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Biomedical subjects

J Janzen

Publications and source records attributed to J Janzen.

At least 19 recordsLinked to original sources
PubMed2006

Insufficient arteriovenous fistulae in hemodialysis patients.

BACKGROUND: For an accurate assessment of structural changes in arteriovenous fistulae (AVF) a microscopic analysis is mandatory. METHODS: 25 insufficient AVF were analyzed with the light microscope using standard histological and immunohistochemical techniques. RESULTS: In 7 patients (28%) atherosclerotic lesions as causes of AVF insufficiency were found. The other 18 patients (72%) had an inhomogeneous spectrum of nonatherosclerotic lesions, for instance intimal hyperplasia. CONCLUSIONS: Histopathologic analysis of insufficient AVF helps clarify the underlying changes in the structure of the vessel wall.

Aneurysm↗
PubMed2004

Intrathoracic and intraabdominal locations of a cystic benign tumor: congenital etiology due to embryological diaphragm development?

A rare case of a benign cystic two-cavity tumor with intrathoracic and intraabdominal localisation is presented. The tumor's embryological etiology, embryological development of the diaphragm and the occurrence of embryonic tumors in general, are discussed. To our knowledge this is the first documented case of a benign two-cavity tumor in childhood and infancy.

Abdominal Neoplasms↗
PubMed2004

Fibromuscular dysplasia of the renal artery responsible for renovascular hypertension: a histological presentation based on a series of 102 patients.

BACKGROUND: Fibromuscular dysplasia (FMD) is a rare non-atherosclerotic and non-inflammatory disease in the arterial system. The purpose of the study was a retrospective analysis of FMD in the renal artery. PATIENTS AND METHODS: A total number of 102 patients (mean age: 36.9 years) who suffered from renovascular hypertension underwent a surgical therapy. The operative specimens of the renal arteries were analysed with the lightmicroscop using histological and immunohistochemical methods. RESULTS: 101 patients (99.02%) presented a medial FMD (extensive-medial subtype in 56 patients, 54.9%, subadventitial subtype in 29 patients, 28.4% and combined subtype in 16 patients, 15.7%). In 1 patient (0.98%) an adventitial FMD was found. We observed the following complications: true and dissecting aneurysms (75 patients, 74.5%), arterio-venous fistulae (2 patients, 1.96%) and chronic thrombosis (10 patients, 9.8%). CONCLUSIONS: With the progress in angioplasty, not all patients suffering from FMD undergo a primary surgical therapy and therefore this lesion is less seen in the daily work of the histopathologist.

Adult↗
PubMed2004

[Radiologic-histopathologic correlation of microcalcifications from 11g vacuum biopsy: analysis of 3196 core biopsies].

PURPOSE: To perform a statistical evaluation of microcalcifications (MC) from suspicious breast lesions detected by radiography and histopathology. MATERIALS AND METHODS: Histological and radiological detection of calcifications were compared from 116 biopsies in 96 women. Lesions with identical description of calcifications detected in histopathology and radiography were considered concordant, patients with obvious discrepancies discordant. If histological and radiological groups of calcifications were identical in number but differed in location, the case was considered pseudo-concordant. RESULTS: Histopathology classified 24 of 116 lesions as malignant and 92 as benign. A total of 3196 core biopsies were examined, 851 of these contained groups of calcifications or single calcifications. Both modalities detected 579 calcifications, with 169 exclusively detected by radiography and 103 exclusively by histopathology. In 35 cases (30 %) radiologic and pathologic results were concordant, in 6 cases pseudo-concordant (4 %) and in 75 cases (65 %) discordant. The case-based Kappa coefficient was - 0.09 (- 0.24 to 0.07). The 122 calcifications not detected by histopathology were few or single calcifications at the edge of the core that were probably lost during processing, 18 were possible artefacts. Six cores contained calcium oxalate, 3 contained milk of calcium. In 6 cases malignant disease was found after the first examination, hence the cores were not searched thoroughly for the missing calcifications. In the remaining 14 cases, no calcifications were found despite complete processing of the tissue. In 49 of 103 cases of radiologically undetected microcalcifications, the retrospect analysis showed dense tissue areas that probably contained the calcification. The remaining 54 cases contained calcifications, which were too small to be detected radiologically. SUMMARY: Discordant results from pathological and radiological examinations of biopsies can mainly be explained by calcifications at the edge of the specimen lost during processing, which are therefore not detected in histopathology, and calcifications too small to be visualized radiologically.

Adult↗
PubMed2004

ABIN-2 forms a ternary complex with TPL-2 and NF-kappa B1 p105 and is essential for TPL-2 protein stability.

NF-kappa B1 p105 forms a high-affinity, stoichiometric interaction with TPL-2, a MEK kinase essential for TLR4 activation of the ERK mitogen-activated protein kinase cascade in lipopolysaccharide (LPS)-stimulated macrophages. Interaction with p105 is required to maintain TPL-2 metabolic stability and also negatively regulates TPL-2 MEK kinase activity. Here, affinity purification identified A20-binding inhibitor of NF-kappa B 2 (ABIN-2) as a novel p105-associated protein. Cotransfection experiments demonstrated that ABIN-2 could interact with TPL-2 in addition to p105 but preferentially formed a ternary complex with both proteins. Consistently, in unstimulated bone marrow-derived macrophages (BMDMs), a substantial fraction of endogenous ABIN-2 was associated with both p105 and TPL-2. Although the majority of TPL-2 in these cells was complexed with ABIN-2, the pool of TPL-2 which could activate MEK after LPS stimulation was not, and LPS activation of TPL-2 was found to correlate with its release from ABIN-2. Depletion of ABIN-2 by RNA interference dramatically reduced steady-state levels of TPL-2 protein without affecting levels of TPL-2 mRNA or p105 protein. In addition, ABIN-2 increased the half-life of cotransfected TPL-2. Thus, optimal TPL-2 stability in vivo requires interaction with ABIN-2 as well as p105. Together, these data raise the possibility that ABIN-2 functions in the TLR4 signaling pathway which regulates TPL-2 activation.

Adaptor Proteins, Signal Transducing↗
PubMed2004

Non-invasive evaluation of atherosclerosis with contrast enhanced 16 slice spiral computed tomography: results of ex vivo investigations.

OBJECTIVE: To evaluate the diagnostic accuracy of 16 slice computed tomography (CT) in determining plaque morphology and composition in an experimental setting. The results were compared with histopathological analysis as the reference standard. METHODS: Nine human popliteal arteries derived from amputations because of atherosclerotic disease were investigated with multislice spiral CT (MSCT). Atherosclerotic lesions were morphologically classified (completely or partially occlusive, concentric, eccentric), and tissue densities were determined within these plaques. In addition, vessel dimensions were quantitatively measured. RESULTS: The results were compared with histological analysis. The concordance index kappa for morphological classification was 0.88. Plaque density (n = 51 lesions) was significantly different (p < 0.0001) between lipid rich, fibrotic, and calcified lesions (Stary stage III: n = 2, 58 (8) Hounsfield units (HU); Stary V: n = 11, 50 (21) HU; Stary VI: n = 14, 96 (42) HU; Stary VII: n = 6, 858 (263) HU; Stary VIII: n = 18, 126 (99) HU). The concordance index kappa for the classification of plaques based on density was 0.51. Vessel dimensions had a good correlation (r = 0.98). CONCLUSIONS: 16 slice CT was found to be a reliable non-invasive imaging technique for assessing atherosclerotic plaque morphology and composition. Although calcified lesions can be differentiated from non-calcified lesions, the diagnostic accuracy in further subclassifying non-calcified plaques as lipid rich and fibrotic is low, even under experimental conditions.

Contrast Media↗
PubMed2004

The microscopic transitional zone between elastic and muscular arteries.

The microscopic transitional zone (TZ) is a segment of the arterial tree, where elastic-type wall architecture is relayed by one of muscular type. Since arterial TZ's are often sites of atherosclerotic and non-atherosclerotic lesions, this histologic anatomic substrate should be considered in the etiology and pathogenesis of vascular diseases. Herein, the topography and fine structure of TZ in renal arteries and carotid bifurcation (tripod) is described, based on randomly collected human autopsy specimens. The average length of the TZ was found to be 10 mm in the renal arteries. The TZ In the carotid tripod was localised only in the postbifurcational segments, where the length varied between 5 and more than 20 mm. In accordance with previous data from the literature, our results confirm a different ratio of scleroprotein components (elastin, collagen) and vascular smooth muscle cells (VSMC) in the microscopic TZ of arteries. Immunohistochemistry for lymphomonocytic antigens revealed no underlying inflammatory condition, especially no evidence of active cellular scavenging and an increased apoptotic rate of VSMC. We perceive the TZ as an arterial segment of reduced architectural compliance and, therefore, as a potential site of mechanotransductional failure leading to vascular diseases.

Actins↗
PubMed2004

Sebaceous glands in the uterine cervix: two new cases.

The authors report on two new cases of sebaceous glands in the uterine cervix. This extremely rare histological observation was found on biopsy specimens of the uterine cervix because of unclear colposcopic findings and of recurrent CIN II. The etiology of this entity is discussed including a brief review of the medical literature.

Adolescent↗
PubMed2002

CD40 regulates the processing of NF-kappaB2 p100 to p52.

The nf-kb2 gene encodes the cytoplasmic NF-kappaB inhibitory protein p100 from which the active p52 NF-kappaB subunit is derived by proteasome-mediated proteolysis. Ligands which stimulate p100 processing to p52 have not been defined. Here, ligation of CD40 on transfected 293 cells is shown to trigger p52 production by stimulating p100 ubiquitylation and subsequent proteasome-mediated proteolysis. CD40-mediated p52 accumulation is dependent on de novo protein synthesis and triggers p52 translocation into the nucleus to generate active NF-kappaB dimers. Endogenous CD40 ligation on primary murine splenic B cells also stimulates p100 processing, which results in the delayed nuclear translocation of p52-RelB dimers. In both 293 cells and primary splenic B cells, the ability of CD40 to trigger p100 processing requires functional NF-kappaB-inducing kinase (NIK). In contrast, NIK activity is not required for CD40 to stimulate the degradation of IkappaBalpha in either cell type. The regulation of p100 processing by CD40 is likely to be important for the transcriptional regulation of CD40 target genes in adaptive immune responses.

Active Transport, Cell Nucleus↗
PubMed2001

Direct phosphorylation of NF-kappaB1 p105 by the IkappaB kinase complex on serine 927 is essential for signal-induced p105 proteolysis.

The p105 precursor protein of NF-kappaB1 acts as an NF-kappaB inhibitory protein, retaining associated Rel subunits in the cytoplasm of unstimulated cells. Tumor necrosis factor alpha (TNFalpha) and interleukin-1alpha (IL-1alpha) stimulate p105 degradation, releasing associated Rel subunits to translocate into the nucleus. By using knockout embryonic fibroblasts, it was first established that the IkappaB kinase (IKK) complex is essential for these pro-inflammatory cytokines to trigger efficiently p105 degradation. The p105 PEST domain contains a motif (Asp-Ser(927)-Gly-Val-Glu-Thr), related to the IKK target sequence in IkappaBalpha, which is conserved between human, mouse, rat, and chicken p105. Analysis of a panel of human p105 mutants in which serine/threonine residues within and adjacent to this motif were individually changed to alanine established that only serine 927 is essential for p105 proteolysis triggered by IKK2 overexpression. This residue is also required for TNFalpha and IL-1alpha to stimulate p105 degradation. By using a specific anti-phosphopeptide antibody, it was confirmed that IKK2 overexpression induces serine 927 phosphorylation of co-transfected p105 and that endogenous p105 is also rapidly phosphorylated on this residue after TNFalpha or IL-1alpha stimulation. In vitro kinase assays with purified proteins demonstrated that both IKK1 and IKK2 can directly phosphorylate p105 on serine 927. Together these experiments indicate that the IKK complex regulates the signal-induced proteolysis of NF-kappaB1 p105 by direct phosphorylation of serine 927 in its PEST domain.

Amino Acid Sequence↗
PubMed2001

Arterial calcifications: morphological aspects and their pathological implications.

Morphological aspects of calcifications are identical whatever their site in the arterial layers: fine granular deposits, plates, rings. Occurrence of complications: fibrosis with foreign body type granuloma, thrombosis, and embolism mainly depend on the site and the amount of calcification. Clinicians should be aware of these complications when performing angioplasty.

Arteriosclerosis↗
PubMed2001

Variable extension of the transitional zone in the medial structure of carotid artery tripod.

BACKGROUND: The goal of our study was to demonstrate the extension of the transitional zone (TZ) between elastic and muscular medial structure in carotid artery tripod. PATIENTS AND METHODS: A histologic study of 56 probes from 8 carotid artery tripods was performed. The probes were obtained from autopsies of 4 adults (mean age: 47.5 years, range 38 to 55 years) and were taken from 7 different topographic sites. RESULTS: At each level of the CCA (at 1 cm and 2 cm proximal to the bifurcation as well as at the bifurcation) we observed an elastic arterial type in 24 (42.8%) probes with 11 to 20 (medium 15.0) elastic fibers per view field (200 x magnification) in the media. In contrast the histologic structure of the ICA and ECA varied as follows: in 8 sections (14.3%) elastic arterial type with 11 to 16 (medium 13.1) elastic fibers, in 11 sections (19.6%) muscular arterial type with 2 to 5 (medium 3.5) elastic fibers and in 9 sections (16.1%) a transitional arterial type with 6 to 8 (medium 6.7) elastic fibers in the media. Atherosclerotic lesions have prevented the assessment of the arterial type in 4 probes (7.1%). The TZ in the medial structure of carotid artery tripods is exclusively localized in the ICA/ECA but not in the CCA. The ICA/ECA presented a TZ with a length up to 0.5 cm (4 probes; 25%), up to 1.5 cm (4 probes; 25%) and longer than 1.5 cm (6 probes; 37.5%). CONCLUSIONS: In this study we confirmed that in the carotid artery tripod, a TZ--an arterial segment with transition from elastic to muscular type--does exist, involving a variable length. Furthermore studies on the impact of the biomechanical properties of the TZ as a potential factor in atherosclerotic disease are justified. In addition, the complex biomechanical behavior of the TZ should be considered prior to interventional procedures.

Adult↗
PubMed2001

Urinary bladder biopsies in spinal cord injured patients.

STUDY DESIGN: A series of 94 urinary bladder biopsies in spinal cord injured (SCI) patients were histopathologically and statistically analysed. OBJECTIVES: The following hypotheses were examined: (1) The number of clinical bladder infections per year in each patient does not influence the histopathological type of inflammation of the urinary bladder; (2) The duration of the spinal cord lesion does not have a strong effect on the type of inflammation; (3) The different neurological levels (upper and lower motor neuron lesions) do not relate to a specific histopathology. SETTINGS: All patients received their treatment at the Swiss Paraplegic Centre in Nottwil, near Lucerne (Switzerland). METHODS: The samples were taken from the bladder fundus during endoscopic urologic operations. Histopathological standard procedures were carried out. Statistical analysis including Kruskal-Wallis and Chi-square tests were performed. RESULTS: Histopathological analysis showed abnormal alterations of the urinary bladder mucosa in 86 SCI-patients: (91.5%). 63 cases (67.0%) showed a chronic type and 23 cases (24.5%) showed a subacute type of inflammation. A normal urinary bladder was found in eight cases (8.5%). The three hypotheses were statistically not rejected. CONCLUSION: Results demonstrated no correlation between the number of bladder infections per year, the period since injury, the neurologic level of the spinal cord lesion and the histopathology of the urinary bladder mucosa.

Adolescent↗
PubMed2000

Cholesterol depletion disrupts lipid rafts and modulates the activity of multiple signaling pathways in T lymphocytes.

Lipid rafts are specialized plasma membrane microdomains, in which glycosphingolipids and cholesterol are major structural components. In T lymphocytes, several signaling proteins are associated with lipid rafts including the protein tyrosine kinase LCK and the adapter protein LAT. To investigate their importance in T cell signaling, lipid rafts were disrupted by depleting cholesterol with methyl-beta-cyclodextrin (MbetaCD). This transiently induced tyrosine phosphorylation of multiple proteins, including the ZAP-70 tyrosine kinase, its associated T cell antigen receptor zeta chain, LAT and phospholipase Cgamma1. Tyrosine phosphorylation was dependent on expression of LCK in lipid rafts. Depletion of cholesterol also resulted in activation of the Ras-ERK pathway. This was largely dependent on phorbol ester-sensitive protein kinase C (PKC) and the PKC-theta isoform translocated to the plasma membrane following MbetaCD treatment. MbetaCD did not stimulate intracellular Ca2+ fluxes; however, consistent with its ability to stimulate Ras, MbetaCD synergized with a Ca2+ ionophore to induce formation of the transcription factor NF-AT. These data indicate a crucial role for cholesterol in the regulation of signaling pathways in T cells, which is likely to reflect its importance in the formation of plasma membrane lipid rafts.

Antibodies, Monoclonal↗
PubMed2000

The transitional zone in the tunica media of renal arteries has a maximal length of 10 millimetres.

BACKGROUND: The goal of our study was to demonstrate and to determine the length of the transitional zone in the tunica media in renal arteries. The majority of renal artery atherosclerotic stenotic lesions occurs in this segment. PATIENTS AND METHODS: Anatomical and histological studies were performed on 26 renal arteries from 13 adults at autopsy (mean age 61.6 years, range 33 to 87 years). RESULTS: In the macroscopical examination the right renal arteries (RRA) were longer with a median 53.8 mm (range 38 to 65 mm) than the left renal arteries (LRA) with a median 47.6 mm (range 35 to 63 mm), the circumferences were nearly the same: RRA 10.9 mm (range 5 mm to 15 mm) and LRA 11 mm (range 5 mm to 15 mm). Probes for histological examinations were taken from three different regions of each renal artery (origin, 5 mm and 10 mm distal to the origin). We observed a typical elastic arterial structure at the origin and muscular types at the distal 10 mm region. At the distal 5 mm region variable ratios of elastic tissue (ET) and smooth muscle cells (SMC) were found as follows: 15 arteries presented an equal ratio of EM:SMC, 7 arteries presented ET > SMC and 4 arteries presented ET < SMC ratios. CONCLUSIONS: In this study we confirmed that in renal arteries, a transitional zone (TZ) that is an arterial segment with transition from elastic to muscular type, does exist, involving the maximal length of 10 mm. Further studies on the impact of the biomechanical properties of the transitional zone as a potential localizing factor in renal atherosclerotic disease are justified. In addition, the complex biomechanical behavior of the TZ of the arterial wall should be taken into consideration when interventional procedures are planned.

Adult↗
PubMed2000

Detection of red cell aggregation by low shear rate viscometry in whole blood with elevated plasma viscosity.

The viscosity of whole blood measured at low shear rates is determined partly by shear resistance of the red cell aggregates present, stronger aggregation increasing the viscosity in the absence of other changes. Effects of cell deformability can confound interpretation and comparison in terms of aggregation, however, particularly when the plasma viscosity is high. We illustrate the problem with a comparison of hematocrit-adjusted blood from type 1 diabetes patients and controls in which it is found the apparent and relative viscosities at a true shear rate of 0.20 s-1 are lower in the patient samples than age matched controls, in spite of reports that aggregation is increased in such populations. Because the plasma viscosities of the patients were higher on average than controls, we performed a series of experiments to examine the effect of plasma protein concentration and viscosity on normal blood viscosity. Dilution or concentration by ultrafiltration of autologous plasma and viscosity measurements at low shear on constant hematocrit red cell suspensions showed (a) suspension viscosity at 0.25 and 3 s-1 increased monotonically with plasma protein concentration and viscosity but (b) the relative viscosity increased, in concert with the microscopic aggregation grade, up to a viscosity of approximately 1.25 mPa-s but above this the value the relative viscosity no longer increased as the degree of aggregation increased in concentrated plasmas. It is suggested that in order to reduce cell deformation effects in hyperviscous pathological plasmas, patient and control plasmas should be systematically diluted before hematocrit is adjusted and rheological measurements are made. True shear rates should be calculated. Comparison of relative viscosities at low true shear rates appears to allow the effects of red cell aggregation to be distinguished by variable shear rate viscometry in clinical blood samples.

Adult↗