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91.
92.
K R Burnett G L Wolf E J Goldstein 《Physiological chemistry and physics and medical NMR》1985,17(1):123-129
A series of experiments was performed to evaluate the accuracy and reproducibility of relaxation values obtained by two RADX table-top spectrometers operating at 5 MHz (R5) and 10 MHz (R10) respectively. The output (T1, T2, and proton content) of each machine was compared (for tissue specimens and paramagnetic solutions) to reference spectrometers. In the range of tissue T1's, R5 overestimates T1 by approx. 10% and R10 underestimates by approx. 23%. For tissue specimens, the T2 output of both machines is within 3% of the reference facility. Proton content values correlate well with the % wet weight of tissues (y = .46x + 24, r = .85) but accuracy deteriorates badly if tissue T1 greater than 400 msec or T2 greater than 300 msec. The output of both machines is accurate and reproducible within 5% over the range of tissue relaxation values (biological fluids excluded). 相似文献
93.
Base Composition and Hybridization Studies of the Three Double-Stranded RNA Segments of Bacteriophage φ6 总被引:4,自引:3,他引:1 下载免费PDF全文
The three double-stranded ribonucleic acid (dsRNA) segments of the bacteriophage phi6 were isolated and shown to have similar melting temperatures and base compositions. RNA:RNA hybridization experiments with the isolated segments eliminate the possibility that the two smaller dsRNA segments arise from a cleavage of the large dsRNA segment. The two smaller RNA segments reanneal rapidly even at low temperatures; in contrast, the large dsRNA reannealed only at higher temperatures. Evidence is also presented which suggests that the dsRNAs may contain a short single-stranded RNA tail. 相似文献
94.
95.
F.-Nora Vögtle Björn Brändl Austin Larson Manuela Pendziwiat Marisa W. Friederich Susan M. White Alice Basinger Cansu Kücükköse Hiltrud Muhle Johanna A. Jähn Oliver Keminer Katherine L. Helbig Carolyn F. Delto Lisa Myketin Dirk Mossmann Nils Burger Noriko Miyake Audrey Burnett Ingo Helbig 《American journal of human genetics》2018,102(4):557-573
96.
Bett Nolan N. Hinch Scott G. Bass Arthur L. Braun Douglas C. Burnett Nicholas J. Casselman Matthew T. Cooke Steven J. Drenner S. Matthew Gelchu Ahmed Harrower William L. Ledoux Roxx Lotto Andrew G. Middleton Collin T. Minke-Martin Vanessa Patterson David A. Zhang Wenming Zhu David Z. 《Hydrobiologia》2022,849(2):385-405
Hydrobiologia - Many of the world’s rivers are dammed, altering the physiology, behaviour, ecology and survival of fish. Integrative research has the potential to improve our understanding of... 相似文献
97.
Crustacean gills function in gas exchange, ion transport, and immune defense against microbial pathogens. Hemocyte aggregates that form in response to microbial pathogens become trapped in the fine vasculature of the gill, leading to the suggestion by others that respiration and ion regulation might by impaired during the course of an immune response. In the present study, injection of the pathogenic bacterium Vibrio campbellii into Callinectes sapidus, the Atlantic blue crab, caused a dramatic decline in oxygen uptake from 4.53 to 2.56 micromol g-1 h-1. This decline in oxygen uptake is associated with a large decrease in postbranchial PO2, from 16.2 (+/-0.46 SEM, n=7) to 13.1 kPa (+/-0.77 SEM, n=9), while prebranchial PO2 remains unchanged. In addition, injection of Vibrio results in the disappearance of a pH change across the gills, an indication of reduced CO2 excretion. The hemolymph hydrostatic pressure change across the gill circulation increases nearly 2-fold in Vibrio-injected crabs compared with a negligible change in pressure across the gill circulation in saline-injected, control crabs. This change, in combination with stability of heart rate and branchial chamber pressure, is indicative of a significant increase in vascular resistance across the gills that is induced by hemocyte nodule formation. A healthy, active blue crab can eliminate most invading bacteria, but the respiratory function of the gills is impaired. Thus, when blue crabs are engaged in the immune response, they are less equipped to engage in oxygen-fueled activities such as predator avoidance, prey capture, and migration. Furthermore, crabs are less fit to invade environments that are hypoxic. 相似文献
98.
Meldrum KK Meldrum DR Sezen SF Crone JK Burnett AL 《American journal of physiology. Regulatory, integrative and comparative physiology》2001,281(1):R359-R364
Heat shock produces cellular tolerance to a variety of adverse conditions; however, the protective effect of heat shock on renal cell ischemic injury remains unclear. Protein kinase C (PKC) has been implicated in the signaling mechanisms of acute preconditioning, yet it remains unknown whether PKC mediates heat shock-induced delayed preconditioning in renal cells. To study this, renal tubular cells (LLC-PK1) were exposed to thermal stress (43 degrees C) for 1 h and heat shock protein (HSP) 72 induction was confirmed by Western blot analysis. Cells were subjected to simulated ischemia 24 h after thermal stress, and the effect of heat shock (delayed preconditioning) on ischemia-induced apoptosis (terminal deoxynucleotidyl transferase dUTP nick-end labeling) and B cell lymphoma 2 (Bcl(2)) expression (Western) was determined. Subsequently, the effect of PKC inhibition on HSP72 induction and heat stress-induced ischemic tolerance was evaluated. Thermal stress induced HSP72 production, increased Bcl(2) expression, and prevented simulated ischemia-induced renal tubular cell apoptosis. PKC inhibition abolished thermal induction of HSP72 and prevented heat stress-induced ischemic tolerance. These data demonstrate that thermal stress protects renal tubular cells from simulated ischemia-induced apoptosis through a PKC-dependent mechanism. 相似文献
99.
Xu KY Kuppusamy SP Wang JQ Li H Cui H Dawson TM Huang PL Burnett AL Kuppusamy P Becker LC 《The Journal of biological chemistry》2003,278(43):41798-41803
Nitric oxide (NO.) generated from nitric oxide synthase (NOS) isoforms bound to cellular membranes may serve to modulate oxidative stresses in cardiac muscle and thereby regulate the function of key membrane-associated enzymes. Ischemia is known to inhibit the function of sarcolemmal enzymes, including the (Na+ + K+)-ATPase, but it is unknown whether concomitant injury to sarcolemma (SL)-associated NOS isoforms may contribute to this process by reducing the availability of locally generated NO. Here we report that nNOS, as well as eNOS (SL NOSs), are tightly associated with cardiac SL membranes in several different species. In isolated perfused rat hearts, global ischemia caused a time-dependent irreversible injury to cardiac SL NOSs and a disruption of SL NO. generation. Pretreatment with low concentrations of the NO. donor 1-hydroxy-2-oxo-3-(N-3-methyl-aminopropyl)-3-methyl-1-triazene (NOC-7) markedly protected both SL NOS and (Na+ + K+)-ATPase functions against ischemia-induced inactivation. Moreover, ischemia impaired SL Na+/K+ binding, and NOC-7 significantly prevented ischemic injury to the ion binding sites on (Na+ + K+)-ATPase. These novel findings indicate that NO. can protect cardiac SL NOSs and (Na+ + K+)-ATPase against ischemia-induced inactivation and suggest that locally generated NO. may serve to regulate SL Na+/K+ ion active transport in the heart. 相似文献
100.
Segregation of a single outboard left-end origin is essential for the viability of parvovirus minute virus of mice 下载免费PDF全文
During DNA replication, the hairpin telomeres of Minute Virus of Mice (MVM) are extended and copied to create imperfectly palindromic duplex junction sequences that bridge adjacent genomes in concatameric replicative-form DNA. These are resolved by the viral initiator protein, NS1, but mechanisms employed at the two telomeres differ. Left-end:left-end junctions are resolved asymmetrically at a single site, OriLTC, by NS1 acting in concert with a host factor, parvovirus initiation factor (PIF). Replication segregates doublet and triplet sequences, initially present as unpaired nucleotides in the bubble region of the left-end hairpin stem, to either side of the junction. These act as spacers between the NS1 and PIF binding sites, and their asymmetric distribution sets up active (OriLTC) and inactive (OriLGAA) forms of OriL. We used a reverse genetic approach to disrupt this asymmetry and found that neither opposing doublets nor triplets in the hairpin bubble were tolerated. Viable mutants were isolated at low frequency and found to contain second-site mutations that either restored the asymmetry or crippled one PIF binding site. These mutations either inactivated the inboard or activated the outboard form of OriL, a polarity that strongly suggests that, in the genus Parvovirus, an active inboard OriL is lethal. 相似文献