Hispanic Ethnicity Differences in Birth Characteristics, Maternal Birthplace, and Risk of Early-Onset Hodgkin Lymphoma: A Population-Based Case-Control Study.

BACKGROUND: Hispanic ethnicity differences in the risk of early-onset Hodgkin lymphoma diagnosed at <40 years are understudied. We conducted a population-based case-control study to evaluate associations between birth characteristics and early-onset Hodgkin lymphoma with a focus on potential ethnic differences. METHODS: This study included 1,651 non-Hispanic White and 1,168 Hispanic cases with Hodgkin lymphoma endorsing a range of races diagnosed at the age of 0 to 37 years during 1988-2015 and 140,950 controls without cancer matched on race/ethnicity and year of birth from the California Linkage Study of Early-Onset Cancers. OR and 95% confidence intervals (CI) were estimated from multivariable logistic regression models. RESULTS: Having a foreign-born mother versus a United States-born mother (i.e., the reference group) was associated with an increased risk of early-onset Hodgkin lymphoma among non-Hispanic Whites (OR = 1.52; 95% CI, 1.31-1.76; P < 0.01) and a decreased risk among Hispanics (OR = 0.78; 95% CI, 0.69-0.88; P < 0.01). Among both race groups, risk of early-onset Hodgkin lymphoma increased with birthweight and maternal age (all Ptrends < 0.01). Among non-Hispanic Whites, each 5-year increase in maternal age (OR = 1.11; 95% CI, 1.04-1.18; Ptrend < 0.01) and paternal age (OR = 1.07; 95% CI, 1.02-1.13; Ptrend < 0.01) was associated with increased risk of early-onset Hodgkin lymphoma. Compared with female Hispanics, male Hispanics had an increased risk of early-onset Hodgkin lymphoma (OR = 1.26; 95% CI, 1.12-1.42; P < 0.01). CONCLUSIONS: Maternal birthplace may play a role in risk of early-onset Hodgkin lymphoma that differs by ethnicity. IMPACT: The ethnic differences observed between certain birth characteristics, maternal birthplace, and early-onset Hodgkin lymphoma raise questions about the underlying biological, generational, lifestyle, residential, and genetic contributions to the disease.

Chronic Porphyromonas gingivalis lipopolysaccharide induces adverse myocardial infarction wound healing through activation of CD8+ T cells.

Oral and gum health have long been associated with incidence and outcomes of cardiovascular disease. Periodontal disease increases myocardial infarction (MI) mortality by sevenfold through mechanisms that are not fully understood. The goal of this study was to evaluate whether lipopolysaccharide (LPS) from a periodontal pathogen accelerates inflammation after MI through memory T-cell activation. We compared four groups [no MI, chronic LPS, day 1 after MI, and day 1 after MI with chronic LPS (LPS + MI); n = 68 mice] using the mouse heart attack research tool 1.0 database and tissue bank coupled with new analyses and experiments. LPS + MI increased total CD8+ T cells in the left ventricle versus the other groups (P < 0.05 vs. all). Memory CD8+ T cells (CD44 + CD27+) were 10-fold greater in LPS + MI than in MI alone (P = 0.02). Interleukin (IL)-4 stimulated splenic CD8+ T cells away from an effector phenotype and toward a memory phenotype, inducing secretion of factors associated with the Wnt/ß-catenin signaling that promoted monocyte migration and decreased viability. To dissect the effect of CD8+ T cells after MI, we administered a major histocompatibility complex-I-blocking antibody starting 7 days before MI, which prevented effector CD8+ T-cell activation without affecting the memory response. The reduction in effector cells diminished infarct wall thinning but had no effect on macrophage numbers or MertK expression. LPS + MI + IgG attenuated macrophages within the infarct without effecting CD8+ T cells, suggesting these two processes were independent. Overall, our data indicate that effector and memory CD8+ T cells at post-MI day 1 are amplified by chronic LPS to potentially promote infarct wall thinning.NEW & NOTEWORTHY Although there is a well-documented link between periodontal disease and heart health, the mechanisms are unclear. Our study indicates that in response to circulating periodontal endotoxins, memory CD8+ T cells are activated, resulting in an acceleration of macrophage-mediated inflammation after MI. Blocking activation of effector CD8+ T cells had no effect on the macrophage numbers or wall thinning at post-MI day 1, indicating that this response was likely due in part to memory CD8+ T cells.

Optimal break structures and cooling strategies to mitigate heat stress during a Rugby League match simulation.

OBJECTIVES: To examine, 1) optimal structure of break periods to mitigate physiological heat strain during rugby league play (Stage 1); and ii) effectiveness of three different cooling strategies applied during breaks (Stage 2). DESIGN: Counter-balanced crossover design. METHODS: In 37 °C, 50% RH, 11 males completed six simulated 80-min (two 40-min halves) rugby league matches on a treadmill with different break structures: regular game (RG) (12-min halftime), 1-min or 3-min "quarter-time" breaks halfway through each half with a 12-min halftime break (R1C and R3C), a 20-min halftime break (EH), or 1-min or 3-min quarter-time breaks with a 20-min halftime break (E1C and E3C) [Stage 1]. Nine participants completed Stage 2, which assessed the application of either ice towels (ICE), an electric fan (FAN) or a misting fan (MST) during breaks in the E3C protocol which, in Stage 1, prevailed as the optimal break structure. RESULTS: Stage 1: Irrespective of quarter-time break duration, reductions in rectal temperature (-0.24 °C ±â€¯0.24) and heart rate (-61 ±â€¯10 bpm) during the halftime break were greater with a 20-min compared to a 12-min break (-0.08 ±â€¯0.13 °C, p = 0.005; -55 ±â€¯-9 bpm, p = 0.021). Stage 2: End-game rises in rectal temperature were smaller (p < 0.006) in MST (1.41 ±â€¯0.22 °C), FAN (1.55 ±â€¯0.36 °C) and ICE (1.60 ±â€¯0.21 °C) than in CON (1.80 ±â€¯0.39 °C). The end-halftime heart rate was lower (p < 0.001) in ICE (89 ±â€¯13 bpm), MST (90 ±â€¯10 bpm) and FAN (92 ±â€¯13 bpm) than in CON (99 ±â€¯18 bpm). CONCLUSIONS: Combining an extended halftime period and quarter-time breaks with MST application is the optimal cooling strategy for rugby league players in hot, humid conditions.

Ad libitum water consumption off-sets the thermal and cardiovascular strain exacerbated by dehydration during a 3-h simulated heatwave.

PURPOSE: To assess whether ad libitum water ingestion of different temperatures is sufficient to prevent dehydration-related exacerbations of thermal and cardiovascular strain, during exposure to conditions representative of a heatwave. METHODS: Twelve participants (mean ± SD; 25 ± 4 years) exercised for 180 min at 3 METs in 40.1 ± 0.6 °C, 40.4 ± 2.1%RH four times: (i) consuming 20 °C water ad libitum (AL20); (ii) consuming 4 °C water ad libitum (AL4); (iii) replacing no fluids (NOFR); (iv) replacing sweat losses (FULLFR). Fluid consumption (FC), dehydration (%DEH), rectal temperature (Tre), rate-pressure product (RPP), forearm blood flow (FBF), mean skin temperature (Tsk), and local sweat rate (LSR) were measured/determined. RESULTS: FC was greater in AL20 (1.30 ± 0.41 L) than AL4 (1.03 ± 0.32 L; P = 0.003). %DEH was lower (P < 0.001) in AL20 (0.11 ± 0.76%), AL4 (0.43 ± 0.64%), and FULLFR (0.01 ± 0.12%) compared to NOFR (1.93 ± 0.28%). %DEH was lower in AL20 than AL4 (P = 0.003). In NOFR, end-trial changes in Tre were greater (P < 0.001) (1.05 ± 0.27 °C) compared to all other trials, but similar among AL20 (0.72 ± 0.30 °C), AL4 (0.76 ± 0.25 °C) and FULLFR (0.74 ± 0.35 °C). End-trial RPP was higher (P < 0.001) in NOFR (12,389 ± 1578 mmHg·bpm) compared to all other trials, but similar among FULLFR (11,067 ± 1292 mmHg·bpm), AL20 (11,214 ± 2078 mmHg·bpm) and AL4 (11,089 ± 1795 mmHg·bpm). No differences in Tsk or LSR were observed among trials, but FBF was lower in NOFR compared to FULLFR (2.84 ± 0.69 vs. 3.52 ± 0.96 ml/100 ml/min; P = 0.029). CONCLUSION: 4 °C or 20 °C ad libitum water ingestion prevented dehydration levels that exacerbate thermal/cardiovascular strain, despite blunted fluid intake with 4 °C water. Higher core temperatures with NOFR are attributed to impaired internal heat distribution secondary to a lower FBF.

Blogging as 'therapy'? Exploring personal technologies for smoking cessation.

This article presents some early, design-oriented research findings from a study that introduced mobile blogging technologies to four people who wished to make a health-related life change--giving up smoking. We wanted to establish the nature of the relationship between blogging and quitting smoking (if any), inspired by some earlier work in the domain showing that social technologies may help with the quit process. We present an account of three participants, documenting details of how blogging technologies fitted into their (changing) lives and examples of digital content they produced. We describe, using examples from participant blogs, instances of self-expression, replacement and self-awareness. We suggest, despite all participants failing in their quit attempts, that there are possible provisional, therapeutic characteristics to such social technologies. Finally, we suggest this therapeutic process can be understood better through a concept of personal translucence.