Mean and fluctuating velocity contours and acoustic characteristics of subsonic and supersonic jets

Shadowgraph photographs of subsonic and supersonic jet

Event-related potentials and cognition in Parkinson's disease: An integrative review

Cognitive impairment is a common non-motor symptom of Parkinson’s disease (PD), but the nature of cognitive changes varies considerably between individuals. According to the dual-syndrome hypothesis, one cluster of patients is characterized by deficits in executive function that may be related to fronto-striatal dysfunction. Other patients primarily show non-frontal cognitive impairments that progress rapidly to PD dementia (PDD). We provide a comprehensive review of event-related potential (ERP) studies to identify ERP measures substantiating the heterogeneity of cognitive impairment in PD. Our review revealed evidence for P3b and mismatch-negativity alterations in PDD, but not in non-demented PD, indicating that alterations of these ERPs constitute electrophysiological markers for PDD. In contrast, ERP correlates of executive functions, such as NoGo-P3, N2, and error(-related) negativity (Ne/ERN), appear to be attenuated in non-demented PD patients in a dopamine-dependent manner. Hence, ERP measures confirm and yield distinct electrophysiological markers for the heterogeneity of cognitive impairment in PD. We discuss limitations and open questions of the ERP approach and provide directions and predictions for future ERP research

Movement-related potentials in Parkinson's disease

To date, many different approaches have been used to study the impairment of motor function in Parkinson's disease (PD). Event-related potentials (ERPs) are averaged amplitude fluctuations of the ongoing EEG activity that are time locked to specific sensory, motor or cognitive events, and as such can be used to study different brain processes with an excellent temporal resolution. Movement-related potentials (MRPs) are ERPs associated with processes of voluntary movement preparation and execution in different paradigms. In this review we concentrate on MRPs in PD. We review studies recording the Bereitschaftspotential, the Contingent Negative Variation, and the lateralized readiness potential in PD to highlight the contributions they have made to further understanding motor deficits in PD. Possible directions for future research are also discussed

The Vehicle, June 1960, Vol. 2 no. 3

Vol. 2, No. 3 To the ReaderRobert Mills Frenchpage 2 Blue-Nosed RobinThomas McPeakpage 3 Forest EtudeJames M. Jenkinsonpage 7 Chant For The MenJerry Whitepage 8 It\u27s OK Now, Chief J.B. Youngpage 9 Magic WordsKathleen Ferreepage 11 SpurnedRay Hoopspage 12 Danger!A. Seerpage 13 GenecideGeorge Fosterpage 14 To a Stern ParentC.E.S.page 14 ReservationNeil O. Parkerpage 14 The Worm and IRichard Blairpage 15 One Way -- Non-TransferableRobert Mills Frenchpage 15 NorthlightEDSpage 16https://thekeep.eiu.edu/vehicle/1007/thumbnail.jp

Effect of reproductive factors on stage, grade and hormone receptor status in early-onset breast cancer

INTRODUCTION: Women younger than 35 years who are diagnosed with breast cancer tend to have more advanced stage tumors and poorer prognoses than do older women. Pregnancy is associated with elevated exposure to estrogen, which may influence the progression of breast cancer in young women. The objective of the present study was to examine the relationship between reproductive events and tumor stage, grade, estrogen receptor and progesterone receptor status, and survival in women diagnosed with early-onset breast cancer. METHODS: In a population-based, case–case study of 254 women diagnosed with invasive breast cancer at age under 35 years, odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using unconditional logistic regression with tumor characteristics as dependent variables and adjusting for age and education. Survival analyses also examined the relationship between reproductive events and overall survival. RESULTS: Compared with nulliparous women, women with three or more childbirths were more likely to be diagnosed with nonlocalized tumors (OR = 3.1, 95% CI = 1.3–7.7), and early age (<20 years) at first full-term pregnancy was also associated with a diagnosis of breast cancer that was nonlocalized (OR = 3.0, 95% CI = 1.2–7.4) and of higher grade (OR = 3.2, 95% CI 1.0–9.9). The hazard ratio for death among women with two or more full-term pregnancies, as compared with those with one full-term pregnancy or none, was 2.1 (95% CI = 1.0–4.5), adjusting for stage. Among parous women, those who lactated were at decreased risk for both estrogen receptor and progesterone receptor negative tumors (OR = 0.2, 95% CI = 0.1–0.5, and OR = 0.4, 95% CI = 0.2–0.8, respectively). CONCLUSION: The results of the present study suggest that pregnancy and lactation may influence tumor presentation and survival in women with early-onset breast cancer

Combining Clinical, Pathological, and Demographic Factors Refines Prognosis of Lung Cancer: A Population-Based Study

In the treatment of lung cancer, an accurate estimation of patient clinical outcome is essential for choosing an appropriate course of therapy. It is important to develop a prognostic stratification model which combines clinical, pathological and demographic factors for individualized clinical decision making.A total of 234,412 patients diagnosed with adenocarcinomas or squamous cell carcinomas of the lung or bronchus between 1988 and 2006 were retrieved from the SEER database to construct a prognostic model. A model was developed by estimating a Cox proportional hazards model on 500 bootstrapped samples. Two models, one using stage alone and another comprehensive model using additional covariates, were constructed. The comprehensive model consistently outperformed the model using stage alone in prognostic stratification and on Harrell's C, Nagelkerke's R(2), and Brier Scores in the whole patient population as well as in specific treatment modalities. Specifically, the comprehensive model generated different prognostic groups with distinct post-operative survival (log-rank P<0.001) within surgical stage IA and IB patients in Kaplan-Meier analyses. Two additional patient cohorts (n = 1,991) were used as an external validation, with the comprehensive model again outperforming the model using stage alone with regards to prognostic stratification and the three evaluated metrics.These results demonstrate the feasibility of constructing a precise prognostic model combining multiple clinical, pathologic, and demographic factors. The comprehensive model significantly improves individualized prognosis upon AJCC tumor staging and is robust across a range of treatment modalities, the spectrum of patient risk, and in novel patient cohorts

High prevalence of lung cancer in a surgical cohort of lung cancer patients a decade after smoking cessation

<p>Abstract</p> <p>Background</p> <p>This study was designed to assess the prevalence of smoking at time of lung cancer diagnosis in a surgical patient cohort referred for cardiothoracic surgery.</p> <p>Methods</p> <p>Retrospective study of lung cancer patients (n = 626) referred to three cardiothoracic surgeons at a tertiary care medical center in Southern California from January 2006 to December 2008. Relationships among years of smoking cessation, smoking status, and tumor histology were analyzed with Chi-square tests.</p> <p>Results</p> <p>Seventy-seven percent (482) had a smoking history while 11.3% (71) were current smokers. The length of smoking cessation to cancer diagnosis was <1 year for 56 (13.6%), 1-10 years for 110 (26.8%), 11-20 years for 87 (21.2%), 21-30 years for 66 (16.1%), 31-40 years for 44 (10.7%), 41-50 years for 40 (9.7%) and 51-60 years for 8 (1.9%). The mean cessation was 18.1 ± 15.7 years (n = 411 former smokers). Fifty-nine percent had stage 1 disease and 68.0% had adenocarcinoma. Squamous cell carcinoma was more prevalent in smokers (15.6% vs. 8.3%, p = 0.028); adenocarcinoma was more prevalent in never-smokers (79.9% versus 64.3%, p = 0.0004). The prevalence of adenocarcinoma varied inversely with pack year (p < 0.0001) and directly with years of smoking cessation (p = 0.0005).</p> <p>Conclusions</p> <p>In a surgical lung cancer cohort, the majority of patients were smoking abstinent greater than one decade before the diagnosis of lung cancer.</p

Male tobacco smoke load and non-lung cancer mortality associations in Massachusetts

<p>Abstract</p> <p>Background</p> <p>Different methods exist to estimate smoking attributable cancer mortality rates (Peto and Ezzati methods, as examples). However, the smoking attributable estimates using these methods cannot be generalized to all population sub-groups. A simpler method has recently been developed that can be adapted and applied to different population sub-groups. This study assessed cumulative tobacco smoke damage (smoke load)/non-lung cancer mortality associations across time from 1979 to 2003 among all Massachusetts males and ages 30–74 years, using this novel methodology.</p> <p>Methods</p> <p>Annual lung cancer death rates were used as smoke load bio-indices, and age-adjusted lung/all other (non-lung) cancer death rates were analyzed with linear regression approach. Non-lung cancer death rates include all cancer deaths excluding lung. Smoking-attributable-fractions (SAFs) for the latest period (year 2003) were estimated as: 1-(estimated unexposed cancer death rate/observed rate).</p> <p>Results</p> <p>Male lung and non-lung cancer death rates have declined steadily since 1992. Lung and non-lung cancer death rates were tightly and steeply associated across years. The slopes of the associations analyzed were 1.69 (95% confidence interval (CI) 1.35–2.04, r = 0.90), and 1.36 (CI 1.14–1.58, r = 0.94) without detected autocorrelation (Durbin-Watson statistic = 1.8). The lung/non-lung cancer death rate associations suggest that all-sites cancer death rate SAFs in year 2003 were 73% (Sensitivity Range [SR] 61–82%) for all ages and 74% (SR 61–82%) for ages 30–74 years.</p> <p>Conclusion</p> <p>The strong lung/non-lung cancer death rate associations suggest that tobacco smoke load may be responsible for most prematurely fatal cancers at both lung and non-lung sites. The present method estimates are greater than the earlier estimates. Therefore, tobacco control may reduce cancer death rates more than previously noted.</p

A simple algebraic cancer equation: calculating how cancers may arise with normal mutation rates

<p>Abstract</p> <p>Background</p> <p>The purpose of this article is to present a relatively easy to understand cancer model where transformation occurs when the first cell, among many at risk within a colon, accumulates a set of driver mutations. The analysis of this model yields a simple algebraic equation, which takes as inputs the number of stem cells, mutation and division rates, and the number of driver mutations, and makes predictions about cancer epidemiology.</p> <p>Methods</p> <p>The equation [<it>p </it>= 1 - (1 - (1 - (1 - <it>u</it>)^<it>d</it>)^<it>k</it>)^{<it>Nm </it>}] calculates the probability of cancer (<it>p</it>) and contains five parameters: the number of divisions (<it>d</it>), the number of stem cells (<it>N </it>× <it>m</it>), the number of critical rate-limiting pathway driver mutations (<it>k</it>), and the mutation rate (<it>u</it>). In this model progression to cancer "starts" at conception and mutations accumulate with cell division. Transformation occurs when a critical number of rate-limiting pathway mutations first accumulates within a single stem cell.</p> <p>Results</p> <p>When applied to several colorectal cancer data sets, parameter values consistent with crypt stem cell biology and normal mutation rates were able to match the increase in cancer with aging, and the mutation frequencies found in cancer genomes. The equation can help explain how cancer risks may vary with age, height, germline mutations, and aspirin use. APC mutations may shorten pathways to cancer by effectively increasing the numbers of stem cells at risk.</p> <p>Conclusions</p> <p>The equation illustrates that age-related increases in cancer frequencies may result from relatively normal division and mutation rates. Although this equation does not encompass all of the known complexity of cancer, it may be useful, especially in a teaching setting, to help illustrate relationships between small and large cancer features.</p