Temperament and body weight from ages 4 to 15 years.

BACKGROUND/OBJECTIVES: In adulthood, conscientiousness and neuroticism are correlates of body weight and weight gain. The present research examines whether the childhood antecedents of these traits, persistence and negative reactivity, respectively, are associated with weight gain across childhood. We likewise examine sociability as a predictor of childhood weight gain and whether these three traits are associated with weight concerns and weight-management strategies in adolescence. SUBJECTS/METHODS: Participants (N=4153) were drawn from the Longitudinal Study of Australian Children, an ongoing, population-based study of child and family health and well-being. At the baseline assessment, caregivers reported on their child's temperament. At every assessment from ages 4-5 to 14-15 years, study children were weighed and measured by trained staff; there were up to six biennial assessments of body mass index and waist circumference. At ages 14-15 years, study children (n=2975) also self-reported on their weight concerns and weight-management strategies. RESULTS: Study children rated lower in persistence or higher in negative reactivity in early childhood gained more weight between the ages of 4 and 15 years. Sociability was associated with weight gain among girls but not among boys. Lower persistence and higher negative reactivity at ages 4-5 years were also associated with greater weight concerns, restrained eating and use of unhealthy weight-management strategies at ages 14-15 years. CONCLUSIONS: Childhood traits related to conscientiousness and neuroticism are associated with objective weight gain across childhood and with concerns and strategies to manage weight in adolescence. These results are consistent with a lifespan perspective that indicates that trait psychological functioning contributes to health-related markers from childhood through old age.

Photolysis of formaldehyde as a hydrogen atom source in the lower atmosphere.

The rates of formaldehyde photodecomposition into hydrogen and formyl radicals and hydrogen and carbon monoxide molecules in sunlightirradiated atmospheres have been estimated from extinction data and photochemical results. These data should prove useful in the development of models for the chemical changes that take place in the polluted atmosphere.

Interleukin 1 alpha (IL-1) and macrophage colony-stimulating factor (M-CSF) accelerate recovery from multiple drug-induced myelosuppression.

Interleukin 1 alpha (IL-1) and macrophage colony-stimulating factor (M-CSF) interact synergistically to enhance the restoration of stem and progenitor subpopulations in murine marrow and, vis-a-vis, to accelerate hematopoietic recovery in 5FU myelosuppressed mice. Similarly, IL-1 is reported to accelerate recovery following myelosuppressive treatment with doxorubicin (AdR), cis-platinum (DDP) and cyclophosphamide (CTx). Studies were carried out in C57Bl/6 mice in order to determine whether IL-1 (+/- M-CSF) intervention was as effective against the myelosuppression experienced following 5FU-based multiple drug combinations. Maximal-tolerated doses (MTD) of AdR (10 mg/kg), DDP (8 mg/kg) or CTx (250 mg/kg) were administered either alone or in combination with 150 mg/kg 5FU. Cytokine intervention (q24 hours x 2) was initiated 24 hours later. Hematopoietic recovery was assessed by measuring the femoral content of the more primitive [IL-1 + IL-3 + M-CSF-responsive] HPP-CFC and the total granulocyte levels in the animals over a ten-day interval following treatment. MTDs of AdR, DDP and CTx, when compared with 5FU, produced only marginal levels of myelosuppression. As a result, cytokine intervention in animals treated with AdR, DDP or CTx resulted in only a modest, transient increase in the HPP-CFC and total granulocyte subpopulations when compared with their effect on 5FU--treated animals. Neither AdR, DDP nor CTx interacted with 5FU to significantly increase the cytotoxic effects of 5FU on the HPP-CFC or granulocyte subpopulations, and both IL-1 and IL-1 + M-CSF effectively stimulated hematopoietic recovery in all animals that received the 5FU--based drug combinations. However, the significant advantage (p < 0.05) achieved by combining IL-1 + M-CSF (vs. IL-1 alone) was only observed in animals that were treated with 5FU and either AdR or DDP. Furthermore, the initial stimulation of HPP-CFC recovery by IL-1 + M-CSF in animals that received DDP + 5FU, when compared with 5FU alone, was subsequently dampened. Although there were subtle, drug-related differences in the temporal response of the more primitive HPP-CFC and granulocyte populations to cytokine therapy, the data from this study demonstrated that abbreviated cytokine interaction can effectively accelerate hematopoietic recovery after combination drug therapy.

Campylobacter colitis in ranch mink in Ontario.

Outbreaks of colitis, where Campylobacter jejuni and Campylobacter coli were the only pathogens isolated occurred in weanling mink (Mustella vision) on two commercial mink ranches in Ontario. Lesions were restricted to the proximal colon and were characterized by multiple 1 mm focal or 1 mm linear erosions/ulcers in the region 2 cm distal to the ileal-colonic junction. Histological changes included thickening of the colonic mucosa, inflammatory cell infiltrate in the lamina propria and submucosa, cellular debris and inflammatory exudate within cryptal lumens and multiple areas of mucosal erosion/ulceration. Four C. jejuni negative mink were challenged with 5.1 X 10(9) colony forming units of C. jejuni by oral inoculation. Three of four experimentally infected mink developed diarrhea by day 4 postinfection with lesions grossly and microscopically similar to mink in the naturally occurring outbreak. Examination of lesions by transmission electron microscope failed to show evidence of C. jejuni invasion of intestinal epithelium. Feeding uncooked slaughterhouse chicken offal was the likely source of C. jejuni in the naturally occurring outbreaks.

Quinacrine binds to the lipid-protein interface of the Torpedo acetylcholine receptor: a fluorescence study.

It has been argued both that there is a high affinity noncompetitive inhibitor binding site in the lumen of the acetylcholine receptor and that this lumen exists on the central axis of the receptor. Such a site would be expected to be 20-40 A from the membrane lipids. We tested whether, in fact, quinacrine, a potent fluorescent noncompetitive inhibitor, binds to such a site. We measured quenching of receptor-bound quinacrine fluorescence by fluorescence dipolar energy transfer to lipid probes, 5-(N-dodecanoylamino)eosin and N-(3-sulfopropyl)-4-(p-didecylaminostyryl)pyridinium, or by collision with paramagnetic lipid probes 2,2,6,6-tetramethylpiperidine-1-oxyl and 3-doxyl-17 beta-hydroxy-5 alpha-androstane (spin-labeled androstane). Initial control experiments established that in the presence of carbamylcholine, quinacrine binds to a phencyclidine-sensitive site on the Torpedo receptor with a Kd equal to 0.14 microM and with a quantum yield of 0.18. Fluorescence energy transfer from receptor-bound quinacrine had a magnitude consistent with quinacrine being less than 10 A from the lipid fluorescent probes. 2,2,6,6-Tetramethylpiperidine-1-oxyl and spin-labeled androstane were two to five times more effective at quenching receptor-bound quinacrine fluorescence than the fluorescence from membrane-partitioned 5-(dodecanoylamino)fluorescein. These results suggest that the quinacrine binding site is too close to the lipid domain to be in the lumen of the receptor, and therefore it is probably located on the outer surface of the membrane-spanning domain of the acetylcholine receptor.

Identification of cyclic ADP-ribose-binding proteins by photoaffinity labeling.

We have synthesized 8-azido-cyclic ADP-ribose (8N3-cADPR) and [32P]8-azido-cyclic ADP-ribose ([32P]8N3-cADPR) in order to characterize cyclic ADP-ribose-(cADPR) binding sites in sea urchin egg homogenates. 8N3-cADPR was an antagonist of cADPR since it did not induce Ca2+ release from egg microsomes but did inhibit the ability of cADPR to do so. The effect of 8N3-cADPR was reversible and could be overcome by high concentrations of cADPR, suggesting that both were acting on the same site. This was supported by the fact that 8N3-cADPR effectively competed for [32P]cADPR binding to microsomes. Reciprocally, binding of [32P]8N3-cADPR could also be selectively displaced by cADPR and 8N3-cADPR, but not by ADP-ribose. These results indicate that 8N3-cADPR binds specifically to the cADPR-binding sites and inhibits cADPR from releasing Ca2+. Photolysis of microsomes preincubated with [32P]8N3-cADPR resulted in specific labeling of proteins of 140 and 100 kDa, which could be prevented by 8N3-cADPR or nanomolar concentrations of cADPR, but not by micromolar concentrations of ADP-ribose, AMP, ADP, ATP, cyclic AMP or inositol 1,4,5-trisphosphate. Caffeine, an agonist of Ca(2+)-induced Ca2+ release, preferentially inhibited the labeling of the 100 kDa as compared to the 140-kDa protein. These results suggest that cADPR may not interact directly with the ryanodine receptor, but may instead, exert its effect through intermediate proteins.

Modulation of phencyclidine-sensitive ethidium binding to the Torpedo acetylcholine receptor: interaction of noncompetitive inhibitors with carbamylcholine and cobra alpha-toxin.

Ethidium is one of two fluorescent ligands known to bind to the noncompetitive inhibitor (NCI) site in the central ion channel of the Torpedo acetylcholine receptor with a micromolar dissociation constant. To further characterize heterotropic allosteric regulation of ligand binding in general, and of ethidium binding in particular, to the Torpedo receptor, we measured the effects of three liquid anesthetics (diethyl ether, halothane, and butanol), two barbiturates (secobarbital and thiamylal), and urethane. The phencyclidine-sensitive chromatic shift and the quantum yield increase associated with ethidium binding to the channel NCI site were used as indicators of ethidium binding. In the absence of other ligands, halothane, diethyl ether, and butanol increased the affinity of ethidium toward the channel NCI site to the same extent as carbamylcholine (400-600-fold), whereas the barbiturates and urethane were without effect. Cobra alpha-toxin blocked anesthetic-induced ethidium binding, confirming that cobra alpha-toxin stabilizes the AcChR in the resting-like state. In the presence of carbamylcholine, when ethidium was bound to the channel NCI site, several ligand-dependent effects were observed. 1) Without affecting further the affinity of ethidium for the NCI binding site, diethyl ether and halothane increased and butanol had no effect on the fluorescence emission of channel-bound ethidium. This indicated that there is little relation between the affinity and the quantum yield of the channel-bound ethidium. 2) Addition of secobarbital and thiamylal had no effect, beyond the effect of carbamylcholine, on ethidium binding to the channel NCI site, indicating that the barbiturates did not bind to the channel NCI site. 3) Urethane inhibited carbamylcholine-induced ethidium binding to the channel NCI binding site, suggesting direct interaction of urethane with the channel NCI binding site, at least when the receptor is in a desensitized state. The results confirm the conformational sensitivity of ethidium binding to the channel NCI binding site and demonstrate at least three different modes of action of anesthetics to inhibit the Torpedo receptor noncompetitively.

Effect of polyethylene glycol on lipid peroxidation in cold-stored rat hepatocytes.

A mechanism suggested to cause injury to preserved organs is the generation of oxygen free radicals either during the cold-storage period or after transplantation (reperfusion). Oxygen free radicals can cause peroxidation of lipids and alter the structural and functional properties of the cell membranes. Methods to suppress generation of oxygen free radicals of suppression of lipid peroxidation may lead to improved methods of organ preservation. In this study we determined how cold storage of rat hepatocytes affected lipid peroxidation by measuring thiobarbituric acid reactive products (malondialdehyde, MDA). Hepatocytes were stored in the UW solution +/- glutathione (GSH) or +/- polyethylene glycol (PEG) for up to 96 h and rewarmed (resuspended in a physiologically balanced saline solution and incubated at 37 degrees C under an atmosphere of oxygen) after each day of storage. Hepatocytes rewarmed after storage in the UW solution not containing PEG or GSH showed a nearly linear increase in MDA production with time of storage and contained 1.618 +/- 0.731 nmol MDA/mg protein after 96 h. When the storage solution contained PEG and GSH there was no significant increase in MDA production after up to 72 h of storage and at 96 h MDA was 0.827 +/- 0.564 nmol/mg protein. When freshly isolated hepatocytes were incubated (37 degrees C) in the presence of iron (160 microM) MDA formation was maximally stimulated (3.314 +/- 0.941 nmol/mg protein). When hepatocytes were stored in the presence of PEG there was a decrease in the capability of iron to maximally stimulate lipid peroxidation. The decrease in iron-stimulated MDA production was dependent upon the time of storage in PEG (1.773 nmol/mg protein at 24 h and 0.752 nmol/mg protein at 48 h).(ABSTRACT TRUNCATED AT 250 WORDS)

Response to rimiterol and salbutamol aerosols administered by intermittent positive-pressure ventilation.

The bronchodilator and cardiac effects produced by aerosols of 0.5% salbutamol and 0.5% and 1% rimiterol administered for three minutes in 40% oxygen by intermittent positive-pressure ventilation (I.P.P.V.) were compared in 15 asthmatic patients. Salbutamol and both the concentrations of rimiterol were equipotent in peak bronchodilator effect, but salbutamol had a significantly longer duration of bronchodilator action. There was significantly less increase in heart rate after rimiterol than after salbutamol. Aerosols of 0.5% rimiterol, 0.5% salbutamol, and saline were administered by I.P.P.V. to 10 normal volunteers. There was no difference between the mean heart rates after 0.5% rimiterol and saline but a highly significant increase in mean heart rate was observed after 0.5% salbutamol. It was concluded that 0.5% rimiterol was an effective short-acting bronchodilator drug with little or no cardiac beta(1)-adrenergic activity when administered for three minutes by I.P.P.V. in 40% oxygen.

[Glycogen storage of the liver: a determining factor of initial function of the hepatic graft]. / Réserves glycogéniques du foie: un facteur déterminant de la fonction initiale du greffon hépatique.

In this study we have investigated the effects of hepatocytes glycogen storage on the quality of livers for transplantation. Rats were fed or fasted for 24 h and hepatocytes isolated and cold stored in UW solution for 24 and 48 hours. Viability of the cells was analyzed by LDH release after 2 hours incubation in L15 with O2. Also, rabbits were fed, fasted (48 h) or glucose fed (48 h) and livers cold stored for 6, 24 and 48 h in UW solution. Functions of the livers were analyzed by isolated perfusion for 2 hours. Hepatocytes from fasted rats released significantly more LDH than hepatocytes from fed rats after 24 and 48 h cold storage. In rabbit livers, fasting depleted glycogen by 85% but had no effect on ATP or glutathione concentration. Livers from fasted rabbits produced similar amount of bile, released similar concentrations of lactate dehydrogenase and aspartate transaminase into the perfusate, maintained similar concentrations of glutathione after 24 hours preservation when compared to fed animals. After 48 h preservation livers from fasted animals were less viable than livers from fed animals and the decrease of liver functions in livers from fasted animals preserved for 48 hours was prevented by feeding glucose. This study shows that liver glycogen storage in hepatocyte is an important metabolite for successful liver preservation. Glycogen may be a source for ATP and antioxydant synthesis during the early period of reperfusion.

Hypothermic preservation of hepatocytes. III. Effects of resuspension media on viability after up to 7 days of storage.

Hepatocyte suspensions provide a rapid method to determine how hypothermic storage affects liver cell metabolism and viability. Using these studies, improved methods of hypothermic liver preservation for transplantation may be developed. In this study, rat hepatocytes were cold-stored for up to 7 days in University of Wisconsin liver preservation solution. At the end of each day of storage hepatocytes were resuspended in Krebs-Henseleit buffer or tissue-culture medium (Liebovitz-15; Fischer's; modified Fischer's, which was similar to Fischer's but with glycine and cysteine added; or Waymouth's medium). Hepatocyte viability was assessed by rewarming and oxygenating the suspensions and measuring the percentage of leakage of lactate dehydrogenase from the cells, the cellular concentration of potassium and the stimulation of respiration by succinate, all measures of plasma membrane integrity. Additionally, concentrations of ATP and glutathione after rewarming and reoxygenation in the various resuspension media were measured. Hepatocyte permeability to lactate dehydrogenase did not increase during cold storage of 1 to 7 days (7.2% +/- 2% leakage), indicating that most of the hepatocytes remained viable during cold storage. However, when rewarmed, loss of viability (leakage of lactate dehydrogenase) was dependent on the composition of the resuspension media. In Krebs-Henseleit buffer, viability was reduced after 2 and 3 days of storage (lactate dehydrogenase leakage on rewarming = 70% to 90%). Leakage of lactate dehydrogenase was reduced significantly after resuspension in tissue-culture media. After 6 days of storage, lactate dehydrogenase leakage from hepatocytes stored in Liebovitz- 15 or modified Fischer's was only about 30%.(ABSTRACT TRUNCATED AT 250 WORDS)