Hypertensive patients' use of blood pressure monitors stationed in pharmacies and other locations: a cross-sectional mail survey

<p>Abstract</p> <p>Background</p> <p>Blood pressure (BP) monitors are commonly stationed in public places such as pharmacies, but it is uncertain how many people with hypertension currently use them. We sought to estimate the proportion of hypertensive patients who use these types of monitors and examine whether use varies by demographic or health characteristics.</p> <p>Methods</p> <p>We conducted a cross-sectional mail survey of hypertensive adults enrolled in a practice based research network of 24 primary care practices throughout the state of North Carolina. We analyzed results using descriptive statistics and examined bivariate associations using chi-square and independent associations using logistic regression.</p> <p>Results</p> <p>We received 530 questionnaires (76% response rate). Of 333 respondents (63%) who reported checking their BP in locations other than their doctor's office or home, 66% reported using a monitor stationed in a pharmacy. Younger patients more commonly reported using pharmacy monitors (48% among those < 45 years vs 35% of those over 65, p = 0.04). Blacks reported using them more commonly than whites (48% vs 39%, p = 0.03); and high school graduates more often than those with at least some college (50% vs 37%, p = 0.02). In multivariate analysis, younger age (aOR 1.49; 95% CI 1.00–2.21 for those age 45 to 65 years vs those > 65 years old) and high school education (aOR 1.74; 95% CI 1.13–2.58) were associated with use of pharmacy-stationed monitors, but Black race was not. Patients with diabetes, heart disease, or stroke were not more likely to use pharmacy-stationed monitors.</p> <p>Conclusion</p> <p>Hypertensive patients' use of BP monitors located in pharmacies is common. Younger patients, Blacks, and those with high school education were slightly more likely to report using them. Because use of these monitors is so common, efforts to ensure their accuracy are important.</p

Different genes interact with particulate matter and tobacco smoke exposure in affecting lung function decline in the general population

BACKGROUND: Oxidative stress related genes modify the effects of ambient air pollution or tobacco smoking on lung function decline. The impact of interactions might be substantial, but previous studies mostly focused on main effects of single genes. OBJECTIVES: We studied the interaction of both exposures with a broad set of oxidative-stress related candidate genes and pathways on lung function decline and contrasted interactions between exposures. METHODS: For 12679 single nucleotide polymorphisms (SNPs), change in forced expiratory volume in one second (FEV(1)), FEV(1) over forced vital capacity (FEV(1)/FVC), and mean forced expiratory flow between 25 and 75% of the FVC (FEF(25-75)) was regressed on interval exposure to particulate matter >10 microm in diameter (PM10) or packyears smoked (a), additive SNP effects (b), and interaction terms between (a) and (b) in 669 adults with GWAS data. Interaction p-values for 152 genes and 14 pathways were calculated by the adaptive rank truncation product (ARTP) method, and compared between exposures. Interaction effect sizes were contrasted for the strongest SNPs of nominally significant genes (p(interaction)>0.05). Replication was attempted for SNPs with MAF<10% in 3320 SAPALDIA participants without GWAS. RESULTS: On the SNP-level, rs2035268 in gene SNCA accelerated FEV(1)/FVC decline by 3.8% (p(interaction) = 2.5x10(-6)), and rs12190800 in PARK2 attenuated FEV1 decline by 95.1 ml p(interaction) = 9.7x10(-8)) over 11 years, while interacting with PM10. Genes and pathways nominally interacting with PM10 and packyears exposure differed substantially. Gene CRISP2 presented a significant interaction with PM10 (p(interaction) = 3.0x10(-4)) on FEV(1)/FVC decline. Pathway interactions were weak. Replications for the strongest SNPs in PARK2 and CRISP2 were not successful. CONCLUSIONS: Consistent with a stratified response to increasing oxidative stress, different genes and pathways potentially mediate PM10 and tobac smoke effects on lung function decline. Ignoring environmental exposures would miss these patterns, but achieving sufficient sample size and comparability across study samples is challengin

Stretchable and wearable colorimetric patches based on thermoresponsive plasmonic microgels embedded in a hydrogel film

Stimuli-responsive colorimetric sensors are promising for various industrial and medical applications due to the capability of simple, fast, and inexpensive visualization of external stimuli. Here we demonstrate a thermoresponsive, smart colorimetric patch based on a thermoresponsive plasmonic microgel embedded in a stretchable hydrogel film. To achieve a fast and efficient thermoresponsive color change, raspberry-shaped plasmonic microgels were fabricated by decorating gold nanoparticles (AuNPs) on poly(N-isopropylacrylamide) (PNIPAM) microgels, which exhibit reversible and strain-insensitive color shifts (between red and grayish violet) in response to a temperature change. The smart colorimetric patch containing a plasmonic microgels exhibits a significant extinction peak shift (176 nm) in a short time (1 s), with a temperature-sensing resolution of 0.2 degrees C. Moreover, the transition temperature of the plasmonic microgel can be finely tuned by additives and comonomers, so that the exquisite temperature visualization can be conducted over a wide temperature range of 25-40 degrees C by assembling plasmonic microgel films with different transition temperatures into an array patch. For proof-of-concept demonstrations, a freestanding smart colorimetric patch was utilized as a spatial temperature scanner and a colorimetric thermometer for a thermoresponsive actuator, which is potentially applicable in smart, wearable sensors and soft robotics

Cell death regulation during influenza A virus infection by matrix (M1) protein: a model of viral control over the cellular survival pathway

During early infection, viruses activate cellular stress-response proteins such as heat-shock proteins (Hsps) to counteract apoptosis, but later on, they modulate these proteins to stimulate apoptosis for efficient viral dissemination. Hsp70 has been attributed to modulate viral entry, transcription, nuclear translocation and virion formation. It also exerts its anti-apoptotic function by binding to apoptosis protease-activating factor 1 (Apaf-1) and disrupting apoptosome formation. Here, we show that influenza A virus can regulate the anti-apoptotic function of Hsp70 through viral protein M1 (matrix 1). M1 itself did not induce apoptosis, but enhanced the effects of apoptotic inducers. M1-small-interfering RNA inhibits virus-induced apoptosis in cells after either virus infection or overexpression of the M1 protein. M1 binds to Hsp70, which results in reduced interaction between Hsp70 and Apaf-1. In a cell-free system, the M1 protein mediates procaspase-9 activation induced by cytochrome c/deoxyadenosine triphosphate. A study involving deletion mutants confirmed the role of the C-terminus substrate-binding domain (EEVD) of Hsp70 and amino acids 128–165 of M1 for this association. The M1 mutants, which did not co-immunoprecipitate with Hsp70, failed to induce apoptosis. Overall, the study confirms the proapoptotic function of the M1 protein during influenza virus infection

The Rotterdam Study: 2010 objectives and design update

The Rotterdam Study is a prospective cohort study ongoing since 1990 in the city of Rotterdam in The Netherlands. The study targets cardiovascular, endocrine, hepatic, neurological, ophthalmic, psychiatric and respiratory diseases. As of 2008, 14,926 subjects aged 45 years or over comprise the Rotterdam Study cohort. The findings of the Rotterdam Study have been presented in close to a 1,000 research articles and reports (see www.epib.nl/rotterdamstudy). This article gives the rationale of the study and its design. It also presents a summary of the major findings and an update of the objectives and methods

The Rotterdam Study: 2012 objectives and design update

The Rotterdam Study is a prospective cohort study ongoing since 1990 in the city of Rotterdam in The Netherlands. The study targets cardiovascular, endocrine, hepatic, neurological, ophthalmic, psychiatric, dermatological, oncological, and respiratory diseases. As of 2008, 14,926 subjects aged 45 years or over comprise the Rotterdam Study cohort. The findings of the Rotterdam Study have been presented in over a 1,000 research articles and reports (see www.erasmus-epidemiology.nl/rotterdamstudy). This article gives the rationale of the study and its design. It also presents a summary of the major findings and an update of the objectives and methods

Variability of the chronic obstructive pulmonary disease key epidemiological data in Europe: systematic review

<p>Abstract</p> <p>Background</p> <p>Chronic obstructive pulmonary disease (COPD) is predicted to become a major cause of death worldwide. Studies on the variability in the estimates of key epidemiological parameters of COPD may contribute to better assessment of the burden of this disease and to helpful guidance for future research and public policies. In the present study, we examined differences in the main epidemiological characteristics of COPD derived from studies across countries of the European Union, focusing on prevalence, severity, frequency of exacerbations and mortality, as well as on differences between the studies' methods.</p> <p>Methods</p> <p>This systematic review was based on a search for the relevant literature in the Science Citation Index database via the Web of Science and on COPD mortality rates issued from national statistics. Analysis was finally based on 65 articles and Eurostat COPD mortality data for 21 European countries.</p> <p>Results</p> <p>Epidemiological characteristics of COPD varied widely from country to country. For example, prevalence estimates ranged between 2.1% and 26.1%, depending on the country, the age group and the methods used. Likewise, COPD mortality rates ranged from 7.2 to 36.1 per 10⁵inhabitants. The methods used to estimate these epidemiological parameters were highly variable in terms of the definition of COPD, severity scales, methods of investigation and target populations. Nevertheless, to a large extent, several recent international guidelines or research initiatives, such as GOLD, BOLD or PLATINO, have boosted a substantial standardization of methodology in data collection and have resulted in the availability of more comparable epidemiological estimates across countries. On the basis of such standardization, severity estimates as well as prevalence estimates present much less variation across countries. The contribution of these recent guidelines and initiatives is outlined, as are the problems remaining in arriving at more accurate COPD epidemiological estimates across European countries.</p> <p>Conclusions</p> <p>The accuracy of COPD epidemiological parameters is important for guiding decision making with regard to preventive measures, interventions and patient management in various health care systems. Therefore, the recent initiatives for standardizing data collection should be enhanced to result in COPD epidemiological estimates of improved quality. Moreover, establishing international guidelines for reporting research on COPD may also constitute a major contribution.</p