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Biomedical subjects

J Janzen

Publications and source records attributed to J Janzen.

At least 19 recordsLinked to original sources
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↗
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↗
PubMed1999

Takayasu's arteritis and fibromuscular dysplasia as causes of acquired atypical coarctation of the aorta: retrospective analysis of seven cases.

Coarctation of the aorta usually occurs in the aortic isthmus: however, 2% of all coarctation is localized at atypical sites such as the aortic arch and the thoracic and/or abdominal aorta. Causal therapy involves vascular surgery, and during the procedure, biopsies of the involved vessels should be taken to establish the etiology. This study involved the retrospective analysis of clinical and histopathological findings for seven patients who underwent vascular surgical procedures (age range, 10-37 years; male/female ratio 3:4). Histopathological analysis of specimens revealed two pathological processes taking place with different localization in the aortic wall as the cause of the atypical coarctation of the aorta: (1) fibrosis/scarification in the tunica media and adventitia compatible with chronic lesions of Takayasu's arteritis (four cases); (2) fibromuscular dysplasia in the tunica media (three cases).

Adolescent↗
PubMed1998

Inhibition of liposome-induced complement activation by incorporated poly(ethylene glycol)-lipids.

Complement activation causes opsonization of foreign particles leading to particle elimination from the blood. Complement-mediated opsonization of charged and large liposomes presents a fundamental problem in their use to deliver therapeutic agents in vivo. To prolong the circulation half-lives of such liposomes, complement activation must be curtailed. The aim of this study was to assess the ability of poly(ethylene glycol)-lipids (PEG-lipids) to inhibit the in vitro activation of the classical pathway of complement in human serum by anionic liposomes. Incorporation of cholesterol-PEG600 (CH-PEG600), cholesterol-PEG1000 (CH-PEG1000), or phosphatidylethanolamine-PEG2000 (PE-PEG2000) resulted in dose-dependent inhibition of C1q binding and complement activation. The dose of PEG-lipid at which complement activation was blocked was inversely related to the PEG chain length. Complement activation was strongly inhibited when 15 mole% of CH-PEG600, 10 mole% CH-PEG1000, or 5 mole% PE-PEG2000 was incorporated into 100-nm anionic liposomes. PEG-lipid incorporation into larger liposomes (240 nm) was also successful in blocking C1q binding and complement activation. Radiolabeled cholesterol-PEG approximately 1400 was prepared and used to determine both the percentage of CH-PEG incorporated into the liposomes and the percentage maintained in the liposomes in the presence of 50% human serum at 37 degrees C for up to 24 h.

Cholesterol↗
PubMed1998

Bladder tissue biopsies in spinal cord injured patients: histopathologic aspects of 61 cases.

It was the aim of this histopathologic study to examine and compare results of bladder tissue biopsies in spinal cord injured (SCI) patients. The study group consisted of 61 SCI patients who received treatment at the Swiss Paraplegic Centre in Nottwil, near Lucerne, Switzerland. The mean age of the study group was 41 years (range, 17-73) and the mean duration of spinal cord lesion was 10 years and 4 months (range, 5 months to 44 years). The male:female ratio was 57:4. Bladder infections had occurred in each patient one to six times per year (median, 3.2). All samples were taken from the trigone of the bladder during endoscopic urologic procedures with a flexible cystoscope. Histopathologic analysis showed abnormal alterations of bladder tissue in 56 SCI patients (91.8%). Forty-six SCI patients (75.4%) had a chronic type and 10 SCI patients (16.4%) a subacute type of inflammation. Normal bladder tissue was found in five cases (8.2%). Further observation revealed the presence of fibrosis (34.4%), edema (9.8%), and lymphoid hyperplasia (6.6%). A t-test for independent samples showed a lack of significant correlation between the number of clinical bladder infections per year, the duration of injury, the neurologic level of the spinal cord lesion, and histopathologic types of infections.

Adolescent↗
PubMed1997

Glutamate transporter EAAC-1-deficient mice develop dicarboxylic aminoaciduria and behavioral abnormalities but no neurodegeneration.

Four L-glutamate neurotransmitter transporters, the three Na(+)-dependent GLAST-1, GLT-1 and EAAC-1, and the Cl(-)-dependent EAAT-4, form a new family of structurally related integral plasma membrane proteins with different distribution in the central nervous system. They may have pivotal functions in the regulation of synaptic L-glutamate concentration during neurotransmission and are believed to prevent glutamate neurotoxicity. To investigate the specific physiological and pathophysiological role of the neuronal EAAC-1, which is also expressed in kidney and small intestine, we have generated two independent mouse lines lacking EAAC-1. eaac-1(-/-) mice develop dicarboxylic aminoaciduria. No neurodegeneration has been observed during a period of >12 months, but homozygous mutants display a significantly reduced spontaneous locomotor activity.

Amino Acid Sequence↗