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Biomedical subjects

J Horn

Publications and source records attributed to J Horn.

151 records · Page 9Linked to original sources
PubMedDate not supplied

Evidence of complement catabolism in acute pancreatitis.

Active proteolytic enzymes are released into the gland parenchyma and surrounding tissues during episodes of acute pancreatitis. Since complement components are potential substrates for active proteases and may be the source of biologically active peptides capable of mediating tissue injury, we have examined sera obtained from 12 patients during 13 episodes of acute pancreatitis for evidence of complement catabolism. In 8 of 13 acute phase sera, there were decreased levels of CH50, C3, C4, or some combination thereof as well as degradation products of C3 (revealed by crossed immunoelectrophoresis). In convalescent sera, levels of complement components were normal or elevated. Measurements of alpha1-antitrypsin, alpha2-macroglobulin, and trypsin inhibitory capacity failed to reveal evidence of protease-antiprotease imbalance. These findings provide evidence of complement catabolism in acute pancreatitis and suggest the possibility that activated complement components may play a role in the pathogenesis of some systemic pathologic changes which occur in this disease.

Acute Disease↗
PubMedDate not supplied

Aluminum in parenteral nutrition solution--sources and possible alternatives.

The extent of aluminum (Al) contamination in parenteral nutrition (PN) solutions for infants is not known. Aluminum was measured in 136 samples from various commercially available components that are used with PN. Results showed Al content varied widely among different components. The same chemical may have a different Al content depending on the manufacturer. However, Al contents were similar among lots from the same manufacturer for the same chemical. Aluminum contamination was arbitrarily classified as high (greater than 500 micrograms Al/liter), intermediate (51-500 micrograms Al/liter) or low (less than or equal to 50 micrograms Al/liter). The high group included most calcium and phosphorus containing salts, 1 multivitamin preparation, folic acid, ascorbic acid and concentrated (25%) albumin. The intermediate group included sodium lactate, potassium phosphates, zinc and chromium chloride, multitrace metal preparation, and 5% plasma protein. The low group included amino acids, sterile water and dextrose water, chloride salts of sodium, potassium, calcium, copper and chromium, sodium phosphates, magnesium sulphate, zinc sulphate, vitamin B12, vitamin K1, 1 multivitamin preparation, soybean oil emulsion and heparinized (2 U/ml) saline. PN solutions made from high Al components may contain up to 300 micrograms Al/liter. Calcium gluconate contributed greater than 80% of the total Al load from PN. Lowering of Al content in calcium gluconate in addition to use of specific low Al components offers the opportunity to significantly lower the Al concentration of the final PN solution and theoretically may achieve an Al content as low as 12 micrograms/l.(ABSTRACT TRUNCATED AT 250 WORDS)

Aluminum↗
PubMedDate not supplied

Parenteral nutrition for infants: effect of high versus low calcium and phosphorus content.

Calcium (Ca) and phosphorus (P) homeostasis were determined in 18 infants (birth weight, 2,810 +/- 135 g; gestational age, 37.4 +/- 0.5 weeks; mean +/- SEM) who received high or low Ca and P content (Ca, P) parenteral nutrition (PN) with a fixed, low dose of vitamin D (25 IU/dl). Nine infants were randomized into low (standard) Ca, P (20 mg Ca and 15.5 mg P/dl) and nine into high Ca, P (60-80 mg Ca and 46.5-62 mg P/dl) PN, and then were studied for up to 6 weeks. The high Ca, P group had stable serum 1,25 dihydroxyvitamin D [1,25(OH)2D], which consistently remained within the normal range (less than 116 pg/ml). Tubular reabsorption of phosphorus (TRP) also was stable and remained consistently less than 90%. The low Ca, P group had elevated and higher 1,25(OH)2D (p = 0.03) than the high Ca, P group. The mean serum 1,25(OH)2D concentration rose from 32 to 112, 115, and 133 pg/ml over a period of 6 weeks. TRP also was higher (p = 0.02) and remained consistently greater than 90%. There were no significant differences between groups in serum parathyroid hormone, calcitonin, Ca, Mg, P, alkaline phosphatase, vitamin D binding protein, and 25 hydroxyvitamin D concentrations; urine Ca/creatinine and Mg/creatinine ratios, and fractional excretion of sodium (Na). Thus, a "high" Ca (60 mg/dl) and P (46.5 mg/dl) content in PN solutions can result in stable serum 1,25(OH)2D and TRP, presumably reflecting minimal stress to Ca and P homeostatic mechanisms without further increase in urinary Ca excretion.

Calcium↗
PubMedDate not supplied

A sudden death syndrome induced in poults and chicks fed diets containing Fusarium fujikuroi with known concentrations of moniliformin.

A sudden death syndrome was induced in chicks and poults fed diets containing Fusarium fujikuroi, formulated to contain 0-330 mg/kg moniliformin (M) with or without the maximum recommended therapeutic concentration of monensin. Lesions of monensin toxicosis were not observed. Clinical signs were referable to cardiac dysfunction (sudden death, dyspnea, cyanosis, depression). Poults and chicks dying early in the study had no gross lesions or had lesions of right ventricular dilation. Treated poults and chicks dying late in the study or euthanatized at termination of the study had lesions of bilateral myocardial hypertrophy, usually concentric. Absolute heart weights and relative heart weights, expressed as a percentage of body weight, were significantly greater in treated birds than controls (P < 0.05), whereas body weights were significantly less (P < 0.05). Microscopically, lesions progressed from acute myocardial degeneration to necrosis, fibrosis, and hypertrophy. Ultrastructural findings were consistent with the gross and microscopic lesions. Serum pyruvate concentrations were a useful indicator of M-induced cardiotoxicosis. Concentrations of serum pyruvate increased with increased concentration of dietary M, but were not affected by addition of monensin to the diet. In chicks ingesting 40-300 mg/kg M, serum pyruvate concentrations were significantly greater (P > 0.05) than those in controls (controls, 0.28 +/- 0.08 mmol/liter; exposed 0.38 +/- 0.11-0.55 +/- 0.13 mmol/liter). Poults ingesting 80-330 mg/kg M had significantly greater serum pyruvate concentrations than controls (controls 0.33 +/- 0.09 mmol/liter; exposed 0.43 +/- 0.13-1.00 +/- 0.006 mmol/liter). The Vetronics System was used to evaluate electrocardiographic alterations in a limited number of chicks and poults surviving to the end of the feeding trial. Electrocardiographic alterations in poults and chicks fed diets containing > or = 40 mg/kg and > or = 160 mg/kg M, respectively, were consistent with ventricular hypertrophy, myocardial injury, and hypoxia. Electrocardiographic alterations were more striking in poults than in chicks. Altered myocardial metabolism due to M toxicosis, in conjunction with the unusual susceptibility of domestic poultry to altered cardiac metabolism, is believed to be the cause of the organ-specific lesions in these birds. These findings suggest that cardiac injury with subsequent alterations in cardiac electrical conductance may be a cause of the sudden deaths observed in poultry chronically intoxicated with dietary M.

Animals↗