Biomedical subjects

H Heinz

Publications and source records attributed to H Heinz.

18 recordsLinked to original sources

PubMed2003

[Familial versus sporadic prostate cancer in the German population. Clinical and pathological characteristics in patients after radical prostatectomy].

Family history is one of the strongest epidemiological risk factors for the development of prostate cancer. The impact on the clinical presentation and prognosis, however, is controversial. In the present study, we analyzed 464 familial and 492 sporadic prostate cancer patients following radical prostatectomy. The average age at onset was 62.1 years in the familial group and 64.2 years in the sporadic controls (p<0.001). The screening attitude, DRE findings and the PSA values at diagnosis the pT- and pN-stages, and the tumor grade did not differ between both groups. With a median follow-up of 3.3 years, the 5- and 10-year progression-free survival rates were 76.2% and 56.5% in familial and 70.8% and 55.5% in sporadic patients, respectively (n.s.). A multiple logistic regression analysis revealed that family history did not have an influence on disease recurrence. In our population there was no association between a familial predisposition and clinical features or clinical course of the disease. Whether hereditary prostate cancer is distinct from sporadic forms cannot be determined before the underlying genetic alterations are identified.

Adult↗

PubMed2003

Association between the clinical presentation and epidemiological features of familial prostate cancer in patients selected for radical prostatectomy.

OBJECTIVE: We evaluated if epidemiological features of familial prostate cancer are associated with certain clinical or histopathological characteristics of the disease. METHODS: 463 German patients with familial prostate cancer who underwent radical prostatectomy were stratified according to several epidemiological criteria: (1). the apparent mode of disease transmission, (2). the average age of onset and (3). number of affected relatives/family, (4). whether or not they met the Johns Hopkins criteria of hereditary prostate cancer. The variables analysed included the Prostate Specific Antigen (PSA) and the digital rectal examination at diagnosis, histopathological characteristics of the prostatectomy specimen and relapse free 5-year survival rates. These characteristics were compared within the subsets of familial patients and compared to 492 control patients with sporadic prostate cancer. RESULTS: Age of onset was the only clinical parameter differentiating familial and sporadic prostate cancer. Otherwise there was no association between epidemiological features of familial predisposition and the clinical presentation or outcome of the disease. CONCLUSIONS: Familial and sporadic prostate cancer seem to be the same disease. Alternatively it may be concluded that the common epidemiological features of familial prostate cancer are not useful to tell tumours that are based on inherited susceptibility apart from those that are not. Whether hereditary prostate cancer is clinically distinct from sporadic forms cannot be determined before the underlying genetic alterations are identified.

Age of Onset↗

PubMed2002

Ambient and biological monitoring of coke plant workers -- determination of exposure to polycyclic aromatic hydrocarbons.

OBJECTIVES: The aims of this study were to determine external and internal polycyclic aromatic hydrocarbon (PAH) exposure in a coke plant and to contribute to the evaluation of biological limit values. METHODS: Personal air sampling was carried out on a study population of 24 coke plant workers. In detail, 16 PAHs were determined, among them phenanthrene, pyrene and benzo[ a]pyrene. For the determination of internal exposure, post-shift urine samples from the workers were examined for hydroxylated metabolites of pyrene (1-hydroxypyrene, 1-OHP) and phenanthrene (1-, 2+9-, 3-, 4-hydroxyphenanthrene, 1-, 2+9-, 3-, 4-OHPhe). In both cases, approved HPLC methods were used. RESULTS: The workers were classified into three groups. The group most exposed was that on the top side of the coke oven, with a mean value of 491.2 microg/m(3) for the sum of all sixteen PAHs. The mean value at the bench side was 26.61 microg/m(3), while it was 76.18 microg/m(3) in the group of workers with no dedicated location (=complete area). Both the excretion of 1-OHP and the sum of hydroxyphenanthrenes had the highest mean levels in the top side group of workers (mean: 19.70 microg/g creatinine (crea.) and 39.18 microg/g crea.), followed by the bench-side workers (mean: 7.01 microg/g crea. and 12.95 microg/g crea.) and the whole-area workers (mean: 3.57 microg/g crea. and 8.70 micorg/g crea.). The concentrations of all urinary metabolites correlated significantly with benzo[ a]pyrene (BaP) in the air. CONCLUSIONS: According to these correlations, urinary concentrations of 8 and 11 microg 1-OHP/g crea., respectively 16 and 23 microg/g crea. for the sum of hydroxyphenanthrenes, correspond to BaP concentrations in air of 2 and 5 micorg/m(3), the German technical guiding concentration (TRK value). Our results are in line with others reported in the literature. That means that it should be possible today to define a standard of occupational hygiene and medicine in coke plants using the elimination of hydroxyphenanthrenes and hydroxypyrene in urine as markers for internal PAH exposure.

Adult↗

PubMed2001

Simple and accurate computations of solvatochromic shifts in pi --> pi* transitions of aromatic chromophores.

A new approach is introduced for calculating the spectral shifts of the most bathochromic pi --> pi* transition of an aromatic chromophore in apolar environments. As an example, perylene in solid and liquid n-alkane matrixes was chosen, and all shifts were calculated relative to one well-defined solid-inclusion system. It was shown that a simple two-level treatment of the solute using Hückel theory yields spectral shifts in excellent agreement with experimental results for the most prominent inclusion sites of perylene in solid n-alkane surroundings and for the dilute solutions in liquid n-alkanes. The idea is general enough to be applied to any aromatic chromophore in a nonpolar solvent matrix. In contrast to earlier treatments, this approach is based on geometry- and environment-dependent polarizabilities, employs an r(-4) dependence for the dispersion energy, and is conceptually very simple and computationally very efficient.

Journal Article↗

PubMed2000

Induction of necrosis and apoptosis of neutrophil granulocytes by Streptococcus pneumoniae.

Apoptosis followed by macrophage phagocytosis is the principal mechanism by which neutrophil granulocytes (PMN) are removed from the site of inflammation. To investigate whether Streptococcus pneumoniae causes apoptosis of PMN, we exposed PMN to viable and heat-killed pneumococci and purified pneumococcal cell walls (PCW). The occurrence of PMN cell death was quantified by flow cytometry using annexin V/propidium iodide labelling of the cells. Intracellular histone-associated DNA fragments were quantified by ELISA. The presence of apoptosis was confirmed by in situ tailing. Exposure of PMN to viable pneumococci caused necrosis of the cells. The pneumococcal cytotoxin pneumolysin, the bacterial production of hydrogen peroxide, and PCW contributed to necrosis. Heat-killed pneumococci accelerated the process of apoptosis observed in cultivated non-stimulated PMN in vitro. These results demonstrated that pneumococci induce PMN cell death. Depending on the intensity of the stimulus, PMN necrosis and apoptosis were observed.

Apoptosis↗

PubMed1994

Proteins induced by recombinant equine interferon-beta 1 within equine peripheral blood mononuclear cells and polymorphonuclear neutrophilic granulocytes.

Peripheral blood mononuclear cells (PBMC) and polymorphonuclear neutrophilic granulocytes (PMN) as well as embryonic equine dermal fibroblasts and the equine fibroblast line E. Derm which were used as controls, were treated with recombinant equine interferon-beta 1 (rEqIFN-beta 1) in vitro which induced the expression of different proteins in these cells. A 74 kDa protein was induced in PBMC and an 82 kDa protein was additionally found in the equine fibroblast E. Derm cell line following treatment with rEqFN-beta 1. Both proteins reacted with anti-mouse and anti-human Mx protein antisera in immunoblot tests. The 74 kDa and perhaps the 82 kDa components may thus represent equine 'Mxanalogous proteins'. The 74 kDa protein was only detected in PBMC of ten out of 20 horses examined. The induction of Mx protein in the horse by Type 1 interferon may therefore resemble that in the mouse, where Mx protein is involved in selective resistance to influenza virus. The influence of rEqIFN-beta 1 on protein expression in equine PBMC and PMN was monitored by metabolic labeling and 2-D gel electrophoresis. Proteins of 82, 74, 58 and 40 kDa were induced in PBMC following exposure to rEqIFN-beta 1. A constitutively expressed 35 kDa protein, however, was no longer demonstrable upon treatment with interferon. None of the proteins induced within PBMC was found in highly purified PMN treated with interferon. PMN exposed to rEqIFN-beta 1 synthesized four proteins in the range of 25 to 27 kDa. These proteins have not been described in interferon-treated PMN of any other species.

Animals↗

PubMed1994

Kinetics of inhibition of replication of vesicular stomatitis virus in blood mononuclear cells of horses after in vitro and in vivo treatment with recombinant equine interferon-beta 1.

Recombinant equine interferon-beta 1 (reqIFN-beta 1) induces an antiviral state in blood mononuclear cells (BMC) of horses. Maximal protection against replication of vesicular stomatitis virus is achieved 6 hours after treatment with IFN in vitro and in vivo. Duration of the protective effect depends on the dose of IFN in vitro and in vivo. Availability of reqIFN-beta 1 in cultures of BMC for up to 48 hours does not prolong the antiviral state. The protective effect on BMC after treatment with IFN has similar duration in vivo and in vitro. Monitoring of the effect of IFN in vivo is, thus, simplified because the antiviral state may be recorded by testing cells twice (ie, before and 6 hours after application of interferon). All further tests may be performed in vitro. Multiple administration of reqIFN-beta 1 do not prolong duration of the protective phases after each administration. Duration of the antiviral state depends only on the dose of reqIFN-beta 1.

Animals↗

PubMed1992

"Discordant" influence of equine recombinant interferon-beta 1 on the cytotoxic capacity of equine polymorphonuclear neutrophils and peripheral blood mononuclear cells in vitro and in vivo.

The influence of recombinant equine interferon-beta 1 (rEqIFN-beta 1) on mononuclear cells of peripheral blood (PBMC) and polymorphonuclear neutrophilic granulocytes (PMN) was tested under in vitro and ex vivo conditions. Treatment of equine PBMC with IFN in vitro enhanced the antibody-independent cytotoxicity (AICC) and antibody-dependent cytotoxicity (ADCC) while there was no significant effect on the cytotoxic capacity of PMN treated with rEqIFN-beta 1 in vitro. Ex vivo there was an increased capacity of AICC and ADCC upon single or multiple application of rEqIFN-beta 1 in PMN, only. Treatment with rEqIFN-beta 1 thus induced an increased cellular cytotoxicity in vitro and in vivo but in different populations of peripheral blood cells. In vivo rEqIFN-beta 1 causes a pronounced activation of PMN but not of PBMC as cytotoxic effector cells. This might be achieved indirectly, e.g., by cytokines produced by IFN-sensitive cells.

Animals↗

PubMed1992

A method for the assay of "difficult" interferons exemplified with recombinant equine interferon-beta 1.

We wished to assay recombinant equine interferon-beta 1 (rEqIFN-beta 1) but could not obtain satisfactory results with previously described methods. Therefore, we developed a yield-reduction assay, using primary horse peripheral blood mononuclear cells (PBMC) with vesicular stomatitis virus (VSV) for challenge, which proved consistently satisfactory and highly sensitive. It is suggested that this method of assay may be useful for IFNs from other animals where problems are encountered.

Animals↗

PubMed1992

Monitoring of effects induced by recombinant equine interferon-beta 1 in whole blood and separated fractions of peripheral blood of horses.

Interferon is known to induce antiviral mechanisms and to exert immunoregulatory capacities on various cell types. The antiviral capacity of recombinant equine interferon-beta 1 (rEqIFN-beta 1) is most sensitively monitored by indirect quantitation of multiplication of vesicular stomatitis virus (VSV) in blood cells of horses. As few as 0.5 pg rEqIFN-beta 1/ml can be assessed by means of 90% reduction of VSV-replication in whole blood (w.b.) as well as in isolated mononuclear blood cells (MNC) in spite of individual variations. The immunoregulatory influence of 20-50 pg rEqIFN-beta 1/ml is sufficient to cause at least a 50% reduction of mitogen-induced lymphocyte proliferation in MNC, while higher concentrations are needed in w.b. Of the mitogens tested the best stimulation of proliferation on the equine lymphoid cells was obtained with staphylococcal enterotoxin B (SEB). Release of reactive oxygen species (ROS) from phagocytic cells in w.b. or from isolated polymorphonuclear cells (PMN) as monitored by chemiluminescence (CL) does not seem suitable for evaluation of rEqIFN-beta 1-induced immunoregulation as only very high rEqIFN-beta 1-concentrations (10(3)-10(4) pg/ml) result in a minute increase (up to 20%) of CL. Comparative studies on w.b. and isolated leukocyte fractions from identical specimens of individual horses suggest that monitoring of antiviral and distinct immunoregulatory capacities of rEqIFN-beta 1 can be performed on w.b. without loss of information and sensitivity as compared to isolated MNC.

Animals↗

PubMed1973