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Biomedical subjects

J Bachmann

Publications and source records attributed to J Bachmann.

At least 19 recordsLinked to original sources
PubMed2006

The effect of organotin compounds on gender specific androstenedione metabolism in the freshwater ramshorn snail Marisa cornuarietis.

In a recent study, we demonstrated that androstenedione was mainly converted to testosterone (T) and 5alpha-dihydrotestosterone (DHT) by digestive gland/gonad complex microsomal fractions isolated from male Marisa cornuarietis, whereas it was primarily metabolized to 5alpha-dihydroandrostenedione (DHA) by females. In the present work, the sexual dimorphic metabolism of androstenedione was further investigated, and attributed to a higher 17beta-hydroxysteroid dehydrogenase activity in males than in females. Thereafter, the hypothesis was tested that the metabolism of androstenedione might be affected by exposure to tributyltin (TBT) and triphenyltin (TPT), which are known to induce the development of imposex in several gastropod species. The in vitro metabolism of androstenedione, particularly the formation of DHA and DHT, was inhibited by both compounds. However, in vivo experiments showed no significant alteration in the metabolism of androstenedione in males, but a marginal (TBT) and a significant (TPT) inhibition of the formation of DHA in females exposed for 150 days to concentrations that had significantly induced the development of imposex. The ratio DHT+T/DHA, a possible indicator of metabolic androgenization, tended to increase (0.43 versus 0.35, p=0.06) in TPT exposed females. However, this ratio never reached values comparable to those found in males (11+/-1).

Androstenedione↗
PubMed2006

Some chemical contaminant of surface sediments at the Baltic Sea coastal region with special emphasis on androgenic and anti-androgenic compounds.

Androgenic and anti-androgenic compounds including p,p'-DDE, Diuron, Linuron, Fenarimol, Vinclozolin, 1-(3,4-dichlorophenyl) urea (DCPU), 1-(3,4-dichlorophenyl)-3-methylurea, (DCPMU), tributyltin (TBT) and triphenyltin (TPT) and their metabolites (DBT, MBT, DPT, MPT) as well as metallic elements (Ni, Cu, Zn, As, Cd, Pb, Co, Tl, Cr, Fe, Mn, Al, K, Mg, Na, Ca, Ba, Ti, Sn), PAHs (16 indicator compounds), DDTs and PCBs have been quantified in top layer (0-10 cm) of up to 37 surface sediment samples collected from several sites in costal zone of the Gulf of Gdańsk, an inland freshwater area of Brdyujście in Poland and the tidal flats of the Norderney Island, Wadden Sea in 2002-2003. These sites differed in the degree of anthropogenic activities, including chemical pollution and related impact on biota. Especially in sediments near shipyards, ship repair facilities, harbours, other industrial activities or close to municipal sewage treatment plant outlets butyltins, PAHs and some metallic elements were found at high concentrations. Diuron, Linuron and DCPMU were detected at a few sites, Fenarimol only once, while Vinclozolin and DCPU were not detected. DDT concentrations in the sediments from the Gdańsk and Gdynia region of the Gulf show a stepwise decrease following the ban for production and use, while diffusion of PCBs at some industrial sites seems to continue. Elevated PAH concentrations in sediments seem to be mainly due to pyrogenic and less to mixed pyrogenic and petrogenic sources, while for a few sites rather petrogenic sources dominated. The reference sites in the Norderney Island, Wadden Sea showed similar or slightly higher loads of DDTs, BTs, PAHs, PCBs and metallic elements when compared to sediments from the least contaminated sites in the coastal Gulf of Gdańsk area, while phenyltins were not detected at both spatially distant European areas.

Androgen Antagonists↗
PubMed2001

Use and misuse of nitrogen in agriculture: the German story.

Nitrogen (N) fertilization in agriculture has been discussed controversially in Germany for almost two centuries. The agronomist Carl Sprengel, who published his theory on the mineral nutrition of plants in 1828, advocated the use of mineral N fertilizers. Chemist Justus von Liebig, on the other hand, vehemently denied around 1850 the need for N fertilization. Although it soon became evident that Sprengel was right and Liebig was wrong, not much synthetic N fertilizer was used in German agriculture until around 1915, when the Haber-Bosch technique enabled the commercial production of NH3. The use of N fertilizers since then has grown, especially since 1950. To increase agricultural productivity, German governments have promoted, directly and indirectly, the use of N in crop and in animal production. Unfortunately, it was overlooked that N surpluses in agriculture increased rapidly; around 1980 they amounted yearly to more than 100 kg ha(-1). The extensive use of N in agriculture is causing environmental damage and is contributing substantially to the external costs of present agriculture. The main N compounds that affect the environment are N2O, NH3, and NO3. These compounds are considered to contribute one third to the external costs of agriculture. Additionally, the high rate of human intake of animal proteins and lipids has adversely affected the health of the country's population. Fundamental corrections in German farm policy appear inevitable.

Agriculture↗
PubMed2000

Genomic differentiation of Neanderthals and anatomically modern man allows a fossil-DNA-based classification of morphologically indistinguishable hominid bones.

Southern blot hybridizations of genomic DNA were introduced as a relatively simple fossil-DNA-based approach to classify remains of Neanderthals. When hybridized with genomic DNA of either human or Neanderthal origin, DNA extracted from two Neanderthal finds-the Os parietale, from Warendorf-Neuwarendorf, Germany, and a clavicula, from Krapina, Croatia-was shown to yield hybridization signals that differ by at least a factor of two compared to the signals obtained with the use of fossil DNA of an early Homo sapiens from the Vogelherd cave (Stetten I), Germany. When labeled chimpanzee DNA was used as a probe, Neanderthal and human DNA, however, revealed hybridization signals of similar intensity. Thus, the genome of Neanderthals is expected to differ significantly from the genome of anatomically modern man, because of the contrasting composition of repetitive DNA. These data support the hypothesis that Neanderthals were not ancestors of anatomically modern man.

Animals↗
PubMed2000

Evolutionary dynamics of the SGM transposon family in the Drosophila obscura species group.

SGM (Drosophila subobscura, Drosophila guanche, and Drosophila madeirensis) transposons are a family of transposable elements (TEs) in Drosophila with some functional and structural similarities to miniature inverted-repeat transposable elements (MITEs). These elements were recently active in D. subobscura and D. madeirensis (1-2 MYA), but in D. guanche (3-4 MYA), they gave rise to a species-specifically amplified satellite DNA making up approximately 10% of its genome. SGM elements were already active in the common ancestor of all three species, giving rise to the A-type specific promoter section of the P:-related neogene cluster. SGM sequences are similar to elements found in other obscura group species, such as the ISY elements in D. miranda and the ISamb elements in Drosophila ambigua. SGM elements are composed of different sequence modules, and some of them, i.e., LS and LS-core, are found throughout the Drosophila and Sophophora radiation with similarity to more distantly related TEs. The LS-core module is highly enriched in the noncoding sections of the Drosophila melanogaster genome, suggesting potential regulatory host gene functions. The SGM elements can be considered as a model system elucidating the evolutionary dynamics of mobile elements in their arms race with host-directed silencing mechanisms and their evolutionary impact on the structure and composition of their respective host genomes.

Animals↗
PubMed1999

SYFPEITHI: database for MHC ligands and peptide motifs.

The first version of the major histocompatibility complex (MHC) databank SYFPEITHI: database for MHC ligands and peptide motifs, is now available to the general public. It contains a collection of MHC class I and class II ligands and peptide motifs of humans and other species, such as apes, cattle, chicken, and mouse, for example, and is continuously updated. All motifs currently available are accessible as individual entries. Searches for MHC alleles, MHC motifs, natural ligands, T-cell epitopes, source proteins/organisms and references are possible. Hyperlinks to the EMBL and PubMed databases are included. In addition, ligand predictions are available for a number of MHC allelic products. The database content is restricted to published data only.

Amino Acid Motifs↗
PubMed1998

Adenosine(5') oligophospho-(5') guanosines and guanosine(5') oligophospho-(5') guanosines in human platelets.

We isolated and identified nucleoside(5') oligophospho-(5') nucleosides containing adenosine and guanosine (ApnG; n = 3-6) as well as diguanosine polyphosphates (GpnG; n = 3-6) in human platelets. For identification, UV spectrometry, matrix-assisted laser desorption/ionization, postsource decay matrix-assisted laser desorption/ionization mass spectrometry, and enzymatic cleavage experiments were used. The adenosine(5') oligophospho-(5') guanosines act as vasoconstrictors and growth factors. The diguanosine polyphosphates are potent modulators of growth in vascular smooth muscle cells, but do not affect vascular tone.

Adenosine↗
PubMed1997

[Follow-up studies of routine health screening in Vorarlberg 1986-1994].

In this longitudinal study we observed a sample of people who participated in the general health screening program in Vorarlberg between 1986 and 1994. The aim was to analyse the changes in the parameters, body-mass index, diastolic and systolic blood pressure, blood glucose, cholesterol, gamma-GT and triglycerides of 1205 women and 718 men over this period. Using the baseline values recorded in 1986 as reference the sample was divided into groups with normal, slightly increased and highly increased values for the parameters. On average, the risk factors of people with highly increased baseline values decreased on both a short-term (1986-1988), and a long-term basis (1986-1994). The only exception was the body-mass index, which showed a slight reduction in the first two years and a slight increase in the long run. The normal baseline values rose in all the variables within the period of observation. Sex differences must be considered with regard to body-mass index, cholesterol and triglycerides, age differences are significant with regard to body-mass index, systolic blood pressure and cholesterol. The results of the study point to the usefulness of regular participation in general health screening programs. They show, in particular, that the risk factors for civilization-induced diseases diminish visibly in the group of highly endangered people.

Adult↗
PubMed1997

Diadenosine polyphosphates' action on calcium and vessel contraction.

The effects of the endogenous, platelet-derived vasoactive compounds, diadenosine tetraphosphate (AP4A), diadenosine pentaphosphate (AP5A), and diadenosine hexaphosphate (AP6A) on the vasoconstriction of isolated rat renal resistance vessels and rat aortic strips were measured using a vessel myograph. In addition, the effects of AP4A, AP5A, and AP6A on the cytosolic free calcium concentration ([Ca2+]i) were evaluated in cultured rat vascular smooth muscle cells (VSMC) using the fluorescent dye technique. Diadenosine polyphosphates dose-dependently increased the force of renal resistance vessels and isolated aortic strips. The administration of 10 mumol/L AP4A, AP5A, or AP6A significantly increased the force of isolated renal resistance vessels by 3.48+/-0.43 mN (n = 8), 2.14+/-0.40 mN (n = 12), or 2.70+/-0.31 mN (n = 11, each P < .01 compared with resting tension), respectively. The administration of 10 micromol/L AP4A, AP5A, or AP6A significantly increased the force of isolated aortic strips by 2.45+/-0.97 mNewton (n = 10), 2.70+/- 0.30 mN (n = 6), or 1.48+/-0.20 mN (each P < .01 compared with resting tension), respectively. The administration of 10 micromol/L AP4A, AP5A, or AP6A significantly increased [Ca2+]i in VSMC to a peak concentration of 314+/-60 nmol/L (n = 6), 247+/-25 nmol/L (n = 15), or 332+/-100 nmol/L (n = 5), respectively (each P < .01 compared with resting value). Both the diadenosine polyphosphate-induced vasoconstriction and [Ca2+]i increase was significantly reduced in the absence of extracellular calcium or after administration of a specific inhibitor of P2 purinoceptors. It is concluded that diadenosine polyphosphates increase [Ca2+]i and hence cause vessel constriction.

Animals↗
PubMed1996

Apoptosis of monocytes cultured from long-term hemodialysis patients.

Monocyte apoptosis in vitro was studied in patients on long-term hemodialysis, CAPD, and in predialytic uremia to gain insight into the high susceptibility of these patients to infections. Monocytes from dialysis and control subjects were cultured for 24 to 120 hours in vitro to analyze the level and progression of DNA fragmentation as a hallmark of apoptosis. After an incubation time of 48 hours chromatin fragmentation of 48.5 +/- 7.7% was found in monocytes from dialysis patients, which significantly exceeded DNA fragmentation of control monocytes (23.1 +/- 9.1%; N = 12; P < 0.01). Over longer culture periods of up to 5 days, a continuous progression of apoptosis occurred with a similar slope of percent DNA fragmentation in the two studied groups. Monocyte viability was > 95% both in the dialysis and control group. Hemodialysis patients also showed elevated levels of monocyte apoptosis when programmed cell death was evaluated by transmission electron microscopy or DNA electrophoresis of cleaved chromatin. To test the functional relevance of monocyte apoptosis, a significant reduction of Candida growth inhibition by monocytes of dialysis patients was found with a strong linkage between percentage of DNA fragmentation and impaired microbicidal capacity. Monocytes obtained from patients after the hemodialysis session and from CAPD patients showed normal DNA fragmentation levels similar to controls. Differences of monocyte apoptosis between patients on cuprophane and high-flux polysulphone dialysis were not found. Uremic predialytic patients also exerted an increased monocyte DNA fragmentation of 44.2 +/- 1.5% (N = 7; P < 0.05 compared to controls). Enhanced apoptosis of uremic monocytes was accompanied by a reduced formation of TNF-alpha over 48 hours, revealing a significant negative correlation between chromatin fragmentation and monokine synthesis. Supplementation of monocyte cultures from dialysis patients with exogenous TNF-alpha turned increased apoptosis back to baseline levels, suggesting that inflammatory mediators may modulate monocyte senescence. In summary, the elevated degree of monocyte apoptosis in end-stage renal failure may contribute to the impaired cellular host defense seen in these patients.

Adult↗
PubMed1995

Biotinidase Km-variants: detection and detailed biochemical investigations.

We describe a simple method for the detection of biotinidase Km-variants and detailed biochemical investigations in 5 such patient. They were detected among 103 patients with plasma biotinidase activity which ranged from undetectable to 30% of the mean normal value. Two different types of biotinidase Km-variants were found. (1) In 3 infants biotinidase had a single 105-430-fold elevated Km for biocytin. Biotinidase showed very low activities (0.2-4% of the mean normal value) in the routine colorimetric assay and was not functional in vivo. Accordingly, these patients presented with classical clinical illness. (2) In two patients biotinidase showed biphasic kinetics indicating the presence of one component with a normal Km and reduced Vmax (1.7% and 12%), and another with 330- and 59-fold elevated Km, respectively. In these two patients, biotinidase proved to be at least partially functional in vivo. However, the first patient developed severe symptoms and biotin deficiency late, at the age of 10-15 years, and the second had marginal biotin deficiency at the age of 2 years but no clinical symptoms. Comparative studies revealed that both patients had more severe biotin deficiency than age-matched patients with similar levels of residual biotinidase activity and a single normal Km. Therefore, all patients with residual biotinidase activity should be evaluated for the presence of a Km-mutation, since such patients should be treated with biotin. These can easily be detected by including a second substrate concentration (1.5 mmol/L) in the routine colorimetric biotinidase assay which is performed with 0.15 mmol/L biotin. Increased activity with the higher substrate concentration indicates the presence of a Km-mutation. Detailed kinetic studies are needed to evaluate the distinct forms of Km-variants.

Amidohydrolases↗
PubMed1995

Differential gene expression of renin and angiotensinogen in the TGR(mREN-2)27 transgenic rat.

Transgenic rats carrying the murine Ren-2 gene represent a monogenetic model of hypertension characterized by low plasma renin and high extrarenal expression of the transgene. The hypothesis has been raised that stimulated local reninangiotensin systems may be responsible for the development of hypertension in this model. This study analyzes the effects of the converting enzyme inhibitor lisinopril, which specifically interferes with the renin-angiotensin system, and the direct vasodilator dihydralazine on the renal and extrarenal expression of renin and angiotensinogen. A comparison of gene expression between heterozygous and homozygous transgenic and normal Sprague-Dawley rats was also performed. We demonstrate high sensitivity of blood pressure toward converting enzyme inhibition in transgenic TGR(mREN-2)27 rats. In the kidney, expression of the transgene and the endogenous renin gene increased, suggesting that both are modulated by lisinopril in a similar manner. On the other hand, blood pressure reduction by dihydralazine did not abolish renal renin suppression in transgenic rats, indicating that mechanisms different from direct effects of blood pressure account for renin suppression. Homozygosity for the transgene led to increased Ren-2 expression and higher blood pressure and had opposite effects on angiotensinogen expression compared with heterozygous rats. Cardiac hypertrophy was reduced by lisinopril but not dihydralazine and was positively correlated with cardiac angiotensinogen expression. Increased angiotensin II in the adrenal gland of TGR(mREN-2)27 rats, which overexpresses the transgene, provides evidence that this leads to enhanced generation of tissue angiotensin II. We conclude that expression of the mouse transgene, the endogenous rat renin gene, and the angiotensinogen gene is subject to differential tissue-specific regulation. Reversal of cardiovascular damage with the converting enzyme inhibitor but not dihydralazine suggests that angiotensin II generated locally may be involved in the pathogenesis of hypertension and structural changes in TGR(mREN-2)27 rats.

Angiotensin II↗
PubMed1995

Coenzyme A glutathione disulfide. A potent vasoconstrictor derived from the adrenal gland.

The adrenal gland is involved in the regulation of vascular tone by secretion of vasoactive agents such as catecholamines, neuropeptide Y, or endogenous ouabain. A further potent vasoconstrictor is isolated from bovine adrenal glands and is identified by chromatography, mass spectrometry, UV spectroscopy, and enzymatic cleavage as coenzyme A glutathione disulfide (CoASSG). CoASSG is found in chromaffin granules of adrenal glands and is released from adrenal medulla slices by carbachol. At a concentration of 10(-12) mol/L CoASSG increases renal vascular resistance. Intra-aortic injection of 5 x 10(-10) mol CoASSG increases blood pressure in the intact animal. Besides its vasopressor properties, this substance potentiates the effects of angiotensin II on vascular tone. It is concluded that CoASSG could play a role in blood pressure regulation not only by direct effects but also by modulation of the action of angiotensin II.

Adrenal Glands↗
PubMed1995

Hyperhomocysteinemia and the risk for vascular disease in hemodialysis patients.

The objective of this study was to examine if hyperhomocysteinemia is associated with occlusive vascular disease in hemodialysis patients. The study design included risk factor analysis and determination of serum homocysteine in hemodialysis patients. Fifty chronic uremic patients on regular hemodialysis treatment were studied. Twenty-four patients had coronary, cerebral, or peripheral signs of occlusive vascular disease. Cerebral vascular disease was diagnosed by computed tomography, arterial angiography, or Doppler sonography of the carotid and vertebral arteries. Coronary vascular disease was diagnosed by documented history of myocardial infarction or by coronary angiography. The diagnosis of peripheral vascular disease was established by angiography of the lower limb arteries. In all control patients, Doppler sonography of the carotid, vertebral, and lower limb arteries and thallium-201 exercise imaging were without pathologic results. Measurements included blood pressure, body mass index, smoking behavior, serum homocysteine (measured by gas chromatography/mass spectrometry), serum total, low-density lipoprotein, and high-density lipoprotein cholesterol, lipoprotein (a), triglycerides, and plasma fibrinogen. In a stepwise multiple logistic regression analysis, high serum homocysteine was significantly associated with occlusive arterial disease (R = 0.23; P = 0.031). Furthermore, hypertension (R = 0.18; P = 0.058), but not serum total, low-density lipoprotein, and high-density lipoprotein cholesterol, lipoprotein (a), triglycerides, diabetes mellitus, body mass index, plasma fibrinogen, and smoking behavior, was significantly associated with atherosclerosis. Our results support the hypothesis that hyperhomocysteinemia is an independent risk factor for vascular disease in hemodialysis patients.

Adult↗
PubMed1995

Diadenosine polyphosphate-induced increase in cytosolic free calcium in vascular smooth muscle cells.

OBJECTIVE: To evaluate the effects of two new endogenous vasoconstricting substances, diadenosine pentaphosphate (AP5A) and diadenosine hexaphosphate (AP6A) on the cytosolic free calcium concentration in vascular smooth muscle cells. METHODS: Spectrofluorophotometric measurements of cytosolic Ca2+ were conducted in monolayers of cultured rat vascular smooth muscle cells using the calcium-sensitive fluorescent dye fura-2. RESULTS: The resting Ca2+ concentration in vascular smooth muscle cells was 80 +/- 5 nmol/l (mean +/- SEM; n = 39). The addition of 10 mu mol/l AP5A or AP6A significantly increased Ca2+ in vascular smooth muscle cells to 248 +/- 55 and 358 +/- 124 nmol/l, respectively. The sustained increase in Ca2+ after administration of AP5A or AP6A was 143 +/- 40 and 148 +/- 57 nmol/l, respectively. Diadenosine polyphosphates induce a transplasmamembrane calcium influx as detected by experiments in the absence of external calcium or by using the manganese quenching technique to report unidirectional calcium fluxes. The effects of diadenosine polyphosphates were compared to those of the well known vasoconstrictor angiotensin II, which increased Ca2+ in vascular smooth muscle cells by 1053 +/- 174 nmol/l. CONCLUSIONS: Diadenosine polyphosphates increase Ca2+ in vascular smooth muscle cells, thereby regulating the contractility of vascular smooth muscle and subsequently blood pressure.

Animals↗
PubMed1994

Studies of the vessel wall properties in hemodialysis patients.

Compliance is an important property of the arterial system and abnormalities in compliance can greatly affect cardiovascular function. The elastic properties of the common carotid artery were therefore studied in 24 normotensive hemodialysis patients and 24 healthy normotensives using a noninvasive technique. The hemodialysis patients and the control subjects were matched for blood pressure. Arterial distension was measured by Doppler analysis of the vessel wall movements and blood pressure was recorded by finger-phlethysmography (Finapres). The vessel wall distensibility (DC: 2.49 +/- 0.23 10(-3)/mm Hg; mean +/- SEM) was significantly reduced and the end diastolic diameter (d: 7.3 +/- 0.3 mm) was significantly increased in younger hemodialysis patients (36.3 +/- 2.0 years) when compared with age-related controls (DC: 3.44 +/- 0.24 10(-3)/mm Hg; d: 6.3 +/- 0.3 mm; mean +/- SEM). In older hemodialysis patients (60.2 +/- 2.3 years), there was no significant difference in vessel wall distensibility (DC: 1.55 +/- 0.15 10(-3)/mm Hg) and vessel diameter (d: 7.8 +/- 0.3 mm) as compared with age-matched controls (DC: 1.77 +/- 0.14 10(-3)/mm Hg; d: 7.2 +/- 0.3 mm). The results show that vessel wall distensibility of the common carotid artery is decreased in younger hemodialysis patients as compared with age-matched healthy subjects. The volume expanded state in hemodialysis patients cannot account for the decreased arterial distensibility, since volume depletion by hemodialysis was not associated with a significant change of arterial distensibility (DC 2.14 +/- 0.44 10(-3)/mm Hg before, DC 2.26 +/- 0.45 10(-3)/mm Hg after ultrafiltration, NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Increased cytosolic sodium and reduced Na,K-ATPase activity in transgenic rats.

The transgenic rat TGR(mRen2)27 is a new monogenetic model in hypertension research that develops fulminant hypertension after the mouse Ren-2d renin gene has been integrated into its genome. To evaluate the molecular mechanism of development of hypertension in this animal model, we measured cytosolic free sodium concentration in intact lymphocytes from seven transgenic rats and eight age-matched normotensive Sprague-Dawley rats using the novel sodium-sensitive fluorescent dye sodium-binding benzofuranisophthalate. Resting cytosolic sodium was significantly higher in transgenic rats compared with Sprague-Dawley rats (31.7 +/- 2.2 versus 18.2 +/- 0.4 mmol/L, mean +/- SEM, P < .001). Inhibition of Na,K-ATPase by 0.5 mmol/L ouabain for 5 minutes significantly increased lymphocytic cytosolic sodium in Sprague-Dawley rats to 36.5 +/- 3.4 mmol/L (P < .001 compared with resting value), whereas no significant change could be observed in transgenic rats (35.4 +/- 0.6 mmol/L), indicating that Na,K-ATPase is less responsive in transgenic rats. The Na,K-ATPase activity from erythrocytes was measured with an enzyme-linked assay. Na,K-ATPase activity was significantly reduced in transgenic rats compared with Sprague-Dawley rats (4.0 +/- 0.3 versus 8.1 +/- 0.6 U/L, P < .001). We concluded that reduced Na,K-ATPase activity leads to elevated cytosolic sodium in this model of genetic hypertension.

Animals↗