Image processing in swallowing and speech research

An image processing system for application to studies of the temporal and spatial parameters of movement during swallowing and speech is described. Image sequences from videotape are digitized for computerized manipulation and analysis in an attempt to improve on conventional visual inspection. The system is “interactive” or “event-driven”: after executing a function, the computer waits for guidance from the user who controls the program through keyboard and mouse input, selecting options from menus and responding to prompts. The analyst alters image clarity by the application of filters and heightens contrast through video enhancement. A technique called “remapping” reduces head motion and provides uniform spatial scaling. Animated sequences of images are used, as opposed to frame-by-frame analysis, to preserve temporal context and increase efficiency of measurement. Low cost off-the-shelf personal computer hardware is used along with original software tailored to the application.     

Intraoperative ultrasound imaging of the entire brain through unilateral exploratory burr holes after severe head injury: technical note

A portable ultrasound unit with a 3.5-MHz probe allows accurate imaging of both cerebral hemispheres and partial imaging of the posterior fossa through unilateral exploratory burr holes or a craniotomy. In patients with clinical signs of transtentorial herniation after severe head injury, this unilateral technique can detect extraaxial and intraparenchymal mass lesions more accurately than is possible with bilateral exploratory burr holes.     

Effects of ambient air pollution on symptom severity and medication use in children with asthma.

BACKGROUND: Exposure to air pollutants has been investigated as a possible cause of asthma attacks in children. OBJECTIVE: To investigate the short-term effects of air pollutants on a panel of 133 children with asthma who enrolled in the Childhood Asthma Management Program. METHODS: During screening, the children completed daily diary cards for an average of 58 days to indicate their medication use and asthma severity. We used ordinal logistic regression to compare the odds of a more serious relative to a less serious asthma attack, and we used a Poisson model to analyze medication use. In both analyses we accommodate dependence in the data and different periods of observation for study subjects. RESULTS: Our results indicate that a 10-microg/m3 increase in particulate matter less than or equal to 2.5 microm (PM2.5) lagged 1 day was associated with a 1.20 times increased odds of having a more serious asthma attack [95% confidence interval (CI), 1.05 to 1.37] and a 1.08-fold increase in medication use (95% CI, 1.01 to 1.15). A 10-microg/m3 increase in particulate matter less than or equal to 10 microm (PM10) increased the odds of a more serious asthma attack (odds ratio = 1.12; 95% CI, 1.04 to 1.22) and also increased medication use (relative risk = 1.05; 95% CI, 1.00 to 1.09). CONCLUSIONS: Increases in PM2.5 and PM10 are significantly associated with an increased risk of more severe asthma attacks and medication use in Seattle area children with asthma. We also found associations with carbon monoxide, but we believe that carbon monoxide is a marker for exposure to combustion byproducts.     

Examination of potential mechanism(s) of metallothionein induction by diethyl maleate.

Diethyl maleate (DEM) is a glutathione-depleting agent that can increase the levels of the sulfhydryl-rich protein metallothionein (MT) in liver. The purpose of the present study was to examine the mechanism(s) by which DEM increases mouse hepatic MT levels. DEM appears to be an indirect MT inducer as suggested by the lack of increase in MT levels when cultured mouse hepatocytes were exposed to DEM. Four possible mechanisms by which indirect MT inducers may cause an elevation in MT concentrations in liver were examined. Zn levels did not increase prior to the increase in hepatic MT, thus, a Zn redistribution to the liver is not the cause of the liver MT induction by DEM. The adrenal gland products were not required for MT induction in liver, as adrenalectomy did not abolish the increase in hepatic MT caused by DEM. The elevation in liver MT does not appear to be due solely to the decrease in liver glutathione (60%) in the initial hour after DEM, because phorone, which decreases liver glutathione (80%), produced only a fourfold increase in hepatic MT. Activation of macrophages does not seem to account for the rise in liver MT levels, as there was no increase in abundance of cytokine mRNAs for TNF-alpha, IL-1 beta, or IL-6 in the liver. These data suggest that the induction of hepatic MT by DEM does not occur in response to (1) an increase in liver Zn that precedes the increase in liver MT, (2) release of adrenal gland products, (3) decrease in liver glutathione, or (4) increased cytokine gene expression.     

Prenatal lead exposure in relation to gestational age and birth weight: A review of epidemiologic studies

Although the adverse effect on pregnancy outcomes at high levels of lead exposure in the workplace has been recognized for years, there is uncertainty regarding the impact of exposure at the lower community exposure levels commonly encountered today. This review summarizes the epidemiologic literature and discusses pertinent methodologic issues and possible sources of interstudy variation. The authors conclude that prenatal lead exposure is unlikely to increase the risk of premature membrane rupture but does appear to increase the risk of preterm delivery. Whether prenatal lead exposure decreases gestational age in terms of infants is unclear. Prenatal lead exposure also appears to be associated with reduced birth weight, but results vary in relation to study design and degree of control for confounding. Adjustment for gestational age, a possible confounder of the birth weight-lead exposure association, did not yield clearer results.     

Canadian Association of General Surgeons Evidence Based Reviews in Surgery. 6. "GERD" as a risk factor for esophageal cancer. Symptomatic gastroesophageal reflux as a risk factor for esophageal adenocarcinoma.

Question: Is gastroesophageal reflux a risk factor for the development of esophageal adenocarcinoma? Design: A case control study. Setting: A population-based study in Sweden between 1994 and 1997. Participants: Cases included all patients with gastric or esophageal adenocarcinoma and half of all patients with esophageal squamous cell cancer, under the age of 80 years and living in Sweden between Dec. 1, 1994, and Dec. 31, 1997. Controls were selected randomly from among persons matched for age (within 10 yr) and sex in the entire Swedish population, through the use of a population register, which is computerized and updated continuously. Assessment of risk factors: Symptomatic reflux was assessed according to the severity of the symptoms (heartburn only, regurgitation only, heartburn and regurgitation combined, nightly symptoms), frequency and duration. Adjustment was made for age, sex, body mass index, smoking history, alcohol ingestion, socioeconomic status, intake of fruit and vegetables, overall energy intake, posture and the degree of physical activity both at work and during leisure. Main outcome measures: Gastric and esophageal adenocarcinoma and esophageal squamous cell cancer. Main results: Among participants with recurrent symptoms of reflux, as compared with those without such symptoms, the odds ratios were 7.7 (95% CI, 5.3–11.4) for development of esophageal adenocarcinoma and 2.0 (95% CI, 1.4–2.9) for adenocarcinoma of the cardia. The more frequent, more severe and longer duration the symptoms of reflux were, the greater was the risk. Among persons with long-standing, severe symptoms of reflux, the odds ratios were 43.5 (95% CI, 18.3–103.5) for development of esophageal adenocarcinoma and 4.4 (95% CI, 1.7–11.0) for adenocarcinoma of the cardia. The risk of esophageal squamous cell carcinoma was not increased with reflux (odds ratio, 1.1; 95% CI, 0.7–1.9). Conclusion: The study identified a strong and probably causal relation between symptomatic reflux as a strong risk factor for esophageal adenocarcinoma and a relatively weak risk factor for adenocarcinoma of the gastric cardia.