To study the role of formula as a cause of rickets, we randomly assigned 46 very-low-birth-weight (VLBW) infants (less than or equal to 1,500 gm) to one of three groups receiving either Isomil, a soy isolate formula, Similac with Iron, a common milk-based formula, or Similac 24 LBW, a hypercaloric milk-based formula designed for low-birth-weight infants during the first three to four months of life. Postnatal changes in serum calcium, phosphorus, alkaline phosphatase, and albumin were monitored during this study. Radiologic diagnosis of rickets was made in 60% of infants fed Isomil and 5% fed Similac with Iron. Significantly low levels of serum phosphorus and high levels of serum alkaline phosphatase were also seen in infants fed Isomil. The exact cause of the biochemical changes and the high incidence of rickets among infants fed Isomil is not clear. Poor solubility and possibly the decreased bioavailability of minerals in soy isolate formula may be important. We conclude that rickets occurs with high frequency among VLBW infants fed soy isolate, but not milk-based formulas. We suggest that prolonged feeding of soy isolate formulas should be avoided in VLBW infants.
Cerebrospinal fluid (CSF) lactate dehydrogenase was determined in 19 control infants without asphyxia (Group I), 24 infants with perinatal asphyxia (Group II), and 26 asphyxiated infants with seizures (Group III). Mean birthweights, gestational ages, CSF glucose, protein and red blood cells, and the ages at which the lumbar punctures were performed were not significantly different among the three groups. Mean CSF lactate dehydrogenase was significantly higher in Group III than in Groups I and II. Isoenzyme patterns indicated that the origin of the CSF lactate dehydrogenase was neuronal tissue, or a plasma transudate from increased permeability of the blood-brain barrier. There were 10 deaths due to anoxic encephalopathy in Group III, but none in Groups I or II. Follow-up of survivors at 10 to 30 months of age revealed neurological sequelae in three infants in Group I, two in Group II and five in Group III. Mean CSF lactate dehydrogenase in those with sequelae had not been significantly different from that of normal survivors; however, the mean was significantly higher in infants who died with anoxic encephalopathy compared with normal infants. These data indicate that CSF lactate dehydrogenase is significantly elevated in infants with fatal anoxic brain damage, and suggest that determinations may be of prognostic value in non-fatal cerebral hypoxia.
This research is carried out to investigate pre-existing repair cracks in cement mortar using the microbiologically induced calcium carbonate precipitation (MICP) technology. In the study, 20-cylinder mortar samples (45 mm in diameter and 40 mm in length) were split to have cracked width of various sizes. Out of twenty cracked samples, sixteen samples of average crack width ranging from 0.12 to 1.3 mm were repaired using the MICP method, while four cracked samples, with an average crack width ranging from 0.16 to 1.55 mm were soaked under distilled water. The water permeability and split tensile strength (STS) of these repaired mortars were tested. The amount of CaCO3 precipitated on the cracked mortar surfaces was evaluated. The results indicated that the MICP repair technique clearly reduced the water permeability of the cracked samples within the range of 73 to 84 %; while water-treated samples were too weak to undergo test. MICP-repaired samples had STS ranging from 29 to 380 kPa after 24 rounds of treatment. A relationship between the STS and percentage amount of CaCO3 precipitated was observed for samples with an average crack width between 0.29 and 1.1 mm, which indicated that STS increased with percentage increase in CaCO3 precipitated on the crack surfaces.
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