Association between visual status and mental health status in Thai rural elderly: a community-based study

AIM: To evaluate the association between visual impairment (VI) and mental health or social engagement in older adults living in rural Thailand. METHODS: Data for this cross-sectional study were drawn from a community survey conducted in 2015 in Saraburi Province, Thailand. Participants were 327 adults aged ≥50y. VI was assessed using presenting distance visual acuity. Mental health and social engagement were evaluated in face-to-face interviews using validated questionnaires. After determining the prevalence of VI and relevant sociodemographic characteristics, multivariate regression analysis was used to evaluate the impact of VI on mental health and social engagement. RESULTS: The prevalence of VI was 18.3%. Major causes were refractive error (58.3%) and cataract (35%). Factors associated with VI in the crude analysis were: older age [odds ratio (OR) 8.08], unemployment (OR 2.72), widowhood (OR 2.47), being divorced/separated (OR 3.27), smoking (OR 2.09) and disability in activities of daily living (OR 2.35). Protective factors were undergoing eye screening at least once a year (P=0.029) and obesity (P=0.005). VI was significantly associated with low social engagement (adjusted OR 4.13) but not with poor mental health (P>0.05). CONCLUSION: Although VI older adults reported less participation in social activities, there is no significant association between VI and poor mental health. Annual eye examinations may prevent VI in older adults. Information about employment and anti-smoking should be targeted to older adults with VI.     

Randomized Controlled Trial of Online Acceptance and Commitment Therapy for Fibromyalgia

In this study, 67 participants (95% female) with fibromyalgia (FM) were randomly assigned to an online acceptance and commitment therapy (online ACT)?and?treatment as usual (TAU; ACT + TAU) protocol or a TAU control condition. Online ACT?+?TAU participants were asked to complete 7 modules over an 8-week period. Assessments were completed at pre-treatment, post-treatment, and 3-month follow-up periods and included measures of FM impact (primary outcome), depression, pain, sleep, 6-minute walk, sit to stand, pain acceptance (primary process variable), mindfulness, cognitive fusion, valued living, kinesiophobia, and pain catastrophizing. The results indicated that online ACT?+?TAU participants significantly improved in FM impact, relative to TAU (P?<.001), with large between condition effect sizes at post-treatment (1.26) and follow-up (1.59). Increases in pain acceptance significantly mediated these improvements (P?=?.005). Significant improvements in favor of online ACT?+?TAU were also found on measures of depression (P?=?.02), pain (P?=?.01), and kinesiophobia (P?=?.001). Although preliminary, this study highlights the potential for online ACT to be an efficacious, accessible, and cost-effective treatment for people with FM and other chronic pain conditions.

Tie2-Cre-induced inactivation of a conditional mutant Nf1 allele in mouse results in a myeloproliferative disorder that models juvenile myelomonocytic leukemia

Neurofibromatosis type one (NF1) is a common genetic disorder affecting 1:4000 births and is characterized by benign and malignant tumors. Children with NF1 are predisposed to juvenile myelomonocytic leukemia. The Nf1 gene encodes neurofibromin, which can function as a Ras GTPase-activating protein. Neurofibromin deficiency in mice leads to mid-gestation lethality due to cardiovascular defects. We have previously shown that conditional inactivation of Nf1 using Tie2-Cre recapitulates the heart defects seen in Nf1(-/-) embryos. Tie2-Cre transgenic mice express Cre recombinase in all endothelial cells. Here, we show that Tie2-Cre-mediated deletion of Nf1 also leads to excision of Nf1 in the hematopoietic lineage. Surviving mice exhibit a myeloproliferative disorder similar to juvenile myelomonocytic leukemia seen in NF1 patients. These mice provide a useful model to study neurofibromin deficiency in hematopoiesis. Furthermore, defects in Tie2-Cre-expressing progenitors that result in heart and blood defects suggest that related heart and blood disorders in NF1 and other syndromes represent disorders of the hemangioblast.     

Notch activity synergizes with B-cell-receptor and CD40 signaling to enhance B-cell activation

How diverse environmental cues are integrated to regulate B-cell activation and development remains poorly understood. Here we show that Notch activity synergizes with B-cell receptor (BCR) and/or CD40 signaling to enhance several aspects of B-cell activation and function. We find that costimulation of follicular B cells with the Notch ligand Delta-like-1 leads to significant increases in BCR- and CD40-mediated proliferation and enhances production of IgG1(+) cells in vitro and in vivo. We further find that coengagement of Notch and the BCR results in increased activation of the MAPK pathway, and MAPK and Notch inhibitors prevent B-cell activation events mediated by coengagement of Notch and the BCR. These data suggest that the BCR and CD40 signaling pathways collaborate with the Notch pathway to optimize B-cell activation.     

An essential role for Notch in neural crest during cardiovascular development and smooth muscle differentiation

The cardiac outflow tract develops as a result of a complex interplay among several cell types, including cardiac neural crest cells, endothelial cells, and cardiomyocytes. In both humans and mice, mutations in components of the Notch signaling pathway result in congenital heart disease characterized by cardiac outflow tract defects. However, the specific cell types in which Notch functions during cardiovascular development remain to be defined. In addition, in vitro studies have provided conflicting data regarding the ability of Notch to promote or inhibit smooth muscle differentiation, while the physiological role for Notch in smooth muscle formation during development remains unclear. In this study, we generated mice in which Notch signaling was specifically inactivated in derivatives of the neural crest. These mice exhibited cardiovascular anomalies, including aortic arch patterning defects, pulmonary artery stenosis, and ventricular septal defects. We show that Notch plays a critical, cell-autonomous role in the differentiation of cardiac neural crest precursors into smooth muscle cells both in vitro and in vivo, and we identify specific Notch targets in neural crest that are implicated in this process. These results provide a molecular and cellular framework for understanding the role of Notch signaling in the etiology of congenital heart disease.