Measuring arterial strain induced by endovascular stents

Endovascular stents are expandable, fenestrated tubes that are threaded in their collapsed state through an artery to a site of occlusion, plastically enlarged and left as permanent implants to scaffold the artery open. The stent induces largescale vascular strains that are difficult to measure in vivo and yet can be critical determinants of stent-vessel biology. A method is developed to measure the strain tensor developed on the surface of an artery as a stent is expanded in vivo. Arterial sections are marked with reference points and imaged as the stent is expanded. An axially symmetric parametric model of the artery is determined for each expansion timepoint, and these reference points are backprojected onto this surface. The backprojected reference points are grouped and analysed to determine the circum-ferential, axial and torsional strain tensor components in each arterial subsection. The method is characterised in vitro using bovine artery segments and a latex phantom, and is then tested on rabbits to demonstrate its feasibility in vivo. In vitro experiments on stented bovine arteries show typical post-stenting strains of 0.60, −0.26, and 0.08 mm mm⁻¹ in the circumferential, axial and torsional directions, respectively, sampled every 1 mm along the length of the stented region. Phantom experiments characterise the RMS error of system measurements as 0.1 mm mm⁻¹. The system is shown capable of measuring strains of straight, accessible vessels in the presence of respiratory/cardiac motion and visual glare in vivo.     

Evaluation of the tumor board as a Continuing Medical Education (CME) activity: Is it useful?

BACKGROUND: Although it has been previously reported that offering continuing medical education (CME) credit is not a major factor in tumor board attendance, the results/utility of the Accreditation Council for Continuing Medical Education mandated evaluations of those tumor boards offering CME credit has not been studied. METHODS: We reviewed the CME evaluations of our University Gastrointestinal Tumor Board; this meeting was chosen because it is multidisciplinary, well attended, and offers CME credit contingent on completing a standard CME evaluation form each session. RESULTS: Of the 2736 attendees, 660 (24%) at the 79 consecutive conferences studied completed the evaluation for CME credit. Reported satisfaction was high; the average response on the 4-question satisfaction survey was 5 (Excellent) on a 5-point Likert scale, only 6% of attendees perceived any commercial bias, and only 3 attendees stated that the conference did not achieve the stated objectives. Of the respondents, 42% indicated that the tumor board information would change their practice, although few specific examples were given. A minority of responders provided specific feedback. CONCLUSIONS: A minority of attendees at this tumor board utilized CME credit. Although satisfaction and impact ratings were high, potential response set bias, lack of specific feedback, and nonresponse bias were limitations to the evaluations.     

Left ventricular chamber function during inhaled nitric oxide in patients with dilated cardiomyopathy.

Inhaled nitric oxide is a potent and selective pulmonary vasodilator. However, when used in patients with congestive cardiac failure, the decrease in pulmonary vascular resistance is associated with an increase in pulmonary capillary wedge pressure (PCWP). This study examined load-independent indexes of left ventricular chamber function during inhaled nitric oxide in 10 patients with dilated cardiomyopathy (mean ejection fraction, 30.2+/-7.8%, mean +/- SD). Etiology of cardiomyopathy was idiopathic in six and ischemic in four. Pulmonary hemodynamics in seven patients revealed normal resting pulmonary vascular resistance. Chamber function was defined by recording pressure-volume loops at steady state and during inferior vena caval occlusion during inhalation of 20 ppm nitric oxide for 10 min. We found no effect of inhaled nitric oxide on steady-state left ventricular pressures, volumes, contractility (end-systolic elastance or preload recruitable stroke work), contraction duration, or active (tau, dP/dt(min)) or passive (end-diastolic pressure-volume relation) diastolic function. Right heart filling pressures did not change. We therefore conclude that 20 ppm inhaled nitric oxide does not affect left ventricular chamber function in patients with controlled heart failure. Previously described elevations in PCWP during inhaled nitric oxide are most likely due to altered left ventricular loading conditions related to secondary pulmonary hypertension in severe heart failure.     

Occurrence of arsenic in seafoods from fast foods analyzed by X-ray fluorescence

Arsenic was detected in 22 of 525 samples of fruits, vegetables, grain products, fast foods, dairy products, and seafoods analyzed by a multielement X-ray fluorescence method. The arsenic occurrences corresponded almost completely and exclusively with seafoods, and the correspondence was confirmed by additional analyses of separated parts of fast-food fish sandwiches. The geometric mean arsenic concentration for all seafoods was 2.1 μg/g (dry weight), with a geometric standard deviation of 3.2. Relative analytical precisions averaged 5.9% standard deviation, and arsenic inhomogeneity among sample aliquots averaged 4.5%. Accuracies validated by six National Institute of Standards and Technology reference materials averaged within 0.2 μg/g, or 5.1 % of certified values, with a net bias of less than 0.1 μg/g. Total arsenic contents in single servings of the seafoods (geometric MEAN = 109 μg) may account completely for the average U.S. arsenic intake if one serving is consumed every 2 to 10 days. Average total arsenic contents are similar among single servings of fish sandwiches, fish fillets, shrimp, and clam chowder; however, variation among specific samples of these seafoods amounts to a factor of 2 to 3. Arsenic concentrations in fish and shrimp agree with values predicted from bioaccumulation from seawater, suggesting consistency with a broader range of seafoods.     

Protection against aflatoxin B1-induced hepatocarcinogenesis in F344 rats by 5-(2-pyrazinyl)-4-methyl-1,2-dithiole-3-thione (oltipraz): predictive role for short-term molecular dosimetry.

Previous studies have demonstrated that dietary administration of the schistosomicidal drug 5-(2-pyrazinyl)-4-methyl-1,2-dithiole-3-thione (oltipraz) ameliorates the hepatotoxicity of aflatoxin B1 (AFB1). Notably, mortality, altered hepatic function, hepatic AFB1-DNA adduct levels, and expression of hepatic enzyme-altered foci were markedly reduced in the rat by concurrent feeding of oltipraz during exposures to AFB1. Collectively, these studies prompted us to evaluate the chemoprotective properties of oltipraz against AFB1-induced liver cancer. In addition, preliminary molecular dosimetry studies were undertaken to determine the utility of measurements of urinary aflatoxin-N7-guanine excretion as a marker of relative risk for hepatocarcinogenesis in AFB1-exposed rats. For the carcinogenesis studies, 5-wk-old male F344 rats were randomly divided into two groups. One group (55 rats) received the AIN-76A diet, and the other group (56 rats) received the AIN-76A diet supplemented with 0.075% oltipraz. The oltipraz-supplemented diet was fed for 4 wk. Beginning 1 wk after starting the experimental diets, all rats in both groups received 25 micrograms of AFB1/rat/day by gavage for 5 days per wk over the next 2 wk. One wk following cessation of dosing with AFB1, oltipraz was removed from the diet, and all rats were fed the AIN-76A diet for the remainder of the experiment. At 3 mo after dosing, livers of ten sentinel rats from each group were analyzed for the burden of gamma-glutamyltranspeptidase-positive foci. In accord with previous findings, rats fed the oltipraz-supplemented diet exhibited substantial reductions in the focal burden (97% reduction; P less than 0.05) of these AFB1-induced lesions. The remaining rats were maintained for the cancer study until they became moribund or the termination of the experiment at 23 mo. Gross liver lesions were identified at autopsy and confirmed by microscopic evaluation. An 11% incidence of hepatocellular carcinoma was observed in the AFB1-treated, control diet-fed rats. An additional 9% of this group had hepatocellular adenomas. Oltipraz afforded complete protection against both AFB1-induced hepatocellular neoplasms. Using Kaplan-Meier survival analyses, rats in the oltipraz group had a significantly (P less than 0.02) longer life span and an increased survival free of liver tumors (P less than 0.0002). Molecular dosimetry studies used rats fed either the oltipraz-supplemented or control diet for 1 wk and then challenged with a single dose of AFB1 to examine the initial rates of 8,9-dihydro-8-(N7-guanyl)-9-hydroxyaflatoxin B1 excreted in the urine.(ABSTRACT TRUNCATED AT 400 WORDS)     

Sex steroids and bone density in premenopausal and perimenopausal women

Bone density begins to decline in women before menopause, and the degree of bone loss is variable. We performed a cross-sectional analysis on the entry data of a 5-yr prospective study of risk factors for osteoporosis to determine the correlation of bone density with serum sex steroid concentrations and body weight. We studied 292 healthy white women, aged 35-50 yr, who were menstruating regularly or had had menses in the past 12 months. Blood samples were drawn in the early follicular phase for estradiol (E2), testosterone (T), dehydroepiandrosterone sulfate, and sex hormone-binding globulin (SHBG). Free levels of E2 (FE2) and T (FT) were calculated based on total T and E2, SHBG, and albumin levels. Women were classified as premenopausal (FSH, less than 12 U/L) and perimenopausal (FSH greater than or equal to 12 U/L; n = 46; 16%). Bone density was measured by dual photon absorptiometry of the lumbar spine (L2-L4) and hip and by single photon absorptiometry of the wrist. Perimenopausal women were older than premenopausal women (45.5 +/- 3.5 and 41.0 +/- 3.9 yr, respectively), but did not differ in height or weight. While bone density did not correlate with age in each group, perimenopausal women had significantly lower bone density at the L2-L4 and femoral neck (L2-L4, 1.18 +/- 0.14 in perimenopausal and 1.24 +/- 0.12 g/cm2 in premenopausal women; femur, 0.84 +/- 0.11 in perimenopausal and 0.90 +/- 0.11 g/cm2 in premenopausal women; P less than 0.005). Body weight showed the strongest positive correlation with bone density. Log FT, percent FT, and FE2 percent correlated positively with bone density, even after controlling for weight. Log SHBG was negatively correlated with bone density in premenopausal women at the hip and wrist after controlling for weight. FSH was inversely correlated with bone density, and E2 and T were lower in perimenopausal than premenopausal women. These data suggest that women who are still menstruating may have relative deficiencies in both E2 and T, with reduced bone densities as a consequence.