Health disparities among older adults following tropical cyclone exposure in Florida.

Tropical cyclones (TCs) pose a significant threat to human health, and research is needed to identify high-risk subpopulations. We investigated whether hospitalization risks from TCs in Florida (FL), United States, varied across individuals and communities. We modeled the associations between all storms in FL from 1999 to 2016 and over 3.5 million Medicare hospitalizations for respiratory (RD) and cardiovascular disease (CVD). We estimated the relative risk (RR), comparing hospitalizations during TC-periods (2 days before to 7 days after) to matched non-TC-periods. We then separately modeled the associations in relation to individual and community characteristics. TCs were associated with elevated risk of RD hospitalizations (RR: 4.37, 95% CI: 3.08, 6.19), but not CVD (RR: 1.04, 95% CI: 0.87, 1.24). There was limited evidence of modification by individual characteristics (age, sex, or Medicaid eligibility); however, risks were elevated in communities with higher poverty or lower homeownership (for CVD hospitalizations) and in denser or more urban communities (for RD hospitalizations). More research is needed to understand the potential mechanisms and causal pathways that might account for the observed differences in the association between tropical cyclones and hospitalizations across communities.

Assessing Adverse Health Effects of Long-Term Exposure to Low Levels of Ambient Air Pollution: Implementation of Causal Inference Methods.

This report provides a final summary of the principal findings and key conclusions of a study supported by an HEI grant aimed at "Assessing Adverse Health Effects of Long-Term Exposure to Low Levels of Ambient Air Pollution." It is the second and final report on this topic. The study was designed to advance four critical areas of inquiry and methods development. First, it focused on predicting short- and long-term exposures to ambient fine particulate matter (PM2.5), nitrogen dioxide (NO2), and ozone (O3) at high spatial resolution (1 km × 1 km) for the continental United States over the period 2000-2016 and linking these predictions to health data. Second, it developed new causal inference methods for estimating exposure-response (ER) curves (ERCs) and adjusting for measured confounders. Third, it applied these methods to claims data from Medicare and Medicaid beneficiaries to estimate health effects associated with short- and long-term exposure to low levels of ambient air pollution. Finally, it developed pipelines for reproducible research, including approaches for data sharing, record linkage, and statistical software. Our HEI-funded work has supported an extensive portfolio of analyses and the development of statistical methods that can be used to robustly understand the health effects of short- and long-term exposure to low levels of ambient air pollution. Our Phase 1 report (Dominici et al. 2019) provided a high-level overview of our statistical methods, data analysis, and key findings, grouped into the following five areas: (1) exposure prediction, (2) epidemiological studies of ambient exposures to air pollution at low levels, (3) sensitivity analysis, (4) methodological contributions in causal inference, and (5) an open access research data platform. The current, final report includes a comprehensive overview of the entire research project.Considering our (1) massive study population, (2) numerous sensitivity analyses, and (3) transparent assessment of covariate balance indicating the quality of causal inference for simulating randomized experiments, we conclude that conditionally on the required assumptions for causal inference, our results collectively indicate that long-term PM2.5 exposure is likely to be causally related to mortality. This conclusion assumes that the causal inference assumptions hold and, more specifically, that we accounted adequately for confounding bias. We explored various modeling approaches, conducted extensive sensitivity analyses, and found that our results were robust across approaches and models. This work relied on publicly available data, and we have provided code that allows for reproducibility of our analyses.Our work provides comprehensive evidence of associations between exposures to PM2.5, NO2, and O3 and various health outcomes. In the current report, we report more specific results on the causal link between long-term exposure to PM2.5 and mortality, even at PM2.5 levels below or equal to 12 µg/m3, and mortality among Medicare beneficiaries (ages 65 and older). This work relies on newly developed causal inference methods for continuous exposure.For the period 2000-2016, we found that all statistical approaches led to consistent results: a 10-µg/m3 decrease in PM2.5 led to a statistically significant decrease in mortality rate ranging between 6% and 7% (= 1 - 1/hazard ratio [HR]) (HR estimates 1.06 [95% CI, 1.05 to 1.08] to 1.08 [95% CI, 1.07 to 1.09]). The estimated HRs were larger when studying the cohort of Medicare beneficiaries that were always exposed to PM2.5 levels lower than 12 µg/m3 (1.23 [95% CI, 1.18 to 1.28] to 1.37 [95% CI, 1.34 to 1.40]).Comparing the results from multiple and single pollutant models, we found that adjusting for the other two pollutants slightly attenuated the causal effects of PM2.5 and slightly elevated the causal effects of NO2 exposure on all-cause mortality. The results for O3 remained almost unchanged.We found evidence of a harmful causal relationship between mortality and long-term PM2.5 exposures adjusted for NO2 and O3 across the range of annual averages between 2.77 and 17.16 µg/m3 (included >98% of observations) in the entire cohort of Medicare beneficiaries across the continental United States from 2000 to 2016. Our results are consistent with recent epidemiological studies reporting a strong association between long-term exposure to PM2.5 and adverse health outcomes at low exposure levels. Importantly, the curve was almost linear at exposure levels lower than the current national standards, indicating aggravated harmful effects at exposure levels even below these standards.There is, in general, a harmful causal impact of long-term NO2 exposures to mortality adjusted for PM2.5 and O3 across the range of annual averages between 3.4 and 80 ppb (included >98% of observations). Yet within low levels (annual mean ≤53 ppb) below the current national standards, the causal impacts of NO2 exposures on all-cause mortality are nonlinear with statistical uncertainty.The ERCs of long-term O3 exposures on all-cause mortality adjusted for PM2.5 and NO2 are almost flat below 45 ppb, which shows no statistically significant effect. Yet we observed an increased hazard when the O3 exposures were higher than 45 ppb, and the HR was approximately 1.10 when comparing Medicare beneficiaries with annual mean O3 exposures of 50 ppb versus those with 30 ppb.institutions, including those that support the Health Effects Institute; therefore, it may not reflect the views or policies of these parties, and no endorsement by them should be inferred.A list of abbreviations and other terms appears at the end of this volume.

Air pollution and COVID-19 mortality in the United States: Strengths and limitations of an ecological regression analysis.

Assessing whether long-term exposure to air pollution increases the severity of COVID-19 health outcomes, including death, is an important public health objective. Limitations in COVID-19 data availability and quality remain obstacles to conducting conclusive studies on this topic. At present, publicly available COVID-19 outcome data for representative populations are available only as area-level counts. Therefore, studies of long-term exposure to air pollution and COVID-19 outcomes using these data must use an ecological regression analysis, which precludes controlling for individual-level COVID-19 risk factors. We describe these challenges in the context of one of the first preliminary investigations of this question in the United States, where we found that higher historical PM2.5 exposures are positively associated with higher county-level COVID-19 mortality rates after accounting for many area-level confounders. Motivated by this study, we lay the groundwork for future research on this important topic, describe the challenges, and outline promising directions and opportunities.

Evaluating the impact of long-term exposure to fine particulate matter on mortality among the elderly.

Many studies link long-term fine particle (PM2.5) exposure to mortality, even at levels below current U.S. air quality standards (12 micrograms per cubic meter). These findings have been disputed with claims that the use of traditional statistical approaches does not guarantee causality. Leveraging 16 years of data-68.5 million Medicare enrollees-we provide strong evidence of the causal link between long-term PM2.5 exposure and mortality under a set of causal inference assumptions. Using five distinct approaches, we found that a decrease in PM2.5 (by 10 micrograms per cubic meter) leads to a statistically significant 6 to 7% decrease in mortality risk. Based on these models, lowering the air quality standard to 10 micrograms per cubic meter would save 143,257 lives (95% confidence interval, 115,581 to 170,645) in one decade. Our study provides the most comprehensive evidence to date of the link between long-term PM2.5 exposure and mortality, even at levels below current standards.

Assessing Adverse Health Effects of Long-Term Exposure to Low Levels of Ambient Air Pollution: Phase 1.

INTRODUCTION: This report provides a summary of major findings and key conclusions supported by a Health Effects Institute grant aimed at "Assessing Adverse Health Effects of Long-Term Exposure to Low Levels of Ambient Pollution." Our study was designed to advance four critical areas of inquiry and methods development. METHODS: First, our work focused on predicting short- and long-term exposures to ambient PM2.5 mass (particulate matter ≤ 2.5µm in aerodynamic diameter) and ozone (O3) at high spatial resolution (1 km × 1 km) for the continental United States during the period 2000-2012 and linking these predictions to health data. Second, we developed new causal inference methods for exposure-response (ER) that account for exposure error and adjust for measured confounders. We applied these methods to data from the New England region. Third, we applied standard regression methods using Medicare claims data to estimate health effects that are associated with short- and long-term exposure to low levels of ambient air pollution. We conducted sensitivity analyses to assess potential confounding bias due to lack of extensive information on behavioral risk factors in the Medicare population using the Medicare Current Beneficiary Survey (MCBS) (nationally representative sample of approximately 15,000 Medicare enrollees per year), which includes abundant data on individual-level risk factors including smoking. Finally, we have begun developing tools for reproducible research - including approaches for data sharing, record linkage, and statistical software. RESULTS: Our HEI-funded work has supported an extensive portfolio of analysis and the development of statistical methods that can be used to robustly understand the health effects of long- and short-term exposure to low levels of ambient air pollution. This report provides a high-level overview of statistical methods, data analysis, and key findings, as grouped into the following four areas: (1) Exposure assessment and data access; (2) Epidemiological studies of ambient exposures to air pollution at low levels; (3) Methodological contributions in causal inference; and (4) Open science research data platform. CONCLUSION: Our body of work, advanced by HEI, lends extensive evidence that short- and long-term exposure to PM2.5 and O3 is harmful to human health, increasing the risks of hospitalization and death, even at levels that are well below the National Ambient Air Quality Standards (NAAQS).

Preservation of root cementum: a comparative evaluation of power-driven versus hand instruments.

OBJECTIVES: The purpose of this study was to evaluate the effects of three distinct periodontal treatment methods in comparison with hand instrumentation on residual cementum of periodontal diseased teeth. Cementum can influence the activities of periodontal cells and may play an important regulatory role in periodontal treatment. The ideal method for periodontal therapy involves removal of biofilm, calculus and endotoxin while preserving root cementum. MATERIAL AND METHODS: Forty-eight caries free, single-rooted teeth in patients diagnosed with severe chronic periodontitis were treated using four different methods prior to extraction. The teeth were instrumented subgingivally at one approximal site either by hand curettes (HC), piezoelectric ultrasonic scalers (U), piezoelectric ultrasonic scalers following air polishing (U + AP) or air polishing (AP) alone. Following extraction of teeth, instrumented and non-instrumented sites were analysed with a dissecting microscope and SEM for measurement of the amount of and surface characteristics of residual cementum. RESULTS: The percentage of coronal cementum remaining following subgingival instrumentation was 84% for U, 80% for U + AP, 94% for AP and 65% for HC. Although subgingival instrumentation of apical portions of the cementum demonstrated 6% less retained cementum in comparison with coronal portions, the amount of retained cementum with AP was still significantly greater than with HC. SEM results found the smoothest root surfaces were produced by the HC followed by the AP, while root surfaces instrumented by U or U + AP presented grooves and scratches. CONCLUSIONS: This study demonstrated that AP was superior to U devices in preserving cementum, whereas HC were the most effective instruments in removing cementum.

Chronic blockade of the AT2 receptor with PD123319 impairs insulin signaling in C57BL/6 mice.

The renin-angiotensin system modulates insulin action. Angiotensin type 1 receptor exerts a deleterious effects while the angiotensin type 2 receptor (AT2R) appears to have beneficial effects providing protection against insulin resistance and type 2 diabetes. Although recent reports indicate that agonism of AT2R ameliorates diabetes and insulin resistance, the phenotype of AT2R-knockout mice seems to be controversial relating this aspect. Thus, in this study we have explored the role of AT2R in the control of insulin action. To that end, C57Bl/6 mice were administered the synthetic AT2R antagonist PD123319 for 21days (10mg/kg/day ip); vehicle treated animals were used as control. Glucose tolerance, metabolic parameters, in vivo insulin signaling in main insulin-target tissues as well as levels of adiponectin, TNF-α, MCP-1 and IL-6 in adipose tissue were assessed. AT2R blockade with PD123319 induced a marginal effect on glucose homeostasis but an important reduction in the insulin-induced phosphorylation of the insulin receptor and Akt in both liver and adipose tissue. Insulin signaling in skeletal muscle remained unaltered after treatment with PD123319, which could explain the minimal effect on glucose homeostasis induced by PD123319. Our current results reinforce the notion that the AT2R has a physiological role in the conservation of insulin action.

Effect of cellulose and lignin on disintegration, antimicrobial and antioxidant properties of PLA active films.

This study reports the effects on antimicrobial, antioxidant, migration and disintegrability activities of ternary nanocomposite films based on poly(lactic acid) incorporating two biobased nanofillers, (cellulose nanocrystals (CNC) and lignin nanoparticles (LNP)), in two different amounts (1 and 3% wt.). Results from antimicrobial tests revealed a capacity to inhibit the Gram negative bacterial growth of Xanthomonas axonopodis pv. vesicatoria and Xanthomonas arboricola pv. pruni along the time, offering innovative opportunities against dangerous bacterial plant pathogens. LNP proved to be highly efficient in antioxidation activity, based on the disappearance of the absorption band at 517nm of the free radical, 2,2-diphenyl-1-picrylhydrazyl (DPPH) upon reduction by an antiradical compound; moreover the combination of LNP and CNC generates a synergistic positive effect in the antioxidation response of PLA ternary films. Furthermore, all the studied formulations showed a disintegrability value up to 90% after 15days of incubation in composting conditions. Migration results showed that the films can be considered suitable for application in food packaging field.

Bionanocomposite films based on plasticized PLA-PHB/cellulose nanocrystal blends.

Optically transparent plasticized poly(lactic acid) (PLA) based bionanocomposite films intended for food packaging were prepared by melt blending. Materials were plasticized with 15wt% of acetyl(tributyl citrate) (ATBC) to improve the material processability and to obtain flexibile films. Poly(hydroxybutyrate) (PHB) was used to increase PLA crystallinity. The thermal stability of the PLA-PHB blends was improved by the addition of 5 wt% of cellulose nanocrystals (CNC) or modified cellulose nanocrystals (CNCs) synthesized from microcrystalline cellulose. The combination of ATBC and cellulose nanocrystals, mainly the better dispersed CNCs, improved the interaction between PLA and PHB. Thus, an improvement on the oxygen barrier and stretchability was achieved in PLA-PHB-CNCs-ATBC which also displayed somewhat UV light blocking effect. All bionanocomposite films presented appropriate disintegration in compost suggesting their possible applications as biodegradable packaging materials.

Nitrosative Stress and Apoptosis by Intravenous Ferumoxytol, Iron Isomaltoside 1000, Iron Dextran, Iron Sucrose, and Ferric Carboxymaltose in a Nonclinical Model.

Iron is involved in the formation as well as in the scavenging of reactive oxygen and nitrogen species. Thus, iron can induce as well as inhibit both oxidative and nitrosative stress. It also has a key role in reactive oxygen and nitrogen species-mediated apoptosis. We assessed the differences in tyrosine nitration and caspase 3 expression in the liver, heart, and kidneys of rats treated weekly with intravenous ferumoxytol, iron isomaltoside 1000, iron dextran, iron sucrose and ferric carboxymaltose (40 mg iron/kg body weight) for 5 weeks. Nitrotyrosine was quantified in tissue homogenates by Western blotting and the distribution of nitrotyrosine and caspase 3 was assessed in tissue sections by immunohistochemistry. Ferric carboxymaltose and iron sucrose administration did not result in detectable levels of nitrotyrosine or significant levels of caspase 3 vs. control in any of the tissue studied. Nitrotyrosine and caspase 3 levels were significantly (p<0.01) increased in all assessed organs of animals treated with iron dextran and iron isomaltoside 1000, as well as in the liver and kidneys of ferumoxytol-treated animals compared to isotonic saline solution (control). Nitrotyrosine and caspase 3 levels were shown to correlate positively with the amount of Prussian blue-detectable iron(III) deposits in iron dextran- and iron isomaltoside 1000-treated rats but not in ferumoxytol-treated rats, suggesting that iron dextran, iron isomaltoside 1000 and ferumoxytol induce nitrosative (and oxidative) stress as well as apoptosis via different mechanism(s).

Multifunctional PLA-PHB/cellulose nanocrystal films: processing, structural and thermal properties.

Cellulose nanocrystals (CNCs) synthesized from microcrystalline cellulose by acid hydrolysis were added into poly(lactic acid)-poly(hydroxybutyrate) (PLA-PHB) blends to improve the final properties of the multifunctional systems. CNC were also modified with a surfactant (CNCs) to increase the interfacial adhesion in the systems maintaining the thermal stability. Firstly, masterbatch pellets were obtained for each formulation to improve the dispersion of the cellulose structures in the PLA-PHB and then nanocomposite films were processed. The thermal stability as well as the morphological and structural properties of nanocomposites was investigated. While PHB increased the PLA crystallinity due to its nucleation effect, well dispersed CNC and CNCs not only increased the crystallinity but also improved the processability, the thermal stability and the interaction between both polymers especially in the case of the modified CNCs based PLA-PHB formulation. Likewise, CNCs were better dispersed in PLA-CNCs and PLA-PHB-CNCs, than CNC.

Central insulin-angiotensin II interaction in blood pressure regulation in fructose overloaded rats.

The aim of the present study was to determine if insulin is able to modulate the pressor response to intracerebroventricularly administered angiotensin II in insulin resistant fructose overloaded rats. Male Sprague-Dawley rats were divided into two groups: 1) Control group (C) with tap water to drink for 6 weeks (n=36); and 2) fructose treated (F), with fructose solution (10% w/v) to drink for 6 weeks (n=36). On the day of the experiment, anesthetized male C and F rats were intracerebroventricularly infused with insulin (12 mU/h, n=15) or Ringer's solution as vehicle (n=15) for 2h. Immediately, changes in mean arterial pressure (MAP) in response to an intracerebroventricular subpressor dose of angiotensin II (5 pmol, n=10) or vehicle (n=5) were measured for 10 min. Then, hypothalami were removed and Akt and ERK1/2 phosphorylation levels were determined. In a subset of C (n=10) and F (n=20) animals, PD98059 (p44/42 MAPK inhibitor) or vehicle was administered intracerebroventricularly at a flow rate of 5 µl/min for 1 min. Ten minutes later, insulin (12 mU/h, n=5 for each group) or vehicle (Ringer's solution, only in the F group, n=5) was perfused for 2h at a flow rate of 4 µl/h, and cardiovascular parameters were measured every 15 min. Immediately, changes in MAP and HR in response to a subpressor dose of Ang II (5 pmol/2 µl) were evaluated for 10 min (n=5 for each group). In other subset of animals (n=6 for each group), AT1 and AT2 hypothalamic receptor levels were measured by Western blotting. Intracerebroventricular insulin pre-treatment increased the pressor response to angiotensin II in C rats. In F rats (with or without insulin pretreatment), the pressor response to angiotensin II was higher than that in vehicle pre-treated C animals, but similar to that observed in C after insulin infusion. In C rats phospho-ERK 1/2 hypothalamic levels significantly increased after angiotensin II injection in insulin pretreated animals compared to vehicle pre-treated rats, suggesting that MAPK activation might be involved in insulin potentiation of blood pressure response to angiotensin II in the brain. Phospho-ERK 1/2 hypothalamic levels were significantly increased in vehicle treated F rats compared to C, suggesting that basal MAPK activation might play a role in the enhanced response to angiotensin II observed in these animals. Finally, in F rats, either after vehicle or insulin infusion, angiotensin II injection was associated with a similar increase in phospho-ERK 1/2 hypothalamic levels, comparable to that observed after angiotensin II injection in insulin pre-treated C animals. ERK 1/2 blockade significantly reduced MAP in F rats compared to C. Moreover, ERK 1/2 inhibition completely abolished the Ang II pressor response in F rats and in insulin pre-treated C animals. All these findings suggest that insulin-angiotensin II interaction at hypothalamic level might be involved in the increase in blood pressure observed in the insulin resistant state.

A preliminary comparison of the effect of 0.3% versus 0.2% chlorhexidine mouth rinse on de novo plaque formation: a monocentre randomized double-blind crossover trial.

OBJECTIVE: Chlorhexidine (CHX) is considered the gold standard against gram-negative microorganisms. Little has been written about the simultaneous influence that both time and concentration could have on antiplaque formation effectiveness of CHX. The aim of this study is to compare the clinical and microbiological effectiveness of two different CHX concentrations and time applications in a 4-day plaque regrowth study model. MATERIAL AND METHODS: Twenty volunteers were enrolled in a randomized double-blind crossover study comparing the effectiveness of CHX 0.3% and CHX 0.2% mouth rinses applied for 15 and 30 s, respectively. Plaque index (PII), total bacterial counts and the detection of specific periopathogens were measured at the 5th day of each mouth rinse application. Taste acceptance was evaluated using a questionnaire. RESULTS: Chlorhexidine 0.3% resulted in a statistically greater reductions (10%) in PIl and periopathogens compared to CHX 0.2%. Furthermore, patients reported comparable taste acceptance in both groups. CONCLUSION: Chlorhexidine is an effective oral antiseptic. The CHX 0.3% mouth rinse formulation used for 15 s resulted in superior clinical and microbiological outcomes compared to the CHX 0.2% formulation, used for 30 s.

Prolonged exposure to GH impairs insulin signaling in the heart.

Acromegaly is associated with cardiac hypertrophy, which is believed to be a direct consequence of chronically elevated GH and IGF1. Given that insulin is important for cardiac growth and function, and considering that GH excess induces hyperinsulinemia, insulin resistance, and cardiac alterations, it is of interest to study insulin sensitivity in this tissue under chronic conditions of elevated GH. Transgenic mice overexpressing GH present cardiomegaly and perivascular and interstitial fibrosis in the heart. Mice received an insulin injection, the heart was removed after 2  min, and immunoblotting assays of tissue extracts were performed to evaluate the activation and abundance of insulin-signaling mediators. Insulin-induced tyrosine phosphorylation of the insulin receptor (IR) was conserved in transgenic mice, but the phosphorylation of IR substrate 1 (IRS1), its association with the regulatory subunit of the phosphatidylinositol 3-kinase (PI3K), and the phosphorylation of AKT were decreased. In addition, total content of the glucose transporter GLUT4 was reduced in transgenic mice. Insulin failed to induce the phosphorylation of the mammalian target of rapamycin (mTOR). However, transgenic mice displayed increased basal activation of the IR/IRS1/PI3K/AKT/mTOR and p38 signaling pathways along with higher serine phosphorylation of IRS1, which is recognized as an inhibitory modification. We conclude that GH-overexpressing mice exhibit basal activation of insulin signaling but decreased sensitivity to acute insulin stimulation at several signaling steps downstream of the IR in the heart. These alterations may be associated with the cardiac pathology observed in these animals.

Morphological observations and Fractological considerations on orthodontics miniscrews.

AIM: The purpose of this study was to evaluate morphological and biomechanical characteristics of a commercial mini-implant. METHODS: Orthodontic low head mini implants, in the two available sizes of 1.5 and 2 mm, have been used. The electronic scanning microscope evaluation has been tested on 3 groups each one composed of 4 samples, observed in numerous enlargements and in the three dimensions of the space. The groups were composed of new mini implants, undamaged mini implants observed after their clinical use and mini-implants broken at the moment of their insertion or removal after their therapeutical use. RESULTS: The microscope analysis of unused mini implants has shown how the diameter reduction of the neck represents the area of greater weakness; such parameter is very important in determining screw resistance to fracture. In fact the fracture observed in vivo always happened to this degree. Some micro carvings and cracks were shown on the surface, these irregularities could facilitate or promote the enlargement of the cracking itself. CONCLUSION: From the results obtained it is clear that the steel is adequate for permanence in the oral cavity, and moreover the material itself is adapted to bear the pressure put on it during therapy. However, it remains advisable to make certain changes to better the surface and geometry of the miniscrews.

Bayesian distributed lag models: estimating effects of particulate matter air pollution on daily mortality.

A distributed lag model (DLagM) is a regression model that includes lagged exposure variables as covariates; its corresponding distributed lag (DL) function describes the relationship between the lag and the coefficient of the lagged exposure variable. DLagMs have recently been used in environmental epidemiology for quantifying the cumulative effects of weather and air pollution on mortality and morbidity. Standard methods for formulating DLagMs include unconstrained, polynomial, and penalized spline DLagMs. These methods may fail to take full advantage of prior information about the shape of the DL function for environmental exposures, or for any other exposure with effects that are believed to smoothly approach zero as lag increases, and are therefore at risk of producing suboptimal estimates. In this article, we propose a Bayesian DLagM (BDLagM) that incorporates prior knowledge about the shape of the DL function and also allows the degree of smoothness of the DL function to be estimated from the data. We apply our BDLagM to its motivating data from the National Morbidity, Mortality, and Air Pollution Study to estimate the short-term health effects of particulate matter air pollution on mortality from 1987 to 2000 for Chicago, Illinois. In a simulation study, we compare our Bayesian approach with alternative methods that use unconstrained, polynomial, and penalized spline DLagMs. We also illustrate the connection between BDLagMs and penalized spline DLagMs. Software for fitting BDLagM models and the data used in this article are available online.

Multiple arm lipomatosis and posterior interosseus nerve palsy.

BACKGROUND: Lipomas are common benign soft tissue tumours which tend to be indolent and risk free. Lipomas rarely spread in the deep soft tissue causing posterior interosseous nerve (PIN) neuropathy. METHODS (CASE DESCRIPTION): We present two patients with multiple lipomatosis of the arms and PIN paralysis, with a brief review of the cases reported in literature. RESULTS AND CONCLUSION: We emphasize the role of electromyographic study as unique methodical capable to reveal an early radial nerve damage, permitting an optimal post-surgical nerve function recovering.

Outcomes of kidneys from donors after cardiac death: implications for allocation and preservation.

Although donation after cardiac death (DCD) kidneys have a high incidence of delayed graft function (DGF) and have been considered marginal, no tool for stratifying risk of graft loss nor a specific policy governing their allocation exist. We compared outcomes of 2562 DCD, 62,800 standard criteria donor (SCD) and 12,812 expanded criteria donor (ECD) transplants reported between 1993 and 2005, and evaluated factors associated with risk of graft loss and DGF in DCD kidneys. Donor age was the only criterion used in the definition of ECD kidneys that independently predicted graft loss among DCD kidneys. Kidneys from DCD donors <50 had similar long-term graft survival to those from SCD (RR 1.1, p = NS). While DGF was higher among DCD compared to SCD and ECD, limiting cold ischemia (CIT) to <12 h decreased the rate of DGF 15% among DCD <50 kidneys. These findings suggest that DCD <50 kidneys function like SCD kidneys and should not be viewed as marginal or ECD, and further, limiting CIT <12 h markedly reduces DGF.

Evidence of altered motor axon properties of the ulnar nerve in carpal tunnel syndrome.

OBJECTIVE: To analyse recruitment properties of ulnar nerve motor axons in 60 CTS patients with negative ulnar nerve electrodiagnostic tests. METHODS: Recruitment properties of the ulnar nerve were studied by analysing the relationship between the intensity of electrical stimulation and the size of motor response, i.e. the stimulus-response curve. Parameters of the curve (threshold, slope and plateau) were compared with those of the corresponding curve of the median nerve and both with parameters of 30 control curves. RESULTS: The ulnar nerve stimulus-response curve was strikingly abnormal and, except for severity, closely resembled that of the median nerve. The slope of the curve was significantly less than that of controls and decreased with increasing abnormalities of the median nerve. This suggested that the pathological process involving the ulnar nerve was contingent with the severity of median nerve involvement. CONCLUSIONS: We propose that the ulnar nerve may be subject to compression in Guyon's canal as a consequence of high pressure in the carpal tunnel of CTS patients. SIGNIFICANCE: Ectopic activity from ulnar axons may contribute to clinical spread of symptoms outside the median nerve territory in CTS. This does not exclude possible involvement of central plasticity mechanisms in producing extra-median symptoms in CTS patients.

Changes in the recruitment curve of the soleus H-reflex associated with chronic low back pain.

OBJECTIVE: We investigated whether patients with chronic low back pain (CLBP) manifest changes in the excitability of the soleus H-reflex. METHODS: H-reflex stimulus-response curve was studied in 14 CLBP patients and 14 age-matched healthy subjects. H-threshold, H-maximum size, H-steepness and H-latency were determined for both legs. Homosynaptic depression (HD), following a train of H-reflexes, and presynaptic inhibition (PI) from flexor afferents onto soleus Ia afferents were also evaluated. RESULTS: H-threshold was significantly increased, H-size as a function of stimulus intensity was significantly different, and H-recruitment curve steepness was significantly lower in CLBP patients compared to healthy subjects. No significant difference in the amount of HD and PI of the H-reflex was found between the two groups. H-latency and Hmax/Mmax ratio was comparable between the subjects groups. CONCLUSIONS: In CLBP there is a reduced excitability of group Ia afferent fibres from the soleus muscle to which presynaptic factors do not seem to contribute and that presumably depend on changes in the peripheral sensory input. SIGNIFICANCE: Changes in H-reflex excitability may underlie a decrease in the gain of a peripheral sensor in CLBP. Estimation of soleus H-threshold and H-recruitment curve may contribute to the diagnostic evaluation of CLBP and may be used to monitor the efficacy of treatment.