Biomedical subjects
A Ince
Publications and source records attributed to A Ince.
Breast metastasis from non-Hodgkin's lymphoma: evaluation with color doppler sonography.
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Calcium pyrophosphate dihydrate crystal deposition disease.
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Prolongation of the survival of murine cardiac allografts by the vitamin D3 analogue 1,25-dihydroxy-delta 16-cholecalciferol.
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1,25-Dihydroxyvitamin D3 attenuates the expression of experimental murine lupus of MRL/l mice.
The murine strain MRL/l spontaneously develops a systemic lupus erythematosus (SLE)-like syndrome. An increased number of T cells and polyclonal T helper cell activity has been described in these mice suggesting a potential role for 1,25-dihydroxyvitamin-D3 [1,25-D3], an antiproliferative hormone selecting the T-helper lymphocyte subset. One month old MRL/l mice were submitted or not to 1,25-D3 0.1 microgram for 4 weeks, then 0.15 microgram given i.p. every other day for 18 weeks while maintained on a low calcium chow. Dermatologic lesions, i.e. alopecia, necrosis of the ear and scab formation, were completely inhibited by 1,25-D3 therapy. By 20 weeks, all mice had developed proteinuria. However, the degree of proteinuria was somewhat reduced in treated mice as assessed by urine protein/creatine ratios (less than 4 vs greater than 4 in treated vs untreated mice respectively). Moreover, a trend for a reduction in serum titers for anti-ssDNA antibodies was observed at 18 weeks. The active vitamin D metabolite had no effect on the development of the generalized lymphoid hyperplasia. Hypercalcemia developed when 1,25-D3 was increased to 0.15 microgram (2.62 +/- 0.12 vs 1.97 +/- 0.07 mmol/l, treated vs untreated mice respectively). These results suggest a beneficial role of 1,25-D3 in the prevention or attenuation of some manifestations of murine SLE, a model sharing many immunologic features with human SLE.
Day and full time psychiatric treatment: a controlled comparison.
Ninety-one patients admitted as emergencies, suffering from neurosis, personality disorder, or adjustment reaction, were randomly allocated to day hospital or to continued in-patient care. Follow-up was for up to one year. Clinical outcome was similar in the day care and in-patient groups, but patient satisfaction was significantly greater in day patients. Day hospital care was only about two-thirds of the cost of the cheaper of the two in-patient regimes, even though contact with it was on average twice as long as for in-patients.
Day treatment: suitability and referral procedure.
In a prospective screening of emergency admissions of patients suffering from neurosis, personality disorder or adjustment reaction, 100 were assessed as suitable for early transfer to day hospital treatment, 101 as unsuitable, and 39 as not requiring further intervention. Of the unsuitable patients, 39 were grossly disturbed; the remainder did not differ in severity from those thought suitable, but there was a specific reason against day treatment in all but 13 of the 62--most commonly alcohol abuse, physical problems, social problems or aggression. Patients' attitudes were also important. Recruitment of patients had to be active, with regular visits to the wards by day hospital staff.
Maleic acid-induced reabsorptive dysfunction in the proximal and distal nephron.
Micropuncture and clearance studies were performed to assess reabsorptive function in the proximal and distal nephron of rats with experimental Fanconi's syndrome induced by maleic acid. Anesthetized rats were studied by free-flow micropuncture of the late proximal tubule 90-120 min after continuous intravenous administration of maleic acid, 100 mg X kg-1 X h-1. Compared with control rats, the reabsorption of sodium and phosphate was significantly reduced (P less than 0.001 and less than 0.02, respectively). Tubular fluid-to-ultrafiltrate (TF/UF) chloride concentration ratio was 1.00 +/- 0.02 compared with 1.16 +/- 0.03 (P less than 0.01) in controls, suggesting a nearly total inhibition of proximal bicarbonate reabsorption. Whole kidney fractional excretions of sodium and chloride were increased significantly (P less than 0.02) but could not be explained by enhanced delivery of these solutes out of the late proximal tubule. To assess whether distal nephron reabsorption of sodium and chloride were inhibited by maleic acid, clearance studies were performed during water diuresis in awake rats. During maleic acid administration, 200 mg X kg-1 X h-1, urine flow rate (P less than 0.02) and the fractional excretions of sodium and chloride (P less than 0.001) increased significantly, but fractional free water clearance decreased from 7.16 +/- 0.42 to 4.03 +/- 0.68% (P less than 0.001). In acetazolamide-treated control rats but not in maleic acid-treated rats with similar bicarbonaturia, the magnitude of fractional free water clearance closely approximated the simultaneously measured fractional distal delivery of chloride. These studies suggest that maleic acid inhibits reabsorption at a distal nephron site or sites as well as in the proximal tubule.
The association of renal infarcts with carotid artery catheters used for clearance studies.
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Proximal tubular necrosis associated with maleic acid administration to the rat.
Administration of maleic acid to the rat is used as an experimental model of Fanconi's syndrome. To determine the site and extent of morphologic injury within the kidney after maleic acid administration, we systematically examined renal tissue using light, transmission electron, and scanning electron microscopy. Tissue was studied either immediately or 24 hours after rats received maleic acid, 200 mg. or 400 mg. per kg. of body weight, and was compared with tissue from controls. In kidneys of maleic acid-treated rats, evidence of injury was observed only in cells of the late pars convoluta and the pars recta in the medullary rays of the cortex and in the outer stripe of the medulla. Injured cells were characterized by an increase in cytoplasmic density, accumulation of numerous small vesicles in the apical region of the cells, abnormal-appearing mitochondria with compressed cristal membranes and flocculent densities, and focal loss of microvilli. Injury was apparent immediately after maleic acid administration and progressed to extensive necrosis by 24 hours after either the 200- or 400-mg. per kg. dose. Except for the presence of granular and hyaline casts in the lumena, the loops of Henle and distal convoluted tubules were normal. Collecting ducts in the outer medulla, but not in the cortex, medullary rays, or inner medulla, had significantly increased numbers of dark cells per total cell population when compared with controls (p less than 0.005). This increase in dark cells may represent an adaptive response of the medullary collecting duct to the functional abnormalities of maleic acid-induced Fanconi's syndrome. Collecting ducts showed no evidence of cell injury or necrosis. These observations provide evidence that maleic acid, like many other renal toxins, produces tubular injury and necrosis only in the proximal tubules, primarily in the medullary rays, and outer stripe of the medulla, and not in the distal tubules.
Effect of ionophore RO 2-2985 on the efflux of calcium from the rat nephron.
The effect of the ionophore RO 2-2985 on the efflux of calcium from the renal tubule was studied employing the in vivo microinjection technique. Microinjection solutions contained either RO 2-2985 (E) or its diluent (C). Following microinjections into the early proximal tubule, urinary 45Ca recoveries averaged 10.1 +/- 1.9 (C) and 3.5 +/- 1.4% (E) (P is less than 0.005), while recoveries averaged 32.3 +/- 6.9 (C) and 24.9 +/- 6.5% (E) (P is less than 0.05) following microinjections into the late proximal tubule. To determine if the decreased recovery of calcium was a specific effect, the effect of RO 2-2985 on the efflux of sodium, phosphate, and 3-O-methyl-D-glucose was examined. Compared to controls, RO2-2985 did not affect the urinary recoveries of 22Na, [32P]orthophosphoric acid, or 3-O-methyl-D-[14C]glucose. These studies demonstrate that RO 2-2985 enhances the efflux of calcium microinjected into the proximal portions of the rat nephron.
Renal tubular transport of organic acids. Studies with oxalate and para-aminohippurate in the rat.
The renal handling of oxalate was examined by free-flow micropuncture, intratubular microinjection, and droplet precession techniques in the rat. After the sustained i.v. infusion of [(14)C]oxalate, the fractional delivery of oxalate from the early portions of the proximal tubule was 120.1+/-4.4%, indicating net secretion. Fractional delivery rates from the late proximal tubule (124.6+/-6.1), distal tubule (120.9+/-2.9), and final urine (126.2+/-2.9%) were not different from that of the early proximal tubule. Direct intratubular microinjections of oxalate into the early proximal tubule and late proximal tubule yielded urinary recovery rates of 85+/-3% and 101+/-2%, respectively, suggesting that oxalate absorption does occur in the mid-portions of the proximal tubule. Droplet precession studies confirmed a secretory flux for oxalate. In contrast to oxalate, para-aminohippurate (PAH), the more traditional marker for organic acid transport, was secreted in the late portions of the proximal tubule and in large measure at a site between the late proximal and distal tubules, presumably the pars recta. Probenecid inhibited PAH secretion but was without effect on net oxalate transport, oxalate absorption, or oxalate secretion. These studies demonstrate that net oxalate secretion occurs in the early portions of the proximal convoluted tubule, undergoes bidirectional transport of approximately equal magnitude in later segments of the proximal tubule, and probably is not transported in more distal nephron sites. The secretory mechanism for oxalate differs from that of PAH in that it is located in a different segment of the nephron and is not inhibited by probenecid. These differences suggest that the early portions of the proximal tubule are important in the renal metabolism of some organic acids.
[One-stage revision of shoulder arthroplasty in the case of periprosthetic infection].
AIM: Infection of shoulder arthroplasties is rare, but represents a potentially devastating complication. The aim of this work is to show the value of various diagnostic procedures, specify causative pathogens and present the results of one-stage revised patients. METHOD: We performed a retrospective analysis of our 16 consecutive patients with an infected shoulder arthroplasty. RESULTS: In 13 of 16 cases a causative pathogen could be established preoperatively. Staphylococcus and Propioni spp. dominated. Only 9 patients could be followed up because two died, two were lost and three patients were revised because of non-infectious complications. The follow-up time was 5.8 years (13 months-13.25 years). The Constant-Murley score was 33.6 of 100. Eradication of infection was achieved in all patients. In the follow-up time no reinfection has occurred. CONCLUSION: Culturing of the preoperative joint fluid aspirate and the determination of CRP provide an early diagnosing of shoulder arthroplasty infection. One-stage revision arthroplasty with radical debridement and application of antibiotics to the bone cement provide an accurate therapy of periprosthetic shoulder infection.
Behçet's disease: does lack of knowledge result in under-diagnosis?
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