On the Effect of Lubricant on Pool Boiling Heat Transfer Performance

   For typical vapor compression processes, lubricant oil is very essential for lubricating and sealing the sliding parts and the lubricant also takes part in cushioning cylinder valves. However lubricants may migrate to the evaporator to alter the heat transfer characteristics. This is can be made clear from the viscosity and surface tension of lubricant since the viscosity of lubricant oil is about two to three orders higher than that of refrigerant whereas the corresponding surface tension of lubricant is approximately one order higher. Typically, the presence of lubricant may deteriorate heat transfer performance, yet this phenomenon becomes more severe when the lubricant mass fraction is higher. However, some previous literatures had clearly showed that the presence of lubricant oil may favor the heat transfer performance at a low lubricant fraction and the heat transfer performance may peak at a specific oil concentration. In this study, the authors aim at clarifying this phenomenon subject to pool boiling condition. Various parameters affecting the heat transfer coefficient, such as viscosity, surface tension, critical solution temperature and other thermodynamic and transport properties will be examined.    During pool boiling process, the lubricant accumulates on the surface since the refrigerant is preferential to evaporate. Hence, excess lubricant enrichment on the surface results in a thin lubricant excess layer and a thermal boundary layer, which influence the heat transfer performance, either enhancement or degradation. The excess layer may bring about a liquid-solid surface energy reduction which increases site density and reduces the bubble departure diameter, causing enhancement and degradation in heat transfer performance, respectively. However, the effect of the bubble departure diameter normally surpasses the influence of site density. This may be the crucial reason that gives rise to an occurrence of the plateau of heat transfer coefficient and followed by an apparent decline of heat transfer coefficient with a further increase of lubricant concentration.    Moreover, with the preferential evaporation of the refrigerant, a surface tension gradient is formed, which induces the Marangoni effect through which refrigerant/lubricant mixtures is supplied toward the contact line. From the phase equilibrium diagram, the maximum of the Marangoni number may occur at the low lubricant concentration with a maximum temperature difference. Hence, the presence of Marangoni effect may also be the favor the heat transfer accordingly. Also, a small fraction of lubricant will increase a larger viscosity that provide a thicker thermal boundary layer which may activate more site density, and enhances the heat transfer performance. Furthermore, miscibility may also play a crucial factor that affects the pool boiling heat transfer performance. The fluid with a smaller difference between the bulk fluid temperature and critical solution temperature may yield a better heat transfer performance by drawing superheated liquid onto the bubble sides.

The Enamel Phenotype in Homozygous Fam83h Truncation Mice

BackgroundTruncation FAM83H mutations cause human autosomal dominant hypocalcified amelogenesis imperfecta (ADHCAI), an inherited disorder characterized by severe hardness defects in dental enamel. No enamel defects were observed in Fam83h null mice suggesting that Fam83h truncation mice would better replicate human mutations.MethodsWe generated and characterized a mouse model (Fam83hTr/Tr) expressing a truncated FAM83H protein (amino acids 1â 296), which recapitulated the ADHCAIâ causing human FAM83H p.Tyr297* mutation.ResultsDay 14 and 7â week Fam83hTr/Tr molars exhibited rough enamel surfaces and slender cusps resulting from hypoplastic enamel defects. The lateral third of the Fam83hTr/Tr incisor enamel layer was thinner, with surface roughness and altered enamel rod orientation, suggesting disturbed enamel matrix secretion. Regular electron density in mandibular incisor enamel indicated normal enamel maturation. Only mildly increased posteruption attrition of Fam83hTr/Tr molar enamel was observed at 7â weeks. Histologically, the Fam83hTr/Tr enamel organ, including ameloblasts, and enamel matrices at sequential stages of amelogenesis exhibited comparable morphology without overt abnormalities, except irregular and less evident ameloblast Tomes’ processes in specific areas.ConclusionsConsidering Fam83hâ /â mice showed no enamel phenotype, while Fam83hTr/Tr (p.Tyr297*) mice displayed obvious enamel malformations, we conclude that FAM83H truncation mutations causing ADHCAI in humans disturb amelogenesis through a neomorphic mechanism, rather than haploinsufficiency.FAM83H truncation mutations cause inherited enamel malformations in humans. Previously we showed that no enamel malformations are observed in Fam83h null mice. Here we demonstrate that truncation of FAM83H in mice causes enamel malformations. This figure shows how the lateral incisor enamel (on the left) is thinner in the Fam83h truncation mouse than it is in wild-type.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/149571/1/mgg3724-sup-0004-DataS4.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/149571/2/mgg3724-sup-0003-DataS3.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/149571/3/mgg3724-sup-0001-DataS1.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/149571/4/mgg3724-sup-0002-DataS2.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/149571/5/mgg3724_am.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/149571/6/mgg3724.pd

Pioglitazone retrieves hepatic antioxidant DNA repair in a mice model of high fat diet

<p>Abstract</p> <p>Background</p> <p>Pioglitazone was reported to improve hepatic steatosis and necroinflammation in human studies. To investigate whether the hepato-protective effect of pioglitazone was associated with an improvement of antioxidant defense mechanism, oxidative DNA damage and repair activity were determined in a high fat diet model. Male C57BL/6 mice were respectively fed with a 30% fat diet, the same diet with pioglitazone 100 mg/kg/day, or a chow diet as control for 8 weeks. Tissue oxidative stress was indicated by malondialdehyde concentration. Oxidative DNA damage was detected by immunohistochemical 8-oxoG staining. Enzymatic antioxidant defense was detected by the real-time PCR of superoxide dismutase (<it>Sod1, Sod2</it>) and DNA glycosylase (<it>Ogg1, MutY</it>). Oxidative DNA repair was detected by immunohistochemical staining and western blotting of OGG1 expression.</p> <p>Results</p> <p>Our results show that hepatic steatosis was induced by a high-fat diet and improved by adding pioglitazone. Malondialdehyde concentration and 8-oxoG staining were strongly increased in the high-fat diet group, but attenuated by pioglitazone. Gene expressions of antioxidant defense mechanism: <it>Sod1, Sod2, Ogg1 </it>and <it>MutY </it>significantly decreased in the high-fat diet group but reversed by pioglitazone co-administration.</p> <p>Conclusion</p> <p>The attenuation of hepatic oxidative DNA damage by pioglitazone in a high-fat diet may be mediated by up-regulation of the antioxidant defense mechanism and oxidative DNA repair activity. The diminution of oxidative damage may explain the clinical benefit of pioglitazone treatment in patients with non-alcoholic fatty liver disease.</p

Creating two-dimensional solid helium via diamond lattice confinement

The universe abounds with solid helium in polymorphic forms. Therefore, exploring the allotropes of helium remains vital to our understanding of nature. However, it is challenging to produce, observe and utilize solid helium on the earth because high-pressure techniques are required to solidify helium. Here we report the discovery of room-temperature two-dimensional solid helium through the diamond lattice confinement effect. Controllable ion implantation enables the self-assembly of monolayer helium atoms between {100} diamond lattice planes. Using state-of-the-art integrated differential phase contrast microscopy, we decipher the buckled tetragonal arrangement of solid helium monolayers with an anisotropic nature compressed by the robust diamond lattice. These distinctive helium monolayers, in turn, produce substantial compressive strains to the surrounded diamond lattice, resulting in a large-scale bandgap narrowing up to ~2.2 electron volts. This approach opens up new avenues for steerable manipulation of solid helium for achieving intrinsic strain doping with profound applications

A long non-coding RNA protects the heart from pathological hypertrophy

The role of long noncoding RNA (lncRNA) in adult hearts is unknownalso unclear is how lncRNA modulates nucleosome remodeling. An estimated 70% of mouse genes undergo antisense transcription, including myosin heavy chain 7 (Myh7) that encodes molecular motor proteins for heart contraction. Here, we identify a cluster of lncRNA transcripts from Myh7 loci and show a new lncRNA–chromatin mechanism for heart failure. In mice, these transcripts, which we named Myosin Heavy Chain Associated RNA Transcripts (MyHEART or Mhrt), are cardiac-specific and abundant in adult hearts. Pathological stress activates the Brg1-Hdac-Parp chromatin repressor complex to inhibit Mhrt transcription in the heart. Such stress-induced Mhrt repression is essential for cardiomyopathy to develop: restoring Mhrt to the pre-stress level protects the heart from hypertrophy and failure. Mhrt antagonizes the function of Brg1, a chromatin-remodeling factor that is activated by stress to trigger aberrant gene expression and cardiac myopathy. Mhrt prevents Brg1 from recognizing its genomic DNA targets, thus inhibiting chromatin targeting and gene regulation by Brg1. Mhrt binds to the helicase domain of Brg1, and this domain is crucial for tethering Brg1 to chromatinized DNA targets. Brg1 helicase has dual nucleic acid-binding specificities: it is capable of binding lncRNA (Mhrt) and chromatinized—but not naked—DNA. This dual-binding feature of helicase enables a competitive inhibition mechanism by which Mhrt sequesters Brg1 from its genomic DNA targets to prevent chromatin remodeling. A Mhrt-Brg1 feedback circuit is thus crucial for heart function. Human MHRT also originates from MYH7 loci and is repressed in various types of myopathic hearts, suggesting a conserved lncRNA mechanism in human cardiomyopathy. Our studies identify the first cardioprotective lncRNA, define a new targeting mechanism for ATP-dependent chromatin-remodeling factors, and establish a new paradigm for lncRNA–chromatin interaction

Risk factors for fatal candidemia caused by Candida albicans and non-albicans Candida species

BACKGROUND: Invasive fungal infections, such as candidemia, caused by Candida species have been increasing. Candidemia is not only associated with a high mortality (30% to 40%) but also extends the length of hospital stay and increases the costs of medical care. Sepsis caused by Candida species is clinically indistinguishable from bacterial infections. Although, the clinical presentations of the patients with candidemia caused by Candida albicans and non-albicans Candida species (NAC) are indistinguishable, the susceptibilities to antifungal agents of these species are different. In this study, we attempted to identify the risk factors for candidemia caused by C. albicans and NAC in the hope that this may guide initial empiric therapy. METHODS: A retrospective chart review was conducted during 1996 to 1999 at the Veterans General Hospital-Taipei. RESULTS: There were 130 fatal cases of candidemia, including 68 patients with C. albicans and 62 with NAC. Candidemia was the most likely cause of death in 55 of the 130 patients (42.3 %). There was no significant difference in the distribution of Candida species between those died of candidemia and those died of underlying conditions. Patients who had one of the following conditions were more likely to have C. albicans, age ≧ 65 years, immunosuppression accounted to prior use of steroids, leukocytosis, in the intensive care unit (ICU), and intravascular and urinary catheters. Patients who had undergone cancer chemotherapy often appeared less critically ill and were more likely to have NAC. CONCLUSION: Clinical and epidemiological differences in the risk factors between candidemia caused by C. albicans and NAC may provide helpful clues to initiate empiric therapy for patients infected with C. albicans versus NAC

Transcriptomic analyses of regenerating adult feathers in chicken

Transcriptome Expression Data. Table of mapped reads to Galgal4 transcripts for all 15 data sets. FPKM (Fragments per kilobase of exon per million fragments mapped): normalized transcript abundance values for each gene in the indicated tissues. (CSV 1314 kb

The Yuan-Tseh Lee Array for Microwave Background Anisotropy

The Yuan-Tseh Lee Array for Microwave Background Anisotropy (AMiBA) is the first interferometer dedicated to studying the cosmic microwave background (CMB) radiation at 3mm wavelength. The choice of 3mm was made to minimize the contributions from foreground synchrotron radiation and Galactic dust emission. The initial configuration of seven 0.6m telescopes mounted on a 6-m hexapod platform was dedicated in October 2006 on Mauna Loa, Hawaii. Scientific operations began with the detection of a number of clusters of galaxies via the thermal Sunyaev-Zel'dovich effect. We compare our data with Subaru weak lensing data in order to study the structure of dark matter. We also compare our data with X-ray data in order to derive the Hubble constant.Comment: accepted for publication in ApJ (13 pages, 7 figures); a version with high resolution figures available at http://www.asiaa.sinica.edu.tw/~keiichi/upfiles/AMiBA7/pho_highreso.pd

IKKβ Suppression of TSC1 Links Inflammation and Tumor Angiogenesis via the mTOR Pathway

SummaryTNFα has recently emerged as a regulator linking inflammation to cancer pathogenesis, but the detailed cellular and molecular mechanisms underlying this link remain to be elucidated. The tuberous sclerosis 1 (TSC1)/TSC2 tumor suppressor complex serves as a repressor of the mTOR pathway, and disruption of TSC1/TSC2 complex function may contribute to tumorigenesis. Here we show that IKKβ, a major downstream kinase in the TNFα signaling pathway, physically interacts with and phosphorylates TSC1 at Ser487 and Ser511, resulting in suppression of TSC1. The IKKβ-mediated TSC1 suppression activates the mTOR pathway, enhances angiogenesis, and results in tumor development. We further find that expression of activated IKKβ is associated with TSC1 Ser511 phosphorylation and VEGF production in multiple tumor types and correlates with poor clinical outcome of breast cancer patients. Our findings identify a pathway that is critical for inflammation-mediated tumor angiogenesis and may provide a target for clinical intervention in human cancer

Core Site-Moiety Maps Reveal Inhibitors and Binding Mechanisms of Orthologous Proteins by Screening Compound Libraries

Members of protein families often share conserved structural subsites for interaction with chemically similar moieties despite low sequence identity. We propose a core site-moiety map of multiple proteins (called CoreSiMMap) to discover inhibitors and mechanisms by profiling subsite-moiety interactions of immense screening compounds. The consensus anchor, the subsite-moiety interactions with statistical significance, of a CoreSiMMap can be regarded as a “hot spot” that represents the conserved binding environments involved in biological functions. Here, we derive the CoreSiMMap with six consensus anchors and identify six inhibitors (IC50<8.0 µM) of shikimate kinases (SKs) of Mycobacterium tuberculosis and Helicobacter pylori from the NCI database (236,962 compounds). Studies of site-directed mutagenesis and analogues reveal that these conserved interacting residues and moieties contribute to pocket-moiety interaction spots and biological functions. These results reveal that our multi-target screening strategy and the CoreSiMMap can increase the accuracy of screening in the identification of novel inhibitors and subsite-moiety environments for elucidating the binding mechanisms of targets