Search PubMed⌕ Search

Biomedical subjects

U Jonas

Publications and source records attributed to U Jonas.

297 records · Page 17Linked to original sources
PubMedDate not supplied

Transformation of 2-hydroxydibenzofuran by laccases of the white rot fungi Trametes versicolor and Pycnoporus cinnabarinus and characterization of oligomerization products.

Laccase, a ligninolytic enzyme, was secreted by each of the white rot fungi Trametes versicolor and Pycnoporus cinnabarinus during growth in a nitrogen-rich medium under agitated conditions. After addition of 2-hydroxydibenzofuran to cell-free supernatants of the cultures, yellow precipitates were formed. These precipitates were poorly soluble in water and therefore readily separated from the supernatant. The products formed were more hydrophobic than the substrate, as indicated by their longer retention times on a reverse phase high-performance liquid chromatography column. Mass spectrometric analysis of the purified products indicated the formation of oligomers. Analysis of the mixture of products by gas chromatography and mass spectrometry after derivatization with diazomethane suggested the formation of at least three dimeric and nine trimeric products. Carbon-carbon and carbon-oxygen bonds were identified in the dimers and trimers, respectively. The nuclear magnetic resonance spectrum of the main dimer suggested coupling of the two monomers at the carbon one position.

Basidiomycota↗
PubMedDate not supplied

Rejuvenation in the early 20th century.

The first theoretical reflections concerning the relation of hormone production with the ageing process stemmed from Charles Edouard Brown-Séquard (1817 1894). At the age of 72 years he experimented on himself with an injection of animal testicular extract. The Viennese physiologist Eugen Steinach (1861 1944) gained world-wide acknowledgement for his theory of 'autoplastic' treatment of ageing. He deduced that after vasoligation, an increased incretory hormonal production would ensue following the cessation of the secretory output of the gonads. The first operation was performed in 1918 and resulted in a vasectomy boom over the next two decades. The Russian Serge Voronoff (1866 1951), working in Paris, was one of the first to transplant testicular tissue from a monkey into a human reproductive gland in 1920. Five years later he had already performed this procedure on 300 patients and attracted patients from all over the world. In America early efforts of human testicular transplantation were performed by Frank Lydston and V.D. Lespinasse. Steinach's vasoligation was taken over by many American doctors, e.g., Harry Benjamin and Charles H. Chetwood. Among the patients who underwent a rejuvenation operation according to Steinach's method were Sigmund Freud (1856 1939) and the Irish poet and Nobel Prize winner William Butler Yeats (1865-1939). Two caricatures from the German magazine Simplicissimus published in 1927, confirm that the rejuvenation operations were constantly in the limelight of the printed media. From 1935 onwards rejuvenation operations gradually lost their appeal due to the introduction of artificial androgens.

Europe↗
PubMedDate not supplied

Functional aspects of vascular tenascin-C expression.

The arterial tenascin C expression in vivo and in vitro has been studied using immunohistochemistry. The functional relevance of localized tenascin C expression was assessed in vitro using various human cell types involved in the progression of vascular disease. Normotensive and hypertensive rats exhibited age-dependent patterns of vascular (aorta) tenascin expression, but the lumen-to-media-directed progression of tenascin induction was accelerated in hypertensive rats. Tenascin-rich neointimal lesions (spontaneous) were observed at branching sites of aorta from aged (80 weeks) hypertensive rats. Subendothelial tenascin foci contained lipid-laden smooth muscle cells and monocytes/macrophages. Medial tenascin foci encaged smooth muscle cells which synthesized DNA. Tenascin was expressed both in vivo and in vitro by endothelial and smooth muscle cells but not by monocytes/macrophages; angiotensin II, oxidized-low density lipoprotein and transforming growth factor beta 1 induced expression of tenascin transcripts and glycoprotein in vitro. Endothelial and smooth muscle cells, but not monocytes, adhered to tenascin substrata. Tenascin reduced focal adhesion integrity in confluent endothelial and smooth muscle cell cultures. Angiotensin II-induced migration of endothelial and smooth muscle cells was accompanied by tenascin deposition within extracellular matrix migration trails. Tenascin may function both as a defense against monocyte invasion and medial smooth muscle replication, as well as a substratum for directed endothelial and smooth muscle cell migration.

Animals↗
PubMedDate not supplied

Analysis of the cyclin-dependent kinase inhibitor p27Kip1 in muscle invasive bladder cancer.

It has been suggested that a deregulated cell cycle control contributes to the development of human malignancies due to the loss of critical antiproliferative mechanisms. The cell cycle is controlled at two checkpoints, one at the G1-S and another at the G2-M transition. Several genes including the structurally related p21WAF/CIP1 gene, the downstream mediator of the p53 tumor suppressor gene, and the p27Kip1 gene have been identified as inducers of cell cycle arrest at the G1 checkpoint when substantial DNA damage has occurred to avoid further replication of the altered genome. Recently, a heat stable 27 kDa protein, the transcript of the p27Kip1 gene, has been identified and was suggested to substantially participate in cell cycle control at the G1 checkpoint. Previous investigations have correlated decreased expression of the p27Kip1 protein with an increased biological aggressiveness of breast and small cell lung cancer. However, the molecular-genetic analysis of a variety of human malignancies including prostate cancer failed to identify any alteration at the p27Kip1 gene locus, therefore suggesting a loss of p27Kip1 protein expression to result from post-transcriptional/post-translational events or from so far unknown regulatory mechanisms. So far, bladder cancer specimens have neither been investigated for p27Kip1 alterations on the DNA level, nor has the result of molecular genetic analysis been correlated with an immunohistochemically detected expression of the gene product, the p27Kip1 protein. The present study is the first to describe p27Kip1 gene alterations on the DNA level in 3 of 42 muscle invasive bladder cancer specimens. In contrast, loss of p27Kip1 protein expression was observed in 14 of 42 (33%) tumors. According to the previously reported observation in a variety of human malignancies, in bladder cancer loss of p27Kip1 protein expression seems to result from post-transcriptional or post-translational events.

Adult↗
PubMedDate not supplied

Prognostic value of p27Kip1 and p21WAF/Cip protein expression in muscle invasive bladder cancer.

Two genes, namely p27Kip1 and p21WAF/Cip1 that reveal distinct structural homology, have been identified as inductors of cell cycle arrest at the G1-checkpoint to prevent entry of somatic cells into the S phase of the cell cycle when substantial DNA damage has occurred. It was demonstrated that the p21WAF/Cip1 gene is induced by pathways dependent and independent from a functionally intact p53 tumour suppressor protein. It has been suggested that decreased expression both of the p21WAF/Cip1 and p27Kip1 protein may contribute to the development of human malignancies due to loss of critical antiproliferative mechanisms. So far, the role of altered p21WAF/Cip1 and mainly of a decreased p27Kip1 protein expression in patients with muscle invasive bladder cancer has not been investigated. In the present study, 50 tumour specimens from 50 patients undergoing radical cystectomy (T2-T4) were investigated for different biological and clinical characteristics as possible prognostic factors: age, depth of tumour infiltration (T-stage), histological grading (G), lymph node status as well as immunohistochemical staining for the p21WAF/Cip1 and p27Kip1 proteins. The median recurrence-free survival for patients with and without retained p21WAF/Cip1 protein expression was 54 months (3-86 months) and 13 months (1-40 months), respectively (p=0.07). During univariate analysis, loss of p21WAF/Cip1 protein expression (p=0.02), T-stage (p=0.02) and histological grading (p=0.03) were significant prognostic factors for survival, among which a negative reaction for the p21WAF/Cip1 protein (p=0.02) as well as T-stage (p=0.005) remained independent significant predictors during multivariate analysis. Loss of p27Kip1 protein expression was not correlated with the recurrence-free or the overall survival of the patients. Prospective studies are needed to confirm the independent prognostic potential of cell-cycle associated proteins such as p21WAF/Cip1 in patients with muscle invasive bladder cancer. The availability of more refined prognostic factors should assist decision making regarding the value of more aggressive treatment options, such as adjuvant or neoadjuvant chemotherapy, for defined subgroups of patients.

Adult↗
PubMedDate not supplied

Predictive value of altered p27Kip1 and p21WAF/Cip1 protein expression for the clinical prognosis of patients with localized prostate cancer.

The p21WAF/Cip and the p27Kip1 genes have been identified as inductors of cell cycle arrest at the G1-checkpoint. Alterations of both genes have been suggested to be involved in the development of a variety of human malignancies due to a loss of critical antiproliferative mechanisms. To evaluate the prognostic importance of these alterations for patients with clinically localized prostate cancer, in 86 specimens (T1-T4) from 86 patients undergoing radical prostatectomy at the Department of Urology at Hannover University Medical School, were investigated. The immunohistochemical expression of the p27Kip1 and p21WAF/Cip protein was correlated to recurrence-free and long-term survival, age, depth of tumour infiltration, histological grade and lymph node status in these patients. After a median follow-up of 71 months (1-198 months), 14 of 20 (70%) patients (Group 1) with loss of p27Kip1 protein expression or a relative amount of < 10% of positively stained tumour cells developed recurrent disease in contrast to 18 of 66 (27%) patients (Group 2) with retained p27Kip1 protein expression (> or = 10% of positively stained tumour cells). The median recurrence-free survival times were 39 (4-134) months and 67 (4-198) months for patients in Groups 1 and 2 (p < 0.01), respectively. In multivariate analysis, loss of p27Kip1 protein expression was identified as the only independent prognostic parameter for recurrence-free survival. Univariate analysis (log-rank test) identified histological grading (p < 0.01) and reactivity for p27Kip1 (p = 0.046) (> or = 10% positivity) as prognostic factors for disease-specific long-term survival. However, during multivariate analysis none of the biological variables investigated retained independent prognostic importance regarding overall survival. Neither a low or a high expression of p21Waf/Cip could be correlated with the clinical prognosis of the patients following radical prostatectomy. This study confirms the independent prognostic value of decreased p27Kip1 protein expression in patients with localized prostate cancer, while a prognostic importance of p21Waf/Cip in addition to established patients' and tumour characteristics like tumour stage and histological grading appears rather unlikely.

Adenocarcinoma↗
PubMedDate not supplied

General anesthesia for ureteral measurements in the rabbit.

Literature search and in vitro studies on ureteral function in humans and rabbits have proven that the rabbit is a suitable animal model for the investigation of the effect of smooth muscle relaxing substances on the ureter. One of the main problems encountered was to find an appropriate anesthetic protocol for this animal model. Application of barbiturates as a monotherapy proved to be unsuitable to allow painfree preparation of the abdomen. Intravenous (iv) anesthesia consisting of ketamine-HCl/xylazine-HCl could not be considered due to interference with ureteral smooth muscle tone. Intravenous administration of ketamine-HCl induced immediate ureteral contractions with increased frequency of ureteral activity. Xylazine-hydrochloride, a mixed alpha 2-, alpha 1-adrenoceptor agonist inhibits the increase in synthesis of 3'5'-cAMP. Since the test substances used are phosphodiesterase-IV-inhibitors (rolipram and its two enantiomers), which increase 3'5'-cAMP, this type of anesthesia would interfere with the pharmacological effect to be investigated. General anesthesia using a combination of nitrous oxide (2 l/min) and oxygen (1 l/min) and a very small amount (2 mg/kg b.w.) of pentobarbital i.v. every 30 minutes, was found to be the most suitable form of anesthesia. It resulted in much more stable circulatory conditions, sufficient depth of anesthesia and the possibility to test muscle relaxing substances (PDE-IV-inhibitor) without any influence from anesthesia on their efficacy.

Anesthesia, General↗
PubMedDate not supplied

The MXI1 tumor suppressor gene is not mutated in primary prostate cancer.

For prostate cancer, allelic deletions from the long arm of chromosome 10 (#10q23-25), the locus of the putative tumor suppressor gene MXI1 (#10q24-25), have been identified as a frequently occurring genetic event. During the development of several human malignancies, the c-myc proto-oncogene has been identified to enhance cellular transformation, mitogenesis and cell proliferation. The MXI1 gene, belonging to the helix-loop-helix (bHLH) gene family, was demonstrated to display tumor suppressor function by antagonizing c-myc induced transcriptional activities. Due to the detection of point mutations in the retained alleles of four primary adenocarcinomas of the prostate, MXI1 gene alterations have been suggested to be involved in the development and/or the progression of prostate cancer. To evaluate the role of MXI1 gene alterations for the development of adenocarcinoma of the prostate, 42 primary prostate cancers of different stage (T1-4) and histological grade (G1-3) were investigated for alterations within exons 4 and 5 of the MXI1 gene (spanning 6 exons in total), encoding for the functional HLH-Zip domain, by RNA-SSCP analysis and direct PCR-DNA-sequencing following the microscopically guided tumor cell dissection from 5 microm fresh-frozen buffer-soaked tissue sections. Even by application of this highly elaborated technical approach, MXI1 gene alterations could not be deleted in any of the tumor specimens investigated. Therefore, a substantial involvement of MXI1 gene alterations in the development of prostate cancer appears unlikely. The newly identified putative tumor suppressor gene PTEN, located at #10q23, might be responsible for the frequently observed allelic deletions from #10q23-25 in prostate cancer.

Adenocarcinoma↗