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SUMMARY Thirty nine very low birthweight neonates (with a birth weight of 820 to 1500 g and gestation of 27 to 34 weeks) who required total parenteral nutrition were randomly assigned to one of three regimens of administration of fat emulsion for a period of eight days. Groups 1 and 2 received the emulsion at a constant rate over 24 and 16 hours, respectively, beginning with a daily dosage of 1 g/kg and increasing daily by 1 g/kg to a maximum of 4 g/kg. Group 3 received the emulsion at a constant rate of 4 g/kg a day over 24 hours. Plasma concentrations of free fatty acids and serum concentrations of total bilirubin, apparent unbound bilirubin, and albumin were measured at regular intervals. Effects of the three regimens on serum bilirubin measurements were determined. The regimen of fat infusion and rate of infusion seemed to have no effect on serum concentrations of total and apparent unbound bilirubin, although there was a trend towards greater variability in apparent unbound concentrations with the intermittent regimen.

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SummaryThe effects of 100% oxygen breathing and constant positive pressure breathing (CPPB) on venous admixture (Qva/Qt) and arterial-alveolar difference for PCOz (aADC02) were examined in seven infants with hyaline membrane disease (HMD). Increasing FIOz from 0.63-0.99 with C P P B constant at 2 cm H z O resulted in significant decrease in Qva/Qt from 0.67-0.47, but produced no change in aADCOz (13.0 torr vs. 15.0 torr). Increasing CPPB to 8 cm H z O with FIOz returned to 0.63 also resulted in decreased Qva/Qt (0.50), but in addition aADCOz decreased significantly to 7.0 torr. The reduction in Qva/Qt with oxygen breathing and with CPPB is interpreted as a reduction in true right-to-left-shunt and a corresponding increase of effective blood flow through the lung. In 100% oxygen the increase in effective pulmonary perfusion occurred in a poorly ventilated compartment and as such was not reflected in the aADC02. On the other hand, with CPPB, the increase in perfusion was accompanic d by an increase in ventilation and, hence, the aADC02 decreased. To illustrate these effects we c0nstructed.a three compartment model for the lung in HMD, calculated the VA/Qc for the well-ventilated compartment in each circumstance, constructed 02-COz diagrams and arrived a t predicted values for the aADCOz for each of the three clinical conditions. These predicted values agree well with those measured, considering the possible errors in our methods and assumptions and considering the absolute changes that may occur with CPPB, namely, increased cardiac output and decreased ventilation. This, in turn, provides strong support for the proposed three compartment model and for the existence of an open, but severely underventilated compartment in HMD. SpeculationIn HMD, the aADCOz seems to be responsive to the effects of CPPB on both ventilation and perfusion, and as such would be valuable clinically in determining optimal levels of CPPB.The Qva/Qt in HMD is due to a true right-to-left shunt (Qs/ Qt) through persistent fetal circulatory pathways (5. 14. 19. 20. 24. 30). pulmonary arteriovenous anastomoses ( 1 8). bronchial veinpulmonary vein communications (20, 37), or capillary perfusion bf atelectatic air spaces (23. 31) or areas of the immature lung where alveolar formation is not yet complete ( 1 8, 37).Previous authors have shown that this shunt is reduced by 100% oxygen breathing (7. 28) and CPPB (2. 4, 8, 12). Recently, it has been suggested that most of this reduction is secondary to relief of hypoxic vascular constriction in an open severely underventilated compartment of the lung with indeterminately low VA/Qc, resulting in increased effective pulmonary blood flow (8. 9).To obtain further evidence for this hypothesis we have examined the effects of oxygen and CPPB on the arterial-alveolar carbon dioxide difference (aADC02), a measurement that is sensitive to changes of blood flow in well-ventilated units of the lung (6, 27). It was predicted that with equivalent changes in Qva/Qt. the a A D C 0 2 would be reduced by CPPB, but not...

Constituents in the feed of reverse osmosis (RO) processes pass into the product by two mechanisms: diffusion through the membrane and advection through defects in the system. While minerals and tracers pass via both mechanisms, pathogens pass only via advection. Using mass and flow balances, a rigorous model is developed to characterize the response of both viruses and tracers in RO systems. The model is used to assess several tracers being considered today. Early virus testing and the commercial requirements of desalination are reviewed, leading to the conclusion that some degree of advection can be expected to be present in RO systems but that commercial incentives can be expected to maintain pathogen removal due to defects somewhat greater than 4.0 log. Model results suggest that the best tracers currently in use can detect defects near this log reduction value but that there is still room for improvement.

The primary objective of this study was the establishment of a postnatal growth curve for the very low-birth-weight infant. Only infants whose size was appropriate for gestational age and whose predominant form of nourishment was enteral were included in the study. Two growth curves were constructed: one for infants weighing less than 900 g (group A, birth weight 799 ± 79 [SD] g, mean gestational age 26.5 weeks), and one for infants weighing 901 to 1,100 g (group B, birth weight 1,023 ± 53 [SD] g, mean gestational age 28.5 weeks). Growth was followed over the first 50 postnatal days. Group A infants gained an average of 10.2 g/d overall during the first 50 postnatal days and group B infants gained an average of 17.1 g/d over the same period. Because the major objective of this study was construction of a growth curve for infants weighing less than 900 g, direct comparison is made with the Dancis grid (1948) as this is the only standard for this group. The growth rates of our infants were found to be more than twice that of the original prediction of Dancis.

W hile calculating the Langelier Saturation Index (LSI) for calcium carbonate for a low-alkalinity mountain supply, it has come to the authors' attention that Method 2330 B for calculating the LSI for calcium carbonate (Rice et al, 2012) includes an incorrect equation for calculating the concentration of bicarbonate ion. The error is of no significance when the pH is below 8 yet becomes of increasing significance as the pH rises above 9. The error can be important to purveyors of low-mineral mountain supplies who seek to understand and manage calcium carbonate saturation in their water supply. Method 2330 B provides the following equation to estimate the bicarbonate ion concentration [HCO -3 ]:It can be shown that the correct form of this equation isAlk t -Alk 0 + 10 (pf m -pH) -10 (pH + pf m -pK w )  1 + 2 × 10 (pH + 3pf m -pK 2 )The definitions for all terms can be found in Method 2330 B.At elevated pH, Eq 1 leads to an underestimate of the saturation pH (pH s ), resulting in an overestimate of the LSI. The magnitude of the error in pH s can be estimated by Eq 3: pH s = log  1 + 2 × 10 (pH + 3pf m -pK 2 )  1 + 0.5 × 10 (pH -pK 2 ) (3) Inspection of Eq 3 will reveal that the magnitude of the error is influenced by the temperature and ionic strength, which can change pf m and pK 2 , but it is not affected by Alk t or Alk 0 . Changes in pH are the dominant influence. The change in the error between pH 8 and 12 is illustrated for an ionic strength of 0.0025 M and a temperature of 22.5°C. (The derivations of Eqs 2 and 3 are presented in the supplemental material to this technical note (on the pages that follow).Trussell Technologies maintains a free, open-source, downloadable tool-CaCO 3 Indices Modeling Spreadsheet (Trussell Technologies, 2015)-on its website. Prior to January 2015, this tool used Eq 1 (Eq 4 in Method 2330 B) to calculate the bicarbonate ion concentration. A revised version of the model has been uploaded, which has been amended to use Eq 2 shown in this note.