are discussed, as well as previous descriptions in the literature relating to course, diagnosis, and therapy.

Aged↗
PubMed2002

[Fulminant course of diffuse alveolar hemorrhage in systemic lupus erythematosus--a case report].

A 31-year old male patient had suffered from systemic lupus erythematosus (SLE) for 21 years. During the last 8 years he exhibited no clinical symptoms and did not receive any medical SLE treatment. He was admitted with a two-day history of dyspnea and fever. Laboratory studies revealed microcytic anemia and elevated levels of inflammation markers. Chest X-ray showed pulmonary infiltrates. The respiratory status rapidly deteriorated and the patient died 16 hours after admission. An autopsy was performed and diffuse alveolar hemorrhage in all parts of the lungs were seen, which was confirmed by microscopic examination. In contrast, lung histology did not show evidence of infection or inflammatory lesions. Additionally, membranous glomerulonephritis could be identified by light and electron microscopy. Diffuse alveolar hemorrhage (DAH) and concomittant lupus nephritis as manifestations of the known SLE were diagnosed. Acute pulmonary hemorrhage was determined as the cause of death. DAH is a rare, but serious manifestation of SLE. The diagnosis is difficult since the occurrence is abrupt and both symptoms and histology of the lesion are non-uniform and unspecific. The present case demonstrates that DAH also develops in patients that have not had clinical symptoms for several years. Since the early diagnosis is essential for the outcome, DAH should be considered in every case of SLE patients with severe pulmonary symptoms. Corticosteroids are the recommended form of therapy for this disorder.

Adult↗
PubMed2002

Characterisation of the cell type-specificity of collagenase 3 mRNA expression in comparison with membrane type 1 matrix metalloproteinase and gelatinase A in the synovial membrane in rheumatoid arthritis.

OBJECTIVE: To study the pattern and cell type-specificity of collagenase 3, membrane-type 1 matrix metalloproteinase (MT1-MMP), and gelatinase A mRNA expression in the synovial membrane in rheumatoid arthritis (RA). METHODS: The mRNA expression of collagenase 3, MT1-MMP, and gelatinase A was characterised by northern blot analysis, reverse transcriptase-polymerase chain reaction, and in situ hybridisation. In situ hybridisation was performed in combination with the immunohistochemical detection of cell type-specific antigens. RESULTS: Synovial membrane specimens from 19 of 21 patients with RA expressing collagenase 3 mRNA were positive for MT1-MMP and gelatinase A mRNA. In control samples from patients without destructive inflammatory joint diseases collagenase 3 mRNA was not expressed and only in two of seven cases was a coexpression of MT1-MMP and gelatinase A mRNA detected. Fibroblast-like cells of the synovial membrane were found to be the predominant source of collagenase 3, MT1-MMP, and gelatinase A mRNA expression in lining and sublining layers as well as at the synovial membrane-cartilage interface. Additionally, the expression of MT1-MMP mRNA was detected in endothelial cells. Collagenase 3 mRNA expression was found in about 5% of CD68 positive macrophages. CONCLUSIONS: Collagenase 3 mRNA is expressed simultaneously with MT1-MMP and gelatinase A mRNA in fibroblast-like cells of the synovial membrane in RA. These results suggest (a) a broad extracellular proteolytic potential of fibroblast-like cells and (b) an important role of cell surface associated procollagenase 3 activation by MT1-MMP and gelatinase A for cartilage degradation by invading fibroblast-like cells.

Arthritis, Rheumatoid↗
PubMed2001

Expression of apoptosis-related proteins, p53, and DNA fragmentation in sarcomas of the pulmonary artery.

BACKGROUND: Apoptosis is a common feature in a variety of pathologic conditions. Induction of apoptosis through apoptotic stimuli such as, chemotherapy or radiation, presents new insights into tumor biology and therapy. In particular, members of the Bcl-2 family as well as the Fas system are known to be involved in the regulation of apoptosis in different tumor entities. METHODS: In the current study, the expression of the apoptosis-related molecules p53, Bax, Bcl-2, Fas (CD95), Fas-Ligand and perforin was examined in 7 patients with a sarcoma of the pulmonary artery. Furthermore, the TUNEL-method for the detection of apoptotic cells was applied as well as sequencing of the p53 gene. RESULTS: In the TUNEL assay, approximately 10% of the sarcoma cells displayed DNA fragmentation. In addition, Bax was expressed in tumor cells. Accumulation of p53 was evident in 4 of 7 patients (pAB 240 antibody), and 2 of them were positive for the pAB 1801 antibody. Only 1 case had a point mutation in Exon 5 of the p53 sequence. A few tumor cells showed a double labeling of Bax and p53. Bcl-2 could be detected only in tumor-associated lymphocytes. Finally, several lymphocytes could be stained with perforin, but none of the specimens showed a reactivity for Fas or Fas-Ligand. CONCLUSION: The expression of Bax indicated a possible role of this molecule in programmed cell death in pulmonary sarcomas. The limited coexpression of Bax and p53 suggested that induction of Bax can occur independently of p53. The detection of perforin in lymphocytes suggested a possible role for this molecule in apoptosis of the sarcoma cells. In contrast, the Fas system did not seem to play an essential role in sarcomas of the great vessels.

Adult↗
PubMed2001

[The frozen shoulder. Arthroscopy, histological findings and transmission electron microscopy imaging].

INTRODUCTION: During a period of 17 months (February 1998 to July 1999) arthroscopy was performed in 172 patients because of pathologic changes of the shoulderjoint. METHODS: From the history and clinical examination, only eleven patients fulfilled the criteria for primary frozen shoulder set up by Lundberg in 1969. Further investigations such as X-ray examination, ultrasonography and MRI scanning showed no changes that could explain the clinical picture of shoulder stiffness. Of the eleven patients with frozen shoulder. additionally in two cases hyperthyroidism, in five cases diabetes type II and in a further five cases a Dupuytren's contracture could be found. Based on the operative procedure, recently published by Habermeyer, Ogilvie and Warner we carried out an arthroscopic arthrolysis of the stiff shoulder. RESULTS: Diagnostic arthroscopy demonstrated synovialitis in the upper and ventral areas of the joint in over 50% of the patients. Interestingly, intraarticular adhesions were not found in any of our patients; in particular, no obliteration of the axillary recess could be seen. Altogether, in seven of the eleven patients with frozen shoulder, a notably contracted biceps tendon was found which obviously applied increased the force on the humeral head, as in corresponding areas cartilage damage could be demonstrated arthroscopically. A significant increase in fibroblast cells next to loose areas of connective tissue could be shown in histological examinations of biopsies of the capsule in the rotatorer interval. We noted thickened vessel walls and an augmentation of the synovial surface, whereas typical inflammation could not be demonstrated in any of the histological specimens. In the transmission-electron microscope examination (TEM) of samples taken from the capsule in the rotatorer interval, structural changes in collagenous tissue were discernible. Typically, a loss of fibril order and a twisting of collagen fibrils were seen. This twirling led to an up to fourfold diameter of the collagenous fibrils, whereby thin, elastin-like filaments could be seen between the thickened bundles of collagen fibrils. CONCLUSION: In stage of the primary frozen shoulder exclusive fibrosis of the joint capsule was found. Electronmicroscopic twists of collagen fibrills were marked.

Aged↗
PubMed2001

[A benign form of osteopetrosis. Case report].

Osteopetrosis is a disease in which a disturbance in the resorption of bone formed by endochondral ossification takes place. The cause of the osteoclast insufficiency is unknown. In the literature, the etiology of the disease is discussed in relation to the complete absence of cathepsin K synthesis, a cysteine protease. In our case report, we demonstrated cathepsin K expression in the osteoclast cells of the benign form of osteopetrosis. We also found the macrophage marker CD 68 in these osteoclast cells, whereas other mononuclear phagocytic cells were not present in the vicinity of osteoclasts. The inhibition of osteoclast cells by phagocytes is unlikely.

Antigens, CD↗
PubMed2001

Detection of mRNA by non-radioactive direct primed in situ reverse transcription.

There are various techniques to detect mRNA in tissue specimens. Among these in situ hybridization is widely applied, and for the detection of small quantities of RNA in situ reverse transcriptase polymerase chain reaction (in situ RT-PCR) has been applied. Furthermore in situ transcription, where signal is produced by direct incorporation of labeled nucleotides during production of a cDNA by reverse transcription, has been shown by a few investigators. We present a non-radioactive in situ reverse transcriptase (in situ RT) protocol which is at least as sensitive as in situ hybridization but avoids probe production and long procedures of preincubation, incubation, and washing. Digoxigenin-labeled UTP is incorporated into a cDNA produced by in situ reverse transcription of mRNA. This method is combined with the fast and sensitive immunogold-silver detection system allowing demonstration of the mRNA within 7 h compared to days in the case of in situ hybridization. Contrary to in situ RT-PCR this new method of in situ RT has no background problems due to non-specific amplification or diffusion of the reaction product.

Animals↗
PubMed2001

Osteopontin expression in primary sarcomas of the pulmonary artery.

Primary tumors of the great vessels (aorta, pulmonal artery, and inferior vena cava) are rare and represent in most cases vascular leiomyosarcomas. Furthermore, there also exists a group of sarcomas arising from the intima, known as intimal sarcomas, associated with early metastasis and a very poor prognosis. Osteopontin (OPN) is an extracellular matrix protein that binds to alphav integrins, thereby promoting cell attachment, chemotaxis, and signal transduction. The reported association of OPN with malignancy and metastasis prompted us to examine the expression of this protein in seven sarcomas of the pulmonary artery. Strong OPN-specific staining could be detected in tumor cells and the adjacent extracellular matrix. Using a double labeling procedure, proliferating cells showed a strong positive reaction with antibodies against OPN. In addition, this protein could be demonstrated in the cytoplasm of macrophages. CD44, a putative receptor of OPN, was expressed on the cellular surface of tumor-associated lymphocytes. The expression of OPN in macrophages and tumor cells indicates that this molecule could possibly mediate cellular adhesion of both cell types in pulmonary sarcomas. The detection in the extracellular matrix shows that OPN is actively secreted and may interact with the corresponding receptor, CD44, on the surface of lymphocytes. Although the function of OPN is not yet fully understood, our data indicate that strong expression of this molecule in poorly differentiated sarcomas could play a role in the progression of malignancy and metastasis as described previously for carcinomas.

Adult↗
PubMed2001

Anderson-Fabry disease: clinical manifestations of disease in female heterozygotes.

Anderson-Fabry disease is a rare, X-chromosomal lipid storage disorder caused by a deficiency of lysosomal alpha-galactosidase A. Clinical manifestations of Anderson-Fabry disease include excruciating pain in the extremities (acroparaesthesia), skin vessel ectasia (angiokeratoma), corneal and lenticular opacity, cardiovascular disease, stroke and renal failure, only renal failure being a frequent cause of death. Heterozygote female carriers have often been reported as being asymptomatic or having an attenuated form of the disease. To evaluate the spectrum of clinical signs in heterozygotes, a comprehensive clinical examination was performed on 20 carriers of Anderson-Fabry disease. This revealed that, in addition to the skin manifestation, various other clinical manifestations of the disease are present, including acroparaesthesia, kidney dysfunction, cerebrovascular disease, and gastrointestinal and heart problems. It therefore appears that Anderson-Fabry disease affects both hemizygotes and heterozyotes and therefore should be considered to be an X-linked dominant disease.

Adolescent↗
PubMed2001

Expression of cysteine proteinases cathepsins B and K and of cysteine proteinase inhibitor cystatin C in giant cell tumor of tendon sheath.

The expression of cysteine proteinases cathepsins B and K and of the endogenous inhibitor of cysteine proteinases, cystatin C, was investigated in tissue specimens of patients with giant cell tumor of tendon sheath (GCTTS). Expression of both enzymes was examined by immunohistochemistry in tissue specimens of 14 patients with GCTTS. Applying double-labeling techniques, the coexpression of cathepsin B and its major endogenous inhibitor cystatin C was additionally studied. Cells expressing the respective proteins were further characterized with the macrophage markers HAM56 and anti-CD68 (clone PG-M1). Cathepsin B could be detected in numerous HAM56-positive mononuclear cells (MC), but only in very few giant cells (GC). In contrast, cathepsin K was predominantly identified in GC that were also strongly immunoreactive for cystatin C and CD68. Coexpression of cathepsin B and cystatin C occurred only in a few MC. The strong expression of both cathepsin B and K suggests that in GCTTS, bone erosion might be mediated not only by pressure of the proliferative tissue, but also by matrix-degrading cysteine proteinases. Because previous studies showed that osteoclasts express high levels of CD68, cathepsin K, and cystatin C but not of cathepsin B, our study contributes to the view that GC of GCTTS and osteoclasts are closely associated.

Adult↗
PubMed2001

Expression of matrix-degrading cysteine proteinase cathepsin K in cholesteatoma.

Cholesteatoma is a nonneoplastic lesion of the middle ear space or mastoid that is histologically characterized by a progressive bone erosion of the ossicles and surrounding bone. Several matrix-degrading enzymes have been implicated as mediators of this bone erosion. Because the novel cysteine proteinase cathepsin K has been shown to play a central role in bone resorption, we examined the expression of this enzyme in tissue specimens of cholesteatoma. Tissue specimens of 9 patients with cholesteatoma were obtained during middle-ear surgery. Expression of cathepsin K mRNA was determined by RT-PCR using specific primers. Immunohistochemical analysis of cathepsin K protein expression in tissue sections was performed by using the streptavidin-alkaline phosphatase technique. Expression of both cathepsin K mRNA and protein was detected in areas affected by cholesteatoma, whereas specimens of nonaffected ear cartilage and surrounding tissue were not positive. In addition, cathepsin K was detected in numerous multinucleated giant cells, particularly osteoclasts at the site of bone degradation. In contrast, keratinized squamous epithelium was negative for cathepsin K. These data demonstrate that the matrix-degrading cysteine proteinase cathepsin K may be involved in bone erosion in cholesteatoma. Strong expression of this collagenolytic enzyme in osteoclasts suggests that these cells are mainly involved in cathepsin K-mediated bone destruction.

Adult↗
PubMed2001

[Drug therapy of carcinoids of the gastrointestinal tract].

Carcinoid tumors are rare and slowly growing neuroendocrine tumors of the foregut, midgut and hindgut. Drug therapy is of special importance in patients with inoperable metastasising disease. This palliative therapy is aimed at reduction of the hormone-dependent symptoms and inhibition of tumor growth. Somatostatin analogues, alpha-interferon and various chemotherapeutic agents are used for this purpose. Drug therapy can be supplemented by surgical and radiological intervention through interdisciplinary cooperation of the surgeon, radiologist, endocrinologist and gastroenterologist.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed2001

Surgical treatment of pulmonary artery sarcoma.

OBJECTIVE: Pulmonary artery sarcomas are rare and usually fatal tumors. The diagnosis is difficult and delayed in most cases. Newer imaging techniques could allow early diagnosis in patients with symptoms of pulmonary vascular obstruction. Surgical resection improves clinical symptoms and offers the only chance of cure. We report the case histories of 7 patients with primary pulmonary artery sarcomas treated by surgical resection with or without adjuvant therapy. METHODS: Seven patients (3 women and 4 men; mean age, 52.3 years; preoperative New York Heart Association functional class III/IV, n = 5/2) underwent operations. Malignancy was preoperatively suspected in 5 patients, and 2 patients had a presumptive diagnosis of chronic pulmonary embolism. Tumor resection with partial or total prosthetic replacement (n = 2), reconstruction (n = 5), or both, of central parts of the pulmonary arteries was performed in 6 patients. Thromboendarterectomy was necessary in 4 patients, and pneumonectomy was necessary in 2 patients. Six patients received adjuvant therapy. RESULTS: There was no perioperative mortality. All patients had a substantial improvement in exercise tolerance and hemodynamics 3 months after their operations. Four patients died 7, 9, 18, and 19 months after their operations because of recurrent tumor or pulmonary metastases. Two patients are alive 21 and 35 months after primary surgical repair, with pulmonary metastases detected by computed tomographic scans. One patient is alive 62 months after resection without clinical or radiologic signs of tumor recurrence or metastasis. CONCLUSIONS: Early diagnosis of primary pulmonary artery sarcomas can be improved by computed tomography and magnetic resonance scanning. Radical surgical resection probably presents the only chance for cure. The role of neoadjuvant or adjuvant treatment modalities has to be defined. Pulmonary artery sarcoma need not necessarily be a fatal diagnosis.

Adult↗
PubMed2001

The expression of cathepsins in osteoclast-like giant cells of an anaplastic thyroid carcinoma with tracheal perforation.

Anaplastic carcinoma of the thyroid gland (ACT) is a rapidly growing neoplasm with a very poor prognosis. In this study, we examined an ACT with osteoclast-like giant cells expressing matrix--degrading cysteine proteinases and their endogeneous inhibitor cystatin C. Bronchoscopic evaluation of a 50-year-old man suffering from hoarseness, dysphagia, and dyspnea revealed an irregular tumor mass infiltrating into the trachea and the cricothyroid ligament region. On histological examination, a necrotizing undifferentiated anaplastic carcinoma with osteoclast-like giant cells was detected. An immunohistochemical study of the tumor tissue was performed using a panel of 15 antibodies, including double labeling techniques. Most of the osteoclast-like multinucleated giant cells (MGC) expressed CD68 and cathepsin K. Colocalization of cathepsin B and its endogenous inhibitor cystatin C occurred in the majority of MGC. Mononuclear cells (MC) were positive for cathepsin B, cystatin C, and CD 68, but only faintly for cathepsin K. Expression of cathepsins B and K in the MGC of the ACT might contribute to the invasive behavior of this tumor, thus promoting metastatic ability and destruction of the cartilagenous trachea.

Biomarkers, Tumor↗
PubMed2001

Temporary warm ischaemia, 5/6 nephrectomy and single uranyl nitrate administration--comparison of three models intended to cause renal fibrosis in rats.

In patients the progression of pathologic renal processes after the treatment of primary disease is a problem of increasing importance and therapeutic strategies are insufficient till now. The aim of this paper was to search for rat models of interstitial fibrosis as a basis for testing therapeutic strategies to prevent end-stage renal failure. Experiments were done on adult female Wistar rats (Han:Wist) to investigate long-term consequences of temporary warm ischaemia, 5/6 nephrectomy (5/6 NX) and single uranyl nitrate (UN) administration (0.3 or 0.5 mg/ 100 g body wt. intraperitoneally). Observation time was 20 weeks after injury in each group. Creatinine clearance, urinary protein excretion and hydroxy-proline (OH-proline) concentration in renal tissue were measured and light microscopic investigations were done to characterise both quality and time course of long-term renal damage in relation to matched control animals. Temporary warm ischaemia and 5/6 NX did not cause any fibrotic changes during the 20 weeks observation period. The higher UN dose led to decreased creatinine clearance, increased urinary protein excretion and enhanced OH-proline concentration in renal tissue. Morphologic investigations showed fibrotic areas containing strongly dilated and atrophic tubules with thickened basal membranes. These effects can be seen from week four after UN administration up to the end of the observation period. In conclusion, administration of one single dose of UN is a simple procedure to induce interstitial renal fibrosis as an experimental model to investigate therapeutic strategies for their prevention.

Animals↗