Social media and youth mental health: Simple narratives produce biased interpretations.

Many academics and pundits contend that social media use is the primary cause of an international youth mental health crisis. However, these claims often rely on correlational evidence, ignoring the confounding effects of developmental, environmental, social, and psychological factors that influence mental health. This oversimplifies the complex etiology of mental health problems.

Does Objectively Measured Social-Media or Smartphone Use Predict Depression, Anxiety, or Social Isolation Among Young Adults?

Despite a plethora of research, the link between digital technology use and psychological distress among young adults remains inconclusive. Findings in this area are typically undermined by methodological limitations related to measurement, study design, and statistical analysis. Addressing these limitations, we examined the prospective, within-person associations between three aspects of objectively-measured digital technology use (smartphone use duration and frequency; social media use duration) and three aspects of psychological distress (depression, anxiety, and social isolation) among a sample of young adults ( = 384).

Social media and well-being: A methodological perspective.

Due to the methodological challenges inherent in studying social media use (SMU), as well as the methodological choices that have shaped research into the effects of SMU on well-being, clear conclusions regarding relationships between SMU and well-being remain elusive. We provide a review of five methodological developments poised to provide increased understanding in this domain: (a) increased use of longitudinal and experimental designs; (b) the adoption of behavioural (rather than self-report) measures of SMU; (c) focusing on more nuanced aspects of SMU; (d) embracing effect heterogeneity; and (e) the use of formal modelling and machine learning. We focus on how these advances stand to bring us closer to understanding relations between SMU and well-being, as well as the challenges associated with these developments.

A systematic review and meta-analysis of discrepancies between logged and self-reported digital media use.

There is widespread public and academic interest in understanding the uses and effects of digital media. Scholars primarily use self-report measures of the quantity or duration of media use as proxies for more objective measures, but the validity of these self-reports remains unclear. Advancements in data collection techniques have produced a collection of studies indexing both self-reported and log-based measures.

Opioid use patterns and risk characteristics among injured patients.

Injured patients are at risk for prolonged opioid use after discharge from care. Limited evidence exists regarding how continued opioid use may be related to opioid medication misuse and opioid use disorder (OUD) following injury. This pilot study characterized opioid consumption patterns, health characteristics, and substance use among patients with active prescriptions for opioid medications following injury care.

Omarigliptin (MK-3102): a novel long-acting DPP-4 inhibitor for once-weekly treatment of type 2 diabetes.

In our effort to discover DPP-4 inhibitors with added benefits over currently commercially available DPP-4 inhibitors, MK-3102 (omarigliptin), was identified as a potent and selective dipeptidyl peptidase 4 (DPP-4) inhibitor with an excellent pharmacokinetic profile amenable for once-weekly human dosing and selected as a clinical development candidate. This manuscript summarizes the mechanism of action, scientific rationale, medicinal chemistry, pharmacokinetic properties, and human efficacy data for omarigliptin, which is currently in phase 3 clinical development.

Exposure data for cosmetic products: lipstick, body lotion, and face cream.

Accurate exposure information for cosmetic products and ingredients is needed in order to conduct safety assessments. Essential information includes both the amount of cosmetic product applied, and the frequency of use. To obtain current data, a study to assess consumer use practices was undertaken.

Synthesis and properties of an EGF-like domain (residues 361-406) in the extreme N-terminal region of the mouse EGF precursor.

Various proteins contain EGF-like domains that are not ligands for the EGF receptor. In the present study a cognate polypeptide for residues 361-406 of the mouse EGF precursor was synthesized by the solid-phase method. The product was renatured under oxidative conditions since it probably has an EGF-like array of three cystine disulfide bonds in its native state.

Physiological coupling of growth factor and steroid receptor signaling pathways: estrogen receptor knockout mice lack estrogen-like response to epidermal growth factor.

Past studies have shown that epidermal growth factor (EGF) is able to mimic the uterotropic effects of estrogen in the rodent. These studies have suggested a "cross-talk" model in which EGF receptor (EGF-R) signaling results in activation of nuclear estrogen receptor (ER) and its target genes in an estrogen-independent manner. Furthermore, in vitro studies have indicated the requirement for ER in this mechanism.

Differences in binding of epidermal growth factor to liver membranes of TCDD-resistant and TCDD-sensitive rats after a single dose of TCDD.

Epidermal growth factor (EGF) receptor has been implied as having a role in certain actions of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). After a single dose of TCDD, the receptor has been shown to be downregulated in several tissues including the liver. Two rat substrains, the Han/Wistar (Kuopio; H/W) rat and the Long-Evans (Turku AB; L-E) rat exhibit over a 1000-fold difference in their sensitivity to the lethal effect of TCDD.

A mechanistic model of effects of dioxin on thyroid hormones in the rat.

A physiological dosimetric model of the disposition of TCDD in the rat (Kohn et al., Toxicol. Appl.

Induced gene transcription: implications for biomarkers.

Numerous xenobiotics regulate cellular functions by altering transcription of target genes. Use of sensitive and specific biomarkers based on gene transcript levels may help clarify the shape of the dose-response curve in the low-dose region associated with human exposures to environmental concentrations of chemicals. We have quantified gene transcription induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin in both animal models and humans with the use of Northern analysis and PCR-based methods.

Persistence of TCDD-induced hepatic cell proliferation and growth of enzyme altered foci after chronic exposure followed by cessation of treatment in DEN initiated female rats.

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a potent tumor promoter in two-stage models of hepatocarcinogenesis. This study focuses on the persistence or reversibility of TCDD-mediated changes in livers after 30 weeks of treatment and cessation of treatment. Diethylnitrosamine (DEN) initiated animals (175 mg/kg) were promoted bi-weekly with TCDD at a dose equivalent to 125 ng/kg/day for 30 weeks without or with a following waiting period of 32 weeks before necropsy.

TCDD reduces rat hepatic epidermal growth factor receptor: comparison of binding, immunodetection, and autophosphorylation.

Administration of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), a potent tumor promoter, to rats resulted in a dose-dependent decrease in hepatic plasma membrane epidermal growth factor receptor (EGFR). The present study is the first to quantify and compare alterations in hepatic EGFR levels in female Sprague-Dawley rats 7 days after a single oral gavage dose of TCDD (0, 1, 5, 25, and 50 micrograms/kg) using three different techniques: (1) equilibrium receptor binding, (2) EGF induced receptor autophosphorylation, and (3) Western blot detection with a rabbit anti-rat EGFR polyclonal antibody. All three methods similarly demonstrated that the level of hepatic EGFR is significantly decreased at a dose of TCDD as low as 1 micrograms/kg.