The relationship between process use and stage of change for sugary drinks.

BACKGROUND: Decreasing sugar-sweetened beverage consumption may reduce obesity and obesity-related diseases. To better understand what processes could facilitate a reduction in sugary beverage intake, we examined the relationship between stage-of-change and use of 10 processes of change. Secondarily, reliability of the measure was assessed. METHODS: A cross-sectional study was conducted, using a newly developed stage-of-change and process of change questionnaire. Participants (n = 105; male, n = 28) were aged between 18 and 60 years. A one-way analysis of variance, with Tukey's and Benjamini-Hochberg post hoc tests, was used to compare process use by stages. Paired t-tests were used to compare total cognitive and total behavioural process use within each stage. Cronbach's α coefficient and mean inter-item correlation was used to assess internal consistency. Reliability of repeated items was examined using kappa. RESULTS: Cognitive and behavioural processes were used more in the contemplation/preparation and maintenance stages than in precontemplation (all P < 0.05). Compared to precontemplation, process use was significantly higher in contemplation/preparation for five individual processes, action for four processes and maintenance for five processes. The use of dramatic relief and self liberation was lower in maintenance than contemplation/preparation. Across the stages, the use of eight of the 10 processes differed. The use of consciousness raising, self re-evaluation and self liberation differed between stages more frequently than other processes. CONCLUSIONS: The use of many processes differed by stage and could be incorporated into programmes aiming to assist adults in reducing their consumption of sugary drinks.

Mapping of the phosphorylase kinase alpha subunit gene on the mouse X chromosome.

Phosphorylase kinase is a glycogenolytic enzyme in several animal tissues. Within the last few years all four subunits of the enzyme have been cloned. The beta, gamma, and delta subunits are known to be autosomal. We have mapped the alpha subunit of phosphorylase kinase, recently cloned by Zander et al. (1988), in an interspecific mouse pedigree and localized it on the X chromosome, where it maps between the X-linked zinc finger protein and phosphoglycerate kinase genes, close to the latter. In man and mouse several X-linked disorders of this enzyme have been described. Although the X-linked phosphorylase kinase deficiency in mice may be caused by a mutation in the structural gene for the alpha subunit, mapped here, the existence of a separate regulatory locus, important in the normal expression or function of the enzyme in muscle, still remains a possibility.

Chromosomal localization of GABAA receptor subunit genes: relationship to human genetic disease.

Hybridization of GABAA receptor probes to human chromosomes in situ and to DNA from sorted human chromosomes has localized the genes encoding a beta subunit and three isoforms of the alpha subunit. The alpha 2 and beta genes are both located on chromosome 4 in bands p12-p13 and may be adjacent. The alpha 1 gene is on chromosome 5 (bands q34-q35) and the alpha 3 gene is on the X chromosome. The alpha 3 locus was mapped also on the mouse X chromosome using genetic break-point analysis in an interspecies pedigree. The combined results locate the human alpha 3 gene within band Xq28, in a location that makes it a candidate gene for the X-linked form of manic depression.

The molecular basis of muscular dystrophy in the mdx mouse: a point mutation.

The mdx mouse is an X-linked myopathic mutant, an animal model for human Duchenne muscular dystrophy. In both mouse and man the mutations lie within the dystrophin gene, but the phenotypic differences of the disease in the two species confer much interest on the molecular basis of the mdx mutation. The complementary DNA for mouse dystrophin has been cloned, and the sequence has been used in the polymerase chain reaction to amplify normal and mdx dystrophin transcripts in the area of the mdx mutation. Sequence analysis of the amplification products showed that the mdx mouse has a single base substitution within an exon, which causes premature termination of the polypeptide chain.

Localization of the mdx mutation within the mouse dystrophin gene.

We have mapped human and mouse X chromosome-specific genomic and cDNA probes through an interspecies Mus musculus/spretus pedigree which contains the mdx mutation. The positions of these markers relative to one another and to the mdx mutation were delineated. Using probes corresponding to segments of the human Duchenne muscular dystrophy (DMD) gene transcript, the position of a cross-hybridizing mouse equivalent gene (mDMD) was located. In more than 200 animals mapped, three were identified which show recombination within this mDMD gene. Analysis of these three animals shows that the mDMD gene is oriented with its 5' end centromeric and its 3' end telomeric on the mouse X chromosome. Furthermore, their recombinational breakpoints are on either side of the mdx mutation, thus providing the first unequivocal demonstration that the mdx mutation is located within the mDMD gene and defining limits within that gene between which the mutation must lie. Within that segment the evidence indicates that there is no major deletion of an exon as detectable by Southern blot analysis in mdx animals. The mdx mouse becomes important as an animal model for the study of the expression of the DMD gene and its developmental consequences, for transgenic and other corrective manipulations.

Variation in the biologic and biochemical characteristics of human menopausal gonadotropin.

Lot differences in the biopotency of human menopausal gonadotropin (hMG) were evaluated and the potential biochemical basis was investigated. The in vivo biopotency of hMG was assessed by a unique bioassay that evaluates the number of ova shed in the cyclic hamster in response to hMG administration. Significant variation in hMG lots was observed using this assay. When subjected to chromatofocusing, hMG displayed five immunoreactive follicle-stimulating hormone (FSH) isohormones and nine luteinizing hormone (LH) isohormones. The relative distribution of FSH, but not LH isohormones, was slightly but significantly different between the lots tested. These data indicate that significant differences exist in the ability of commercially available hMG to stimulate follicular development and ovulation. The biochemical basis for these differences in in vivo biopotency remains to be elucidated.

Analysis of chromatin proteins from human placenta.

Low-salt extracts of chromatin from human term placenta have been examined for the presence of the high mobility group (HMG) proteins. Based upon salt-dissociation characteristics, solubilities in trichloroacetic acid and electrophoretic behaviour on sodium dodecyl sulphate-polyacrylamide gel electrophoresis (SDS-PAGE) and non-equilibrium pH gradient gel electrophoresis (NEPHGE), each of the HMG proteins is present, including HMG-1, -2, -E, -14, and -17. A remarkably large amount of HMG-E is present in term human placenta. Additionally, a protein not previously recognized, which we designate HMG-PL, is present in term placenta. Electrophoretic comparison of the HMG proteins from placentae of varying gestational age, using NEPHGE, demonstrates that all of the placental HMG proteins exhibit multiplicity, reminiscent of chicken erythrocyte HMG proteins. Specifically, we found HMG-E to be unaltered in amounts relative to HMG-1 and -2 in placentae varying from 20 to 40 weeks of gestation. HMG-PL, however, is differentially expressed, increasing in amounts as gestation proceeds past 34 weeks. HMG-PL was purified and subjected to amino acid analysis. Its composition supports the notion that HMG-PL is a member of the HMG-1 family.

Implications of ethnicity in the care of the terminally ill.

A holistic approach to the care of the terminally ill must include considerations of ethnic variables and cultural traditions influencing views of death. The implications of ethnicity for health care delivery, direct patient care, and interpretation of patient and family responses are discussed.