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A condition on the Hamiltonian of an isospectral time-dependent quantum mechanical system is derived, which, if satisfied, implies optimal adiabaticity (defined later). The condition is expressed in terms of the Hamiltonian and the evolution operator related to it. Because the latter depends in a complicated way on the Hamiltonian, it is not yet clear how the condition can be used to extract useful information about the optimal Hamiltonian analytically. The condition is tested on an exactly-soluble time-dependent problem (a spin in a magnetic field), where perfectly adiabatic evolution can be easily identified. PACS Nos: 03.65.Aa, 03.65.Ta Nous avons developpe une condition applicable au Hamiltonien d'un systeme physique quantique isospectral et dependant du temps, qui, si elle est satisfaite, implique une adiabaticite optimale (definie plus tard). La condition est exprimee en fonction du Hamiltonien et de l'operateur d'evolution qui lui est relie. Puisque ce dernier depend du Hamiltonien d'une facon compliquee, il n'est pas encore clair comment cette condition peut etre utilisee pour extraire de l'information utile sur le Hamiltonien optimal. Nous testons la condition sur un probleme dependant du temps a solution exacte (un spin dans un champ magnetique), oU on peut identifier facilement une evolution parfaitement adiabatique. [Traduit par la Redaction], 1. Introduction The adiabatic theorem in quantum mechanics was developed when quantum mechanics was still in its infancy [1]. (See ref. 2 for an early English-language reference, and ref. 3 [...]

Background: The COVID-19 pandemic has required family physicians to rapidly address increasing mental health problems with limited resources. Vulnerable home-based seniors with chronic physical conditions and commonly undermanaged symptoms of anxiety and depression were recruited in this pilot study to compare two brief self-care intervention strategies for the management of symptoms of depression and/or anxiety., Methods: We conducted a pilot RCT to compare two tele-health strategies to address mental health symptoms either with 1) validated CBT self-care tools plus up to three telephone calls from a trained lay coach vs. 2) the CBT self-guided tools alone. The interventions were abbreviated from those previously trialed by our team, to enable their completion in 2 months. Objectives were to assess the feasibility of delivering the interventions during a pandemic (recruitment and retention); and assess the comparative acceptability of the interventions across the two groups (satisfaction and tool use); and estimate preliminary comparative effectiveness of the interventions on severity of depression and anxiety symptoms. Because we were interested in whether the interventions were acceptable to a wide range of older adults, no mental health screening for eligibility was performed., Results: 90 eligible patients were randomized. 93% of study completers consulted the self-care tools and 84% of those in the coached arm received at least some coaching support. Satisfaction scores were high among participants in both groups. No difference in depression and anxiety outcomes between the coached and non-coached participants was observed, but coaching was found to have a significant effect on participants' use and perceived helpfulness of the tools., Conclusion: Both interventions were feasible and acceptable to patients. Trained lay coaching increased patients' engagement with the tools. Self-care tools offer a low cost and acceptable remote activity that can be targeted to those with immediate needs. While effectiveness results were inconclusive, this may be due to the lack of eligibility screening for mental health symptoms, abbreviated toolkit, and fewer coaching sessions than those used in our previous effective interventions., Trial Registration: ClinicalTrials.gov Identifier: NCT0460937., Competing Interests: The authors have declared that no competing interests exist., (Copyright: © 2024 Yaffe et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)

Rationale: Smoking status and smoking history remain poorly accounted for as variables that could affect the efficacy of new drugs being tested in chronic obstructive pulmonary disease (COPD) patients. As a proof of concept, we used a pre-clinical model of cigarette smoke (CS) exposure to compare the impact of treatment during active CS exposure or during the cessation period on the anti-inflammatory effects IL-1α signaling blockade. Methods: Mice were exposed to CS for 2 weeks, followed by a 1-week cessation, then acutely re-exposed for 2 days. Mice were treated with an anti-IL-1α antibody either during CS exposure or during cessation and inflammatory outcomes were assessed. Results: We found that mice re-exposed to CS displayed reduced neutrophil counts and cytokine levels in the bronchoalveolar lavage (BAL) compared to mice exposed only acutely. Moreover, we found that treatment with an anti-IL-1α antibody during the initial CS exposure delayed inflammatory processes and interfered with pulmonary adaptation, leading to rebound pulmonary neutrophilia, increased BAL cytokine secretion (CCL2) and upregulated Mmp12 expression. Conversely, administration of anti-IL-1α during cessation had the opposite effect, improving BAL neutrophilia, decreasing CCL2 levels and reducing Mmp12 expression. Discussion: These results suggest that pulmonary adaptation to CS exposure dampens inflammation and blocking IL-1α signaling during CS exposure delays the inflammatory response. More importantly, the same treatment administered during cessation hastens the return to pulmonary inflammatory homeostasis, strongly suggesting that smoking status and treatment timing should be considered when testing new biologics in COPD., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Milad, Pineault, Tremblay, Routhier, Lechasseur, Beaulieu, Aubin and Morissette.)

Treatment of the cigarette smoke-associated lung diseases, such as chronic obstructive pulmonary disease (COPD), has largely focused on broad-spectrum anti-inflammatory therapies. However, these therapies, such as high-dose inhaled corticosteroids, enhance patient susceptibility to lung infection and exacerbation. Our objective was to assess whether the cationic host defense peptide, human β-defensin 2 (hBD-2), can simultaneously reduce pulmonary inflammation in cigarette smoke-exposed mice while maintaining immune competence during bacterial exacerbation. Mice were exposed to cigarette smoke acutely (4 days) or chronically (5 days/wk for 7 wk) and administered hBD-2 intranasally or by gavage. In a separate model of acute exacerbation, chronically exposed mice treated with hBD-2 were infected with nontypeable Haemophilus influenzae before euthanasia. In the acute exposure model, cigarette smoke-associated pulmonary neutrophilia was significantly blunted by both local and systemic hBD-2 administration. Similarly, chronically exposed mice administered hBD-2 therapeutically exhibited reduced pulmonary neutrophil infiltration and downregulated proinflammatory signaling in the lungs compared with vehicle-treated mice. Finally, in a model of acute bacterial exacerbation, hBD-2 administration effectively limited neutrophil infiltration in the lungs while markedly reducing pulmonary bacterial load. This study shows that hBD-2 treatment can significantly attenuate lung neutrophilia induced by cigarette smoke exposure while preserving immune competence and promoting an appropriate host-defense response to bacterial stimuli.

Vaping is increasingly popular among the young and adult population. Vaping liquids contained in electronic cigarettes (e-cigarettes) are mainly composed of propylene glycol and glycerol, to which nicotine and flavors are added. Among several biological processes, glycerol is a metabolic substrate used for lipid synthesis in fed state as well as glucose synthesis in fasting state. We aimed to investigate the effects of glycerol e-cigarette aerosol exposure on the aspects of glycerol and glucose homeostasis. Adult and young male and female mice were exposed to e-cigarette aerosols with glycerol as vaping liquid using an established whole-body exposure system. Mice were exposed acutely (single 2-h exposure) or chronically (2 h/day, 5 days/week for 9 weeks). Circulating glycerol and glucose levels were assessed and glycerol as well as glucose tolerance tests were performed. The liver was also investigated to assess changes in the histology, lipid content, inflammation, and stress markers. Lung functions were also assessed as well as hepatic mRNA expression of genes controlling the circadian rhythm. Acute exposure to glycerol aerosols generated by an e-cigarette increased circulating glycerol levels in female mice. Increased hepatic triglyceride and phosphatidylcholine concentrations were observed in female mice with no increase in circulating alanine aminotransferase or evidence of inflammation, fibrosis, or endoplasmic reticulum stress. Chronic exposure to glycerol e-cigarette aerosols mildly impacted glucose tolerance test in young female and male mice. Fasting glycerol, glucose, and insulin remained unchanged. Increased pulmonary resistance was observed in young male mice. Taken together, this study shows that the glycerol contained in vaping liquids can affect the liver as well as the aspects of glucose and glycerol homeostasis. Additional work is required to translate these observations to humans and determine the biological and potential pathological impacts of these findings., (© 2022 The Authors. Physiological Reports published by Wiley Periodicals LLC on behalf of The Physiological Society and the American Physiological Society.)

Cigarette smoke exposure induces inflammation marked by rapid and sustained neutrophil infiltration, IL-1α, release and altered surfactant homeostasis. However, the extent to which neutrophils and IL-1α contribute to the maintenance of pulmonary surfactant homeostasis is not well understood. We sought to investigate whether neutrophils play a role in surfactant clearance as well as the effect of neutrophil depletion and IL-1α blockade on the response to cigarette smoke exposure. In vitro and in vivo administration of fluorescently labeled surfactant phosphatidylcholine was used to assess internalization of surfactant by lung neutrophils and macrophages during or following cigarette smoke exposure in mice. We also depleted neutrophils using anti-Ly-6G or anti-Gr-1 Abs, or we neutralized IL-1α using a blocking Ab to determine their respective roles in regulating surfactant homeostasis during cigarette smoke exposure. We observed that neutrophils actively internalize labeled surfactant both in vitro and in vivo and that IL-1α is required for smoke-induced elevation of surfactant protein (SP)-A and SP-D levels. Neutrophil depletion during cigarette smoke exposure led to a further increase in SP-A levels in the bronchoalveolar lavage and increased IL-1α, CCL2, GM-CSF, and G-CSF release. Finally, macrophage expression of Mmp12 , a protease linked to emphysema, was increased in neutrophil-depleted groups and decreased following IL-1α blockade. Taken together, our results indicate that neutrophils and IL-1α signaling are actively involved in surfactant homeostasis and that the absence of neutrophils in the lungs during cigarette smoke exposure leads to an IL-1α-dependent exacerbation of the inflammatory response., (Copyright © 2021 by The American Association of Immunologists, Inc.)

Genetic predispositions and environmental exposures are regarded as the main predictors of respiratory disease development. Although the impact of dietary essential nutrient deficiencies on cardiovascular disease, obesity, and type II diabetes has been widely studied, it remains poorly explored in chronic respiratory diseases. Dietary choline and methionine deficiencies are common in the population, and their impact on pulmonary homeostasis is currently unknown. Mice were fed choline- and/or methionine-deficient diets while being exposed to room-air or cigarette smoke for up to 4 wk. Lung functions were assessed using the FlexiVent. Pulmonary transcriptional activity was assessed using gene expression microarrays and quantitative PCR. Immune cells, cytokines, and phosphatidylcholine were quantified in the bronchoalveolar lavage. In this study, we found that short-term dietary choline and/or methionine deficiencies significantly affect lung function in mice in a reversible manner. It also reduced transcriptional levels of collagens and elastin as well as pulmonary surfactant phosphatidylcholine levels. We also found that dietary choline and/or methionine deficiencies markedly interfered with the pulmonary response to cigarette smoke exposure, modulating lung function and dampening inflammation. These findings clearly show that dietary choline and/or methionine deficiencies can have dramatic pathophysiological effects on the lungs and can also affect the pathobiology of cigarette smoke-induced pulmonary alterations. Expanding our knowledge in the field of "nutri-respiratory research" may reveal a crucial role for essential nutrients in pulmonary health and disease, which may prove to be as relevant as genetic predispositions and environmental exposures.

Smoking alters pulmonary reverse lipid transport and leads to intracellular lipid accumulation in alveolar macrophages. We investigated whether stimulating reverse lipid transport with an agonist of the liver X receptor (LXR) would help alveolar macrophages limit lipid accumulation and dampen lung inflammation in response to cigarette smoke. Mice were exposed to cigarette smoke and treated intraperitoneally with the LXR agonist T0901317. Expression of lipid capture and lipid export genes was assessed in lung tissue and alveolar macrophages. Pulmonary inflammation was assessed in the bronchoalveolar lavage (BAL). Finally, cholesterol efflux capacity and pulmonary surfactant levels were determined. In room air-exposed mice, T0901317 increased the expression of lipid export genes in macrophages and the whole lung and increased cholesterol efflux capacity without inducing inflammation or affecting the pulmonary surfactant. However, cigarette smoke-exposed mice treated with T0901317 showed a marked increase in BAL neutrophils, IL-1α, C-C motif chemokine ligand 2, and granulocyte-colony-stimulating factor levels. T0901317 treatment in cigarette smoke-exposed mice failed to increase the ability of alveolar macrophages to export cholesterol and markedly exacerbated IL-1α release. Finally, T0901317 led to pulmonary surfactant depletion only in cigarette smoke-exposed mice. This study shows that hyperactivation of LXR and the associated lipid capture/export mechanisms only have minor pulmonary effects on the normal lung. However, in the context of cigarette smoke exposure, where the pulmonary surfactant is constantly oxidized, hyperactivation of LXR has dramatic adverse effects, once again showing the central role of lipid homeostasis in the pulmonary response to cigarette smoke exposure.

Short bowel syndrome develops when the remnant mass of functioning enterocytes following massive resections cannot support growth or maintain fluid-electrolyte balance and requires parenteral nutrition. Resection itself stimulates the intestine's inherent ability to adapt morphologically and functionally. The capacity to change is very much related to the high turnover rate of enterocytes and is mediated by several signals; these signals are mediated in large part by enteral nutrition. Early initiation of enteral feeding, close clinical monitoring, and ongoing assessment of intestinal adaptation are key to the prevention of irreversible intestinal failure. The length of the functional small bowel remnant is the most important variable affecting outcome. The major objective of intestinal rehabilitation programs is to achieve early oral nutritional autonomy while maintaining normal growth and nutrition status and minimizing total parenteral nutrition related comorbidities such as chronic progressive liver disease. Remarkable progress has been made in terms of survivability and quality of life, especially in the context of coordinated multidisciplinary programs, but much work remains to be done.

Background: Premature infants require high intakes of Ca and P to mimic fetal accretion rates. With the current phosphate salt used, adequate amounts cannot be provided due to the precipitation of Ca and P in TPN solutions., Objective: To compare monobasic potassium phosphate (monobasic regimen) and monobasic plus dibasic potassium phosphate (dibasic regimen) on calcium phosphate solubility in 5 amino acid products, and to determine whether solubility differences observed in these products can be explained by buffering capacity., Methods: TPN solutions were prepared according to standard clinical practice. The following amino acid products were used at 3% concentrations: Primene, Vamin N, TrophAmine, Aminosyn-PF, and Travasol. Dextrose 10%, standard electrolytes, heparin, vitamins and trace elements were added. Calcium (as gluconate) and phosphate (as monobasic or dibasic regimen) were added in one-to-one molar ratios from 0-45 mmol/L. Solutions were inspected macroscopically and microscopically for precipitation under three conditions: immediately, 24 h after preparation at room temperature, and 3 h later in a 37 degrees C water bath. Buffering capacity was determined for each amino acid product by titrating with standardized 0.1 M NaOH., Results: Variations in Ca:P solubility and buffer capacity exist between amino acid solutions. With Primene and Vamin no macroscopic or microscopic precipitation was detected up to 45 mmol/L using monobasic regimen, compared to 25 mmol/L using dibasic regimen with Trophamine. Buffer capacity did not account for the solubility differences observed between the five amino acid products, which were related to the pH of the final solution., Conclusions: These data will allow clinicians to double the current concentrations of calcium and phosphate in neonatal TPN solutions using monobasic regimen. Although this is particularly relevant to situations when fluid intake is restricted, the effect of the acid load needs to be investigated in extremely low birth weight infants.

Objective: To compare the concentrations of peroxides between adult and neonatal total parenteral nutrition (TPN) solutions in response to protection against inducers of peroxidation such as multivitamins and exposure to light or air., Methods: Peroxide concentrations were measured in freshly prepared adult and neonatal solutions of fat-free TPN in four settings: with or without an air inlet, and protected or unprotected from ambient light. An oxygen washout was performed by exposing a fat-free neonatal TPN solution to a continuous flow of nitrogen., Results: Globally, light was the main inducer of peroxides in adult and neonatal solutions. However, in adult solutions the concentration of peroxides remained <15 micromol/L, while in neonatal solutions the peroxide concentration was as high as 300 micromol/L in ambient light. Although the oxygen washout did prevent the generation of peroxides, avoiding air inlet was not as effective as was photoprotection in decreasing the important peroxide load in the neonatal TPN solution., Conclusions: The higher concentration of peroxides found in neonatal solutions compared with adult solutions is explained by the differences in nutrient composition between the two solutions. Contamination of parenteral solutions by air during compounding accounts for the photoinduced generation of peroxides in TPN solutions. It is more convenient to protect TPN solutions from light exposure after the admixture of the multivitamin solution than to avoid contact with oxygen.

In recent years, many studies have been published regarding the link between sodium intake and high blood pressure. Canadian, American and WHO Guidelines on the treatment of hypertension all indicate salt reduction as an efficient non-pharmacologic recommendation. However, due to the lack of clear and specific Canadian legislation on food labelling, consumers are not able to make informed choices of food products on the basis of salt content. The time has come for public health experts to join this debate.

Background: Light exposure induces the generation of peroxides in solutions of total parenteral nutrition (TPN). Peroxide toxicity has been documented in cell, in tissue, and in isolated organs. To decrease the infused peroxide load and to protect the quality of the parenteral nutrients, we tested the photoprotective properties of different infusion sets., Methods: Solutions of fat-free TPN and all-in-one total nutrient admixture (TNA) were run through sets of bags (clear and covered) and tubings (clear and colored: black, orange, and yellow) offering different levels of protection against light. Peroxide levels were determined by ferrous oxidation of xylenol orange, thiol functions by the 5,5,-dithiobis(2-nitrobenzoic acid) technique, and absorbance of tubings by spectroscopy., Results: Protection of only the bag had little effect on peroxide generation. In fat-free TPN solutions kept in covered bags, peroxide concentrations were 1.5 to 2 times higher when run through clear compared with colored tubings. When exposed to phototherapy or in the presence of lipids, peroxides were two to three times higher with the clear compared with the black tubing; meanwhile, orange and yellow tubings offered varying levels of protection related to their light-absorbing properties. Colored tubings offered a greater protection against the disappearance of thiol functions., Conclusions: Covering bags and using orange and yellow tubings may be a practical solution to reduce infused peroxide loads from about 400 to 100 microM. This is especially relevant in patients with an immature or a compromised antioxidant capacity or when phototherapy or preparations of TNA are used.

Objective: The purpose of this study was to determine the optimal parenteral feeding regimen for infants with compromised respiratory function., Methods: We studied the influence of varying the source of energy on respiratory gas exchange in 10 infants who were supported by mechanical ventilation and who received intravenous feedings. Two isoenergetic parenteral regimens were infused consecutively; the level of fat intake was varied inversely with that of glucose. Under similar ventilator settings, transcutaneous partial pressures of oxygen and carbon dioxide, as well as indirect calorimetry were measured during each regimen., Results: Despite the higher carbon dioxide production during the glucose-rich regimen (8.9 +/- 0.7 vs 7.9 +/- 0.4 ml/kg per minute, p < 0.05 by analysis of variance), transcutaneous partial pressure of carbon dioxide remained unaffected, suggesting ventilatory compensation as documented by the increased (p < 0.002) alveolar ventilation. This was not associated with a detectable rise in oxygen consumption, but with a significant change in partial pressure of oxygen (77 +/- 5 vs 66 +/- 3 mm Hg, p < 0.05)., Conclusions: Ventilator-dependent infants with early and mild bronchopulmonary dysplasia, who receive intravenous feedings of a moderate load of glucose-based energy, can compensate for enhanced carbon dioxide production by increasing their respiratory drive, with a beneficial effect on oxygenation compared with that observed when energy is derived from lipid-based solutions.

The objective of this study was to describe fatal occupational electrocutions that occurred in Quebec between 1981 and 1988 and propose a classification suitable for setting up a prevention agenda. Of 63 fatalities, an investigation report was available in 57 (90.5%). They all occurred among males, 70.2% of whom were under the age of 35; 49.1% were performing a task related to the construction sector. A principal factor analysis allowed classification of 90.2% of the fatalities in two categories: victims assigned to electrical tasks indoors and those assigned to non-electrical tasks outdoors. The first group (56.5% of the cases) were electrocuted by direct contact with voltage less than 10 Kvolts and the second by the intermediary of a vector with voltage above 10 Kvolts. The identification of the two patterns of electrocutions provided an additional argument for shifting recommendations for prevention from educating the workers, to reducing the electrical hazards at the source.

There is a general willingness to eliminate sulfites from the diet because of adverse reactions. Because little is known about the biological effects of these antioxidants in vivo, we compared clinical and nutritional parameters in newborn infants receiving two parenteral amino acid solutions containing either 300 mg/dl or no metabisulfite. The primary objective was to verify whether decreasing the sulfur content of parenteral nutrition would diminish the calciuria of newborn infants. In a crossover design, 18 newborn infants received two regimens differing only in their metabisulfite content. Nitrogen and mineral balances; clinical parameters such as mean heart and respiratory rates, body temperature, and transcutaneous PO2 and PCO2 (n = 7); and energy expenditure were similar in both regimens. Withdrawing bisulfites from the diet did not change calciuria, put an extra burden on the infant's metabolic adaptation, or cause short-term clinical repercussions.

The hypothesis that a high-fat parenteral regimen was beneficial for respiratory gas exchanges, in comparison with a high-glucose regimen, was tested in a paired crossover design. Ten parenterally fed newborn infants with no respiratory problems received two 5-day isoenergetic and isonitrogenous regimens that differed in their nonprotein source of energy; the level of fat intake (low fat (LF) 1 gm.kg-1.day-1; high fat (HF) 3 gm.kg-1.day-1) varied inversely with that of glucose. Continuous transcutaneous PO2 (tcPO2) and PCO2 (tcPCO2), respiratory gas exchange (indirect calorimetry), and plasma arachidonate metabolites were measured at the end of each regimen. Oxygen consumption and resting energy expenditure were not affected by modification of the source of energy. However, carbon dioxide production (VCO2) was higher during LF than during HF (6.9 +/- 0.2 vs 6.2 +/- 0.1 ml.kg-1.min-1; p less than 0.01), as was the respiratory quotient (1.08 +/- 0.02 vs 0.96 +/- 0.02; p less than 0.001). Despite the differences in VCO2, the tcPCO2 was not affected, suggesting adequate pulmonary compensation during LF, as documented by the higher minute ventilation (160 +/- 7 vs 142 +/- 5 ml.kg-1.min-1; p less than 0.01). The lower tcPO2 during the HF regimen (73.8 +/- 2.8 vs 68.8 +/- 2.6 mm Hg; p less than 0.015) indicated a disturbance at the alveolocapillary level induced by the lipid emulsion. No differences were found in circulating levels of prostaglandins and thromboxanes. The substitution of glucose for lipid did not modify fat storage (2.1 +/- 0.3 vs 2.1 +/- 0.3 gm.kg-1.day-1). We conclude that the supposed beneficial effect of a fat emulsion on respiratory gas exchange is questionable.

Because the monobasic potassium phosphate salt (monobasic) improves the solubility of calcium and phosphorus in amino acid plus dextrose solutions, compared with the current mixtures of monobasic plus dibasic salts (dibasic), we tested the bioavailability and clinical effects of monobasic in 16 parenterally fed low birth weight infants at standard (n = 8) and high levels (n = 8) of mineral intakes. A constant infusion of macronutrients and vitamin D was provided in a crossover design of two four-day periods. With standard intakes of calcium (35 mg/kg/day, 0.9 mmol/kg/day) and phosphorus (30 mg/kg/day, 1 mmol/kg/day), there was no difference between monobasic and dibasic regimens on balance data or plasma biochemical monitoring (calcium, phosphorus, pH, carbon dioxide pressure, base excess, 1,25-dihydroxyvitamin D, 25-hydroxyvitamin D). With the use of the monobasic regimen, the mineral intakes were doubled without precipitation in the infusate: calcium, 70 mg/kg/day (1.8 mmol/kg/day), and phosphorus, 55 mg/kg/day (1.7 mmol/kg/day). This led to increased apparent retention of both calcium (63 +/- 5 mg/kg/day, 1.58 +/- 0.12 mmol/kg/day) and phosphorus (52 +/- 4 mg/kg/day, 1.67 +/- 0.14 mmol/kg/day) compared with that for standard levels of mineral intake. The improvement of calcium-phosphorus balance was accompanied by more severe calciuria (9 +/- 2 mg/kg/day, 0.2 +/- 0.05 mmol/kg/day) and by metabolic compensation for an increased acid load. In addition to the possibility of exceeding the buffering capacity of the infant, this relative acidosis could also be evidence of improved bone mineralization.

The reliability of shorter nitrogen balance determinations was evaluated in order to facilitate the nutritional assessment of parenterally fed infants. The intraindividual day-to-day variations of nitrogen intake, excretion, and retention were analyzed in 23 parenterally fed newborn infants (birth weight: 785-2630 g). Nitrogen retentions measured over 3 consecutive days were highly correlated (r = 0.90-0.96), and the reliability for a single 24-hr collection was estimated by r1 = 0.93. Nitrogen balance data obtained over a 24-hr period are reliable for the purpose of clinical investigations, provided the nutrient intake is constant.

Carbohydrate and lipid intakes have both been found to modulate the metabolism of long-chain fatty acids. To define the respective influence of these two energy substrates on plasma fatty acid concentrations, 32 studies were performed in 16 parenterally fed newborn infants (mean +/- SEM, birth wt: 2.15 +/- 0.1 kg, age: 10 +/- 1 d). In a paired cross-over design, the infants received for a given level of energy (60 versus 80 kcal/kg/d) two 6-d isonitrogenous and isocaloric regimens constructed so that the level of fat intake, 1 or 3 g/kg/d varied inversely with that of glucose. Total plasma fatty acid levels did not reflect the composition of the emulsion and varied with energy substrates. Plasma levels of three fatty acids rose inversely to the lipid intake, during the high glucose regimen: 16:1w7, 20:3w9 biologic markers of essential fatty acid deficiency, and 20:3w6 a derivative of 18:2w6. Glucose intake could exert its influence on 20:3w9 and 20:3w6 via insulin, an activator of delta 6 desaturase. Both glucose and fat should be taken into account when evaluating plasma fatty acid profile.

The nitrogen retention and plasma amino acid concentration were determined in eight preterm infants (mean birth weight 970 +/- 130 g; mean gestational age 28 +/- 1 weeks) receiving successively total parenteral nutrition and their own mother's milk. The nitrogen retention during both regimens was comparable to the fetal accretion rate. Plasma amino acid concentrations were lower during the enteral phase of the study than during parenteral nutrition. The metabolic response of small preterm infants is related to the quality of amino acids as well as to the route of intake.

To evaluate the influence of amino acid preparations on the metabolic response of parenterally fed immature newborn infants, nitrogen retention and plasma amino acid concentrations were compared in very-low-birth-weight infants given two parenteral regimens differing only by the composition of the infused amino acids (Travasol 10% blend B and Vamin 7%). The intakes of fluid, nitrogen, and calories were comparable. The nitrogen retention was 72% +/- 7% with Vamin and 65% +/- 6% with Travasol. The differences in plasma amino acid concentrations were consistent with the composition of the amino acid solutions. During the infusion of Vamin the increased intake of aromatic amino acids resulted in high plasma levels of tyrosine (256 +/- 233 mumol/L, range 67 to 894 mumol/L). The infusion of Travasol resulted in high plasma levels of methionine (114 +/- 39 mumol/L, range 53 to 260 mumol/L) and an elevated load of glycine, which was accompanied by an abnormally high urinary loss of this amino acid. Despite these metabolic imbalances, the growth rate over the whole study was adequate. These results emphasize the importance of the composition of amino acid solutions on the metabolic response of the very immature preterm infant.

To evaluate the metabolic and clinical consequences of changing from high-glucose to high-fat regimens during initiation of parenteral nutrition, we performed 22 studies in 11 newborn infants (birth weight (mean +/- SD) 2.54 +/- 0.54 kg, gestational age 37 +/- 3 weeks, postnatal age 8 +/- 3 days) maintained in a constant thermal environment. In a paired design, two isoproteinic (2.4 +/- 0.2 gm/kg/day) and isocaloric (64 +/- 6 kcal/kg/day) regimens differing by source of energy (high glucose vs high lipid) were infused on consecutive days. Environmental and body temperatures were recorded during a 4-hour period, and 24-hour urinary excretions of catecholamines, nitrogen, and C peptide were measured. Despite constant incubator and average skin temperatures, the rectal and interscapular temperatures rose significantly when the high-glucose regimen was changed to a high-lipid regimen. The specific locations of these changes in body temperature suggested brown fat activation. A significant drop in nitrogen retention (63 +/- 9% vs 56 +/- 10%) during the lipid infusion could be further evidence of a metabolic adaptation to the rapid change in energy substrates.