Developing critical pitter thresholds for canning peaches using the nondestructive Sinclair firmness sensor

The rclationship bctwccn mechanical pitting damage using ihe Alias piner (Atlas Pacific Engineering Ca, l»c > Pueblo, Colorado) over a range of nondestmetive and destruciive firmness measuremems for 'Andross*, Car$on\ and *Ros$* clingsíone peaches was studied, During the two years of woifc, (he percentage of 'Aodiosa1, *Car$on\ and 'Rou' fmit wiih pitung damage increased sharply as nondestmetive firmness sensor Sinclair firmness index valúes fell below 7 0 (SFI) and \\hcn dostructive penelromeief readings fell bdow 3 S pounds (17 N) Even ihough ihere was a low correlation between nondesiruciive and desinictive firmness measuremems. nondestmetive mcasuremcnte appcar to be wcll lelated lo (he piíüng damage These preliminary results encourage ihat further research to ímprove the relationship belween an automatic nondestmetive systcm could give processors ihe opüon to segiegate peaches susceptible lo pitting prior lo processin

The Relationship between Body Composition, Fatty Acid Metabolism and Diet in Spinal Muscular Atrophy

Acknowledgments: I.B. received a studentship from SMA Angels Charity. M.B.’s SMA research isfunded by SMA Angels Charity, Muscular Dystrophy UK, Action Medical Research and SMA UK. S.H.P.’s SMA research is funded by SMA Europe and Anatomical Society.Peer reviewedPublisher PD

Observations from a prototype implementation of the Common APSE Interface Set (CAIS)

This paper presents an overview of the Common Ada Programming Support Environment (APSE) Interface Set (CAIS), its purpose, and its history. The paper describes an internal research and development effort at the Mitre Corporation to implement a prototype version of the current CAIS specification and to rehost existing Ada software development tools onto the CAIS prototype. Based on this effort, observations are made on the maturity and functionality of the CAIS. These observations support the government's current policy of publicizing the CAIS specification as a baseline for public review in support of its evolution into a standard which can be mandated for use as Ada is today

Upper-Ocean Eddy Transports of Heat, Potential Vorticity, and Volume in the Northeastern North Atlantic—“Vivaldi 1991”

Mesoscale eddies in the northeast North Atlantic were investigated using the SeaSoar towed CTD and ADCP data from the 1991 Vivaldi cruise. These data cover an area of 1700 km × 1500 km between 39° and 54°N and between 35° and 10°W. To maximize statistical significance, but retain the possibility of determining north-south gradients, statistics of eddy quantities were calculated separately for the northern and southern halves of the cruise area. The mean flow in the south is essentially zero: in the north the flow is dominated by the North Atlantic Current (NAC) with a mean speed of 6.5 cm s-1. The eddy kinetic energy in the south, 205 cm2 s-2, is, however, only slightly less than in the north, 272 cm2 s-2. The eddy momentum transports, or Reynolds stresses, u′v′, show a poleward decrease, corresponding to an acceleration of the mean eastward flow associated with the NAC of 0.03 cm s-1 day-1. The eddy heat transports, u′T′, are not significantly different from zero in the south but show a clear poleward transport in the north of 5.5 K cm s-1, or 0.1 PW for the 365-m layer 1500 km wide. The depth-averaged eddy potential vorticity fluxes, u′q′, show a convergence toward the source region of the low-potential-vorticity eastern North Atlantic Central Water west of Biscay. The residual or rectified eddy transport velocity implied by the eddy potential vorticity flux. u* = -u′q′/q, is 0.7 cm s-1 toward the southwest in the south, while in the north it is 0.9 cm s-1 toward the northwest crossing the property isolines. The directions correspond to a divergence from the formation region of the eastern North Atlantic Central Water. An assessment of the overall volume transport of the region suggests that the westward eddy volume transport (∼4 Sv; Sv ≡ 106 m3 s-1) is almost balanced by an eastward geostrophic flow (∼3 Sv) with the remainder being supplied by a smaller contribution leaving the northward-flowing eastern boundary current (∼1 Sv)

Phytochemical Assays of Commercial Botanical Dietary Supplements

The growing popularity of botanical dietary supplements (BDS) has been accompanied by concerns regarding the quality of commercial products. Health care providers, in particular, have an interest in knowing about product quality, in view of the issues related to herb-drug interactions and potential side effects. This study assessed whether commercial formulations of saw palmetto, kava kava, echinacea, ginseng and St. John's wort had consistent labeling and whether quantities of marker compounds agreed with the amounts stated on the label. We purchased six bottles each of two lots of supplements from nine manufacturers and analyzed the contents using established commercial methodologies at an independent laboratory. Product labels were found to vary in the information provided, such as serving recommendations and information about the herb itself (species, part of the plant, marker compound, etc.) With regard to marker compound content, little variability was observed between different lots of the same brand, while the content did vary widely between brands (e.g. total phenolic compounds in Echinacea ranged from 3.9–15.3 mg per serving; total ginsenosides in ginseng ranged from 5.3–18.2 mg per serving). Further, the amounts recommended for daily use also differed between brands, increasing the potential range of a consumer's daily dose. Echinacea and ginseng were the most variable, while St. John's wort and saw palmetto were the least variable. This study highlights some of the key issues in the botanical supplement market, including the importance of standardized manufacturing practices and reliable labeling information. In addition, health care providers should keep themselves informed regarding product quality in order to be able to appropriately advise patients utilizing both conventional and herbal medicines

Sonographic identification of an unusual complication of midtrimester pregnancy termination: Unrecognized intra-abdominal extrusion of fetal parts

No Abstract.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/38190/1/1870160210_ftp.pd

Systemic peptide-mediated oligonucleotide therapy improves long-term survival in spinal muscular atrophy.

The development of antisense oligonucleotide therapy is an important advance in the identification of corrective therapy for neuromuscular diseases, such as spinal muscular atrophy (SMA). Because of difficulties of delivering single-stranded oligonucleotides to the CNS, current approaches have been restricted to using invasive intrathecal single-stranded oligonucleotide delivery. Here, we report an advanced peptide-oligonucleotide, Pip6a-morpholino phosphorodiamidate oligomer (PMO), which demonstrates potent efficacy in both the CNS and peripheral tissues in severe SMA mice following systemic administration. SMA results from reduced levels of the ubiquitously expressed survival motor neuron (SMN) protein because of loss-of-function mutations in the SMN1 gene. Therapeutic splice-switching oligonucleotides (SSOs) modulate exon 7 splicing of the nearly identical SMN2 gene to generate functional SMN protein. Pip6a-PMO yields SMN expression at high efficiency in peripheral and CNS tissues, resulting in profound phenotypic correction at doses an order-of-magnitude lower than required by standard naked SSOs. Survival is dramatically extended from 12 d to a mean of 456 d, with improvement in neuromuscular junction morphology, down-regulation of transcripts related to programmed cell death in the spinal cord, and normalization of circulating insulin-like growth factor 1. The potent systemic efficacy of Pip6a-PMO, targeting both peripheral as well as CNS tissues, demonstrates the high clinical potential of peptide-PMO therapy for SMA

Therapeutic strategies for spinal muscular atrophy: SMN and beyond

Spinal muscular atrophy (SMA) is a devastating neuromuscular disorder characterized by loss of motor neurons and muscle atrophy, generally presenting in childhood. SMA is caused by low levels of the survival motor neuron protein (SMN) due to inactivating mutations in the encoding gene SMN1 A second duplicated gene, SMN2, produces very little but sufficient functional protein for survival. Therapeutic strategies to increase SMN are in clinical trials, and the first SMN2-directed antisense oligonucleotide (ASO) therapy has recently been licensed. However, several factors suggest that complementary strategies may be needed for the long-term maintenance of neuromuscular and other functions in SMA patients. Pre-clinical SMA models demonstrate that the requirement for SMN protein is highest when the structural connections of the neuromuscular system are being established, from late fetal life throughout infancy. Augmenting SMN may not address the slow neurodegenerative process underlying progressive functional decline beyond childhood in less severe types of SMA. Furthermore, individuals receiving SMN-based treatments may be vulnerable to delayed symptoms if rescue of the neuromuscular system is incomplete. Finally, a large number of older patients living with SMA do not fulfill the present criteria for inclusion in gene therapy and ASO clinical trials, and may not benefit from SMN-inducing treatments. Therefore, a comprehensive whole-lifespan approach to SMA therapy is required that includes both SMN-dependent and SMN-independent strategies that treat the CNS and periphery. Here, we review the range of non-SMN pathways implicated in SMA pathophysiology and discuss how various model systems can serve as valuable tools for SMA drug discovery

Pulmonary sequestration: Ultrasonic appearance

No Abstract.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/38181/1/1870100612_ftp.pd

Electronic structure, phase stability and chemical bonding in Th2_2Al and Th2_2AlH4_4

We present the results of theoretical investigation on the electronic structure, bonding nature and ground state properties of Th$_2$Al and Th$_2$AlH$_4$ using generalized-gradient-corrected first-principles full-potential density-functional calculations. Th$_2$AlH$_4$ has been reported to violate the "2 \AA rule" of H-H separation in hydrides. From our total energy as well as force-minimization calculations, we found a shortest H-H separation of 1.95 {\AA} in accordance with recent high resolution powder neutron diffraction experiments. When the Th$_2$Al matrix is hydrogenated, the volume expansion is highly anisotropic, which is quite opposite to other hydrides having the same crystal structure. The bonding nature of these materials are analyzed from the density of states, crystal-orbital Hamiltonian population and valence-charge-density analyses. Our calculation predicts different nature of bonding for the H atoms along $a$ and $c$. The strongest bonding in Th$_2$AlH$_4$ is between Th and H along $c$ which form dumb-bell shaped H-Th-H subunits. Due to this strong covalent interaction there is very small amount of electrons present between H atoms along $c$ which makes repulsive interaction between the H atoms smaller and this is the precise reason why the 2 {\AA} rule is violated. The large difference in the interatomic distances between the interstitial region where one can accommodate H in the $ac$ and $ab$ planes along with the strong covalent interaction between Th and H are the main reasons for highly anisotropic volume expansion on hydrogenation of Th$_2$Al.Comment: 14 pages, 9 figure