Excitation energies and spins of a superdeformed band in 194Hg from one-step discrete decays to the yrast line.
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Biomedical subjects
Publications and source records attributed to D Ackermann.
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The health-related and social needs of aged people and their fulfillment are studied. Only a very weak relation is found between the financial situation and the claims for possible financial resources. On the other side education is found to have a key position for the drawing of supplementing pensions. The problems resulting for the assignment of financial support to aged people are discussed.
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An immunoradiometric assay is described for the determination of human anti-idiotypic anti-B72.3 IgG. The latter is formed in ovarian cancer patients after treatment with the murine monoclonal antibody B72.3, which is directed against the tumour-associated glycoprotein 72 (TAG-72). A gel coupled with Fc-specific anti-human IgG antibodies is used as a solid phase for the extraction of serum IgG. The anti-B72.3 IgG is then specifically detected by incubation with radiolabelled B72.3 detector antibodies. Calibration standards were prepared from serum obtained from a patient repeatedly treated with B72.3 antibodies. The concentration of anti-idiotypic anti-B72.3 antibodies was expressed as TAG-72-like arb.units/1. The assay performed with two 60-minute incubation steps is characterized by a high sensitivity (detection limit: 3 x 10(3) arb.units/1) and precision (coefficients of variation: intra-assay = 6.4% and 5.8% at 80 x 10(3) arb. units/1 and 217 x 10(3) arb.units/1, inter-assay = 8.7% and 7.1% at 91 x 10(3) arb.units/1 and 212 x 10(3) arb.units/1) and a good linearity of dilution (recovery after dilution between 99% and 107%). The assay is more specific than previously described methods; no interference was observed by TAG-72 up to 3.3 x 10(7) arb.units/1. Also, non-specific human anti-mouse antibodies did not cross-react up to 34.8 mg/l. The test may be modified for detection of anti-idiotypic antibodies, which are formed after treatment with other monoclonal antibodies.
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To determine whether chronic overconsumption of protein might increase renal mass and cause up-regulation of 1,25-dihydroxyvitamin D3 [1,25-(OH)2D] production, 57 male recurrent idiopathic calcium stone formers (RCSF), 29 with hypercalciuria (HCSF; urinary calcium x V, > 7.50 mmol/day) and 28 with normocalciuria (NCSF), were compared with 15 healthy male controls (C) while consuming a free choice diet. Renal mass in RCSF was measured by the sum of the surface areas of right and left kidneys (square centimeters) on plain films of the abdomen by a computer-assisted sonic stylus; in C, renal mass was assessed sonographically. Serum intact PTH and 1,25-(OH)2D were measured radioimmunometrically. In HCSF, urinary phosphate x V (35.9 +/- 1.2 mmol/day) was higher than that in NCSF (29.3 +/- 1.3 mmol/day; P = 0.0009) or C (28.7 +/- 1.8 mmol/day; P = 0.005); urinary creatinine x V (16.5 +/- 0.5 mmol/day) was also higher in HCSF than in NCSF (15.0 +/- 0.5 mmol/day; P = 0.024) or C (13.8 +/- 0.6 mmol/day; P = 0.002). For identical blood levels of ionized calcium and phosphate, the 1,25-(OH)2D/PTH concentration ratio (an index of regulation of 1,25-(OH)2D production) was higher in HCSF (6.5 +/- 1.0) than in NCSF (4.0 +/- 0.3; P = 0.005). In addition, the sum of the surface areas of right and left kidneys was increased in HCSF (163.4 +/- 2.9 cm2) compared with that in NCSF (140.5 +/- 3.1 cm2; P = 0.0001), and it positively correlated with urinary phosphate x V (r = 0.429; P = 0.001) as well as with urinary creatinine x V (r = 0.294; P = 0.026); no such correlation was noted in C. Calcitriol levels were positively related to renal mass in RCSF (r = 0.316; P = 0.018), but not in C. Finally, urinary calcium x V positively correlated with the serum calcitriol/PTH concentration ratio only in RCSF (r = 0.388; P = 0.003). These findings suggest that protein overconsumption may cause an increase in renal mass and up-regulate calcitriol production in some male RCSF, an effect that would subsequently cause "idiopathic" hypercalciuria.
The calciuric response after an oral calcium load (1000 mg elemental calcium together with a standard breakfast) was studied in 13 healthy male controls and 21 recurrent idiopathic renal calcium stone formers, 12 with hypercalciuria (UCa x V > 7.50 mmol/24 h) and nine with normocalciuria. In controls, serum 1,25(OH)2 vitamin D3 (calcitriol) remained unchanged 6 h after oral calcium load (50.6 +/- 5.1 versus 50.9 +/- 5.0 pg/ml), whereas it tended to increase in hypercalciuric (from 53.6 +/- 3.2 to 60.6 +/- 5.4 pg/ml, P = 0.182) and fell in normocalciuric stone formers (from 45.9 +/- 2.6 to 38.1 +/- 3.3 pg/ml, P = 0.011). The total amount of urinary calcium excreted after OCL was 2.50 +/- 0.20 mmol in controls, 2.27 +/- 0.27 mmol in normocalciuric and 3.62 +/- 0.32 mmol in hypercalciuric stone formers (P = 0.005 versus controls and normocalciuric stone formers respectively); it positively correlated with serum calcitriol 6 h after calcium load (r = 0.392, P = 0.024). Maximum increase in urinary calcium excretion rate, delta Ca-Emax, was inversely related to intact PTH levels in the first 4 h after calcium load, i.e. more pronounced PTH suppression predicted a steeper increase in urinary calcium excretion rate. Twenty-four-hour urine calcium excretion rate was inversely related to the ratio of delta calcitriol/deltaPTHmax after calcium load (r = -0.653, P = 0.0001), indicating that an abnormally up-regulated synthesis of calcitriol and consecutive relative PTH suppression induce hypercalciuria.(ABSTRACT TRUNCATED AT 250 WORDS)
To assess bone mineral density (BMD) in idiopathic calcium nephrolithiasis, dual-energy x-ray absorptiometry was performed at lumbar spine, upper femur (femoral neck, Ward's triangle, and total area), distal tibial diaphysis, and distal tibial epiphysis in 110 male idiopathic calcium stone formers (ICSF); 49 with and 61 without hypercalciuria on free-choice diet). Results were compared with those obtained in 234 healthy male controls, using (1) noncorrected BMD, (2) BMD corrected for age, height, and BMI, and (3) a skeletal score based on a tercile distribution of BMD values at following four sites: lumbar spine, Ward's triangle, tibial diaphysis, and tibial epiphysis. After correction, BMD--and therefore also skeletal score--tended to be lower in the stone formers than in controls at five of the six measurement sites, that is, lumbar spine, upper femur, Ward's triangle, tibial diaphysis, and tibial epiphysis, limit of significance being reached for the last two sites without difference between hypercalciuric (HCSF) and normocalciuric stone formers (NCSF). Estimated current daily calcium intake was significantly lower in patients (616 +/- 499 mg/24 h, mean +/- SEM) than in controls (773 +/- 532, p = 0.02). Of 17 patients who in the past had received a low-calcium diet for at least 1 year, 10 had a low skeletal score (4-6) whereas only 1 had a high score (10-12; p = 0.037). Of the 12 stone formers in the study with skeletal score 4 (i.e., the lowest), 8 had experienced in the past one or more fractures of any kind versus only 19 of the remaining 77 patients with skeletal score 5-12 (p = 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
Stone formation is an uncommon complication in renal allograft recipients. We report a 61-year-old woman who had undergone cadaveric renal transplantation in 1982 because of chronic renal failure due to polycystic kidney disease. Since 1985 she has developed recurrent urinary tract infections with Proteus mirabilis, and persistent microhematuria was detectable from 1988 on. Since renal function remained stable, she was repeatedly treated with antibiotics. Following a septicemia with P mirabilis, a staghorn calculus was discovered and was surgically removed from the allograft. Stone analysis (infrared spectrometry) revealed 60% struvite and 40% carbonate apatite. Since urinary tract infections with urea-splitting bacteria are a more frequent cause of stone formation in transplant patients than in nontransplant patients with kidney stones, stone disease should be considered in every allograft recipient presenting with recurrent urinary tract infection and microhematuria.
Between 1983 and 1992 22 children with urolithiasis were treated at the Department of Paediatric Surgery and Paediatrics of the University Hospital of Berne. There were 8 girls and 14 boys with a mean age of 7.3 years. Metabolic disease was found in 6 children. There were 12 renal stones, 12 ureteral stones, 1 bladder stone and 1 urethral stone. Conservative therapy, ESWL, and surgery were used as treatment each in one third of the children. Studying our patient-group and analyzing the recent literature, the place of the different therapeutic methods of the childhood stones will be discussed.
Risk factors for low urinary citrate excretion were assessed in 34 consecutive male recurrent idiopathic calcium stone formers (RCSF) who collected two 24-h urines while on free-choice diet. Overt hypocitraturia (hypo-cit) was defined as UCit x V < 1.70 mmol/day, and 'low' citraturia (low-cit) as UCit x V between 1.70 and 2.11 mmol/day. Twenty-three RCSF had normocitraturia (normo-cit), six low-cit and five hypo-cit. UCit x V positively correlated with urine volume (VOLUME, r = 0.44, P = 0.009), vegetable fibre intake (fibers, r = 0.46, P = 0.009) and GI-alkali absorption (alkali, r = 0.47, P = 0.006), and volume, fibres and alkali tended to be lower among RCSF with low-/hypo-cit. A 3-day NH4Cl loading test (0.95 mEq/kg BW daily in 3 doses) was performed in RCSF as well as in 14 age-matched healthy male controls (C). On a plot of urine pH versus serum bicarbonate, 10 of 11 RCSF with low-/hypo-cit, but only six of 23 with normo-cit (P = 0.0004) fell off the normal range, indicating incomplete RTA. Two or more risk factors simultaneously occurred in only four of 23 RCSF with normo-cit, but in eight of 11 with low-/hypo-cit (P = 0.002). In conclusion, incomplete RTA is the most prevalent risk factor for low-/hypo-cit in RCSF, and decreases in vegetable fibres and urine volume emerge as two new risk factors for low urinary CIT.
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Catheter embolization was performed in 13 patients with persistent hematuria after an iatrogenic injury of the renal artery (n = 7), due to a vascular malformation (n = 4), or after renal trauma (n = 2). On angiography the following vascular changes were found: extravasation of contrast medium due to a severe vascular laceration (n = 2), pseudoaneurysms (n = 2), arteriovenous fistulas or malformations (n = 3) or combined vascular injuries (n = 2). The embolization was done using the monoaxial technique in nine patients, while in four patients a coaxial technique with micro-catheters was used. The method of choice is the use of micro-catheters with micro-coils. This technique allows the superselective embolization of small renal arteries without damaging the surrounding parenchyma.
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.
Angiography was performed on 6 patients with acute haematuria following percutaneous nephrostomy and nephrolitholapaxy; in 3, vessel damage with leak of contrast into the nephrostomy canal or renal parenchyma was demonstrated and in 3 there were one or more pseudoaneurysms with or without arteriovenous fistula. All patients were successfully treated by catheter embolisation. Various catheter techniques (monaxial, coaxial) and embolic materials (Spongostan, Ivalon, coils) were used. The use of a Tracker-18 catheter with micro coils is the method of choice and permits superselective embolisation of bleeding from small peripheral branches with maximal preservation of the renal parenchyma.
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.