PubMed Health⌕ Search

Biomedical subjects

B Hess

Publications and source records attributed to B Hess.

At least 19 recordsLinked to original sources
PubMed1992

Chromophore of sensory rhodopsin II from Halobacterium halobium.

The photoreceptor sensory rhodopsin II (sR-II) was enriched 120-fold from cell membranes of Halobacterium halobium. The final preparation yields sR-II with a specific content of 3 nmol of sR-II/mg of protein. The spectroscopic measurements were performed on the enriched photoreceptor solubilized in digitonin. In the absolute absorption spectrum of the partially purified receptor, the main peak in the visible range corresponded to sR-II with a maximum at 488 nm. Cytochromes contributed to the spectrum only in a minor band at 415 nm. The extinction coefficient of sR-II was estimated from difference spectra during bleaching with hydroxylamine to be 48,000 M-1 cm-1. The reduced chromophore displayed a pronounced fine structure which is due to the coplanarity of the retinyl residue. The isomeric composition of the chromophore from the enriched photoreceptor was determined in retinal extracts in HPLC. The dark-adapted sR-II contains 80% all-trans- and 20% 13-cis-retinal. After illumination, the ratio changed to 1:1, indicating a trans-cis isomerization during the photocycle of sR-II.

Archaeal Proteins↗
PubMed1992

Immortalization of murine B cells in vitro with oncogene-containing retroviral vectors.

A large panel of oncogene-containing retroviral vectors has been constructed and used to infect activated murine splenic B cells to determine whether particular oncogenes are capable of directly mediating B cell immortalization. Mature B cell lines have been consistently established with some of these retroviral vectors. These B cell lines arose at a low frequency, indicating that more genetic events were required in addition to infection with the retroviral vector for immortalization to occur. All such lines were LPS-dependent and non-tumorigenic. All lines secrete IgG and express surface IgG, but not IgD or IgM. In addition, they are CD11b+ and CD23-. These cells may be derived from the CD5 "lineage" or a related B cell subset and appear to be more susceptible to immortalization than conventional B cells.

Animals↗
PubMed1992

Biochemical and photochemical properties of the photophobic receptors from Halobacterium halobium and Natronobacterium pharaonis.

The phototaxis of Halobacterium halobium is initiated by two photoreceptors, the sensory rhodopsins sR-I and sR-II. An sR-II-like pigment has also been described in Natronobacterium pharaonis. In this work it was shown that N. pharaonis cells are repelled by light with a wavelength of 500 nm. A further comparison of membrane preparations from H. halobium (mutant D1) containing only sR-II and from N. pharaonis [strain SP1(28)] with a chromophoric protein (psR-II) resembling sR-II revealed substantial similarities. The biochemical and photochemical properties of the pigments are quite similar, with psR-II being more stable to external conditions such as pH and ionic strength of the buffer. Both pigments are bleached by low concentrations of hydroxylamine and can be reconstituted by the addition of all-trans-retinal. The absorption spectrum of psR-II is quite similar to sR-II including the shoulder on the short-wavelength side. After light excitation sR-II and psR-II undergo photocycles with at least three intermediates. The earliest intermediate has an absorption maximum above 520 nm and decays to a species which has a characteristic absorption (approximately 380 nm) of a deprotonated Schiff base. The final step is the regeneration of the original ground state via a red-shifted intermediate absorbing around 540 nm. From this cumulative evidence it can be concluded that, not only sR-II, but also the pigment from N. pharaonis is a photophobic photoreceptor.

Archaea↗
PubMed1992

[Toxicity of an organic Germanium compound: deleterious consequences of a "natural remedy"].

Reports mainly from Japan, recommend germanium (Ge)-containing compounds as "anti-cancer" and "immunostimulatory" remedies. We report on a 25-tear-old woman with stage II HIV disease who consumed a total of 47 g Ge as Ge-lactate-citrate 18%. She developed severe renal insufficiency (creatinine clearance 7 ml/min/1.73 m2, proteinuria 0.28 g/d) and hepatomegaly. Biopsies revealed tubulointerstitial nephropathy with vacuolar degeneration, mainly of distal tubular epithelia, and severe liver steatosis. Tissue Ge content in kidney and liver biopsy specimens was increased 68-and 140 fold respectively. In agreement with previous reports, renal dysfunction persisted 9 months later (creatinine clearance 11 ml/min/1.73 m2).

Acute Kidney Injury↗
PubMed1992

Tamm-Horsfall glycoprotein--inhibitor or promoter of calcium oxalate monohydrate crystallization processes?

The processes of calcium oxalate monohydrate (COM) crystal nucleation, growth and aggregation (agglomeration) generally have been studied using a wide variety of assay systems/conditions. This paper reviews the apparently conflicting data on the effects of Tamm-Horsfall glycoprotein (THP) on COM crystallization processes in vitro, with the main emphasis on crystal aggregation. According to its well-known physico-chemical properties, THP has a dual role in modifying crystal aggregation: at high pH and low ionic strength (IS). THP is a powerful crystal aggregation inhibitor. Upon lowering pH and raising IS, THP viscosity increases, leading to reduced crystal aggregation inhibition. In the presence of additional calcium ions, some THPs even become strong promoters of crystal aggregation. This phenomenon seems to be more pronounced in THPs isolated from recurrent calcium stone formers whose proteins exhibit an abnormally high tendency of polymerization. Recent studies suggest an inherited molecular abnormality of THP among some severe recurrent calcium stone formers.

Calcium Oxalate↗
PubMed1992

[Preventive measures in stones due to infection, uric acid and cystine].

General prophylaxis of renal stone formation consists of 1. high fluid intake and 2. modest consumption of protein-rich foods. Specific prophylactic measures are based on pathophysiologic mechanisms of stone formation. In infection-induced renal stones, combined treatment with culture specific antibiotics and complete stone removal is of utmost importance. In all cases where stone fragments cannot be removed completely and/or partial obstruction remains, long-term antibiotics in combination with urine acidification by methionine (urine pH 5.6 to 6.2) are most appropriate. Prophylaxis of uric acid stones primarily consists of reducing purine intake and alkalizing the urine by potassium citrate. Only if this regimen failed or gout occurred, allopurinol should be administered. In patients with cystine stones, urine volume should be increased to greater than 3000 ml/die. Alkalizing the urine to a pH greater than 7.5 rises cystine solubility, whereas cystine excretion may be reduced by a diet low in sodium and/or low in methionine/cysteine. Thiols form mixed thiol-cysteine disulfides that are many times more soluble than cystine in urine; because of their high rate of adverse side-effects, however, these compounds are of lowest priority in the treatment of cystine stones. There is no convincing evidence for the efficacy of high dose ascorbic acid treatment in cystinuria.

Anti-Infective Agents, Urinary↗
PubMed1991

[Physiopathology, etiology and medical treatment of non-calcium lithiasis].

Under the term "non-calcium nephrolithiasis", three types of renal stone formation are considered. (1) Infected nephrolithiasis, which is due to bacteriological ureolysis. Its treatment includes lowering of oversaturation by antibiotics, urease inhibition and/or acidification of the urine; lowering of crystallization by eradicating concomitant infections caused by non-ureolytic organisms; prevention of crystal adherence by exogenous glycosaminoglycans, and prevention of bacterial adherence by glycolipids. (2) Uric acid lithiasis is defined on physico-chemical and physiopathological grounds. Medical treatment consists of increasing water intake, reducing puric acid intake, alkalinizing the urine inhibiting xanthine-oxidase. (3) Cystinuria is described as a nephrolithogenic proximal tubulopathy. Medical treatment includes reduction of urinary cystine concentration by a strong increase of water intake; reduction of urinary cystine excretion by diet and increase of cystine solubility by urinary alkalinization or administration of some thiol compounds.

Cystinuria↗
PubMed1991

Molecular abnormality of Tamm-Horsfall glycoprotein in calcium oxalate nephrolithiasis.

Tamm-Horsfall glycoprotein (THP) inhibits self-aggregation of calcium oxalate monohydrate (COM) crystals and may therefore be part of the natural defenses against deposition of COM in the kidney in the form of stones or nephrocalcinosis. We have studied THP from six patients with severe nephrolithiasis and have found that their THP inhibits COM self-aggregation less than normal THP under conditions of NaCl and THP concentration and pH similar to those of human urine. The reason for the reduced inhibition of COM crystal aggregation seems to be an enhanced self-aggregation of patient THP, which removes it from effective interactions with the COM crystals. In one family, the father and the oldest son both excreted THP that behaved abnormally and in similar ways, whereas THP from the other son and from the wife behaved normally.

Adult↗
PubMed1991

The role of Tamm-Horsfall glycoprotein and Nephrocalcin in calcium oxalate monohydrate crystallization processes.

Theoretical considerations as well as clinical observations suggest that the aggregation of nucleated crystals is the most dangerous step in the formation of calcium oxalate (CaOx) renal stones. The effects of 2 major urinary glycoproteins, Tamm-Horsfall glycoprotein (THP) and Nephrocalcin (NC), on calcium oxalate monohydrate (COM) crystal aggregation in vitro are studied. At low ionic strength (IS) and high pH (within urinary limits), THP is a powerful crystal aggregation inhibitor (90% inhibition at 40 mg/l). Decreasing pH to 5.7 and raising IS to 0.21 increases TRP viscosity, thereby lowering THP crystal aggregation inhibition. Upon addition of calcium (5 mmol/l), some THPs are no more soluble and promote crystal aggregation (up to 70%). In the presence of citrate (5 mmol/l), which is only slightly inhibitory (14%), the promoting effect of THP is reversed into aggregation inhibition (up to 55%). There is evidence for a molecular abnormality in THPs from severe recurrent CaOx stone formers, since they exhibit increased polymerization and reduced solubility. The 14 kD (kilodalton), Gla-containing glycoprotein NC also strongly inhibits crystal aggregation. However, NC isolated from urines of recurrent CaOx stone formers and from CaOx renal stones are 10 times less inhibitory. Both are structurally abnormal in that they lack Gla and are less amphophilic.

Calcinosis↗
PubMed1990

The role of fructose 2,6-bisphosphate in glycolytic oscillations in extracts and cells of Saccharomyces cerevisiae.

Fructose 2,6-bisphosphate is physiologically one of the most potent activators of yeast 6-phosphofructo-1-kinase. The glycolytic oscillation observed in cell-free cytoplasmic extracts of the yeast Saccharomyces cerevisiae responds to the addition of fructose 2,6-bisphosphate in micromolar concentrations by showing a pronounced decrease of both the amplitude and the period. The oscillations can be suppressed completely by 10 microM and above of this activator but recovers almost fully (95%) to the unperturbed state after 3 h. Fructose 2,6-bisphosphate shifts the phases of the oscillations by a maximal +/- 60 degrees. Oscillations in concentration of endogenous fructose 2,6-bisphosphate in the extract were also observed. Fructose 2,6-bisphosphate alters the dynamic properties of 6-phosphofructo-1-kinase which are vital for its role as the 'oscillophore'. However, the minute amount (approximately 0.3 microM) of endogenous fructose 2,6-bisphosphate and the phase relationship of its oscillations compared with other metabolites indicate that this activator is not an essential component of the oscillatory mechanism. Further support for this conclusion is the observation of sustained oscillations in both the extracts and a population of intact cells of a mutant strain (YFA) of S. cerevisiae with no detectable fructose 2,6-bisphosphate (less than 5 nM).

Adenosine Monophosphate↗
PubMed1990

Acute uric acid nephropathy in two gouty patients with moderate hyperuricemia and high urine acidity.

Acute uric acid nephropathy has been described almost uniformly in patients with massive uric acid overload (malignancies with rapid cell destruction, epileptic seizures). Severe hyperuricosuria and intratubular uric acid precipitation result. Here we present two patients with gout, normal uric acid production, and moderate hyperuricemia, both of whom developed acute uric acid nephropathy. Because of pronounced urine acidity (pH values of 4.6 and 5.0 in morning fasting urines), supersaturation with respect to undissociated uric acid exceeded solubility (0.54 mmol/l), despite basal urate secretions of less than 2.2 mmol/24 hours. Additional predisposing factors, such as uricosuric treatment, heavy beer-drinking, over-consumption of purine-rich foods, and hot environment, were superimposed in both cases.

Acute Kidney Injury↗
PubMed1990

High resolution 13C-solid state NMR of bacteriorhodopsin: assignment of specific aspartic acids and structural implications of single site mutations.

Three mutant strains of Halobacterium sp. GRB with the site of mutation in the bacterioopsin gene (PM 326: Asp96----Asn; PM 374: Asp96----Gly; PM 384: Asp85----Glu) were grown in a synthetic medium containing (4-13C)-Asp. The mutant bacteriorhodopsins labeled with (4-13C)-Asp (37%-45%), and owing to the metabolism of Halobacteria also with (11-13C)-Trp (50%-100%), were isolated as purple membranes and 13C Solid State Magic Angle Sample Spinning (MASS) Nuclear Magnetic Resonance (NMR) spectra of the samples were taken. The Asp96 mutants lacked the signal at 171.3 ppm which was previously assigned to a protonated internal Asp (Engelhard et al. 1989a). This observation supports the conclusion that Asp96 is protonated in the ground state. PM 384 (Asp85----Glu) has an absorption maximum at 610 nm. It can be converted into a purple form (lambda max = 540 nm) by treatment with a detergent (CHAPSO). The NMR-spectra of these two species differ from each other and from the wild type. The intensity of the resonance at 173 ppm in the wild type spectrum is reduced in both forms of the mutant protein. It is probable that this signal is caused by Asp85. The amino acid changes result not only in a perturbation of their direct environment but also effects on Trp residues and the chromophore protein interaction can be observed.

Aspartic Acid↗
PubMed1990

Electrooptical studies on proton-binding and -release of bacteriorhodopsin.

Electric field induced pH changes of purple membrane suspensions were investigated in the pH range from 4.1 to 7.6 by measuring the absorbance change of pH indicators. In connection with the photocycle and proton pump ability, three different states of bacteriorhodopsin were used: (1) the native purple bacteriorhodopsin (magnesium and calcium ions are bound, the M intermediate exists in the photocycle and protons are pumped), (2) the cation-depleted blue bacteriorhodopsin (no M intermediate), and (3) the regenerated purple bacteriorhodopsin which is produced either by raising the pH or by adding magnesium ions (the M intermediate exists). In the native purple bacteriorhodopsin there are, at least, two types of proton binding sites: one releases protons and the other takes up protons in the presence of the electric field. On the other hand, blue bacteriorhodopsin and the regenerated purple bacteriorhodopsin (pH increase) show neither proton release nor proton uptake. When magnesium ions are added to the suspensions, the field-induced pH change is observed again. Thus, the stability of proton binding depends strongly on the state of bacteriorhodopsin and differences in proton binding are likely to be related to differences in proton pump activity. Furthermore, it is suggested that the appearance of the M intermediate and proton pumping are not necessarily related.

Bacteriorhodopsins↗
PubMed1990

Prophylaxis of uric acid and cystine stones.

Although they are two very distinct entities, uric acid and cystine stone disease share a common physico-chemical background, i.e. urinary supersaturation with respect to a compound that is poorly soluble in an acid milieu. Therefore, high-fluid intake and urine alkalinization, preferably by potassium citrate, are of utmost importance for prophylaxis. Urinary excretion of uric acid and cystine may be reduced by dietary measures as well as by drug therapy (allopurinol and thiols, respectively).

Cystine↗
PubMed1990

Prophylaxis of infection-induced kidney stone formation.

Lowering supersaturation with respect to struvite and carbonate apatite is the most important prophylactic measure in patients with infection-induced kidney stone disease. This is best achieved by combining culture-specific antibiotics with urinary acidification. Urinary infection with non-urease-producing Escherichia coli, probably promoting struvite particle formation, must be eradicated. Possible measures for improving urothelial anti-adherence properties or reducing bacterial adherence are discussed.

Anti-Bacterial Agents↗