What features of a nutrition resource are important to adolescents of a low socioeconomic status?

OBJECTIVE: To identify the key features of a nutrition resource that are important to adolescents of a low socioeconomic status (SES). DESIGN: Structured interviews were conducted to explore participants' preferences relating to the features of a nutrition resource. Thematic framework analysis was used to determine key themes, subthemes and concepts from the data. SETTING: Streetsport activity sessions, north-east of Scotland. PARTICIPANTS: Eighteen adolescents aged 12-17 years from a low socioeconomic background. RESULTS: The overarching themes identified were barriers and facilitators to engagement with a nutrition resource. Adolescents expressed a preference for an app, and this was mainly attributed to convenience and low cost. There was also an emphasis on the integral role social media has in their lives. Aesthetics was a facilitator for both male and female participants, with a particular focus on weight loss. Behaviour change support, including reminders, access to simple recipes and adopting a 'small change approach', were identified as possible facilitators, whereas cost, environmental influences, and existing eating habits were identified as possible barriers to engaging with a nutrition resource. CONCLUSIONS: A number of subthemes, including aesthetics, cost and convenience, which have previously been reported in adolescents with a higher SES, were prominent in our research. The present study contributes to insights relating to behaviour change tools that should be considered when developing a nutrition resource targeting disadvantaged adolescents. Further research focusing on how mobile phone technology and social media can be utilised to support dietary behaviour change in low SES adolescents is recommended.

The capsaicin analogue SDZ249-665 attenuates the hyper-reflexia and referred hyperalgesia associated with inflammation of the rat urinary bladder.

This study assessed the effects of the systemically administered capsaicin analogue SDZ249-665 in an animal model of visceral pain and hyper-reflexia. The effects of prophylactic administration of SDZ249-665 (in the dose range 0.05-1 mg/kg) on the viscero-visceral hyper-reflexia (VVH) and the referred viscero-somatic hyperalgesia to mechanical stimuli (VSH) associated with turpentine inflammation of the rat urinary bladder were evaluated. SDZ249-665 attenuated both the VVH and the VSH in a dose related fashion. In the VVH model, following solvent control administration, intra-vesical turpentine administration was associated with a significant reduction in micturition threshold to 43.7% (SEM 6.3) of baseline, indicating the presence of a VVH. This effect was not observed when animals were prophylactically treated with SDZ249-665 alone. At a dose of 0.1 mg/kg the micturition threshold was 90.7% (SEM 10.2) of baseline at 1 h after intra-vesical instillation of turpentine. In the VSH model, curves were plotted of the difference in fore and hind limb withdrawal latencies from a mechanical stimulus and the area under these curves (AUCs) were compared between different treatment protocols. Intra-vesical turpentine was associated with a negative deflection of the curve (AUC -5.2x10(3) SEM 1.7) in comparison with naïve animals (AUC -0.02x10(3) SEM 0.6), indicative of a referred hyperalgesia. This was prevented, in a dose-related manner, by prophylactic administration of SDZ249-665. For example, at a dose of 0.5 mg/kg the AUC was +0.4x10(3) (SEM 0.8). These findings support previous work indicating that capsaicin sensitive neurones participate in patho-physiological events occurring following inflammation of the bladder, and provides evidence that systemically active capsaicin based compounds may be developed for use in the clinical setting.

Combinatorial RNA interference indicates GLH-4 can compensate for GLH-1; these two P granule components are critical for fertility in C. elegans.

We report that four putative germline RNA helicases, GLHs, are components of the germline-specific P granules in Caenorhabditis elegans. GLH-3 and GLH-4, newly discovered, belong to a multi-gene glh family. Although GLHs are homologous to Drosophila VASA, a polar granule component necessary for oogenesis and embryonic pattern formation, the GLHs are distinguished by containing multiple CCHC zinc fingers. RNA-mediated interference (RNAi) reveals the GLHs are critical for oogenesis. By RNAi at 20 degrees C, when either loss of GLH-1 or GLH-4 alone has no effect, loss of both GLH-1 and GLH-4 results in 97% sterility in the glh-1/4(RNAi) offspring of injected hermaphrodites. glh-1/4(RNAi) germlines are under-proliferated and are without oocytes. glh-1/4(RNAi) animals produce sperm; however, spermatogenesis is delayed and the sperm are defective. P granules are still present in glh-1/4(RNAi) sterile worms as revealed with antibodies against the remaining GLH-2 and GLH-3 proteins, indicating the GLHs function independently in P granule assembly. These studies reveal that C.elegans can use GLH-1 or GLH-4 to promote germline development.

Hmg-coA reductase gene family in cotton (Gossypium hirsutum L.): unique structural features and differential expression of hmg2 potentially associated with synthesis of specific isoprenoids in developing embryos.

As a first step towards understanding the biosynthesis of isoprenoids that accumulate in specialized pigment glands of cotton at the molecular level, two full-length genes (hmg1 and hmg2) were characterized encoding hmg-coA reductase (HMGR; EC 1.1.1.34), the enzyme that catalyzes the formation of a key isoprenoid precursor. Cotton hmgr genes exhibited features typical of other plant genes, however, hmg2 encodes the largest of all plant HMGR enzymes described to date. HMG2 contains several novel features that may represent functional specialization of this particular HMGR isoform. Such features include a unique 42 amino acid sequence located in the region separating the N-terminal domain and C-terminal catalytic domain, as well as an N-terminal hydrophobic domain that is not found in HMG1 or other HMGR enzymes. DNA blot analysis revealed that hmg1 and hmg2 belong to small subfamilies that probably include homeologous loci in allotetraploid cotton (Gossypium hirsutum L.). Ribonuclease protection assays revealed that hmg1 and hmg2 are differentially expressed in a developmentally- and spatially-modulated manner during morphogenesis of specialized terpenoid-containing pigment glands in embryos. Induced expression of hmg2 coincided with a possible commitment to sesquiterpenoid biosynthesis in developing embryos, although other developmental processes also requiring HMGR cannot be excluded.

Inflammation of the rat urinary bladder is associated with a referred thermal hyperalgesia which is nerve growth factor dependent.

We have assessed whether a referred somatic hyperalgesia to thermal stimulation of the hind limb of rats occurs after inflammation of the urinary bladder. Furthermore, we evaluated whether any such viscero-somatic hyperalgesia (VSH) is dependent on the neurotrophin nerve growth factor (NGF). Limb withdrawal thresholds from thermal stimulation of both fore and hind limbs were assessed simultaneously at baseline and at fixed times for 24 h after various interventions. After plotting curves for the difference in withdrawal time of fore and hind limbs against time, the area under the curve (AUC) was calculated to provide a single measure over the 24-h period. A negative value indicated relative hyperalgesia of the hind limb. With simple catheterization, although there was a trend towards hind limb hyperalgesia, there was no significant difference in this AUC (mean -100.5) compared with naïve control animals (mean AUC +53.6). However, inflammation with 50% turpentine oil was associated with a significant change in AUC (mean -676.8), indicative of relative hyperalgesia of the hind limb. This hyperalgesia was mimicked by intra-vesical instillation of NGF (in place of turpentine) (mean AUC -1418.3 while mean AUC in naïve animals was +439.4). Furthermore, prior administration of an NGF sequestering molecule, trkA-IgG, attenuated turpentine-induced VSH. These findings increase our knowledge of the nature of visceral and referred pain and further implicate NGF in the hyperalgesic response to inflammation of the urinary bladder.

Prenatal ethanol exposure selectively reduces the mRNA encoding alpha-1 thyroid hormone receptor in fetal rat brain.

Some of the developmental defects characteristic of congenital or experimental hypothyroidism are also observed in children or experimental animals prenatally exposed to ethanol, suggesting that a subset of neurological defects attributable to ethanol exposure are produced by interfering with thyroid hormone action. In this article, we tested whether an ethanol treatment regimen known to produce neurological damage in rats can alter the expression of the mRNAs encoding the thyroid hormone receptor isoforms (TR alpha-1, TR alpha-2, and TR beta-1) in the fetal rat brain neocortex and hippocampus. Rats were fed an ethanol-containing diet beginning on gestational day (G) 6 and continuing until sacrifice on G15, G17, or G21; controls included animals pair-fed a liquid control diet or fed lab chow. Ethanol selectively reduced the expression of TR alpha-1 mRNA in the neocortex and hippocampus on G21, compared with pair-fed and control fetuses. In contrast, pair-feeding selectively reduced TR alpha-2 mRNA in both neocortex and hippocampus on G21, and increased TR beta-1 mRNA on G17. These data support the hypothesis that ethanol may interfere with thyroid hormone action during fetal brain development. In addition, these data indicate that ethanol and pair-feeding exert independent effects on thyroid hormone receptor expression in the developing brain.

Automated liver cell processing facilitates large scale isolation and purification of porcine hepatocytes.

An automated method for large scale isolation and purification of porcine hepatocytes is described. Liver cells were harvested by a two-step portal vein perfusion with ethylenediaminetetraacetate and collagenase. Hepatocyte purification was carried out using either a standard manual processing method (Procedure A) or an automated processing method using a filtration chamber and a programmable cell washer (Procedure B). Both methods produced high cell yields (Procedure A: 1.30 +/- 0.55 x 10(10) viable hepatocytes/liver; Procedure B: 1.38 +/- 0.32 x 10(10) viable hepatocytes/liver) and viability (Procedure A: 89 +/- 6.5%; Procedure B: 92 +/- 3.9%). Hepatocyte purity was significantly greater after Procedure B than after Procedure A (93.1 +/- 3.1% versus 83.1 +/- 3%, p < 0.01). Isolated hepatocytes by either method were morphologically intact, as demonstrated by transmission electron microscopy showing integrity of plasma membranes and intracellular organelles. Cultured hepatocytes isolated by either method were functionally intact, although those isolated by Procedure A showed significantly lower activity of microsomal 7-ethoxycoumarin-O-deethylase activity (p < 0.05) and mitochondrial succinate dehydrogenase activity (p < 0.01). In conclusion, use of the automated hepatocyte processing method resulted in efficient large scale preparation of porcine hepatocytes, with higher purity and greater retention of differentiated liver metabolic functions, and was found to be less time consuming and less labor intensive.

Acute prenatal ethanol exposure and luteinizing hormone-releasing hormone messenger RNA expression in the fetal mouse brain.

Ethanol exposure during critical periods of development results in alterations of central nervous system morphology and function. In this study, the effects of acute ethanol exposure on the number of neurons expressing luteinizing hormone-releasing hormone (LHRH) messenger RNA (mRNA) has been analyzed. Also, the expression of LHRH mRNA in the diagonal band of Broca/preoptic area (DBB/POA) was determined. Pregnant C57BL/6J mice were intubated with two doses of a 25% solution of ethanol or water (2.9 g/kg body weight) 4 hr apart on gestation day 7 (G7), G10, or G11. Animals were killed on G18, and in situ hybridization was utilized to detect neurons expressing LHRH mRNA. The number of neurons expressing LHRH mRNA was determined along their migration route from the rostrum into the forebrain. Ethanol exposure on G7 did not significantly change the number of neurons expressing LHRH mRNA on G18 compared with that in control animals. However, the number of neurons expressing LHRH mRNA in the nasal septum area in animals exposed to ethanol on G10 or G11 was significantly less than the number in control animals (p < 0.05). Prenatal ethanol exposure on any of the aforementioned treatment days did not alter the expression of LHRH mRNA at the level of the DBB/POA on G18 in ethanol-treated animals compared with control animals. Also, neuron-specific enolase mRNA expression at the level of the DBB/POA was not altered by prenatal ethanol exposure. Therefore, ethanol exposure on the aforementioned treatment days did not differentially affect LHRH mRNA expression compared with neuron-specific enolase mRNA expression at the level of the DBB/POA.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of in utero ethanol exposure on the development of LHRH neurons in the mouse.

Prenatal ethanol exposure has been shown to result in craniofacial malformations as well as alterations of central nervous system morphology and function. Previous studies have demonstrated that acute ethanol exposure on gestational day 7 in the developing C57BL/6J mouse resulted in craniofacial abnormalities similar to that of children with fetal alcohol syndrome. We investigated the effect of ethanol on the migration and number of immunoreactive LHRH (irLHRH) neurons in this strain of mouse. Pregnant mice were intubated with 2 doses of a 25% solution of ethanol 4 h apart on gestational day 7 (G7). Control animals were intubated with water. Animals were sacrificed on G14 or G18 and immunocytochemistry was used to identify irLHRH neurons that were visualized by light microscopy. Fetal ethanol administration did not substantially affect the migration of the LHRH neurons from the medial nasal placode into the forebrain on G14 or G18. The total number of irLHRH neurons was not significantly different on G14 in ethanol-exposed animals as compared to the number in control animals. However, the total number of irLHRH neurons on G18 was significantly less (P less than 0.03) in 4 neuroanatomical regions in fetal ethanol-exposed mice compared to those in control mice; the nasal septum, the traverse area superior to the cribriform plate and ventromedial to the olfactory bulbs, the arch area which included the olfactory tubercle, medial septal nuclei and anterior hypothalamus in G18 fetuses, and preoptic area of the brain. Coronal investigation of the number of irLHRH neurons on G18 indicates that the loss of irLHRH neurons occurred predominantly in the medial region of the rostrum and brain.

Secretory granule mediator release and generation of oxidative metabolites of arachidonic acid via Fc-IgG receptor bridging in mouse mast cells.

The releases of beta-hexosaminidase, LTC4, LTB4, and PGD2 after the bridging of Fc gamma R3 were assessed in mouse IL-3-dependent bone marrow-derived progenitor mast cells (BMMC), BMMC maintained in coculture with 3T3 fibroblasts separated by a filter to achieve maturation of the granules toward those of a serosal mast cell (SMC), and SMC that are the prototype of a mouse connective tissue mast cell. Bridging of Fc gamma R on BMMC with the 2.4G2 rat anti-Fc gamma RII/III mAb and anti-rat IgG elicited only 4% net release of beta-hexosaminidase and 4, 2, and 1 ng/10(6) cells of immunoreactive LTC4, LTB4, and PGD2, respectively. Bridging of Fc-IgE receptors (Fc epsilon R) on BMMC yielded 35% net release of beta-hexosaminidase and 9, 4, and 3 ng/10(6) cells of immunoreactive LTC4, LTB4, and PGD2, respectively. BMMC maintained in coculture responded to the bridging of Fc gamma R with statistically significant increases in the net percent release of beta-hexosaminidase to 16% and in the generation of immunoreactive LTC4 to 11 ng/10(6) cells, but without a significant change in the production of either LTB4 or PGD2. Bridging of Fc epsilon R on cocultured mast cells yielded a net percent release of beta-hexosaminidase and lipid mediator amounts and profile similar to those for BMMC. Bridging of Fc gamma R on purified mouse SMC resulted in a maximal net percent release of beta-hexosaminidase of 10% and the generation of 4, 1, and 17 ng/10(6) cells of immunoreactive LTC4, LTB4, and PGD2, respectively; the net percent release of beta-hexosaminidase and PGD2 generation were significantly greater than those obtained from BMMC. The Fc epsilon R-mediated net percent release of beta-hexosaminidase from purified SMC was 34%, with PGD2 being the predominant metabolite of arachidonic acid. That the predominant lipid mediator generated with activation by either Fc gamma R or Fc epsilon R is LTC4 for cocultured mast cells and PGD2 for SMC suggests that the mast cell phenotype rather than the receptor class being bridged determines the lipid mediator profile. The responsiveness to Fc gamma R bridging elicited by coculture of BMMC with fibroblasts in vitro and present in SMC derived in vivo relative to BMMC may relate to the previously measured increases in receptor number per cell, but may also involve the acquisition of an enhanced signal transduction capability, possibly through the increased expression of Fc gamma RIII.

Molecular cloning of gp49, a cell-surface antigen that is preferentially expressed by mouse mast cell progenitors and is a new member of the immunoglobulin superfamily.

gp49 is a Mr 49,000 glycoprotein expressed on the surface of mouse bone marrow-derived mast cells, which are progenitors for the major in vivo mast cell subclasses, typified by intestinal mucosal mast cells and serosal mast cells. The amino-terminal amino acid sequence of gp49 was determined after isolation of the solubilized membrane protein by affinity chromatography with the B23.1 anti-gp49 monoclonal antibody. Redundant oligonucleotides were used to isolate a full-length 1.3-kilobase cDNA from a mouse mast cell library. The predicted amino acid sequence contains a signal peptide of 23 residues, an extracellular domain of 215 residues with three potential sites of N-linked glycosylation, a transmembrane domain of 23 residues, and a cytoplasmic tail of 42 residues. Hybridization of the gp49 cDNA was limited to mRNA extracted from those cell types that also bound the B23.1 monoclonal antibody as assessed by cytofluorographic analyses. The predicted extracellular domain of gp49 contains two regions of 48 and 51 amino acids, each flanked by cysteine residues. Both regions meet criteria for being C2-type domains of the immunoglobulin superfamily based upon the alignment of consensus amino acids and their predicted secondary structure organization. Thus, gp49, a membrane glycoprotein preferentially expressed by the progenitor mast cell population, is a new member of the immunoglobulin superfamily.

Differences between the activities of human monoclonal IgG1 and IgG3 anti-D antibodies of the Rh blood group system in their abilities to mediate effector functions of monocytes.

Seven IgG1 and seven IgG3 human monoclonal antibodies derived from heterohybridoma or Epstein-Barr virus-transformed lymphocytes and specific for the D antigen of the human Rh blood group system were tested for their ability to bring about red cell attachment to and phagocytosis by monocytes. The antibodies produced by the heterohybridomas were also investigated for their potency to mediate antibody-dependent cellular cytotoxicity (ADCC) by monocytes. When red cells were sensitized with any of the IgG1 anti-D antibodies, most of them were ingested by the phagocytes. By contrast, many of the red cells coated with any of the IgG3 antibodies remained attached to the monocyte surface while only few underwent phagocytosis. Some of the attached red cells remained on the phagocyte exterior for a considerable length of time. The ADCC activities of the IgG3 anti-D antibodies was greater than that of the IgG1 anti-D antibodies. The results mean that in vitro IgG1 anti-D mediates red cell destruction mainly by phagocytosis, while IgG3 anti-D causes their destruction predominantly by prolonged cytolysis. These differences between the effector functions of human monoclonal IgG1 and IgG3 anti-D antibodies might have important implications for their use in the prophylaxis of haemolytic disease of the new-born.