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Biomedical subjects

B Hess

Publications and source records attributed to B Hess.

At least 37 records · Page 2Linked to original sources
PubMed2000

Periodic patterns in biology.

New physical and computerized techniques for continuous read-out of intra and intercellular signals allow the study of biochemical dynamics of both local and spreading modes. A vast amount of new information in the area of periodic, quasiperiodic, and chaotic reactions is currently being accumulated, some of which is reviewed here to provide typical mechanisms and occurrences on the basis of a wide variety of reaction circuits and target structures. Following a short review of the time windows of temporal pattern, mechanisms and models of period-generating and transmitting systems are presented for both calcium and oligogenic oscillations. Spreading mechanisms of local signal oscillations through intra- and intercellular space yielding periodic patterns are presented for calcium waves in Dictyostelium discoideum, of cardiovascular and neuronal networks, followed by consideration of some of the properties of complex systems behavior.

Animals↗
PubMed2000

[Kidney calculi--is nutrition a trigger or treatment?].

Kidney stones occur in up to 15% of the population. The incidence of stone disease is 0.1-0.4%, i.e. 100 to 400 out of 100,000 people form a kidney stone every year. The recurrence rate is high, reaching 52% within 10 years and 75% within 20 years, respectively. Since urinary supersaturation, the driving force for crystallisation and stone formation, directly depends on nutritional habits, dietary recommendations are an important part of stone treatment. The benefit of urine dilution by means of a high fluid intake (urine volume at least 2.5 L/d) has been established by several studies. On the other hand, incorrect dietary recommendations, such as the restriction of calcium as advocated for decades, can even promote stone formation! Indeed, large prospective trials have clearly demonstrated that the risk for stone formation decreases with increasing daily calcium intake. It is therefore mandatory that low-calcium diet is finally abandoned in patients with calcium kidney stones and replaced by a sufficient calcium consumption, i.e. 1200 mg per day. Furthermore, epidemiological studies confirm that a diet rich in meat protein carries an increased risk for forming upper urinary tract stones; thus, daily protein intake should not exceed 1 g/kg body weight, which corresponds with general recommendations for a healthy diet. Last but not least, more recent studies have shown that the consumption of high quantities of fruits and vegetables may protect against kidney stone formation, since it raises urinary excretion of citrate, an important inhibitor of crystallization. The present review emphasizes on the relations between nutrition and stone formation in the urinary tract and offers convenient and inexpensive measures for the prevention of recurrence of nephrolithiasis.

Calcium, Dietary↗
PubMed2000

Determinants of urinary excretion of Tamm-Horsfall protein in non-selected kidney stone formers and healthy subjects.

BACKGROUND: The aim of the study was to measure urinary excretion of Tamm-Horsfall protein (THP), an important inhibitor of crystallization, and to identify possible determinants of urinary THP excretion in non-selected kidney stone formers (SF) and healthy subjects (C). METHODS: By means of a commercially available ELISA (Pharmacia and Upjohn/Elias, Germany), we measured THP in 24-h urines of 104 SF (74 males/30 females, age 16-74 years) who had formed 8.7+/-2.4 stones (range 1-240), and of 71 C (41 males/30 females, age 22-62 years). Types of stones formed by SF were 88 calcium, eight uric acid, six infection, and two cystine. All values are means+/-SE. RESULTS: The normal range (5th to 95th percentile) of U(THP)xV was 9.3-35.0 mg/day in males and 9.0-36.3 mg/day in females respectively. Mean U(THP)xV was 21.3+/-1.2 mg/day (range 3. 4-51.6) in male and 15.2+/-1.6 mg/day (range 1.8-32.3) in female SF (P=0.008 vs male SF). Since U(THP)xV was positively correlated with C(Crea) (r=0.312, P=0.001) in SF as well as with U(Crea)xV (r=0.346, P=0.0001) and with body surface (r=0.271, P=0.0003) in all study subjects, mean THP/Crea (mg/mmol) was used for all further calculations. Overall, THP/Crea was lower in SF (1.42+/-0.07 vs 1. 68+/-0.08, P:=0.015), mainly due to increased THP/Crea in female C (2.08+/-0.11, P=0.0036 vs female SF, P=0.0001 vs male C and vs male calcium SF), which also explains decreased THP/Crea values in calcium SF (1.46+/-0.08, P=0.041 vs C). In addition, THP/Crea was reduced in uric acid SF (1.11+/-0.21, P=0.049 vs C). Whereas THP/Crea was not related to age, urine volume, intake of dairy calcium, or urinary markers of protein intake, either in C or in SF, it correlated significantly with urinary Citrate/Crea, both in C (r=0.523, P=0.0001) and in SF (r=0.221, P=0.025). In C only, but not in SF, THP/Crea was correlated with urinary Calcium/Crea (r=0. 572, P=0.0001) and with Oxalate/Crea (r=0.274, P=0.022). CONCLUSIONS: Both in C and SF, urinary THP excretion is related to body size, renal function and urinary citrate excretion, whereas dietary habits apparently do not affect THP excretion. Uric acid and calcium stone formation predict reduced THP excretion in comparison with C, whereas female gender goes along with increased urinary THP excretion in C. Possibly most relevant to kidney stone formation is the fact that THP excretion rises only in C in response to increasing urinary calcium and oxalate concentrations, whereas this self-protective mechanism appears to be missing in SF.

Adult↗
PubMed2000

Citrate determines calcium oxalate crystallization kinetics and crystal morphology-studies in the presence of Tamm-Horsfall protein of a healthy subject and a severely recurrent calcium stone former.

BACKGROUND: The aim of this study was to measure the effects of normal (nTHP) and abnormal stone former Tamm-Horsfall protein (SF-THP) on calcium oxalate (CaOx) nucleation and aggregation as well as on crystal morphology, in presence or absence of citrate. METHODS: Nucleation and aggregation of CaOx crystals from a supersaturated, stirred solution (200 mM NaCl, 10 mM Na-acetate, pH 5.70, 5 mM Ca and 0.5 mM Ox) were studied by spectrophotometric time-course measurements of OD at 620 nm (OD(620)). Measured parameters were induction time t(I) (time to induce formation of detectable particles), S(N), (slope of increase of OD(620), mainly due to crystal nucleation), and S(A), (slope of decrease of OD(620) after equilibrium has been reached, due to crystal aggregation). Effects of citrate, nTHP and SF-THP on these parameters were measured, and scanning electron microscopy (SEM) was performed. RESULTS: At 1.5, 2.5 and 3.5 mM, citrate increased t(I) and inhibited crystal nucleation (by 78-87%) as well as aggregation (by 63-70%), and smaller CaOx crystals (length/width ratio 1.7+/-0.1) than under standard conditions (length/width 3.9+/-0.5) were visible (P<0.001). Normal THP at 30 and 40 mg/l inhibited crystal nucleation and, more strongly, aggregation (inhibition 76-81%). SEM revealed a decrease in length/width ratio to 2.6+/-0.4 (P=0.051 vs standard conditions) and less aggregation than without nTHP. At all concentrations tested, SF-THP reduced t(I) (P=0.0001 vs standard conditions) and promoted aggregation (inhibition -48 to -33%); crystals were elongated with a length/width ratio of 4.3+/-0.6 (P<0. 05 vs nTHP). When simultaneously present with nTHP, citrate enhanced the inhibitory effects of nTHP, producing the smallest (length/width 1.5+/-0.1) and least aggregated crystals. Finally, 3.5 mM citrate turned promotory SF-THP into a crystallization inhibitor with abundant small and clustered, but not aggregated crystals. CONCLUSION: Citrate appears to be the main determinant of CaOx crystallization rates and crystal morphology in the presence of nTHP as well as SF-THP. Its effects appear to predominate over those of THP, since even promotory SF-THP is turned into a crystallization inhibitor in the presence of citrate. This re-emphasizes at a morphological level what has been concluded from functional as well from clinical studies, namely that citrate is needed in urine at equimolar concentrations to calcium in order to prevent the formation of large crystal aggregates in presence of abnormal THP.

Adult↗
PubMed2000

Similarities between principal components of protein dynamics and random diffusion

Principal component analysis, also called essential dynamics, is a powerful tool for finding global, correlated motions in atomic simulations of macromolecules. It has become an established technique for analyzing molecular dynamics simulations of proteins. The first few principal components of simulations of large proteins often resemble cosines. We derive the principal components for high-dimensional random diffusion, which are almost perfect cosines. This resemblance between protein simulations and noise implies that for many proteins the time scales of current simulations are too short to obtain convergence of collective motions.

Journal Article↗
PubMed1999

Self-organizing molecular networks.

Strong diffusional mixing and short delivery times typical for micrometer and sub-micrometer reaction volumes lead to a special situation where the turnover times of individual enzyme molecules become the largest characteristic time scale of the chemical kinetics. Under these conditions, populations of cross-regulating allosteric enzymes form molecular networks that exhibit various kinds of self-organized coherent collective dynamics.

Allosteric Regulation↗
PubMed1999

[Antihypertensive therapy in diabetes mellitus].

Approximately 150 million people worldwide have diabetes mellitus, of whom 90% are type II diabetics. It is therefore of no surprise that diabetic nephropathy has become the leading cause of end-stage renal disease. Opposite to what has been known previously, kidney disease is at least as common in type II as in type I diabetes. However, because the majority of type II diabetics has hypertension for many years before diabetes mellitus becomes clinically relevant, renal lesions are often heterogeneous with frequent exclusive presence of ischemic changes. For the treatment of hypertension in diabetics without nephropathy (no microalbuminuria), drugs that exert beneficial effects or are at least neutral with respect to lipid and glucose metabolism, such as ACE inhibitors, angiotensin II-receptor antagonists, non-dihydropyridine-calcium channel blockers and the thiazide-like indapamide, are to be preferred. Although metabolically neutral, dihydropyridine calcium channel blockers should be used with caution, since an increase in cardiovascular morbidity and mortality in type II diabetics treated with these compounds has most recently been described. Once that diabetic nephropathy is established, blood pressure should be lowered to 120/80 mmHg (measured in seated position). Antihypertensive treatment should primarily be based on ACE inhibitors; angiotensin II-receptor antagonists are a valuable alternative if ACE inhibitors are not tolerated. Both ACE inhibitors and angiotensin II-receptor antagonists should be used with high caution in elderly patients with severe atherosclerosis in whom acute renal failure could occur due to the presence of bilateral renal artery stenosis. Newer studies indicate that non-dihydropyridine calcium channel blockers such as verapamil and diltiazem may be as effective as ACE inhibitors in preserving renal function in diabetic nephropathy. A fix-dose combination of the ACE inhibitor trandolapril with verapamil is now available; it should be reserved for patients whose blood pressure and/or proteinuria can not be adequately controlled with ACE inhibitors. Finally, indapamide is the only antihypertensive diuretic with nephroprotective properties.

Antihypertensive Agents↗
PubMed1999

The value of phytoestrogens as a possible therapeutic option in postmenopausal women with coronary heart disease.

Large epidemiological studies have proved that the risk of coronary heart disease in postmenopausal women can be decreased by oestrogen replacement therapy. The effect is triggered by metabolic processes in the liver (decrease of LDL-cholesterol, increase of HDL-cholesterol) as well as by direct impact on the arterial wall (anti-oxidation, relaxation, anti-proliferation). The therapeutical usage of oestrogens is limited by an increased incidence of breast and endometrial cancer. Cyclic application of progestogens virtually eliminates the risk. Unfortunately, progestogens may antagonise the atheroprotective effect of oestrogens. Structurally modified oestrogens as well as selective oestrogen receptor modulators were investigated in clinical trials. They might provide the desired atheroprotective effects of oestrogen without negative side effects on the mammary gland or the endometrium. In this respect isoflavones also known as phytoestrogens, were analysed. They are widespread and occur naturally in many plants, especially in soy products. Cell culture and animal experiments as well as clinical studies revealed that phytoestrogens such as genistein and daidzein act atheroprotectively in the same way as oestrogen. Effects on the mammary gland or the endometrium could not be detected, but positive side effects on the bone metabolism and the decrease of certain types of cancer could be observed. In total, the therapeutical application of phytoestrogens in postmenopausal women seems to be of real and great benefit. We conclude that in women the risk of death from coronary heart disease increases after the onset of menopause. Recently discovered properties of phyto-oestrogens seem to be of great benefit as they do not seem to have any side effects on the mammary gland and the endometrium which are limiting factors for oestrogen replacement therapy.

Journal Article↗
PubMed1999

Effects of a 'common sense diet' on urinary composition and supersaturation in patients with idiopathic calcium urolithiasis.

OBJECTIVES: To test whether dietary advice as the only treatment is able to reduce urinary supersaturation in patients with idiopathic calcium urolithiasis. METHODS: By means of EQUIL 2, we calculated relative supersaturations of calcium oxalate (RS(CaOx)), brushite (RS(Brushite)), apatite (RS(Apatite)) and uric acid (RS(UA)) of 24-hour urine samples of 68 healthy male controls as well as of 47 male idiopathic calcium stone formers (ICSF) before and after individualized dietary advice (DA). Main goals of DA were (1) to keep urine volume > 2,000 ml/day, and (2) to reduce meat protein intake to 1 g/kg body weight per day. Compliance was judged from changes in urine volume and U(Urea)xV. RESULTS: In the whole group of ICSF, DA did not alter supersaturations. Only in those 9 ICSF (19%) with good compliance (increase in volume and decrease in U(Urea)xV), RS(CaOx) and RS(UA) fell by 26 and 49%, respectively. Besides poor compliance, these findings can be explained by positive correlations between changes in volume and U(Urea)xV in ICSF (r = 0. 319, p = 0.037) or U(Na)xV (r = 0.342, p = 0.019). For instance, ICSF with volumes >/= 2,000 ml/day had evidence of elevated protein and salt intake; thus, DA mainly focused on protein and salt intake, but not on volume. This resulted in decreases in U(Urea)xV and U(Na)xV, but also in volume; thus, RS(CaOx) remained unaltered. CONCLUSIONS: DA is able to significantly lower RS(CaOx); however, because intakes of fluid and protein are directly and positively linked to each other, this only can be achieved if high fluid and lower meat protein intake are equally stressed in all ICSF.

Adult↗
PubMed1998

Self-organizing molecular networks.

Strong diffusional mixing and short delivery times typical for micrometer and sub-micrometer reaction volumes lead to a special situation where the turnover times of individual enzyme molecules become the largest characteristic time scale of the chemical kinetics. Under these conditions, populations of cross-regulating allosteric enzymes form molecular networks that exhibit various kinds of self-organized coherent collective dynamics.

Cell Physiological Phenomena↗
PubMed1998

[Severe chronic iron deficiency in a 17-year-old student].

A 17 year old male suffered from iron deficiency of undetermined cause for 2 years. Iron substitution was able to correct it for short periods. With the exception of fatigue and recurring abdominal pain attributed to oral iron therapy no further symptoms were present. The physical status on admission was unremarkable. The laboratory detected intestinal disorders, an anemia of the chronic type without evidence for malignancy or renal failure suggested an inflammatory gastro-intestinal disorder. In spite of a twice negative noninvasive test for gluten-intolerance the clinician favored in his differential diagnosis non tropical sprue over inflammatory bowel disease (IBD, Crohn's disease, Whipple's disease). Histopathology of small bowel specimens did not indicate sprue. An ileo-colonoscopy revealed severe ulcerating ileitis and mild chronic colitis. The histologic specimen revealed a severe ileal inflammation with cosinophilia and the colon specimens epitheloid microgranuloma. These findings are highly compatible with the diagnosis of Crohn's disease. Iron deficiency anemia is common in Crohn's disease. In the current case it is due to disturbed iron uptake. Iron deficiency anemia as sole symptom of Crohn's disease is extremely rare.

Adolescent↗
PubMed1998

[Central lung embolism in chronic interstitial pneumopathy].

An 80 year old patient with known interstitial pneumopathy of unknown etiology was hospitalized because of acute onset and rapid deterioration of dyspnea at rest within days. A foregoing neurologic investigation including CT and EEG because of prior syncopes and cramp attacks had not revealed pathologic findings. Thorax X-ray at admission showed homogenous loss of transparency on the left side, calcified basal plaques on both sides and prominent central pulmonary vessels with jumping caliber. A punctate of the leftsided pleural effusion revealed lymphocytic exsudate, normal pH, low glucose and an elevated LDH. The patient died shortly after a collapse at a bowel visit and pulmonary embolism was suspected in accordance to results from arterial blood gas analysis, ECG and chest X-ray. Neurologic symptoms could be explained by recurrent pulmonary embolism. Pleural plaques together with the punctate suggested a malignant etiology. A mesothelioma was taken into consideration, although there were no anamnestic reports on an exposition to asbestos. Autopsy revealed almost complete central embolism of the left pulmonary artery with acute cor pulmonale thus confirming the clinical suspicion. The embolus showed components of different ages of origin. Besides bronchitic and emphysematous alteration histology of the pulmonary tissue revealed interstitial and septal fibrosis with focal tissue consolidation. In one giant cell a typical asbestos body was found (in 1 out of 10 sections). In spite of missing information on an exposition to asbestos an abnormally high exposition must be taken into consideration because of the finding of an asbestos particle in relation to the amount of tissue studied. Apart from interstitial fibrosis asbestos may also cause consolidation of pulmonary tissue. Histology of plaquelike lesions revealed mesothelioma of fibrous type. This finding supports the suspicion that a major part of the pulmonary lesions was due to exposition to asbestos.

Aged↗
PubMed1998

Metachromatic leukodystrophy: molecular genetics and an animal model.

Metachromatic leukodystrophy (MLD) is a lysosomal storage disorder caused by the deficiency of arylsulphatase A (ASA; EC 3.1.6.8). Deficiency of this enzyme causes intralysosomal storage of the sphingolipid cerebroside sulphate. This lipid is abundant in myelin and it may thus not be surprising that storage mainly affects oligodendrocytes. Patients suffer from a progressive demyelination causing various neurological symptoms. The disease is fatal and treatment is not available. The human ASA gene has been cloned and more than 40 mutations have been analysed that cause metachromatic leukodystrophy. Few of these alleles are frequent among patients, whereas most mutant alleles have only been found in single families. Since MLD has only been described in humans and no naturally occurring animal model has been described, ASA-deficient mice have been generated by homologous recombination. The ASA knockout mice are unable to degrade sulphatide and store the lipid intralysosomally. The pattern of lipid storage in neuronal and non-neuronal tissues resembles that described for patients. In the nervous system, lipid storage is found in oligodendrocytes, astrocytes and some neurons. Animals display an astrogliosis and a decreased average axonal diameter. Purkinje cells and Bergmann glia of the cerebellum are morphologically aberrant. Demyelination is seen in the acoustic ganglion and occurs between the ages of 6 and 12 months. The animals are deaf at this age and display various neuromotor abnormalities. However, compared to humans the mice have a surprisingly mild phenotype, since they have a normal life span and do not develop widespread demyelination. ASA-deficient mice have been transplanted with bone marrow, which was transduced with a retroviral vector expressing arylsulphatase A. The majority of transplanted animals display sustained expression of arylsulphatase A from the retroviral construct up to 5 months after transplantation. However, preliminary data suggest that this therapeutic approach does not reduce storage material.

Animals↗
PubMed1998

High-calcium intake abolishes hyperoxaluria and reduces urinary crystallization during a 20-fold normal oxalate load in humans.

BACKGROUND: The aim of the study was to test whether increasing dietary calcium intake lowers intestinal oxalate absorption and thereby prevents hyperoxaluria and urinary crystallization during a 20-fold normal oxalate load in healthy subjects. METHODS: Fourteen healthy male volunteers (age 23-44 years, BMI 21.5-27.7 kg/m2) collected 24-h urines while on free-choice diet as well as on two standardized diets. The latter contained 2545 kcal, 2500 ml of mineral water, 102 g of protein, 13.6 g of sodium chloride and 2220 mg of oxalate (approximately 20-fold content of an average diet). Subjects were studied twice while on the standardized diet, once while eating a normal amount of calcium (1211 mg/day, oxalate-rich diet), and once while eating 3858 mg of calcium/day (calcium and oxalate-rich diet). RESULTS: Compared with the free-choice diet (322+/-36 micromol/d), UOx x V increased to 780+/-72 micromol/d on the oxalate-rich diet (P=0.001) and fell again to 326+/-31 micromol/d on calcium and oxalate-rich diet (P=0.001 vs oxalate-rich diet). Urinary glycolate (a metabolic precursor of Ox) always remained below the upper limit of the normal range and did not change between different diets, indicating that changes in UOX x V reflect respective variations in intestinal absorption of Ox. Uca x V was 4.60+/-0.45 mmol/d on the free-choice diet and 3.20+/-0.32 mmol/d on the oxalate-rich diet (P=0.011 vs free-choice diet); it increased to 7.28+/-0.74 mmol/d on the calcium- and oxalate-rich diet (P=0.001 vs free-choice and oxalate-rich diets). As indicated by the AP (CaOx) index (Tiselius), urinary supersaturation did not vary significantly between the three diets. In freshly voided morning urines (studied in 8/14 subjects) on the oxalate-rich diet, CaOx crystals or crystal aggregates of up to 80 microm diameter were found in 5/8 urines, whereas this never occurred on the free-choice diet and only t once on the calcium- and oxalate-rich diet. CONCLUSION: . Increasing calcium intake while eating Ox-rich food prevents dietary hyperoxaluria and reduces CaOx crystallization in healthy subjects. This further illustrates that dietary counseling to idiopathic calcium-stone formers should ensure sufficient calcium intake, especially during oxalate-rich meals.

Adult↗
PubMed1998

Malnutrition-induced hypokalemic myopathy in chronic alcoholism.

CASE REPORT: A 42-year-old man with a history of Billroth II-gastrectomy, chronic alcoholism, and malnutrition developed acute tetraparesis, two days before admission. He presented with bilateral, proximal upper and lower limb weakness, limb girdle wasting, bilaterally reduced Achilles tendon reflexes, and bilateral stocking-type sensory disturbances. Laboratory data revealed hypokalemia (2.2 mmol/L), elevated creatine kinase (7282 U/L), metabolic alkalosis and reduced urine potassium, albumin, and total protein. Muscle biopsy showed atrophic, necrotic, and regenerating fibers, endomysial macrophages, and vacuolar degeneration, interpreted as hypokalemic myopathy. With the correction of the serum potassium, tetraparesis rapidly resolved. With other causes excluded, malnutrition and gastrectomy were considered responsible for hypokalemia in this patient with acute tetraparesis and chronic alcoholism.

Acute Disease↗