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B Hess

Publications and source records attributed to B Hess.

At least 91 records · Page 5Linked to original sources
PubMed1993

[Urinary specific gravity--comparative measurements using reagent strips and refractometer in 340 morning urine samples].

The specific gravity of urine (SG) indicates the number and weight of solute particles in urine; its measurement is helpful in interpreting proteinuria detected by dipstick tests and in monitoring adequate hydration in patients with nephrolithiasis. Four methods for measuring SG or osmolality of urine are currently available (depression of the freezing-point, urometry, refractometry, cation exchange on a reagent strip). Using a recently developed reagent strip, we have measured SG in morning urines of 340 non-selected outpatients and compared the results with SG measurements by refractometry of the same urines. In 86.2% of all urines, a good positive correlation between SG measured by reagent strip and refractometry was noted (r = 0.913, p = 0.0001). In 13.8% of the urines, however, the SG measured by reagent strip deviated by more than +/- 5 from the value obtained by refractometry; in 90% of these urines, glucosuria (reagent strip values too low or too high), proteinuria (values too high), or bacteriuria/leukocyturia (values too low or too high) could be found. In alkaline urine (pH > 7.0), SG values obtained by reagent strip have to be corrected by +5.

Female↗
PubMed1993

Tubulointerstitial nephropathy persisting 20 months after discontinuation of chronic intake of germanium lactate citrate.

Two young human immunodeficiency virus (HIV)-infected patients, a 25-year-old woman and a 26-year-old man, consumed large amounts of germanium lactate citrate 18% as an "immunostimulant" for 9 months. The woman, who had stage II HIV infection, developed severe renal dysfunction (creatinine clearance, 7 mL/min/1.73 m2) and slight proteinuria (0.28 g/d) after ingesting 260 g germanium lactate citrate 18%. Hepatomegaly with liver dysfunction (SGOT, 102 U/L; gamma-glutamyl transferase (GT), 159 U/L) and lactic acidosis (plasma lactate, 7.3 mmol/L) developed simultaneously. Renal biopsy revealed tubulointerstitial nephropathy with vacuolar cell degeneration and periodic acid-Schiff-positive intracellular deposits mainly in distal tubules. Liver biopsy disclosed severe hepatic steatosis; liver function tests returned to normal within 5 weeks. Since renal failure persisted for 2 years after ingestion of germanium (creatinine clearance, 14 mL/min/1.73 m2; proteinuria, 0.84 g/d), a second renal biopsy was performed, which showed marked but focal distal tubular atrophy and slight interstitial fibrosis. The male patient, who had stage III HIV infection, had ingested the same compound; he presented with a creatinine clearance of 43 mL/min/m2 and proteinuria of 0.36 g/d. Renal biopsy disclosed tubulointerstitial changes similar to those found in the female patient. After 9 months off germanium, creatinine clearance remained unchanged. Neutron activation analysis of all biopsy specimens in both cases documented germanium concentrations 10 to 70 times normal in renal tissue and 140 times normal in liver tissue.

Adult↗
PubMed1993

Citrate and calcium effects on Tamm-Horsfall glycoprotein as a modifier of calcium oxalate crystal aggregation.

We measured the effects of Tamm-Horsfall glycoprotein (THP) on calcium oxalate monohydrate (COM) crystal aggregation (Ac) in vitro as well as intrinsic viscosities (Vi) of THP at pH 5.7 and 200 mM NaCl and studied the effects of calcium and citrate on these parameters. THP were isolated from 24-h urines of seven male recurrent calcium stone formers (RCSF) and eight age-matched male healthy volunteers (N, normal). At basal conditions, RCSF-THP inhibited Ac by 28 +/- 10% and normal THP by 60 +/- 6% (P = 0.028). In the presence of calcium, increasing THP concentrations from 16 to 28 and 40 mg/l progressively lowered inhibition by RCSF-THP, but not by N-THP. At 40 mg/l, inhibition by N-THP was 27 +/- 9% vs. -43 +/- 8% by RCSF-THP (P = 0.001), i.e., all stone former THP promoted Ac. With an additional 3.5 mM of citrate, inhibition of Ac was 56 +/- 5% by normal and 34 +/- 6% by stone former THP (P = 0.021), and all seven stone former THP again inhibited Ac. Vi of RCSF-THP was higher than that of N at basal conditions (162 +/- 21 vs. 93 +/- 15 ml/g, P = 0.021) and in the presence of 5 mM calcium (352 +/- 54 vs. 118 +/- 17 ml/g, P = 0.001), i.e., RCSF-THP were more self-aggregated, but not when citrate was added (185 +/- 29 vs. 123 +/- 19 ml/g). (ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Relative hypoparathyroidism and calcitriol up-regulation in hypercalciuric calcium renal stone formers--impact of nutrition.

The issue of secondary hyperparathyroidism in idiopathic hypercalciuria (IH) was addressed in 61 male idiopathic calcium stone formers (SF) who underwent metabolic evaluation on a free-choice diet as well as bone mineral density (BMD) measurements by dual-energy X-ray absorptiometry. They were divided into hypercalciurics (HCSF, n = 30, UCa X V > 7.5 mmol/day) and normocalciurics (NCSF, n = 31, UCa X V < 7.5 mmol/day). At identical blood Ca2+ levels, parathyroid hormone (PTH) was lower in HCSF (25.3 +/- 1.8 pg/ml) than in NCSF (31.4 +/- 1.8 pg/ml, p = 0.017). Since neither fasting urinary hydroxyproline nor pyridinoline/deoxypirdinoline excretions nor BMD values were different between HCSF and NCSF, chronic bone dissolution as the cause of relative hypoparathyroidism in HCSF could be excluded. Despite lower PTH in the face of similar phosphate, Ca2+ and IGF-1 blood levels, however, serum 1,25-dihydroxyvitamin D3 (calcitriol) concentrations were slightly (though not significantly) higher in HCSF than in NCSF (52.8 +/- 3.2 vs. 47.3 +/- 2.9 pg/ml, p = NS), and calcitriol/PTH ratio was elevated in HCSF (2.52 +/- 0.29) vs. NCSF (1.66 +/- 0.15, p = 0.001). Creatinine clearance, significantly higher in HCSF than in NCSF (113 +/- 4 vs. 92 +/- 3 ml/min/1.73 m2, p = 0.0001), was positively correlated with excretion rates of urinary markers of both protein and NaCl intake. Since serum calcitriol levels were positively correlated with creatinine clearance (r = 0.350, slope = 0.288, p = 0.006), up-regulation of calcitriol synthesis with subsequent relative hypoparathyroidism in HCSF is-at least partly-explained by exaggerated protein and sodium consumption.

Absorptiometry, Photon↗
PubMed1993

The tale of parathyroid function in idiopathic hypercalciuria.

At the origin, idiopathic hypercalciuria has been described as a syndrome consisting of normocalcemia, low plasma phosphate levels and abnormally high urinary calcium excretion. The cause of this syndrome was subject to many investigations throughout the years. Two main pathophysiologic hypotheses have been proposed: a) primary intestinal hyperabsorption of calcium, leading to depression of parathyroid hormone (PTH) secretion ("absorptive" hypercalciuria); and b) primary renal tubular leak of calcium which stimulates PTH secretion (secondary hyperparathyroidism). Most of the published studies indicate that intestinal hyperabsorption of calcium with subsequent relative hypoparathyroidism is the primary event causing idiopathic hypercalciuria, and that this occurs as a consequence of increased production of 1,25(OH)2-vitamin D3 (calcitriol). Fasting hypercalciuria, originally taken as evidence for a "renal leak" of calcium, appears to be, at least in part, the consequence of relative hypoparathyroidism.

Calcitriol↗
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

Simultaneous monitoring of light-induced changes in protein side-group protonation, chromophore isomerization, and backbone motion of bacteriorhodopsin by time-resolved Fourier-transform infrared spectroscopy.

Absorbance changes in the infrared and visible spectral range were measured in parallel during the photocycle of light-adapted bacteriorhodopsin, which is accompanied by a vectorial proton transfer. A global fit analysis yielded the same rate constants for the chromophore reactions, for protonation changes of protein side groups, and for the backbone motion. From this result we conclude that all reactions in various parts of the protein are synchronized to each other and that no independent cycles exist for different parts. The carbonyl vibration of Asp-85, indicating its protonation, appears with the same rate constant as the Schiff base deprotonation. The carbonyl vibration of Asp-96 disappears, indicating most likely its deprotonation, with the same rate constant as for the Schiff base reprotonation. This result supports the proposed mechanism in which the protonated Schiff base, a deprotonated aspartic acid (Asp-85) on the proton-release pathway, and a protonated aspartic acid (Asp-96) on the proton-uptake pathway act as internal catalytic proton-binding sites.

Journal Article↗
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↗