Evidence review of technology and dietary assessment.

SIGNIFICANCE: Diets high in fruit and vegetable consumption are associated with a decrease in chronic diseases. Dietary factors are linked to 4 of the 10 leading noncommunicable causes of death: cardiovascular disease, some cancers, stroke, and type 2 diabetes. Accurately measuring dietary patterns has many challenges. Dietary intake measurement has traditionally relied on self-report instruments such as 24-hour recall, food record, and food frequency questionnaires to record consumption history. These methods have inherent limitations in detecting small but important changes in fruit and vegetable consumption patterns. Promising advances in technology have made more sophisticated techniques for recording dietary intake possible. Computers and Web-based programs, handheld personal digital assistants with cameras and telephone cards, smart phones, cameras, and video recorders options may reduce the burden of recording what has been consumed. Furthermore, technology-based methods of dietary assessment may provide a higher degree of reliability and validity in visually determining fruit and vegetable consumption, and additional study is warranted. PURPOSE: The purpose of this article is to present a review of the evidence on the effectiveness of technology-based methods for dietary assessment, which included fruit and vegetable consumption. APPROACH: One hundred and eighty-seven articles published between 1998 and 2008 were initially identified. Fifteen met the study inclusion criteria and were evaluated by an interdisciplinary team using the Stetler Strength of Evidence Scale. RESULTS: Six technology-based methods for dietary assessment were identified. Findings from validity and reliability testing of technology-based methods are encouraging and need replication. Clinically important features offered through technology may reduce reporting burden and offer behavioral feedback to users. Methodologically sound, empirical research into using technology-based application for dietary assessment in a variety of populations of sufficient size is needed.

Hepatocyte-Specific Deletion of Mouse Lamin A/C Leads to Male-Selective Steatohepatitis.

BACKGROUND & AIMS: Lamins are nuclear intermediate filament proteins that comprise the major components of the nuclear lamina. Mutations in LMNA, which encodes lamins A/C, cause laminopathies, including lipodystrophy, cardiomyopathy, and premature aging syndromes. However, the role of lamins in the liver is unknown, and it is unclear whether laminopathy-associated liver disease is caused by primary hepatocyte defects or systemic alterations. METHODS: To address these questions, we generated mice carrying a hepatocyte-specific deletion of Lmna (knockout [KO] mice) and characterized the KO liver and primary hepatocyte phenotypes by immunoblotting, immunohistochemistry, microarray analysis, quantitative real-time polymerase chain reaction, and Oil Red O and Picrosirius red staining. RESULTS: KO hepatocytes manifested abnormal nuclear morphology, and KO mice showed reduced body mass. KO mice developed spontaneous male-selective hepatosteatosis with increased susceptibility to high-fat diet-induced steatohepatitis and fibrosis. The hepatosteatosis was associated with up-regulated transcription of genes encoding lipid transporters, lipid biosynthetic enzymes, lipid droplet-associated proteins, and interferon-regulated genes. Hepatic Lmna deficiency led to enhanced signal transducer and activator of transcription 1 (Stat1) expression and blocked growth hormone-mediated Janus kinase 2 (Jak2), signal transducer and activator of transcription 5 (Stat5), and extracellular signal-regulated kinase (Erk) signaling. CONCLUSIONS: Lamin A/C acts cell-autonomously to maintain hepatocyte homeostasis and nuclear shape and buffers against male-selective steatohepatitis by positively regulating growth hormone signaling and negatively regulating Stat1 expression. Lamins are potential genetic modifiers for predisposition to steatohepatitis and liver fibrosis. The microarray data can be found in the Gene Expression Omnibus repository (accession number: GSE93643).

Ethanol and Acetaminophen Synergistically Induce Hepatic Aggregation and TCH346-Insensitive Nuclear Translocation of GAPDH.

The glycolytic enzyme glyceraldehyde-3-phosphate dehydrogenase (GAPDH) signals during cellular stress via several post-translational modifications that change its folding properties, protein-protein interactions and sub-cellular localization. We examined GAPDH properties in acute mouse liver injury due to ethanol and/or acetaminophen (APAP) treatment. Synergistic robust and time-dependent nuclear accumulation and aggregation of GAPDH were observed only in combined, but not individual, ethanol/APAP treatments. The small molecule GAPDH-targeting compound TCH346 partially attenuated liver damage possibly via mitochondrial mechanisms, and independent of nuclear accumulation and aggregation of GAPDH. These findings provide a novel potential mechanism for hepatotoxicity caused by combined alcohol and acetaminophen exposure.

Patients' health beliefs and adaptation to carpal tunnel syndrome based on duration of symptomatic presentation.

The purpose of this paper was to examine the health beliefs and adaptation of patients receiving hand therapy treatment for carpal tunnel syndrome (CTS). A maximum variation sample of five patients referred for treatment of CTS was used to provide a diverse group of patients with varied backgrounds of age, gender, race, and occupation. Qualitative interviews based on the Health Beliefs model were conducted at the initial evaluation. Adaptive comments were recorded throughout the process. A grounded theory method was used to code and analyze the information gathered. Four themes emerged as to why and when persons wait to seek treatment for CTS: 1) denial of symptoms; 2) work/positioning the cause; 3) life changes; and 4) last resort. In conclusion, a low level of perceived seriousness and a low level of perceived susceptibility to CTS appeared to interfere with persons' seeking treatment for CTS.