Joint Associations of Diet and Device-measured Physical Activity with Mortality and Incident CVD and Cancer: a prospective analysis of the UK Biobank Study.

BACKGROUND: We examined the joint associations of diet and device-measured intensity-specific PA with all-cause mortality (ACM), cardiovascular disease (CVD) and cancer incidence. METHODS: We used data from 79,988 participants from the UK Biobank, a population-based prospective cohort study. Light PA (LPA), moderate-to-vigorous PA (MVPA), vigorous PA (VPA) and total PA (TPA) were measured using a wrist-worn accelerometer. Diet Quality Score (DQS) was based on 10 foods and ranged from 0 (unhealthiest) to 100 (healthiest) points. We derived joint PA and diet variables. Outcomes were all-cause mortality, CVD and cancer incidence including PA, diet and adiposity-related (PDAR) cancer. RESULTS: During a median follow-up of 8 years, 2,863 deaths occurred, 11,053 participants developed CVD, 7,005 developed cancer and 3,400 developed PDAR cancer. Compared with the least favourable referent group (bottom PA tertile/low DQS), participants with middle and high (total and intensity specific) PA, except for LPA, had lower all-cause mortality risk and incident CVD risk, regardless of DQS. For example, among middle and high VPA and high DQS groups, CVD HR were 0.79 (95%CI 0.74-0.86) and 0.75 (95%CI 0.69-0.82), respectively. The pattern of cancer results was less pronounced but in agreement with the ACM and CVD incidence findings (e.g. HR 0.90, 95%CI 0.81-0.99; 0.88,0.79-0.98 and 0.82,0.74-0.92 among high VPA for low, moderate and high DQS group, respectively). CONCLUSIONS: Device-measured PA reveals novel joint associations with diet on health outcomes. IMPACT: Our results emphasize the crucial role of PA in addition to a healthy diet for reducing chronic diseases and mortality risk.

Association between Protein Intake and Diabetes Complications Risk Following Incident Type 2 Diabetes: The EPIC-Potsdam Study.

Our knowledge about the connection between protein intake and diabetes-related complications comes largely from studies among those already diagnosed with type 2 diabetes (T2D). However, there is a lack of information on whether changing protein intake after diabetes diagnosis affects complications risk. We aimed to explore the association between protein intake (total, animal, and plant) and vascular complications in incident T2D patients considering pre-diagnosis intake and changes in intake after diagnosis. This prospective cohort study included 1064 participants from the European Prospective Investigation into Cancer and Nutrition (EPIC)-Potsdam cohort who developed T2D during follow-up (physician-verified). Dietary protein intake was measured with a food frequency questionnaire at baseline and follow-up. We included physician-reported incident diabetes complications (myocardial infarction, stroke, nephropathy, and neuropathy). A total of 388 participants developed complications, 82 macrovascular complications, and 343 microvascular complications. Substituting carbohydrates with protein showed a trend towards lower complications risk, although this association was not statistically significant (hazard ratio (HR) for 5% energy (E) substitution: 0.83; 95% confidence intervals (CI): 0.60-1.14). Increasing protein intake at the expense of carbohydrates after diabetes diagnosis was not associated with total and microvascular complications (HR for 5% E change substitution: 0.98; 95% CI: 0.89-1.08 and HR for 5% E change substitution: 1.02; 95% CI: 0.92-1.14, respectively). Replacing carbohydrates with protein did not elevate the risk of diabetes complications in incident T2D cases.

Intracranial granuloma in a patient with granulomatosis with polyangiitis under rituximab maintenance: A case report.

BACKGROUND: Rituximab (RTX) is being used for both induction and maintenance of anti-neutrophil cytoplasmic antibody (ANCA) -associated vasculitis. However, the efficacy of RTX for the granulomatous findings of granulomatosis with polyangiitis (GPA) has not been demonstrated as clearly as its vasculitic manifestations. CASE SUMMARY: A 46-year-old man was diagnosed in 2019 with GPA with constitutional symptoms, bilateral mastoiditis, prostatic necrosis, nodules in both lungs, pauci-immune necrotizing glomerulonephritis and high level of PR3-ANCA. He reached clinical remission after induction with high-dose corticosteroids and intravenous cyclophosphamide pulses at the 3rd month. Two months following the second cycle of RTX as maintenance, he developed multiple cranial mass lesions, and excisional biopsy revealed necrotizing vasculitis with granuloma formation. Remission was achieved with long-term high-dose corticosteroid therapy after surgical excision. CONCLUSION: We observed a relapse of GPA with intracranial granulomatous lesions in a patient under RTX maintenance. Limited efficacy of RTX should be considered for mainly granulomatous manifestations in patients with GPA.

Modification of incident cancer risk with changes in metabolic syndrome status: A prospective cohort study in Taiwan.

PURPOSE: We aimed to investigate the effect of altered metabolic syndrome (MetS) status on cancer risk. METHODS: From 2002 through 2008 of the Taiwan MJ cohort, there were 111,616 adults who had repeated MetS measurements performed 3.3 years apart and were followed up for cancer incidence over 11.8 years. Cancer was confirmed based on histopathological reports. RESULTS: Participants were categorized as MetS-free (n = 80,409; no MetS at the first or last health screening), MetS-developed (n = 9833; MetS absence at the first screening and presence at the last screening), MetS-recovered (n = 8958; MetS presence at the first screening and absence at the last screening), and MetS-persisted (n = 12,416; MetS presence at the first and last screenings). We used the Fine-Gray sub-distribution method, with death as competing risk, to determine the association between MetS changes and incident cancer risk. During 1320,796 person-years of follow-up, 5862 individuals developed cancer. The incidence rate of cancer per 1000 person-years was 3.89 in the MetS-free, 5.26 in MetS-developed, 4.61 in MetS-recovered, and 7.33 in MetS-persisted groups (P < .001). Compared with the MetS-free group, MetS-persisted individuals had a higher risk of incident cancer. CONCLUSIONS: Persistent MetS was found to be associated with a high risk of incident cancer.

Body mass index and cancer risk among adults with and without cardiometabolic diseases: evidence from the EPIC and UK Biobank prospective cohort studies.

BACKGROUND: Whether cancer risk associated with a higher body mass index (BMI), a surrogate measure of adiposity, differs among adults with and without cardiovascular diseases (CVD) and/or type 2 diabetes (T2D) is unclear. The primary aim of this study was to evaluate separate and joint associations of BMI and CVD/T2D with the risk of cancer. METHODS: This is an individual participant data meta-analysis of two prospective cohort studies, the UK Biobank (UKB) and the European Prospective Investigation into Cancer and nutrition (EPIC), with a total of 577,343 adults, free of cancer, T2D, and CVD at recruitment. We used Cox proportional hazard regressions to estimate multivariable-adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) for associations between BMI and incidence of obesity-related cancer and in turn overall cancer with a multiplicative interaction between BMI and the two cardiometabolic diseases (CMD). HRs and 95% CIs for separate and joint associations for categories of overweight/obesity and CMD status were estimated, and additive interaction was quantified through relative excess risk due to interaction (RERI). RESULTS: In the meta-analysis of both cohorts, BMI (per ~ 5 kg/m2) was positively associated with the risk of obesity-related cancer among participants without a CMD (HR: 1.11, 95%CI: 1.07,1.16), among participants with T2D (HR: 1.11, 95% CI: 1.05,1.18), among participants with CVD (HR: 1.17, 95% CI: 1.11,1.24), and suggestively positive among those with both T2D and CVD (HR: 1.09, 95% CI: 0.94,1.25). An additive interaction between obesity (BMI ≥ 30 kg/m2) and CVD with the risk of overall cancer translated into a meta-analytical RERI of 0.28 (95% CI: 0.09-0.47). CONCLUSIONS: Irrespective of CMD status, higher BMI increased the risk of obesity-related cancer among European adults. The additive interaction between obesity and CVD suggests that obesity prevention would translate into a greater cancer risk reduction among population groups with CVD than among the general population.

Associations of changes in physical activity and diet with incident obesity and changes in adiposity: Longitudinal findings from the UK Biobank.

We examined the association of changes in physical activity and diet with obesity development and changes in body fat percentage, body mass index, and waist circumference. 31,344 adults without obesity at baseline (age = 56.0 ± 7.5 years; female = 49.1%) from the UK Biobank were included. Physical activity was categorised based on public health guidelines as: inactive; insufficient; and sufficient. Diet category was assigned based on an established composited score that included consumption of fruits, vegetables, fish, red meat (unprocessed), and processed meat. Diet was categorised as: poor; reasonable; and good. Physical activity and diet changes were categorised based on changes in category: worsened; stable; increased (physical activity)/improved (diet). During a mean follow up of 6.8 (SD = ±2.3) years, 1354 (4.3%) participants developed obesity. Compared to stable physical activity-diet, increasing physical activity was associated with the lowest obesity odds, across diet changes (e.g., OR [95%CI]: diet worsened (0.89 [0.69, 1.15]); diet improved (0.65 [0.48, 0.89])). Increasing physical activity with improved diet was associated with the largest difference in body fat percentage (ß:-0.62 [-0.82, -0.41]), body mass index (-0.37 [-0.47, -0.28]), and waist circumference (-1.21 [-1.63, -0.79]). Excluding adults with a history of smoking, or major illness, lowered obesity odds among participants with increased physical activity by an additional 11%-21%. In those who decreased physical activity obesity was attenuated when combined with diet improvement. Improvements in physical activity or diet mutually attenuated the deleterious associations of the other behaviour's deterioration. In most analyses, increases in physical activity conferred consistent positive associations against the development of obesity, across dietary change groups.

Joint association of alcohol consumption and adiposity with alcohol- and obesity-related cancer in a population sample of 399,575 UK adults.

Obesity and alcohol consumption are both important modifiable risk factors for cancer. We examined the joint association of adiposity and alcohol consumption with alcohol- and obesity-related cancer incidence. This prospective cohort study included cancer-free UK Biobank participants aged 40-69 years. Alcohol consumption was categorised based on current UK guidelines into four groups. We defined three markers of adiposity: body fat percentage (BF %), waist circumference and BMI and categorised each into three groups. We derived a joint alcohol consumption and adiposity marker variable with twelve mutually exclusive categories. Among 399 575 participants, 17 617 developed alcohol-related cancer and 20 214 developed obesity-related cancer over an average follow-up of 11·8 (SD 0·9) years. We found relatively weak evidence of independent associations of alcohol consumption with cancer outcomes. However, the joint association analyses showed that across all adiposity markers, above guideline drinkers who were in the top two adiposity groups had elevated cancer incidence risk (e.g. HR for alcohol-related cancer was 1·53 (95 % CI (1·24, 1·90)) for within guideline drinkers and 1·61 (95 % CI (1·30, 2·00)) for above guideline drinkers among participants who were in the top tertile BF %. Regardless of alcohol consumption status, the risk of obesity-related cancer increased with higher adiposity in a dose-response manner within alcohol consumption categories. Our study provides guidance for public health priorities aimed at lowering population cancer risk via two key modifiable risk factors.

Body shape phenotypes of multiple anthropometric traits and cancer risk: a multi-national cohort study.

BACKGROUND: Classical anthropometric traits may fail to fully represent the relationship of weight, adiposity, and height with cancer risk. We investigated the associations of body shape phenotypes with the risk of overall and site-specific cancers. METHODS: We derived four distinct body shape phenotypes from principal component (PC) analysis on height, weight, body mass index (BMI), waist (WC) and hip circumferences (HC), and waist-to-hip ratio (WHR). The study included 340,152 men and women from 9 European countries, aged mostly 35-65 years at recruitment (1990-2000) in the European Prospective Investigation into Cancer and Nutrition (EPIC) study. Cox proportional hazards regression was used to estimate multivariable-adjusted hazard ratios (HRs) and 95% confidence intervals (CIs). RESULTS: After a median follow-up of 15.3 years, 47,110 incident cancer cases were recorded. PC1 (overall adiposity) was positively associated with the risk of overall cancer, with a HR per 1 standard deviation (SD) increment equal to 1.07 (95% confidence interval 1.05 to 1.08). Positive associations were observed with 10 cancer types, with HRs (per 1 SD) ranging from 1.36 (1.30-1.42) for endometrial cancer to 1.08 (1.03-1.13) for rectal cancer. PC2 (tall stature with low WHR) was positively associated with the risk of overall cancer (1.03; 1.02-1.04) and five cancer types which were not associated with PC1. PC3 (tall stature with high WHR) was positively associated with the risk of overall cancer (1.04; 1.03-1.05) and 12 cancer types. PC4 (high BMI and weight with low WC and HC) was not associated with overall risk of cancer (1.00; 0.99-1.01). CONCLUSIONS: In this multi-national study, distinct body shape phenotypes were positively associated with the incidence of 17 different cancers and overall cancer.

Changes in physical activity and adiposity with all-cause, cardiovascular disease, and cancer mortality.

BACKGROUND: The relationship between joint changes in physical activity and adiposity with mortality is not well understood. We examined the association of changes in these two established risk factors with all-cause (ACM), cardiovascular disease (CVD), and cancer mortality. METHODS: We used longitudinal data from Taiwan's MJ Cohort, comprising 116,228 general population adults recruited from 1998-2013 with repeated measures 4.6 y (2.5) apart and followed up for mortality for 11.9 y (3.5). Physical activity, body mass index (BMI), waist circumference (WC), and body fat percentage (BF%) groups and changes were based on public health and clinical guidelines. RESULTS: Compared to stable-insufficient physical activity, increasing physical activity from any baseline level was associated with lower ACM (HR [95%CI]): 0.85 [0.74, 0.96]) and CVD mortality (0.72 [0.55, 0.93]) risk. This was approximately equal to meeting physical activity guidelines at both timepoints (eg: 0.71 [0.58, 0.88] for CVD mortality). Compared to stable-overweight/moderate adiposity, decreasing adiposity level attenuated but did not offset mortality risk for all three outcomes (eg: BMI = 0.95 [0.76, 1.16] for CVD mortality). Only maintaining a healthy adiposity level at both timepoints offset mortality risk (BMI = 0.75 [0.61, 0.89]) for CVD mortality). In the joint changes analyses, lower mortality risk was a consequence of increases in physical activity across adiposity change groups (eg: WC decrease = 0.57 [0.48, 0.67]; WC stability = 0.73 [0.66, 0.80], WC increase = 0.83 [0.72, 0.97] for ACM). Decreasing adiposity attenuated the negative associations of decreased physical activity (BF% = 1.13 [0.95, 1.35] for ACM). CONCLUSIONS: We found a lower risk for ACM, CVD, and cancer mortality from increasing physical activity and an attenuation from decreasing adiposity regardless of baseline levels. The beneficial associations of joint changes were primarily driven by physical activity, suggesting lower mortality risk may be more immediate through physical activity improvements compared to adiposity improvements alone.

Migratory and anti-fibrotic programmes define the regenerative potential of human cardiac progenitors.

Heart regeneration is an unmet clinical need, hampered by limited renewal of adult cardiomyocytes and fibrotic scarring. Pluripotent stem cell-based strategies are emerging, but unravelling cellular dynamics of host-graft crosstalk remains elusive. Here, by combining lineage tracing and single-cell transcriptomics in injured non-human primate heart biomimics, we uncover the coordinated action modes of human progenitor-mediated muscle repair. Chemoattraction via CXCL12/CXCR4 directs cellular migration to injury sites. Activated fibroblast repulsion targets fibrosis by SLIT2/ROBO1 guidance in organizing cytoskeletal dynamics. Ultimately, differentiation and electromechanical integration lead to functional restoration of damaged heart muscle. In vivo transplantation into acutely and chronically injured porcine hearts illustrated CXCR4-dependent homing, de novo formation of heart muscle, scar-volume reduction and prevention of heart failure progression. Concurrent endothelial differentiation contributed to graft neovascularization. Our study demonstrates that inherent developmental programmes within cardiac progenitors are sequentially activated in disease, enabling the cells to sense and counteract acute and chronic injury.

Effect of severe compared with moderate energy restriction on physical activity among postmenopausal female adults with obesity: a prespecified secondary analysis of the Type of Energy Manipulation for Promoting optimum metabolic health and body composition in Obesity (TEMPO) Diet randomized controlled Trial.

BACKGROUND: An under-explored strategy for increasing physical activity is the dietary treatment of obesity, but empirical evidence is lacking. OBJECTIVES: We aimed to compare the effects of weight loss via severe as opposed to moderate energy restriction on physical activity over 36 mo. METHODS: A total of 101 postmenopausal female adults (45-65 y, BMI 30-40 kg/m2, <180 min/wk of structured exercise) were randomly assigned to either 12 mo of moderate energy restriction (25%-35% of energy requirement) with a food-based diet, or a severe intervention involving 4 mo of severe energy restriction (65%-75% of energy requirement) with a total meal replacement diet, followed by 8 mo of moderate energy restriction. Physical activity was encouraged, but no tailored or supervised exercise prescription was provided. Physical activity was assessed with an accelerometer worn for 7 d before baseline (0 mo) and 0.25, 1, 4, 6, 12, 24, and 36 mo after intervention commencement. RESULTS: Compared with the moderate group, the severe group exhibited greater mean: total volume of physical activity; duration of moderate-to-vigorous-intensity physical activity (MVPA); duration of light-intensity physical activity; step counts, as well as lower mean duration of sedentary time. All these differences (except step counts) were apparent at 6 mo [e.g., 1006 metabolic equivalent of task (MET)-min/wk; 95% CI: 564, 1449 MET-min/wk for total volume of physical activity], and some were also apparent at 4 and/or 12 mo. There were no differences between groups in the 2 other outcomes investigated (self-efficacy to regulate exercise; and proportion of participants meeting the WHO's 2020 Physical Activity Guidelines for MVPA). When the analyses were adjusted for weight at each time point, the differences between groups were either attenuated or abolished. CONCLUSIONS: Among female adults with obesity, including a dietary component to reduce excess body weight-notably one involving severe energy restriction-could potentially enhance the effectiveness of physical activity interventions.This trial was registered at www.anzctr.org.au as ACTRN12612000651886.

Alcohol drinking in one's thirties and forties is associated with body mass index in men, but not in women: A longitudinal analysis of the 1970 British Cohort Study.

Our objective was to investigate longitudinal associations between alcohol drinking and body mass index (BMI). Alcohol drinking (exposure), BMI (outcome), smoking habit, occupation, longstanding illness, and leisure time physical activity (potential confounders) were assessed at ages 30, 34, 42, and 46 in the 1970 British Birth Cohort Study. Multilevel models were used to cope with the problem of correlated observations. There were 15,708 observations in 5931 men and 14,077 observations in 5656 women. Drinking was associated with BMI in men. According to the regression coefficients, BMI was expected to increase by 0.36 (95% confidence interval: 0.11, 0.60) kg/m2 per year in men who drank once a week and by 0.40 (0.14, 0.15) kg/m2 per year in men who drank most days. In ten years, BMI was expected to increase by 5.4 kg/m2 in men who drank and by 2.9 kg/m2 in men who drank and were physically active. Drinking was not associated with BMI in women. Rather, BMI was expected to increase by 0.25 (0.07, 0.43) kg/m2 per year in women who were former smokers. In ten years, BMI was expected to increase by 4.3 kg/m2 in women who were former smokers and by 0.8 kg/m2 in women who were former smokers and who were physically active. Associations between drinking and BMI were similar after further adjustment for problematic drinking and diet. These longitudinal data suggest that drinking is associated with BMI in men and that drinking is not associated with BMI in women independent of other lifestyle risk factors.

Periodontitis induces endothelial dysfunction in mice.

The treatment of periodontitis has numerous positive effects on established chronic health conditions, including cardiovascular disease and diabetes. However, ethical considerations do limit the establishment of human trials to investigate whether periodontitis promotes the early stages of chronic conditions. Therefore, the aim of this study was to investigate whether periodontitis induces endothelial dysfunction in hyperlipidemic apolipoprotein E gene-deficient (ApoE-/-) mice. Forty-five 8-week-old ApoE-/- mice were challenged by oral lavage with Porphyromonas gingivalis and Streptococcus gordonii for 4 weeks. A subgroup of animals (n = 15-17/group) was placed in a metabolic chamber immediately before euthanasia at 4 weeks to measure VO2/CO2 concentrations and voluntary locomotion. In infected and control animals alveolar bone levels were measured by x-ray imaging and endothelial function was determined by measuring endothelial-dependent vasorelaxation of aortic rings. The mRNA expression levels of serum amyloid A and tumor necrosis factor were determined in liver tissues by qRT PCR and protein concentrations in serum by ELISA. Caecal contents were analysed by sequencing to determine changes to the gut microbiota to investigate linkages between microbiome and systemic changes. The results showed that oral lavage of P. gingivalis and S. gordonii for 4 weeks, initiated periodontitis in ApoE-/- mice, similar to the human situation. The oral inflammation was accompanied by a significant increase in mRNA expression of pro-inflammatory mediators serum amyloid A1 and tumor necrosis factor in the liver. Mice with periodontitis also exhibited impaired endothelial-dependent vasorelaxation responses to acetylcholine. This systemic response was connected to increased energy expenditure, locomotion and respiratory quotient. No differences were detected in caecal microbiota between the infected and control animals. Overall, this is the first report that provide evidence that periodontitis induces endothelial dysfunction in mice. Other systemic responses observed in response to the local reaction need further investigation. The study suggests that early prevention of periodontitis may help limit the early stages of endothelial dysfunction that is linked to atherogenesis in humans.

Lifestyle risk factors and infectious disease mortality, including COVID-19, among middle aged and older adults: Evidence from a community-based cohort study in the United Kingdom.

In this community-based cohort study, we investigated the relationship between combinations of modifiable lifestyle risk factors and infectious disease mortality. Participants were 468,569 men and women (56.5 ± 8.1, 54.6% women) residing in the United Kingdom. Lifestyle indexes included traditional and emerging lifestyle risk factors based on health guidelines and best practice recommendations for: physical activity, sedentary behaviour, sleep quality, diet quality, alcohol consumption, and smoking status. The main outcome was mortality from infectious diseases, including pneumonia, and coronavirus disease 2019 (COVID-19). Meeting public health guidelines or best practice recommendations among combinations of lifestyle risk factors was inversely associated with mortality. Hazard ratios ranged between 0.26 (0.23-0.30) to 0.69 (0.60-0.79) for infectious disease and pneumonia. Among participants with pre-existing cardiovascular disease or cancer, hazard ratios ranged between 0.30 (0.25-0.34) to 0.73 (0.60-0.89). COVID-19 mortality risk ranged between 0.42 (0.28-0.63) to 0.75 (0.49-1.13). We found a beneficial dose-response association with a higher lifestyle index against mortality that was consistent across sex, age, BMI, and socioeconomic status. There was limited evidence of synergistic interactions between most lifestyle behaviour pairs, suggesting that the dose-response relationship among different lifestyle behaviours is not greater than the sum of the risk induced by each behaviour. Improvements in lifestyle risk factors and meeting public health guidelines or best practice recommendations could be used as an ancillary measure to ameliorate infectious disease mortality.

Formation of advanced glycation endproducts in foods during cooking process and underlying mechanisms: a comprehensive review of experimental studies.

Advanced glycation endproducts (AGE) are a group of complex and heterogeneous molecules, sharing some common characteristics such as covalent cross-link formation among proteins, the effect of transforming the colour of food products into yellow-brown colours and fluorescence formation. AGE are linked to many diseases including diabetes, renal diseases, CVD, liver diseases, neuro-degenerative and eye disorders, female reproductive dysfunction, and even cancer. AGE are formed endogenously but are also provided from exogenous sources including diet and tobacco. Western diet, rich in processed and/or heat-treated foods, fat and sugar, increases the exposure to AGE. The foods that contain high levels of fat and protein are generally rich in terms of AGE, and are also prone to AGE formation during cooking compared with carbohydrate-rich foods such as vegetables, fruits, legumes and whole grains. The present article aimed to review the literature about the effects of different cooking methods and conditions on the AGE content of food and AGE formation mechanisms using a comprehensive approach.

Dynamics of activating and repressive histone modifications in Drosophila neural stem cell lineages and brain tumors.

During central nervous system development, spatiotemporal gene expression programs mediate specific lineage decisions to generate neuronal and glial cell types from neural stem cells (NSCs). However, little is known about the epigenetic landscape underlying these highly complex developmental events. Here, we perform ChIP-seq on distinct subtypes of Drosophila FACS-purified NSCs and their differentiated progeny to dissect the epigenetic changes accompanying the major lineage decisions in vivo By analyzing active and repressive histone modifications, we show that stem cell identity genes are silenced during differentiation by loss of their activating marks and not via repressive histone modifications. Our analysis also uncovers a new set of genes specifically required for altering lineage patterns in type II neuroblasts (NBs), one of the two main Drosophila NSC identities. Finally, we demonstrate that this subtype specification in NBs, unlike NSC differentiation, requires Polycomb-group-mediated repression.

Promoting a Healthy Diet in Young Adults: The Role of Nutrition Labelling.

The use of the nutrition facts label has been associated with healthy eating behaviors for adults. However, the relationship between nutrition facts label use and overall diet quality is not well known in young adults, a vulnerable group that acquire lifelong eating behaviors during this period of life. This study aimed to assess if the use of information on the nutrition facts label is associated with a higher diet quality in young adults. In this cross-sectional study, 958 university students aged 18⁻34 years were recruited. Nutrition facts label use was recorded. Dietary intake was assessed using 24-h dietary recall. Healthy Eating Index-2005 (HEI-2005) scores were calculated. HEI-2005 score was significantly associated with using nutrition facts label (p < 0.001). The mean total HEI-2005 score was 60.7 ± 10.11, 62.4 ± 11.43 and 67.1 ± 12.23 respectively for never, sometimes and everytime users of nutrition facts label (p < 0.001). Sub-group scores of HEI-2005 for total fruits, whole fruits, total vegetables, whole grains, milk, oils, saturated fat, and calories from solid fat, alcohol and added sugar (SoFAAS) were significantly higher in regular nutrition facts label users (p < 0.05, for each). This study showed that young adults who regularly use the nutrition facts label have a higher diet quality.

Is aluminum exposure a risk factor for neurological disorders?

Aluminum (Al) is widely found in the nature. Although the relation between Al and neurodegenerative diseases is still controversial, Al is related with many brain diseases including Alzheimer's disease, Parkinson's disease, and multiple sclerosis. Al exposure occurs mainly through environment, occupational, and dietary factors for humans. Al exposure with diet can be through foods, food additives, water, and contamination of Al equipment/utensils. The aim of this review is to summarize various hypotheses, which link Al and neurodegeneration, and to determine the roles of Al exposure through different sources including diet, environment, and occupation. Future studies should be done in vulnerable subgroups of population including children, patients receiving antacid or Al-containing pharmeteucials on a daily basis, patients with reduced renal function, and patients on parenteral nutrition regimens that are likely to be affected by possible adverse health effects of Al. In addition, gender, age, and Al interactions need to be determined. One of the most important challanges in future epidemiological studies is to determine which variables should be controlled. In addition, experimental studies should be more focused and translational. In this context, exposure dose, dose-response effects, and time lapse between exposures and cognitive assessments are very important.

Development of acute pulmonary hypertension after bortezomib treatment in a patient with multiple myeloma: a case report and the review of the literature.

Bortezomib is widely used in treatment of multiple myeloma. In recent years, severe bortezomib-induced lung injury has been reported. The clinical course is generally characterized with fever and dyspnea, followed by respiratory failure with pulmonary infiltrates. Herein, we report a 57-year-old man with newly diagnosed multiple myeloma admitted with dyspnea, fever, and hypotension on the third day of the first dose of bortezomib therapy. He had bilateral jugular venous distention, crackles at the bases of the lungs and hepatomegaly. Transthoracic echocardiography revealed acute pulmonary hypertension (PH) with an estimated pressure of 70 mm Hg. The perfusion scintigraphy ruled out pulmonary embolism, and microbiological examination was negative. On his course, fever, dyspnea, hypoxia, and pulmonary vascular pressure subsided rapidly. The sudden onset of PH and its rapid decrement without any treatment suggests bortezomib as the underlying cause. Subsequently, the patient did not respond to vincristine-doxorubicin-dexamethasone regimen and thalidomide. Bortezomib treatment was repeated, and no pulmonary adverse reactions occurred. Follow-up echocardiographies revealed pulmonary arterial pressures to be maximally of 35 mm Hg. To our knowledge, this is the first case of acute PH after front-line bortezomib therapy. In this report, we review bortezomib-related pulmonary complications in the literature and possible underlying mechanisms.

Two-dimensional strain and strain rate imaging of the left atrium and left ventricle in adult patients with atrial septal defects before and after the later stage of percutaneous device closure.

AIM: Atrial septal defect (ASD) causes chronic volume overload of the right heart. The potential adverse effects of this long-standing volume overload to left atrium (LA) and left ventricle (LV) and their response to ASD closure has been poorly studied. METHODS: We studied 20 ASD patients before the procedure, at the 24-hour and 1 month following the percutaneous closure. Twenty age-matched controls served as the control group. The analysis for atrial deformation was performed on the lateral wall, mid segment of the LA from apical four-chamber view. Peak longitudinal strain (S) and strain rate (SR) during LA reservoir, passive emptying, atrial contraction phases and LV global longitudinal systolic S and SR were measured. RESULTS: Peak S and SR at LA reservoir, conduit and late contraction phases in ASD patients were similar to controls. All of these parameters increased immediately after the closure of the defect. Similarly, SLV and SRLV in ASD patients were not significantly different from the controls and significantly increased after the closure. But LA S, SR and LV S, SR results decreased in 1 month after the closure. SLV in ASD patients was significantly correlated with echocardiographic findings and the invasively measured defect size. CONCLUSION: LA and LV S and SR are not significantly affected in ASD patients. However, correction of the long-standing volume overload by percutaneous closure causes an early increase in LA and LV longitudinal deformation that correlates with the magnitude of the atrial septal defect. But this increase decreased in 1 month after closure.