A Web-Based Health Promotion Program for Older Workers: Randomized Controlled Trial

BackgroundRecent evidence supports the efficacy of programs that promote improvements in the health practices of workers 50 years and older who are at higher risk for chronic diseases than younger workers are. Internet-based programs that promote healthy practices have also shown promise and, therefore, should be especially appropriate for workers aged 50 years and older.ObjectiveThe purpose of the research was to evaluate the effectiveness of HealthyPast50, a fully automated Web-based health promotion program based on social cognitive theory and aimed specifically at workers 50 years and older.MethodsThe randomized controlled trial was conducted across multiple US offices of a large global information technology company. The sample included 278 employees aged 50 to 68 who were recruited online and randomly assigned to the Web-based HealthyPast50 program or to a wait-list control condition. Self-report measures of diet, physical activity, stress, and tobacco use were collected online before and 3 months after the program group was given access to the program. Use data included number of log-ins and number of pages accessed. The primary analysis was multiple linear regression, following intent-to-treat principles with multiple imputation using the Markov chain Monte Carlo (MCMC) approach for nonmonotone missing data. Potential moderators from demographic characteristics and program dosage effects were assessed using multiple linear regression models. Additional analyses were conducted on complete (nonimputed) cases, excluding program participants who used the program for less than 30 minutes.ResultsRetention rates were good for both groups: 80.4% (111/138) for the program group and 94.3% (132/140) for the control group. Program group participants spent a mean of 102.26 minutes in the program (SD 148.32), logged in a mean of 4.33 times (SD 4.28), and viewed a mean of 11.04 pages (SD 20.08). In the analysis of the imputed dataset, the program group performed significantly better than the control group on diet behavioral change self-efficacy (estimated adjusted difference [Δ]=0.16, P=.048), planning healthy eating (Δ=0.17, P=.03), and mild exercise (Δ=1.03, P=.01). Moderator and dosage analyses of the dataset found no significant program effects. Analyses of the nonimputed dataset comparing program users with controls found additional significant program effects on eating practices (Δ=0.09, P=.03), exercise self-efficacy (Δ=0.12, P=.03), exercise planning (Δ=0.18, P=.03), and aging beliefs (Δ=0.17, P=.01). Moderator analysis of this dataset also found significant moderator effects of gender on multiple measures of exercise.ConclusionsA Web-based health promotion program showed promise for making a significant contribution to the short-term dietary and exercise practices of older working adults. Gender effects suggest that the program effects on exercise are due mainly to improvements among women.     

Heritability of the Human Craniofacial Complex

Quantifying normal variation and the genetic underpinnings of anatomical structures is one of the main goals of modern morphological studies. However, the extent of genetic contributions to normal variation in craniofacial morphology in humans is still unclear. The current study addresses this gap by investigating the genetic underpinnings of normal craniofacial morphology. The sample under investigation consists of 75 linear and angular measurements spanning the entire craniofacial complex, recorded from lateral cephalographs of 1,379 participants in the Fels Longitudinal Study. Heritabilities for each trait were estimated using SOLAR, a maximum‐likelihood variance components approach utilizing all pedigree information for parameter estimation. Trait means and mean effects of the covariates age, sex, age², sex × age, and sex × age² were simultaneously estimated in the analytic models. All traits of the craniofacial complex were significantly heritable. Heritability estimates ranged from 0.10 to 0.60, with the majority being moderate. It is important to note that we found similar ranges of heritability occurring across the different functional/developmental components of the craniofacial complex, the splanchnocranium, the basicranium, and the neurocranium. This suggests that traits from different regions of the craniofacial complex are of comparable utility for the purposes of population history and phylogeny reconstruction. At the same time, this genetic influence on craniofacial morphology signals a caution to researchers of nongenetic studies to consider the implications of this finding when selecting samples for study given their project design and goals. Anat Rec, 298:1535–1547, 2015. © 2015 Wiley Periodicals, Inc.     

Endoscopic Management of Bleeding Gastric Varices—an Updated Overview

Endoscopic insertion of enteral feeding tubes is a major advance in the delivery of nutrition therapy. Since the first report of percutaneous endoscopic gastrostomy (PEG) in 1980 (Gauderer et al. J Pediatr Surg. 15:872–5, 1980), insertion techniques and equipment have been refined and improved. Despite this progress, deep jejunal enteral access remains a difficult procedure, and many endoscopists do not have experience with the techniques of nasojejunal (NJ) placement, percutaneous endoscopic gastrojejunostomy (PEGJ), or direct percutaneous endoscopic jejunostomy (DPEJ) (Shike and Latkany, Gastrointest Endosc Clin N Am. 8:569–80, 1998). The difference between an exasperating experience and a rewarding procedure lies in mastering the “tips and tricks” that make insertion easy. While the basic techniques are described elsewhere (McClave and Chang 2011), we review several universal basic principles to enhance deep jejunal access, which should promote a more efficient and successful procedure.     

The ErbB4 Ligand Neuregulin-4 Protects against Experimental Necrotizing Enterocolitis

Necrotizing enterocolitis (NEC) affects up to 10% of premature infants, has a mortality of 30%, and can leave surviving patients with significant morbidity. Neuregulin-4 (NRG4) is an ErbB4-specific ligand that promotes epithelial cell survival. Thus, this pathway could be protective in diseases such as NEC, in which epithelial cell death is a major pathologic feature. We sought to determine whether NRG4-ErbB4 signaling is protective in experimental NEC. NRG4 was used i) in the newborn rat formula feeding/hypoxia model; ii) in a recently developed model in which 14- to 16-day-old mice are injected with dithizone to induce Paneth cell loss, followed by Klebsiella pneumoniae infection to induce intestinal injury; and iii) in bacterially infected IEC-6 cells in vitro. NRG4 reduced NEC incidence and severity in the formula feed/hypoxia rat model. It also reduced Paneth cell ablation–induced NEC and prevented dithizone-induced Paneth cell loss in mice. In vitro, cultured ErbB4^−/− ileal epithelial enteroids had reduced Paneth cell markers and were highly sensitive to inflammatory cytokines. Furthermore, NRG4 blocked, through a Src-dependent pathway, Cronobacter muytjensii–induced IEC-6 cell apoptosis. The potential clinical relevance of these findings was demonstrated by the observation that NRG4 and its receptor ErbB4 are present in human breast milk and developing human intestine, respectively. Thus, NRG4-ErbB4 signaling may be a novel pathway for therapeutic intervention or prevention in NEC.Necrotizing enterocolitis (NEC) is a devastating intestinal disease primarily affecting premature infants. In the United States, NEC afflicts 7% of infants weighing <1500 g.¹ In addition to prematurity, risk factors include hypoxia, bacterial colonization of the intestine, and formula feeding.² The development of NEC seems to be multifactorial, and patients may have any combination of risk factors at the time of presentation. The current disease model is that the immature gut barrier, along with defects in endogenous antimicrobial activity,³ allows bacterial translocation across the epithelium, triggering an inflammatory response that further worsens gut barrier function. Pathogenic bacteria,^{4, 5} inflammatory cytokines such as tumor necrosis factor (TNF),^{6, 7, 8} and Paneth cell dropout³ have all been associated with human NEC and contribute to NEC-like injury in animal models.Available therapy for either prevention or treatment of NEC is limited, and patients currently face a mortality rate of approximately 30%.^{9, 10, 11} Breast-fed infants have a lower risk of NEC than their formula-fed peers,^{12, 13} and a variety of studies have attempted to identify and characterize factors in human milk that confer this protection. Candidate protective molecules to date include immunoglobulins, oligosaccharides, lactoferrin, and soluble growth factors, such as epidermal growth factor (EGF)¹⁴ and heparin-binding EGF-like growth factor (HB-EGF).¹⁵ In rat and mouse models, enteral administration of either EGF^{16, 17} or HB-EGF¹⁸ decreases the incidence and severity of NEC. The primary receptor for both EGF and HB-EGF is EGF receptor (EGFR), the prototypic member of the ErbB receptor tyrosine kinase family. However, HB-EGF also activates ErbB4, a member of the ErbB family whose potential role in the developing gut and NEC is not known.ErbB4 has unique biochemical properties distinguishing it from other ErbB family members. Compared with EGFR, ErbB2, or ErbB3, it recognizes a broader collection of ligands, including the EGF-like growth factors HB-EGF and betacellulin as well as the heregulin/neuregulin molecules.¹⁹ At the same time, the ErbB4 c-terminus contains a distinct and somewhat restricted set of functional docking sites for downstream effectors²⁰ and is thus predicted to elicit divergent cellular effects on activation versus other family members. In fact, we recently demonstrated that neuregulin-4 (NRG4), an ErbB4-specific ligand that does not bind or activate other family members, including EGFR,²¹ specifically promotes survival but not migration or proliferation of mouse colon epithelial cells.²² Thus, ErbB4 is a potentially unique and selective target for therapeutic protection in diseases in which intestinal epithelial cell death is a major pathologic feature.We previously reported that ErbB4 is up-regulated in adult human and murine colon inflammation in vivo²³ and that ErbB4 overexpression protects cultured colonocytes from cytokine-induced apoptosis in a ligand-dependent manner.²⁴ Furthermore, i.p. NRG4 administration reduces the severity of acute murine dextran sulfate sodium colitis.²² Thus, it seems that ErbB4 induction is a natural compensatory response meant to preserve the epithelium rather than part of disease pathology and that ErbB4 activation with exogenous ligand is protective against induced inflammation. However, the role of this signaling pathway in the small intestine, or during development, has not been described. We hypothesized that ErbB4 and its ligands have a protective role in the small bowel during postnatal development, particularly in the setting of NEC-associated acute injury and inflammation. To advance our understanding of ErbB4 biology in intestinal homeostasis and disease, we tested the hypothesis that NRG4-ErbB4 signaling is protective in experimental NEC.