Quality of weight loss advice on internet forums.

BACKGROUND: Adults use the Internet for weight loss information, sometimes by participating in discussion forums. Our purpose was to analyze the quality of advice exchanged on these forums. METHODS: This was a retrospective analysis of messages posted to 18 Internet weight loss forums during 1 month in 2006. Advice was evaluated for congruence with clinical guidelines; potential for causing harm; and subsequent correction when it was contradictory to guidelines (erroneous) or potentially harmful. Message- and forum-specific characteristics were evaluated as predictors of advice quality and self-correction. RESULTS: Of 3368 initial messages, 266 (7.9%) were requests for advice. Of 654 provisions of advice, 56 (8.6%) were erroneous and 19 of these 56 (34%) were subsequently corrected. Forty-three (6.6%) provisions of advice were harmful, and 12 of these 43 (28%) were subsequently corrected. Messages from low-activity forums (fewer messages) were more likely than those from high-activity forums to be erroneous (10.6% vs 2.4%, P < .001) or harmful (8.4% vs 1.2%, P < .001). In high-activity forums, 2 of 4 (50%) erroneous provisions of advice and 2 of 2 (100%) potentially harmful provisions of advice were corrected by subsequent postings. Compared with general weight loss advice, medication-related advice was more likely to be erroneous (P = .02) or harmful (P = .01). CONCLUSIONS: Most advice posted on highly active Internet weight loss forums is not erroneous or harmful. However, clinical and research strategies are needed to address the quality of medication-related advice.

CSF from Parkinson disease patients differentially affects cultured microglia and astrocytes.

BACKGROUND: Excessive and abnormal accumulation of alpha-synuclein (α-synuclein) is a factor contributing to pathogenic cell death in Parkinson's disease. The purpose of this study, based on earlier observations of Parkinson's disease cerebrospinal fluid (PD-CSF) initiated cell death, was to determine the effects of CSF from PD patients on the functionally different microglia and astrocyte glial cell lines. Microglia cells from human glioblastoma and astrocytes from fetal brain tissue were cultured, grown to confluence, treated with fixed concentrations of PD-CSF, non-PD disease control CSF, or control no-CSF medium, then photographed and fluorescently probed for α-synuclein content by deconvolution fluorescence microscopy. Outcome measures included manually counted cell growth patterns from day 1-8; α-synuclein density and distribution by antibody tagged 3D model stacked deconvoluted fluorescent imaging. RESULTS: After PD-CSF treatment, microglia growth was reduced extensively, and a non-confluent pattern with morphological changes developed, that was not evident in disease control CSF and no-CSF treated cultures. Astrocyte growth rates were similarly reduced by exposure to PD-CSF, but morphological changes were not consistently noted. PD-CSF treated microglia showed a significant increase in α-synuclein content by day 4 compared to other treatments (p ≤ 0.02). In microglia only, α-synuclein aggregated and redistributed to peri-nuclear locations. CONCLUSIONS: Cultured microglia and astrocytes are differentially affected by PD-CSF exposure compared to non-PD-CSF controls. PD-CSF dramatically impacts microglia cell growth, morphology, and α-synuclein deposition compared to astrocytes, supporting the hypothesis of cell specific susceptibility to PD-CSF toxicity.

Quality of weight loss advice on internet forums.

BACKGROUND: Adults use the Internet for weight loss information, sometimes by participating in discussion forums. Our purpose was to analyze the quality of advice exchanged on these forums. METHODS: This was a retrospective analysis of messages posted to 18 Internet weight loss forums during 1 month in 2006. Advice was evaluated for congruence with clinical guidelines; potential for causing harm; and subsequent correction when it was contradictory to guidelines (erroneous) or potentially harmful. Message- and forum-specific characteristics were evaluated as predictors of advice quality and self-correction. RESULTS: Of 3368 initial messages, 266 (7.9%) were requests for advice. Of 654 provisions of advice, 56 (8.6%) were erroneous and 19 of these 56 (34%) were subsequently corrected. Forty-three (6.6%) provisions of advice were harmful, and 12 of these 43 (28%) were subsequently corrected. Messages from low-activity forums (fewer messages) were more likely than those from high-activity forums to be erroneous (10.6% vs 2.4%, P < .001) or harmful (8.4% vs 1.2%, P < .001). In high-activity forums, 2 of 4 (50%) erroneous provisions of advice and 2 of 2 (100%) potentially harmful provisions of advice were corrected by subsequent postings. Compared with general weight loss advice, medication-related advice was more likely to be erroneous (P = .02) or harmful (P = .01). CONCLUSIONS: Most advice posted on highly active Internet weight loss forums is not erroneous or harmful. However, clinical and research strategies are needed to address the quality of medication-related advice.

B cells in ADA deficiency

Deficiency of the enzyme adenosine deaminase (ADA) results in severe lymphopenia in humans. Mice with an inactivating mutation in the ADA gene also exhibit profound lymphopenia, as well as pulmonary insufficiency and ribcage abnormalities. In fact, the mouse model has a phenotype that is remarkably similar to that of the human disease, making the mice valuable tools for unraveling the mechanism of lymphocyte destruction in absence of this housekeeping gene. T cell deficiency in ADA deficiency has been extensively studied by others, revealing a block in early thymocyte development. In contrast, our studies revealed that early B cell development in the bone marrow is normal. ADA-deficient mice, however, exhibit profound defects in germinal center formation, preventing antigen-dependent B cell maturation in the spleen. ADA-deficient spleen B cells display significant defects in proliferation and activation signaling, and produce more IgM than their normal counterparts, suggesting that extrafollicular plasmablasts are overrepresented. B cells from ADA-deficient mouse spleens undergo apoptosis more readily than those from normal mouse spleens. Levels of ADA's substrates, adenosine and 2′-deoxyadenosine, are elevated in both bone marrow and spleen in ADA-deficient mice. S ′-adenosyihomoeysteine hydrolase (SAH hydrolase) activity is significantly inhibited in both locales, as well. dATP levels, though, are only elevated in spleen, where B cell development is impaired, and not in bone marrow, where B cell ontogeny is normal. This finding points to dATP as the causative agent of lymphocyte death in ADA deficiency. ADA deficiency results in inhibition of the enzyme ribonucleotide reductase, thereby depleting nucleoside pools needed for DNA repair. Another mouse model that lacks a functional gene encoding a protein involved in DNA repair and/or cell cycle checkpoint regulation, p53-binding protein 1, exhibits blocks in T and B cell development that are similar to those seen in ADA-deficient mice. Unraveling the mechanisms of lymphocyte destruction in ADA deficiency may further understanding of lymphocyte biology, facilitate better chemotherapeutic treatment for lymphoproliferative diseases, and improve gene and enzyme therapy regimens attempted for ADA deficiency. ^

Roadmap for implementing the Chronic Care Model for weight management: Healthcare Institution's Response to Obesity (HIRO)

Background. Excess weight and obesity are at epidemic proportions in the United States and place individuals at increased risk for a variety of chronic conditions. Rates of diabetes, high blood pressure, coronary artery disease, stroke, cancer, and arthritis are all influenced by the presence of obesity. Small reductions in excess weight can produce significant positive clinical outcomes. Healthcare organizations have a vital role to play in the identification and management of obesity. Currently, healthcare providers do not adequately diagnose and manage excess weight in patients. Lack of skill, time, and knowledge are commonly cited as reasons for non-adherence to recommended standards of care. The Chronic Care Model offers an approach to healthcare organizations for chronic disease management. The model consists of six elements that work together to empower both providers and patients to have more productive interactions: the community, the health system itself, self-management support, delivery system design, decision support, and clinical information systems. The model and its elements may offer a framework through which healthcare organizations can adapt to support, educate, and empower providers and patients in the management of excess weight and obesity. Successful management of excess weight will reduce morbidity and mortality of many chronic conditions. Purpose. The purpose of this review is to synthesize existing research on the effectiveness of the Chronic Care Model and its elements as they relate to weight management and behaviors associated with maintaining a healthy weight. Methods: A narrative review of the literature between November 1998 and November 2008 was conducted. The review focused on clinical trials, systematic reviews, and reports related to the chronic care model or its elements and weight management, physical activity, nutrition, or diabetes. Fifty-nine articles are included in the review. Results. This review highlights the use of the Chronic Care Model and its elements that can result in improved quality of care and clinical outcomes related to weight management, physical activity, nutrition, and diabetes. Conclusions. Healthcare organizations can use the Chronic Care Model framework to implement changes within their systems to successfully address overweight and obesity in their patient populations. Specific recommendations for operationalizing the Chronic Care Model elements for weight management are presented.^