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Hyperpolarization activated cation current (If) in cardiac myocytes from pulmonary vein sleeves in the canine with atrial fibrillation

Jia-Yue Li,Hong-Juan Wang,Bin Xu,Xue-Ping Wang,Yi-Cheng Fu,Mei-Yan Chen,De-Xian Zhang,Yan Liu,Qiao Xue,Yang Li,

老年心脏病学杂志(英文版) , 2012,
Developing of chromium cast steel on sleeves of heavy machines  [PDF]
J. Kilarski,A. Studnicki,J. Suchoń
Archives of Foundry Engineering , 2010,
Abstract: The results of investigations of hardness, impact resistance, abrasive and corrosive wear of selected chromium cast steel with destination on sleeves of heavy machines were introduced in the article. First results of exploational investigations talked over on the end.
Investigation of Causes of Scrap Occurrence in Thread Cutting on Steel Sleeves for Motorcar Industry  [PDF]
Maru?i?, V.,Budi?, I.,?ari?, T.
Metalurgija , 2007,
Abstract: This paper studies causes of scrap occurrence, wear and breakage of cutters during thread cutting of steel sleeves poured in Al die castings of motor car engine components. It was concluded that the reason for occurrence of problems with thread cutting of sleeves most probably should be attributed to the fact whether hardness value reaches 200 HB or over 250 HB. The most probable reason for over wear and consequently to breakage of cutters and scrap occurrence, although castings display top quality, lies in the fact that the internal diameter of sleeves frequently falls down under minimally allowed tolerances for threaded sleeves.
Regressive Changes of the Myocardial Sleeves in Elderly Victims of Sudden Bathtub Death  [PDF]
Fumiko Satoh, Yoshihisa Seto, Akio Tsuboi, Motoki Osawa
Forensic Medicine and Anatomy Research (FMAR) , 2015, DOI: 10.4236/fmar.2015.32011
Abstract: In Japan, most sudden deaths occurring during bathing happen in the winter, and predominantly to elderly people. One can infer a relation to physical conditions that are specific to aging. Atrial fibrillation, an arrhythmia, increases with age. This study examined histological changes in the pulmonary vein myocardial sleeves of sudden bathtub death victims and compared them with those of control individuals. We investigated 35 sudden deaths that occurred during bathing and 34 accidental deaths or deaths caused by diseases unrelated to cardiopathies. Pulmonary veins were excised cross-sectionally from the hilar side to the venoatrial junction. Then they were stained with hematoxylin and eosin, resorcin-fuchsin van Gieson, and Congo-red stains. Amyloid deposits in the pulmonary vein myocardial sleeves, as well as the range and severity of scarring, were graded microscopically on a scale of 0-3. In the sudden bathtub death victims, severe scarring was found in the myocardial sleeves of the four pulmonary veins (mean score, 2.0), which was significantly different (p < 0.05) from the control subjects (mean score, 1.4). Cardiomegaly was found in 28 out of the autopsied individuals. In subjects with cardiomegaly, the mean value of pulmonary vein myocardial sleeve scarring was 2.1. In subjects without cardiomegaly, the mean value was 1.8. Comparison revealed that cardiomegaly was associated significantly with scarring progression and degeneration of the myocardial sleeves. Scarring of the pulmonary vein myocardial sleeves was more advanced in victims of sudden bathtub death than in controls without heart disease. Elderly people with scarring of the pulmonary vein myocardial sleeves are likely to develop degenerative variations in their intra-atrial excitation conduction. These results demonstrate that taking hot baths might induce supraventricular arrhythmias such as atrial fibrillation.
Expression and intracellular localization of duck enteritis virus pUL38 protein
Jun Xiang, Guangpeng Ma, Shunchuan Zhang, Anchun Cheng, Mingshu Wang, Dekang Zhu, Renyong Jia, Qihui Luo, Zhengli Chen, Xiaoyue Chen
Virology Journal , 2010, DOI: 10.1186/1743-422x-7-162
Abstract: Duck enteritis virus (DEV) is a natural pathogen of ducks and causes duck viral enteritis, an acute, contagious, and lethal disease affecting waterfowl belonging to the family Anatidae [1]. DEV is a member of the family Herpesviridae. The DEV virion is enveloped, and the genome consists of double-stranded DNA segments packaged in an icosahedral capsid [2]. The gene library of the DEV CHv strain was constructed in our laboratory, and more than 72 major open reading frames (ORFs) were found [3], coding for enzymes, structural proteins, and scaffolding proteins. However, the functional characteristics of most of these proteins are still unknown. To date, only the kinetics of expression and intracellular location of pUL24 [4], pUL31 [5,6], pUL51 [7,8], pUS3 [9], and dUTPase [10] have been investigated. Using bioinformatic tools, some putative glycoproteins and enzymes of the virus were characterized, such as gC [11], gE [12], gI, gD [13], and helicase pUL5 [14]. The identity of other components remains obscure. The DEV pUL38 protein has been suggested to be a putative structural protein. Computational predictions have revealed that DEV pUL38 mainly targets the cytoplasm and nucleus [15]. Immunological assays are an essential part of studies aimed at determining the kinetics of expression and the cellular location of DEV pUL38 in vitro. In this study, we obtained rabbit anti-pUL38 polyclonal sera, which were shown to be functional in immunofluorescence and western blotting assays.The DEV CHv strain used throughout this study was grown in duck embryo fibroblast (DEF) cells. Cell cultures were maintained in modified Eagle's medium (MEM) supplemented with 10% fetal bovine serum (FBS) and antibiotics [16]. In a previous study, we had amplified the ORF of pUL38 (1398 bp) from the DEV genome [15]. The amplified product was cloned between the BamHI and XhoI sites of a pET32(+) plasmid, and a pET32-pUL38 plasmid construct was created.Escherichia coli BL21(DE3) was transformed wi
Decay of nuclear hyperpolarization in silicon microparticles  [PDF]
M. Lee,M. C. Cassidy,C. Ramanathan,C. M. Marcus
Physics , 2011, DOI: 10.1103/PhysRevB.84.035304
Abstract: We investigate the low-field relaxation of nuclear hyperpolarization in undoped and highly doped silicon microparticles at room temperature following removal from high field. For nominally undoped particles, two relaxation time scales are identified for ambient fields above 0.2 mT. The slower, T_1s, is roughly independent of ambient field; the faster, T_1f, decreases with increasing ambient field. A model in which nuclear spin relaxation occurs at the particle surface via a two-electron mechanism is shown to be in good agreement with the experimental data, particularly the field-independence of T_1s. For boron-doped particles, a single relaxation time scale is observed. This suggests that for doped particles, mobile carriers and bulk ionized acceptor sites, rather than paramagnetic surface states, are the dominant relaxation mechanisms. Relaxation times for the undoped particles are not affected by tumbling in a liquid solution.
Fast nuclear spin hyperpolarization of phosphorus in silicon  [PDF]
D. R. McCamey,J. van Tol,G. W. Morley,C. Boehme
Physics , 2008, DOI: 10.1103/PhysRevLett.102.027601
Abstract: We experimentally demonstrate a method for obtaining nuclear spin hyperpolarization, that is, polarization significantly in excess of that expected for a thermal equilibrium. By exploiting a modified Overhauser process, we obtain more than 68% nuclear anti-polarization of phosphorus donors in silicon. This polarization is reached with a time constant of ~150 seconds, at a temperature of 1.37 K and a magnetic field of 8.5 T. The ability to obtain such large polarizations is discussed with regards to its significance for quantum information processing and magnetic resonance imaging.
Human Cytomegalovirus pUL79 Is an Elongation Factor of RNA Polymerase II for Viral Gene Transcription  [PDF]
Yi-Chieh Perng,Jessica A. Campbell,Deborah J. Lenschow,Dong Yu
PLOS Pathogens , 2014, DOI: doi/10.1371/journal.ppat.1004350
Abstract: In this study, we have identified a unique mechanism in which human cytomegalovirus (HCMV) protein pUL79 acts as an elongation factor to direct cellular RNA polymerase II for viral transcription during late times of infection. We and others previously reported that pUL79 and its homologues are required for viral transcript accumulation after viral DNA synthesis. We hypothesized that pUL79 represented a unique mechanism to regulate viral transcription at late times during HCMV infection. To test this hypothesis, we analyzed the proteome associated with pUL79 during virus infection by mass spectrometry. We identified both cellular transcriptional factors, including multiple RNA polymerase II (RNAP II) subunits, and novel viral transactivators, including pUL87 and pUL95, as protein binding partners of pUL79. Co-immunoprecipitation (co-IP) followed by immunoblot analysis confirmed the pUL79-RNAP II interaction, and this interaction was independent of any other viral proteins. Using a recombinant HCMV virus where pUL79 protein is conditionally regulated by a protein destabilization domain ddFKBP, we showed that this interaction did not alter the total levels of RNAP II or its recruitment to viral late promoters. Furthermore, pUL79 did not alter the phosphorylation profiles of the RNAP II C-terminal domain, which was critical for transcriptional regulation. Rather, a nuclear run-on assay indicated that, in the absence of pUL79, RNAP II failed to elongate and stalled on the viral DNA. pUL79-dependent RNAP II elongation was required for transcription from all three kinetic classes of viral genes (i.e. immediate-early, early, and late) at late times during virus infection. In contrast, host gene transcription during HCMV infection was independent of pUL79. In summary, we have identified a novel viral mechanism by which pUL79, and potentially other viral factors, regulates the rate of RNAP II transcription machinery on viral transcription during late stages of HCMV infection.
The Herpes Simplex Virus Protein pUL31 Escorts Nucleocapsids to Sites of Nuclear Egress, a Process Coordinated by Its N-Terminal Domain  [PDF]
Christina Funk?,Melanie Ott?,Verena Raschbichler?,Claus-Henning Nagel?,Anne Binz?,Beate Sodeik?,Rudolf Bauerfeind?,Susanne M. Bailer
PLOS Pathogens , 2015, DOI: 10.1371/journal.ppat.1004957
Abstract: Progeny capsids of herpesviruses leave the nucleus by budding through the nuclear envelope. Two viral proteins, the membrane protein pUL34 and the nucleo-phosphoprotein pUL31 form the nuclear egress complex that is required for capsid egress out of the nucleus. All pUL31 orthologs are composed of a diverse N-terminal domain with 1 to 3 basic patches and a conserved C-terminal domain. To decipher the functions of the N-terminal domain, we have generated several Herpes simplex virus mutants and show here that the N-terminal domain of pUL31 is essential with basic patches being critical for viral propagation. pUL31 and pUL34 entered the nucleus independently of each other via separate routes and the N-terminal domain of pUL31 was required to prevent their premature interaction in the cytoplasm. Unexpectedly, a classical bipartite nuclear localization signal embedded in this domain was not required for nuclear import of pUL31. In the nucleus, pUL31 associated with the nuclear envelope and newly formed capsids. Viral mutants lacking the N-terminal domain or with its basic patches neutralized still associated with nucleocapsids but were unable to translocate them to the nuclear envelope. Replacing the authentic basic patches with a novel artificial one resulted in HSV1(17+)Lox-UL31-hbpmp1mp2, that was viable but delayed in nuclear egress and compromised in viral production. Thus, while the C-terminal domain of pUL31 is sufficient for the interaction with nucleocapsids, the N-terminal domain was essential for capsid translocation to sites of nuclear egress and a coordinated interaction with pUL34. Our data indicate an orchestrated sequence of events with pUL31 binding to nucleocapsids and escorting them to the inner nuclear envelope. We propose a common mechanism for herpesviral nuclear egress: pUL31 is required for intranuclear translocation of nucleocapsids and subsequent interaction with pUL34 thereby coupling capsid maturation with primary envelopment.
Human Cytomegalovirus Protein pUL117 Targets the Mini-Chromosome Maintenance Complex and Suppresses Cellular DNA Synthesis  [PDF]
Zhikang Qian,Van Leung-Pineda,Baoqin Xuan,Helen Piwnica-Worms,Dong Yu
PLOS Pathogens , 2010, DOI: 10.1371/journal.ppat.1000814
Abstract: Modulation of host DNA synthesis is essential for many viruses to establish productive infections and contributes to viral diseases. Human cytomegalovirus (HCMV), a large DNA virus, blocks host DNA synthesis and deregulates cell cycle progression. We report that pUL117, a viral protein that we recently identified, is required for HCMV to block host DNA synthesis. Mutant viruses in which pUL117 was disrupted, either by frame-shift mutation or by a protein destabilization-based approach, failed to block host DNA synthesis at times after 24 hours post infection in human foreskin fibroblasts. Furthermore, pUL117-deficient virus stimulated quiescent fibroblasts to enter S-phase, demonstrating the intrinsic ability of HCMV to promote host DNA synthesis, which was suppressed by pUL117. We examined key proteins known to be involved in inhibition of host DNA synthesis in HCMV infection, and found that many were unlikely involved in the inhibitory activity of pUL117, including geminin, cyclin A, and viral protein IE2, based on their expression patterns. However, the ability of HCMV to delay the accumulation of the mini-chromosome maintenance (MCM) complex proteins, represented by MCM2 and MCM4, and prevent their loading onto chromatin, was compromised in the absence of pUL117. When expressed alone, pUL117 slowed cell proliferation, delayed DNA synthesis, and inhibited MCM accumulation. Knockdown of MCM proteins by siRNA restored the ability of pUL117-deficient virus to block cellular DNA synthesis. Thus, targeting MCM complex is one mechanism pUL117 employs to help block cellular DNA synthesis during HCMV infection. Our finding substantiates an emerging picture that deregulation of MCM is a conserved strategy for many viruses to prevent host DNA synthesis and helps to elucidate the complex strategy used by a large DNA virus to modulate cellular processes to promote infection and pathogenesis.
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