Inhibition of pink color development in cooked, uncured ground turkey through the binding of non-pink generating ligands to muscle pigments

The pink color defect in cooked, uncured turkey is a sporadic problem that can result in economic loss and consumer dissatisfaction. Fourteen ligands were tested in ground turkey samples for their ability to reduce pink color development in control samples and in the presence of 150 ppm sodium nitrite or 1.0% nicotinamide (pink color producing agents). The 14 ligands evaluated were: 3-amino pyridine (AP), 4-benzoylpyridine (BP), diethylenetriamine pentaacetic acid (DA), ethylenedinitrilo-tetraacetic acid disodium salt (EA), 2,3 dihydroxybenzoic acid (DB), 3-ethyl pyridine (EP), trans 1,2-diaminocyclohexane-N,N,N',N' tetraacetic acid monohydrate (HA), calcium reduced nonfat dried milk (NM), 2,3 phthalic acid (PA), 3-picoline (PC), pyrrole (PY), pyridazine (PZ), pyridinedicarboxcylic acid (YA), and pyrazinedicarboxcylic acid (ZA). All ligands were incorporated into ground turkey at 0.20 mg/g (meat weight basis) except for NM (30 mg/g). Color was evaluated using a reflectance spectrophotometer to measure pigment changes (nicotinamide hemochrome, nitrosohemochrome) and with a chroma meter to determine CIE L* a* b* values. Reduction in pink color development was apparent with the addition of the ligand alone and in the presence of sodium nitrite and especially nicotinamide. The four most effective ligands tested were DA, EA, HA, and NM. In general, pink color reduction was highest in the ligand only and the ligand plus nicotinamide samples as was observed by CIE a* and nicotinamide hemochrome value reductions.     

Diazepam-insensitive GABAA receptors on postnatal spiral ganglion neurones in culture

Using dissociated spiral ganglion cell cultures obtained from 3-day-old rat cochlea, we investigated the response of auditory neurones to gamma-aminobutyric acid (GABA) using patch-clamp techniques. In our recording conditions, GABA elicited inward currents in > 95% of the neurones which reversed around 0 mV. Similar inward currents were measured using isoguvacin, a specific agonist of GABAA receptors. GABA-gated currents were reversibly inhibited by the channel blocker picrotoxin and the GABA competitive antagonist bicuculline. These functional GABAA receptors are characterized by an insensitivity to benzodiazepines and a relatively high sensitivity to beta-carbolines and barbiturates. These results show that the GABAA receptor pharmacological properties of spiral ganglion neurones are close to those of cerebellar granule cells.     

Interaction of Interceed oxidized regenerated cellulose with macrophages: a potential mechanism by which Interceed may prevent adhesions

OBJECTIVE: The objective of the study was to determine whether Interceed oxidized regenerated cellulose (Johnson & Johnson Medical, Arlington, Tex.), because of its polyanionic nature, may compete for the macrophage scavenger receptor. STUDY DESIGN: RAW macrophages were incubated with Interceed oxidized regenerated cellulose and known scavenger receptor ligands. The production of interleukin-1beta by mouse peritoneal macrophages was measured in the presence of Interceed cellulose. RESULTS: When macrophages were incubated with Interceed cellulose, increasing concentrations inhibited the uptake of fluorescent acetyl low-density lipoprotein. In the presence of Interceed cellulose there was a decrease in the production of interleukin-1beta by mouse macrophages. CONCLUSION: These results suggest that the interaction of Interceed oxidized regenerated cellulose with macrophages with scavenger receptors may result in a decreased secretion of matrix components, inflammatory mediators, and cellular growth factors. Thus Interceed cellulose may function as a biologic barrier in preventing adhesions.     

Structure and properties of the cell nucleus chromatin in the brain of rats exposed to gamma-radiation]

Exposure of rats to radiation in a dose of 1 Gy changes sensitivity of chromatin in the cerebral cortex cells to the action of DNAase 1, which promotes an increase of the DNA hydrolysis level and content of dissolved chromatin fractions. A day after irradiation the chromatin structure restores only partially and then (7-30 days after irradiation) it passes into a new, less compact state. The irradiation changes the chromatin ability to aggregation in the presence of Mg2+ and spermidine.     

Effects of DHT and EGF on human hyperplastic prostate cells cultured in vitro: growth, morphology and phenotype characterisation

Investigation of Prussak's space and its relationship to adjacent spaces is important in elucidating the cause of retraction pocket and cholesteatoma formation in this space. This study was designed to quantitatively characterize the chronological development of Prussak's space and its relationship to adjacent spaces in temporal bones. One-hundred and forty-nine human temporal bone slides (115 normal, 28 with otitis media with effusion, three with retraction pockets and three with attic type cholesteatoma) including specimens ranging from fetal to adult bones were studied. Prussak's space was formed and sufficient aeration routes established by 4 years of age in normal temporal bones. In temporal bones with otitis media with effusion, however, the growth of Prussak's space was suppressed and few routes for aeration established until 10 years of age. In normal temporal bones, Prussak's space developed with aeration routes sufficient to avert the negative pressure which can result in retraction pocket formation in the pars flaccida of the tympanic membrane.     

Synchrotron infrared microspectroscopy detecting the evolution of Huntington's disease neuropathology and suggesting unique correlates of dysfunction in white versus gray brain matter

Huntington's disease (HD), caused by a mutation of the corresponding gene encoding the protein huntingtin (htt), is characterized by progressive deterioration of cognitive and motor functions, paralleled by extensive loss of striatal neurons. At the cellular level, pathogenesis involves an early and prolonged period of neuronal dysfunction followed by neuronal death. Understanding the molecular events driving these deleterious processes is critical to the successful development of therapies to slow down or halt the progression of the disease. Here, we examined biochemical processes in a HD ex vivo rat model, as well as in a HD model for cultured neurons using synchrotron-assisted Fourier transform infrared microspectroscopy (S-FTIRM). The model, based on lentiviral-mediated delivery of a fragment of the HD gene, expresses a mutant htt fragment in one brain hemisphere and a wild-type htt fragment in the control hemisphere. S-FTIRM allowed for high spatial resolution and distinction between spectral features occurring in gray and white matter. We measured a higher content of β-sheet protein in the striatal gray matter exposed to mutant htt as early as 4 weeks following the initiation of mutant htt exposure. In contrast, white matter tracts did not exhibit any changes in protein structure but surprisingly showed reduced content of unsaturated lipids and a significant increase in spectral features associated with phosphorylation. The former is reminiscent of changes consistent with a myelination deficiency, while the latter is characteristic of early pro-apoptotic events. These findings point to the utility of the label-free FTIRM method to follow mutant htt's β-sheet-rich transformation in striatal neurons ex vivo, provide further evidence for mutant htt amyloidogenesis in vivo, and demonstrate novel chemical features indicative of white matter changes in HD. Parallel studies in cultured neurons expressing the same htt fragments showed similar changes.     

Maturation of peroxisomes in differentiating human hepatoblastoma cells (HepG2): possible involvement of the peroxisome proliferator-activated receptor alpha (PPAR alpha)

Although several variant alleles at the human NAT1 gene locus have been reported, their relationship to phenotypic variations in NAT1 function remains unclear. We have used in-vivo and invitro phenotyping tests, along with PCR-based cloning and heterologous expression, to investigate the extent of variation in NAT1 function and to characterize novel allelic variants at the NAT1 gene locus. The NAT1-selective substrate p-aminosalicylic acid (PAS) was used as a probe for NAT1 function. In-vivo PAS acetylation rates were estimated by determining the ratio of PAS to N-acetylated PAS (AcPAS) in urine and plasma following the oral ingestion of Nemasol Sodium. Excluding outliers, a 65-fold variation in the urinary AcPAS:PAS ratio was observed (n = 144), while a 5.6-fold variation in the plasma AcPAS:PAS ratio was seen in a subset (n = 19) of this sample. Urinary and plasma ratios correlated moderately (r = 0.74, p < 0.0005). One individual (case 244) had a marked impairment of PAS N-acetylation, with 10-fold lower urinary and plasma AcPAS:PAS ratios compared with other subjects. Biochemical investigations in whole blood lysates from case 244 suggested a NAT1 kinetic defect, with a 20-fold increased apparent K(m) for PAS and a 90-fold decreased Vmax for AcPAS formation. We subcloned, sequenced and expressed the protein-coding regions of the NAT1 alleles from case 244 and from seven other selected probands. Sequence analysis revealed the presence of two new variant alleles, designated as NAT1 x 14 and NAT1 x 15, in case 244, as well as one variant, NAT1 x 11, which has been observed in previous investigations. NAT1 x 14 contained a missense mutation (G560-->A) that is predicted to change a single amino acid (Arg187-->Gln), as well as two 3' non-coding region mutations (T1088-->A and C1095-->A) that have previously been observed in the NAT1 x 10 allelic variant. NAT1 x 15 had a single nonsense mutation (C559-->T; Arg187-->stop) and, thus, encodes a truncated protein. The activity of recombinant NAT1 14 mirrored the defective enzyme function in whole blood lysates from case 244, while NAT1 15 was completely inactive. Expressed NAT1 11, on the other hand, had identical activity to the wild type NAT1 4 allele, suggesting that the coding region mutations in this variant are functionally silent. The frequencies of NAT1 x 11, NAT1 x 14 and NAT1 x 15 were 0.021, 0.028 and 0.014 (n = 288 alleles), respectively, suggesting that they are relatively rare in our predominantly Caucasian sample.     

Implementation of the Henry J. Kaiser Family Foundation's Community Health Promotion Grant Program: a process evaluation

The Community Health Promotion Grants Program, sponsored by the Henry J. Kaiser Family Foundation, represents a major health initiative that established 11 community health promotion projects. Successful implementation was characterized by several critical factors: (1) intervention activities; (2) community activation; (3) success in obtaining external funding; and (4) institutionalization. Analysis of the program was based on data from several sources: program reports, key informant surveys, and a community coalition survey. Results indicate that school-based programs focusing on adolescent health problems were the most successful in reaching the populations they were targeting. The majority of the programs were able to attract external funding, thereby adding to their initial resource base. The programs were less successful in generating health promotion activities and in achieving meaningful institutionalization in their communities.