Factors affecting body composition in preterm infants: Assessment techniques and nutritional interventions.

Limited research has been conducted that elucidates the growth and body composition of preterm infants. It is known that these infants do not necessarily achieve extra-utero growth rates and body composition similar to those of their term counterparts. Preterm infants, who have difficulty in achieving these growth rates, could suffer from growth failure. These infants display an increased intra-abdominal adiposity and abnormal body composition when they achieve catch-up growth. These factors affect the quality of weight gain, as these infants are not only shorter and lighter than term infants, they also have more fat mass (FM) and less fat-free mass (FFM), resulting in a higher total fat percentage. This could cause metabolic syndrome and cardiovascular problems to develop later in a preterm infant's life. The methods used to determine body composition in preterm infants should be simple, quick, non-invasive and inexpensive. Available literature was reviewed and the Dauncey anthropometric model, which includes skinfold thickness at two primary sites and nine body dimensions, is considered in this review the best method to accurately determine body composition in preterm infants, especially in resource-poor countries. It is imperative to accurately assess the quality of growth and body composition of this fragile population in order to determine whether currently prescribed nutritional interventions are beneficial to the overall nutritional status and quality of life-in the short- and long-term-of the preterm infant, and to enable timely implementation of appropriate interventions, if required.

Changes in body mass and metabolic profiles in patients with first-episode schizophrenia treated for 12 months with a first-generation antipsychotic.

OBJECTIVES: To assess changes in body mass and metabolic profiles in patients with first-episode schizophrenia receiving standardised, assured treatment and to identify predictors and moderators of the effects. METHODS: We investigated the changes in body mass, fasting blood glucose and lipids in 107 largely antipsychotic naïve, first-episode schizophrenia patients who were treated according to a standard algorithm with long-acting injectable flupenthixol decanoate over 12 months. RESULTS: Eighty-three (78%) participants completed the 12 months of treatment, and 104 (97%) received 100% of the prescribed injections during their participation. There were significant increases in BMI (P<.0001), waist circumference (P=0.0006) and triglycerides (P=0.03) and decrease in HDL (P=0.005), while systolic (P=0.7) and diastolic blood pressure (P=0.8), LDL (P=0.1), cholesterol (P=0.3), and glucose (P=0.9) values did not change over time. The triglyceride: HDL ratio increased by 91%. Change in BMI was only correlated with change in triglycerides (P=.008). The only significant predictor of BMI increase was non-substance abuse (P=.002). CONCLUSIONS: The risks of weight gain and metabolic syndrome associated with antipsychotic treatment in first-episode schizophrenia are not restricted to second generation antipsychotics. This is a global problem, and developing communities may be particularly susceptible.

Tetramethylpiperidine-substituted phenazines inhibit the proliferation of intrinsically multidrug resistant carcinoma cell lines.

The effects of nine new tetramethylpiperidine (TMP)-substituted phenazines on the growth of a human esophageal cancer cell line (WHCO3), two human hepatocellular carcinoma cell lines (PLC and HepG2) and three human colon cancer cell lines (CaCo2, COLO 320DM and HT29) were compared to those of clofazimine, B669 and five standard chemotherapeutic agents. The three most active TMP-substituted phenazines against these cell lines were B3962, B4126 and B4125 with mean IC50 values for all the cancer cell lines tested of 0.36, 0.47 and 0.48 microg/ml respectively. B3962 and B4126, but not B4125 were also the most active against a semi-continuous human fibroblast culture (MRC5). The compound with the highest tumor specificity relative to the fibroblast culture, was B4125. Importantly, there was minimal variation in sensitivity of the different cell lines, including a multidrug resistant cell line (COLO 320DM) expressing high levels of P-glycoprotein, to the TMP-substituted phenazines. This was not the case with the standard chemotherapeutic agents. The efficacy of compounds such as B4125 against a broad spectrum of multidrug resistant cancer cell lines, together with their relatively high tumor specificity, suggests that these agents may be useful in the treatment of intrinsically resistant cancers such as colon and liver cancer.

Clindamycin, erythromycin, and roxithromycin inhibit the proinflammatory interactions of Pseudomonas aeruginosa pigments with human neutrophils in vitro.

The Pseudomonas aeruginosa-derived phenazine pigments pyocyanin and 1-hydroxyphenazine (1-hp) prime human neutrophils for enhanced, stimulus-activated release of superoxide and myeloperoxidase (MPO), respectively. In the present study, the modulatory potentials of the antimicrobial agents clindamycin, erythromycin, and roxithromycin (10 and 20 micrograms/ml) on the prooxidative interactions of pyocyanin and 1-hp (12.5 microM) with human neutrophils have been investigated. Clindamycin, erythromycin, and especially roxithromycin caused dose-related inhibition of the generation of superoxide by both untreated and pyocyanin-treated neutrophils during activation with either the synthetic chemotactic tripeptide N-formyl-L-methionyl-L-leucyl-L-phenylalanine (FMLP) or the calcium ionophore A23187. The antimicrobial agents also inhibited the generation of reactive oxidants by the MPO-H2O2-halide system during activation of both untreated and 1-hp-treated neutrophils by FMLP. These effects appeared to be due to drug-related interference with membrane-associated oxidative metabolism, since none of the antimicrobial agents inhibited the release of MPO by activated neutrophils, nor did they possess oxidant-scavenging properties. These data demonstrate that clindamycin, erythromycin, and especially roxithromycin antagonize the proinflammatory interactions of pyocyanin and 1-hp with neutrophils and indicate a possible therapeutic role for these antimicrobial agents in the prevention of tissue damage in diseases characterized by P. aeruginosa infection.

Proinflammatory interactions of pyocyanin and 1-hydroxyphenazine with human neutrophils in vitro.

The effects of the Pseudomonas aeruginosa-derived pigments, pyocyanin and 1-hydroxyphenazine (1-hp), on membrane-associated oxidative metabolism and release of lysozomal enzymes by human neutrophils were investigated in vitro. Pyocyanin, but not 1-hp, increased the generation of superoxide and the rate and duration of oxygen uptake by activated neutrophils. Both agents increased the myeloperoxidase-mediated iodinating activity of neutrophils, which in the case of 1-hp was due to stimulation of the release of myeloperoxidase by activated neutrophils. 1-hp also increased the release of lysozyme by activated neutrophils. Pyocyanin caused only slight enhancement of the release of myeloperoxidase and lysozyme by stimulated neutrophils but was more potent with respect to the release of the specific granule marker, vitamin B12-binding protein. These data indicate the existence of diverse, proinflammatory interactions of pyocyanin and 1-hp with human phagocytes, which may intensify neutrophil-mediated tissue damage during P. aeruginosa infections.