RESUMEN
This report presents testing of a prototype cantilevered liquid-nitrogen-cooled silicon mirror. This mirror was designed to be the first mirror for the new soft X-ray beamlines to be built as part of the Advanced Light Source Upgrade. Test activities focused on fracture, heat transfer, modal response and distortion, and indicated that the mirror functions as intended.
RESUMEN
Amelanchier alnifolia (Nutt.) Nutt. ex M. Roem., commonly known as juneberry or Saskatoon serviceberry, was historically a widely used prairie fruit that is native to the Northern Great Plains, southern Yukon and Northwest Territories (4). While juneberry is an important fruit crop in the prairie provinces of Canada, small commercial plantings also occur throughout the northern United States (2), including Michigan. On July 18, 2009, severe rust symptoms were observed on plants in a 2-year-old field of A. alnifolia 'Northline' in Northport, MI. The plants had been sourced as seedlings from a nursery in Alberta, Canada in 2007. Signs and symptoms were present on fruits and leaves on virtually all of the plants. Symptomatic fruit were still immature, and on average, more than 70% of the fruit surface was covered with tubular, whitish aecia with conspicuous orange aeciospores. Portions of twigs also showed fusiform swellings (1 to 3 cm long) covered with aecia. Aecia were hypophyllous, fructicolous and caulicolous, roestelioid, and 2 to 4 mm high. The peridium was cylindric and tapering toward the apex, dehiscent at the apex, retaining a tubular shape for a long time and at times becoming lacerated on the sides with age. Peridial cells were linear rhomboidal, 50 to 105 µm long, hyaline to brownish, outer walls smooth, inner walls with small papillae, and side walls delicately verrucose-rugose with elongate papillae having variable lengths. Aeciospores were globoid, 20 to 35 × 25 to 38 µm (average 30.7 × 32.5 µm), orange to cinnamon brown, and densely verrucose with walls 2.5 to 3.5 µm thick. On the basis of these morphological characters, the host, and comparison with a reference specimen (BPI 122010), the pathogen was identified as Gymnosporangium nelsonii Arthur (1,3). The 5' region of the 28S rDNA was sequenced (GenBank Accession No. HM591299.1), confirming the identification as a species of Gymnosporangium, one distinct from previously sequenced specimens available in GenBank. The specimen has been deposited at the U.S. National Fungus Collections (BPI 880671 and 880709). Four other species found previously on Amelanchier spp. in the Midwest differ as follows: G. clavipes and G. clavariiforme have verrucose peridial cells and different 28S rDNA sequences; G. nidus-avis has rugose peridial cells; and G. corniculans has cornute peridia that dehisce from lateral slits while apices remain intact and verrucose peridial walls with verrucae on the side walls (1). The infection was likely caused by basidiospores originating from telia on Juniperus spp. in the area surrounding the field. However, no telia of G. nelsonii were found on junipers in the immediate vicinity. To our knowledge, this is the first report of G. nelsonii on juneberry in Michigan and the Midwest. Because of the devastating impact of this disease on fruit quality, fungicide programs have been devised for disease control and were effective in 2010. Juneberry growers in the Midwest need to be aware of this disease and monitor their crop carefully for symptoms and signs. References: (1) F. D. Kern. A Revised Taxonomic Account of Gymnosporangium. Pennsylvania State University Press, University Park, 1973. (2) K. Laughlin et al. Juneberry for Commercial and Home Use on the Northern Great Plains. North Dakota State University, Fargo 1996. (3) S. K. Lee and M. Kakishima. Mycoscience 40:121, 1999. (4) G. Mazza and C. G. Davidson. Page 516 in: New Crops. Wiley, New York, 1993.
RESUMEN
BACKGROUND: Two principal mechanisms are thought to be responsible for Brugada syndrome (BS): (1) right ventricular (RV) conduction delay and (2) RV subepicardial action potential shortening. This in vivo high-density mapping study evaluated the conduction and repolarization properties of the RV in BS subjects. METHODS AND RESULTS: A noncontact mapping array was positioned in the RV of 18 BS patients and 20 controls. Using a standard S(1)-S(2) protocol, restitution curves of local activation time and activation recovery interval were constructed to determine local maximal restitution slopes. Significant regional conduction delays in the anterolateral free wall of the RV outflow tract of BS patients were identified. The mean increase in delay was 3-fold greater in this region than in control (P=0<0.001). Local activation gradient was also maximally reduced in this area: 0.33+/-0.1 (mean+/-SD) mm/ms in BS patients versus 0.51+/-0.15 mm/ms in controls (P<0.0005). The uniformity of wavefront propagation as measured by the square of the correlation coefficient, r(2), was greater in BS patients versus controls (0.94+/-0.04 versus 0.89+/-0.09 [mean+/-SD]; P<0.05). The odds ratio of BS hearts having any RV segment with maximal restitution slope >1 was 3.86 versus controls. Five episodes of provoked ventricular tachycardia arose from wave breaks originating from RV outflow tract slow-conduction zones in 5 BS patients. CONCLUSIONS: Marked regional endocardial conduction delay and heterogeneities in repolarization exist in BS. Wave break in areas of maximal conduction delay appears to be critical in the initiation and maintenance of ventricular tachycardia. These data indicate that further studies of mapping BS to identify slow-conduction zones should be considered to determine their role in spontaneous ventricular arrhythmias.
