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Background Behavior change is essential for promoting health and preventing illness; yet, motivating individuals to adopt and maintain healthy behaviors remains a significant challenge. Multiple models have been developed in Psychology and Behavioral Sciences to understand and encourage behavior change, including the Capability, Opportunity, Motivation, Behavior model (COM-B model), the Health Belief Model, the Behavior Change Wheel, the Theoretical Domains Framework (TDF), nudge theory, and Behavior Change Techniques (BCTs). Among these, the Fogg Behavior Model (FBM), developed by Dr. BJ Fogg, offers a specific and valuable framework for facilitating behavior change. This scoping review aims to analyze studies that apply the FBM in health, particularly its impact on changing health-related behaviors. By synthesizing the evidence, this review provides valuable insights into the use and impact of the FBM in promoting behavior change in health, with implications for future research and practice. Objective To investigate the application of the FBM within the health domain, focusing on its role in behavior change interventions. Methods A comprehensive search of multiple databases, including MEDLINE/PubMed, Cochrane Library, Epistemonikos, and PsycINFO, was conducted to identify studies applying the FBM in health-related interventions. The search strategy incorporated terms related to the FBM, health behavior change, and relevant health outcomes, with no restrictions on publication date. Unpublished and grey literature was also searched. Eligibility criteria included studies that applied the FBM in health interventions and reported outcomes. The review followed PRISMA-ScR and SAGER guidelines to ensure comprehensive reporting and consideration of sex and gender variables. Data were synthesized using a narrative approach, summarizing findings descriptively and thematically. Results Six studies met the inclusion criteria, covering sexual and reproductive health, vaccination, chronic disease management, general wellness, and healthcare adherence. The FBM was applied through motivation (anticipation, sensation, belonging), ability enhancement (reducing effort, increasing accessibility, integrating behaviors into routines), and prompts (reminders, calls to action, environmental cues). Effectiveness varied across studies. Gestational weight management reduced gestational diabetes (10.34% vs. 34.48%, p = 0.028), hypertension (3.45% vs. 27.59%, p = 0.030), and cesarean rates (41.38% vs. 72.41%, p = 0.017). HPV vaccination interventions increased intent to vaccinate (63.3–96.7%, p < 0.001), with 30% receiving the first dose within three months. Diabetes self-management improved dietary adherence (p = 0.04), physical activity (p = 0.005), and glucose monitoring (p = 0.02). Parental nutrition interventions increased knowledge (d = 1.07), beliefs (d = 0.61), and behavior change (d = 0.59). A vaginal birth intervention raised intention by 29% (p < 0.05). Conclusions Our scoping review highlights the FBM as an effective framework for promoting health behavior change across various domains. By systematically applying motivation, ability, and prompts, FBM-based interventions demonstrated positive outcomes. However, limitations such as the lack of long-term follow-ups and sex- and gender-disaggregated data indicate areas for future research. Expanding its application to diverse populations, integrating digital health technologies, and addressing structural and cultural barriers will enhance its impact. Strengthening methodological rigor and comparative analyses with other behavior change models will further refine its effectiveness for broader public health applications. Despite its potential, the FBM remains underutilized in public health research. Trial registration Open Science Framework osf.io/jpwxg.

Access to scientific data can enable independent reuse and verification; however, most data are not available and become increasingly irrecoverable over time. This study aimed to retrieve and preserve important datasets from 160 of the most highly-cited social science articles published between 2008–2013 and 2015–2018. We asked authors if they would share data in a public repository—the Data Ark—or provide reasons if data could not be shared. Of the 160 articles, data for 117 (73%, 95% CI [67%–80%]) were not available and data for 7 (4%, 95% CI [0%–12%]) were available with restrictions. Data for 36 (22%, 95% CI [16%–30%]) articles were available in unrestricted form: 29 of these datasets were already available and 7 datasets were made available in the Data Ark. Most authors did not respond to our data requests and a minority shared reasons for not sharing, such as legal or ethical constraints. These findings highlight an unresolved need to preserve important scientific datasets and increase their accessibility to the scientific community.

Background.Although antiretroviral therapy has the ability to fully restore a normal CD4+ cell count (>500 cells/mm3) in most patients, it is not yet clear whether all patients can achieve normalization of their CD4+ cell count, in part because no study has followed up patients for >7 years. Methods.Three hundred sixty-six patients from 5 clinical cohorts who maintained a plasma human immunodeficiency virus (HIV) RNA level <1000 copies/mL for at least 4 years after initiation of antiretroviral therapy were included. Changes in CD4+ cell count were evaluated using mixed-effects modeling, spline-smoothing regression, and Kaplan-Meier techniques. Results.The majority (83%) of the patients were men. The median CD4+ cell count at the time of therapy initiation was 201 cells/mm3 (interquartile range, 72–344 cells/mm3), and the median age was 47 years. The median follow-up period was 7.5 years (interquartile range, 5.5–9.7 years). CD4+ cell counts continued to increase throughout the follow-up period, albeit slowly after year 4. Although almost all patients (95%) who started therapy with a CD4+ cell count ⩾300 cells/mm3 were able to attain a CD4+ cell count ⩾500 cells/mm3, 44% of patients who started therapy with a CD4+ cell count <100 cells/mm3 and 25% of patients who started therapy with a CD4+ cell count of 100–200 cells/mm3 were unable to achieve a CD4+ cell count >500 cells/mm3 over a mean duration of follow-up of 7.5 years; many did not reach this threshold by year 10. Twenty-four percent of individuals with a CD4+ cell count <500 cells/mm3 at year 4 had evidence of a CD4+ cell count plateau after year 4. The frequency of detectable viremia (“blips”) after year 4 was not associated with the magnitude of the CD4+ cell count change. Conclusions.A substantial proportion of patients who delay therapy until their CD4+ cell count decreases to <200 cells/mm3 do not achieve a normal CD4+ cell count, even after a decade of otherwise effective antiretroviral therapy. Although the majority of patients have evidence of slow increases in their CD4+ cell count over time, many do not. These individuals may have an elevated risk of non–AIDS-related morbidity and mortality.

Depression affects 20-30% of HIV-infected patients and is associated with worse HIV outcomes. Although effective depression treatment is available, depression is largely untreated or undertreated in this population. We quantified gaps in antidepressant treatment, treatment adjustments, and outcomes among US patients in routine HIV care in the nationally distributed CNICS observational clinical cohort. This cohort combines detailed clinical data with regular, self-reported depressive severity assessments (Patient Health Questionnaire-9, PHQ-9). We considered whether participants with likely depression received antidepressants, whether participants on antidepressants with persistently high depressive symptoms received timely dose adjustments, and whether participants achieved depression remission. We considered a cross-sectional analysis (6,219 participants in care in 2011-2012) and a prospective analysis (2,936 participants newly initiating CNICS care when PHQ-9 screening was active). The cross-sectional sample was 87% male, 53% Caucasian, 25% African American, and 18% Hispanic; the prospective sample was similar. In both samples, 39-44% had likely depression, with 44-60% of those receiving antidepressants. Of participants receiving antidepressants, 20-26% experienced persistently high depressive symptoms; only a small minority of those received antidepressant dose adjustments. Overall, 35-40% of participants on antidepressants achieved full depression remission. Remission among participants with persistently high depressive symptoms was rare regardless of dose adjustments. In this large, diverse cohort of US patients engaged in routine HIV care, we observed large gaps in antidepressant treatment, timely dose adjustment to address persistently high depressive symptoms, and antidepressant treatment outcomes. These results highlight the importance of more effective pharmacologic depression treatment models for HIV-infected patients.

Lyme disease (LD) is the most commonly reported tick-borne illness in the U.S. and Europe, and its geographic distribution is continuously expanding worldwide. Though early LD can be treated with antibiotics, chronic LD is recalcitrant to antibiotic treatments and thus requires multiple courses of antibiotic therapy. Currently, there are no human vaccines nor prophylactic antibiotics to prevent LD. As the causative agent of LD, Borreliella burgdorferi has evolved unique metabolic pathways, some of which are specific and essential for its survival and thus present as ideal targets for developing new therapeutics. By using an approach of genetics, biochemistry, structural biology, drug screening, and animal models, this report provides evidence that lactate dehydrogenase can be a potential target for developing genus-specific metabolic inhibitors against B. burgdorferi and potentially other tick-borne pathogens as well.

The timing of the initiation of antiretroviral therapy in asymptomatic patients with HIV infection is unclear. In this retrospective study involving patients in North America from 1996 through 2005, the deferral of therapy until the patient's CD4+ count had fallen below one of the two thresholds of interest (a range of 351 to 500 cells or >500 cells per cubic millimeter) was associated with a relative hazard of death of 1.69 and 1.94, respectively. In this retrospective study involving patients in North America, deferral of therapy until the patient's CD4+ count had fallen below one of the two thresholds of interest (a range of 351 to 500 cells or >500 cells per cubic millimeter) was associated with an increase in the risk of death of 69% and 94%, respectively. The use of antiretroviral therapy has dramatically reduced disease progression and death among patients with human immunodeficiency virus (HIV) infection, 1 , 2 but the optimal time to begin therapy is uncertain. 3 , 4 Current guidelines recommend treatment for asymptomatic patients who have a CD4+ count of less than 350 cells per cubic millimeter on the basis of accumulating observational data. 5 , 6 However, these guidelines note the lack of data from randomized clinical trials regarding the timing of the initiation of antiretroviral therapy. 3 , 4 Data from randomized trials are limited to an analysis of a subgroup of 477 patients 7 from the Strategies for . . .

To describe disparities along the depression treatment cascade, from indication for antidepressant treatment to effective treatment, in HIV-infected individuals by gender and race/ethnicity. The Center for AIDS Research (CFAR) Network of Integrated Clinical Systems (CNICS) cohort includes 31,000 HIV-infected adults in routine clinical care at 8 sites. Individuals were included in the analysis if they had a depressive symptoms measure within one month of establishing HIV care at a CNICS site. Depressive symptoms were measured using the validated Patient Health Questionnaire-9 (PHQ-9). Indication for antidepressant treatment was defined as PHQ-9 ≥ 10 or a current antidepressant prescription. Antidepressant treatment was defined as a current antidepressant prescription. Evidence-based antidepressant treatment was considered treatment changes based on a person's most recent PHQ-9, in accordance with clinical guidelines. We calculated the cumulative probability of moving through the depression treatment cascade within 24 months of entering CNICS HIV care. We used multivariable Cox proportional hazards models to estimate associations between gender, race/ethnicity, and a range of depression outcomes. In our cohort of HIV-infected adults in routine care, 47% had an indication for antidepressant treatment. Significant drop-offs along the depression treatment cascade were seen for the entire study sample. However, important disparities existed. Women were more likely to have an indication for antidepressant treatment (HR 1.54; 95% CI 1.34, 1.78), receive antidepressant treatment (HR 2.03; 95% CI 1.53, 2.69) and receive evidence-based antidepressant treatment (HR 1.67; 95% CI 1.03, 2.74), even after accounting for race/ethnicity. Black non-Hispanics (HR 0.47, 95% CI 0.35, 0.65), Hispanics (HR 0.63, 95% CI 0.44, 0.89) and other race/ethnicities (HR 0.35, 95% CI 0.17, 0.73) were less likely to initiate antidepressant treatment, compared to white non-Hispanics. In our cohort of HIV-infected adults depressive symptoms were common. Important disparities in the prevalence of depressive symptoms and receipt of antidepressant treatment existed by gender and race/ethnicity.

More than 50 000 people participated in the rescue and recovery work that followed the Sept 11, 2001 (9/11) attacks on the World Trade Center (WTC). Multiple health problems in these workers were reported in the early years after the disaster. We report incidence and prevalence rates of physical and mental health disorders during the 9 years since the attacks, examine their associations with occupational exposures, and quantify physical and mental health comorbidities. In this longitudinal study of a large cohort of WTC rescue and recovery workers, we gathered data from 27 449 participants in the WTC Screening, Monitoring, and Treatment Program. The study population included police officers, firefighters, construction workers, and municipal workers. We used the Kaplan-Meier procedure to estimate cumulative and annual incidence of physical disorders (asthma, sinusitis, and gastro-oesophageal reflux disease), mental health disorders (depression, post-traumatic stress disorder [PTSD], and panic disorder), and spirometric abnormalities. Incidence rates were assessed also by level of exposure (days worked at the WTC site and exposure to the dust cloud). 9-year cumulative incidence of asthma was 27·6% (number at risk: 7027), sinusitis 42·3% (5870), and gastro-oesophageal reflux disease 39·3% (5650). In police officers, cumulative incidence of depression was 7·0% (number at risk: 3648), PTSD 9·3% (3761), and panic disorder 8·4% (3780). In other rescue and recovery workers, cumulative incidence of depression was 27·5% (number at risk: 4200), PTSD 31·9% (4342), and panic disorder 21·2% (4953). 9-year cumulative incidence for spirometric abnormalities was 41·8% (number at risk: 5769); three-quarters of these abnormalities were low forced vital capacity. Incidence of most disorders was highest in workers with greatest WTC exposure. Extensive comorbidity was reported within and between physical and mental health disorders. 9 years after the 9/11 WTC attacks, rescue and recovery workers continue to have a substantial burden of physical and mental health problems. These findings emphasise the need for continued monitoring and treatment of the WTC rescue and recovery population. Centers for Disease Control and Prevention and National Institute for Occupational Safety and Health.

Background. Cross-sectional plasma human immunodeficiency virus (HIV) viral load (VL) measures have proven invaluable for clinical and research purposes. However, cross-sectional VL measures fail to capture cumulative plasma HIV burden longitudinally. We evaluated the cumulative effect of exposure to HIV replication on mortality following initiation of combination antiretroviral therapy (ART). Methods. We included treatment-naive HIV-infected patients starting ART from 2000 to 2008 at 8 Center for AIDS Research Network of Integrated Clinical Systems sites. Viremia copy-years, a time-varying measure of cumulative plasma HIV exposure, were determined for each patient using the area under the VL curve. Multivariable Cox models were used to evaluate the independent association of viremia copy-years for all-cause mortality. Results. Among 2027 patients contributing 6579 person-years of follow-up, the median viremia copy-years was 5.3 log 10 copy × y/mL (interquartile range: 4.9—6.3 log 10 copy × y/mL), and 85 patients (4.2%) died. When evaluated separately, viremia copy-years (hazard ratio [HR] = 1.81 per log 10 copy × y/mL; 95% confidence interval [CI], 1.51—2.18 per log 10 copy × y/mL), 24-week VL (1.74 per log 10 copies/mL; 95% CI, 1.48—2.04 per log 10 copies/mL), and most recent VL (HR = 1.89 per log 10 copies/mL; 95% CI: 1.63—2.20 per log 10 copies/mL) were associated with increased mortality. When simultaneously evaluating VL measures and controlling for other covariates, viremia copy-years increased mortality risk (HR = 1.44 per log 10 copy × y/mL; 95% CI, 1.07—1.94 per log 10 copy × y/mL), whereas no cross-sectional VL measure was independently associated with mortality. Conclusions. Viremia copy-years predicted all-cause mortality independent of traditional, cross-sectional VL measures and time-updated CD4+ T-lymphocyte count in ART-treated patients, suggesting cumulative HIV replication causes harm independent of its effect on the degree of immunodeficiency.

Abstract Background People living with human immunodeficiency virus (HIV; PLWH) have a markedly elevated anal cancer risk, largely due to loss of immunoregulatory control of oncogenic human papillomavirus infection. To better understand anal cancer development and prevention, we determined whether recent, past, cumulative, or nadir/peak CD4+ T-cell count (CD4) and/or HIV-1 RNA level (HIV RNA) best predict anal cancer risk. Methods We studied 102 777 PLWH during 1996–2014 from 21 cohorts participating in the North American AIDS Cohort Collaboration on Research and Design. Using demographics-adjusted, cohort-stratified Cox models, we assessed associations between anal cancer risk and various time-updated CD4 and HIV RNA measures, including cumulative and nadir/peak measures during prespecified moving time windows. We compared models using the Akaike information criterion. Results Cumulative and nadir/peak CD4 or HIV RNA measures from approximately 8.5 to 4.5 years in the past were generally better predictors for anal cancer risk than their corresponding more recent measures. However, the best model included CD4 nadir (ie, the lowest CD4) from approximately 8.5 years to 6 months in the past (hazard ratio [HR] for <50 vs ≥500 cells/µL, 13.4; 95% confidence interval [CI], 3.5–51.0) and proportion of time CD4 <200 cells/µL from approximately 8.5 to 4.5 years in the past (a cumulative measure; HR for 100% vs 0%, 3.1; 95% CI, 1.5–6.6). Conclusions Our results are consistent with anal cancer promotion by severe, prolonged HIV-induced immunosuppression. Nadir and cumulative CD4 may represent useful markers for identifying PLWH at higher anal cancer risk. Among various CD4 or human immunodeficiency virus (HIV) RNA measures, nadir and cumulative CD4 were the best predictors for anal cancer risk, suggesting a key role for severe, prolonged HIV-induced immunosuppression in anal carcinogenesis. Early antiretroviral therapy may help prevent anal cancer.