Efficacy and acceptability of a pilot dietary intervention focusing on self-compassion, goal-setting and self-monitoring.

OBJECTIVE:Overweight and obesity are universal health challenges. Recent evidence emphasises the potential benefits of addressing psychological factors associated with obesity in dietary programmes. This pilot study investigated the efficacy and acceptability of a combined online and face-to-face dietary intervention that used self-compassion, goal-setting and self-monitoring to improve dietary behaviour, as well as psychological factors associated with dietary behaviour. DESIGN:Embedded mixed methods including a 4-week before-after trial and a one-on-one interview. Quantitative outcomes of the study were the levels of self-compassion; eating pathology; depression, anxiety and stress; and dietary intake. Qualitative outcomes were participants' perceptions about the acceptability of the intervention. SETTING:UNSW Kensington campus. PARTICIPANTS:Fourteen participants with overweight and obesity aged between 18 and 55 years old. RESULTS:Results showed that the intervention significantly improved self-compassion and some aspects of dietary intake (e.g. decrease in energy intake) at Week Four compared with Week Zero. Some aspects of eating pathology also significantly decreased (e.g. Eating Concern). However, changes in self-compassion over the 4 weeks did not significantly predict Week Four study outcomes, except for level of stress. Most participants found self-compassion, goal-setting and self-monitoring to be essential for dietary behaviour change. However, participants also indicated that an online programme needed to be efficient, simple and interactive. CONCLUSIONS:In conclusion, the current study provides preliminary but promising findings of an effective and acceptable combined online and face-to-face intervention that used self-compassion, goal-setting and self-monitoring to improve dietary habits. However, the results need to be examined in future long-term randomised controlled trials

Integrin-linked kinase is required for laminin-2–induced oligodendrocyte cell spreading and CNS myelination

Early steps in myelination in the central nervous system (CNS) include a specialized and extreme form of cell spreading in which oligodendrocytes extend large lamellae that spiral around axons to form myelin. Recent studies have demonstrated that laminin-2 (LN-2; α2β1γ1) stimulates oligodendrocytes to extend elaborate membrane sheets in vitro (cell spreading), mediated by integrin α6β1. Although a congenital LN-2 deficiency in humans is associated with CNS white matter changes, LN-2–deficient (dy/dy) mice have shown abnormalities primarily within the peripheral nervous system. Here, we demonstrate a critical role for LN-2 in CNS myelination by showing that dy/dy mice have quantitative and morphologic defects in CNS myelin. We have defined the molecular pathway through which LN-2 signals oligodendrocyte cell spreading by demonstrating requirements for phosphoinositide 3-kinase activity and integrin-linked kinase (ILK). Interaction of oligodendrocytes with LN-2 stimulates ILK activity. A dominant negative ILK inhibits LN-2–induced myelinlike membrane formation. A critical component of the myelination signaling cascade includes LN-2 and integrin signals through ILK

Leading Order Temporal Asymptotics of the Modified Non-Linear Schrodinger Equation: Solitonless Sector

Using the matrix Riemann-Hilbert factorisation approach for non-linear evolution equations (NLEEs) integrable in the sense of the inverse scattering method, we obtain, in the solitonless sector, the leading-order asymptotics as $t$ tends to plus and minus infinity of the solution to the Cauchy initial-value problem for the modified non-linear Schrodinger equation: also obtained are analogous results for two gauge-equivalent NLEEs; in particular, the derivative non-linear Schrodinger equation.Comment: 29 pages, 5 figures, LaTeX, revised version of the original submission, to be published in Inverse Problem

Spontaneous allelic variant in deafness–blindness gene \u3ci\u3eUsh1g\u3c/i\u3e resulting in an expanded phenotype

Relationships between novel phenotypic behaviors and specific genetic alterations are often discovered using target-specific, directed mutagenesis or phenotypic selection following chemical mutagenesis. An alternative approach is to exploit deficiencies in DNA repair pathways that maintain genetic integrity in response to spontaneously induced damage. Mice deficient in the DNA glycosylase NEIL1 show elevated spontaneous mutations, which arise from translesion DNA synthesis past oxidatively induced base damage. Several litters of Neil1 knockout mice included animals that were distinguished by their backwards-walking behavior in open-field environments, while maintaining frantic forward movements in their home cage environment. Other phenotypic manifestations included swim test failures, head tilting and circling. Mapping of the mutation that conferred these behaviors showed the introduction of a stop codon at amino acid 4 of the Ush1g gene. Ush1gbw/bwnull mice displayed auditory and vestibular defects that are commonly seen with mutations affecting inner-ear hair-cell function, including a complete lack of auditory brainstem responses and vestibular-evoked potentials. As in other Usher syndrome type I mutant mouse lines, hair cell phenotypes included disorganized and split hair bundles, as well as altered distribution of proteins for stereocilia that localize to the tips of row 1 or row 2. Disruption to the bundle and kinocilium displacement suggested that USH1G is essential for forming the hair cell\u27s kinocilial links. Consistent with other Usher type 1 models, Ush1gbw/bw mice had no substantial retinal degeneration compared with Ush1gbw/+ controls. In contrast to previously described Ush1g alleles, this new allele provides the first knockout model for this gene

Differential patterns of allelic loss in estrogen receptor-positive infiltrating lobular and ductal breast cancer.

The two main histological types of infiltrating breast cancer, lobular (ILC) and the more common ductal (IDC) carcinoma are morphologically and clinically distinct. To assess the molecular alterations associated with these breast cancer subtypes, we conducted a whole-genome study of 166 archival estrogen receptor (ER)-positive tumors (89 IDC and 77 ILC) using the Affymetrix GeneChip(R) Mapping 10K Array to identify sites of loss of heterozygosity (LOH) that either distinguished, or were shared by, the two phenotypes. We found single nucleotide polymorphisms (SNPs) of high-frequency LOH (>50%) common to both ILC and IDC tumors predominately in 11q, 16q, and 17p. Overall, IDC had a slightly higher frequency of LOH events across the genome than ILC (fractional allelic loss = 0.186 and 0.156). By comparing the average frequency of LOH by chromosomal arm, we found IDC tumors with significantly (P 25% informativity), we identified 78 and 466 individual SNPs with a higher frequency of LOH (P < 0.05) in ILC and IDC tumors, respectively. Hierarchical clustering of these 544 SNPs grouped tumors into four major groups based on their patterns of LOH and retention of heterozygosity. LOH in chromosomal arms 8p and 5q was common in higher grade IDC tumors, whereas ILC and low-grade IDC grouped together by virtue of LOH in 16q

Use of bioanalyzer electropherograms for quality control and target evaluation in microarray expression profiling studies of ocular tissues

Expression profiling with DNA microarrays has been used to examine the transcriptome of a wide spectrum of vertebrate cells and tissues. The sensitivity and accuracy of the data generated is dependent on the quality and composition of the input RNA. In this report, we examine the quality and array performance of over 200 total RNA samples extracted from ocular tissues and cells that have been processed in a microarray core laboratory over a 7-year period. Total RNA integrity and cRNA target size distribution were assessed using the 2100 Bioanalyzer. We present Affymetrix GeneChip array performance metrics for different ocular samples processed according to a standard microarray assay workflow including several quality control checkpoints. Our review of ocular sample performance in the microarray assay demonstrates the value of considering tissue-specific characteristics in evaluating array data. Specifically, we show that Bioanalyzer electropherograms reveal highly abundant mRNAs in lacrimal gland targets that are correlated with variation in array assay performance. Our results provide useful benchmarks for other gene expression studies of ocular systems

Wildlife Reservoirs of Canine Distemper Virus Resulted in a Major Outbreak in Danish Farmed Mink (<em>Neovison vison</em>)

A major outbreak of canine distemper virus (CDV) in Danish farmed mink (Neovison vison) started in the late summer period of 2012. At the same time, a high number of diseased and dead wildlife species such as foxes, raccoon dogs, and ferrets were observed. To track the origin of the outbreak virus full-length sequencing of the receptor binding surface protein hemagglutinin (H) was performed on 26 CDV's collected from mink and 10 CDV's collected from wildlife species. Subsequent phylogenetic analyses showed that the virus circulating in the mink farms and wildlife were highly identical with an identity at the nucleotide level of 99.45% to 100%. The sequences could be grouped by single nucleotide polymorphisms according to geographical distribution of mink farms and wildlife. The signaling lymphocytic activation molecule (SLAM) receptor binding region in most viruses from both mink and wildlife contained G at position 530 and Y at position 549; however, three mink viruses had an Y549H substitution. The outbreak viruses clustered phylogenetically in the European lineage and were highly identical to wildlife viruses from Germany and Hungary (99.29% – 99.62%). The study furthermore revealed that fleas (Ceratophyllus sciurorum) contained CDV and that vertical transmission of CDV occurred in a wild ferret. The study provides evidence that wildlife species, such as foxes, play an important role in the transmission of CDV to farmed mink and that the virus may be maintained in the wild animal reservoir between outbreaks