49 research outputs found
ASME 2004-59928 NUCLEATE BOILING INSIDE THE EVAPORATOR OF THE PLANAR LOOP HEAT PIPE
ABSTRACT The Loop Heat Pipe (LHP) under development is a next generation micro heat transfer device that utilizes the latent heat of a working fluid and has excellent transfer capacity compared with that of standard metallic cooling devices. A typical LHP consists of an evaporator, a reservoir (also called the compensation chamber), vapor and liquid lines, a subcooler, and a condenser. As heat is applied to the evaporator, all of the input energy goes into the evaporation of the liquid in the pores of the primary CPS wick or leak to the bottom. The nucleate boiling, which occurs beneath the primary wick in the evaporator, is a very significant phenomena. It affects critical operating issues, such as dry out of the primary wick. Using a clear evaporator machined from Pyrex glass, the nucleation, which occurred in the evaporator, was studied. De-ionized water was utilized as the working fluid. INTRODUCTION The loop heat pipe (LHP) is a thermal control and heat transport device. LHPs were originally invented and developed in the former Soviet Union in the mid 1980's, and has been employed in a reliable and versatile thermal control system for space applications. LHPs can transport very large thermal power loads over long distances through flexible, small diameter tubes and against high gravitational heads due to capillary forces in the evaporator. LHPs are two-phase heat transfer devices that utilize the latent heat and are completely self-circulating systems that have no mechanical moving parts and add no unwanted vibration to the spacecraft
Engineered Nanostructures for High Thermal Conductivity Substrates
In the DARPA Thermal Ground Plane (TGP)
program[1],we are developing a new thermal technology
that will enable a monumental thermal technological leap
to an entirely new class of electronics, particularly
electronics for use in high-tech military systems. The
proposed TGP is a planar, thermal expansion matched heat
spreader that is capable of moving heat from multiple
chips to a remote thermal sink. DARPA’s final goals
require the TGP to have an effective conductivity of
20,000 W/mK, operate at 20g, with minimal fluid loss of
less than 0.1%/year and in a large ultra-thin planar package
of 10cmx20cm, no thicker than 1mm. The proposed TGP
is based on a heat pipe architecture[2], whereby the
enhanced transport of heat is made possible by applying
nanoengineered surfaces to the evaporator, wick, and
condenser surfaces. Ultra-low thermal resistances are
engineered using superhydrophilic and superhydrophobic
nanostructures on the interior surfaces of the TGP
envelope. The final TGP design will be easily integrated
into existing printed circuit board manufacturing
technology. In this paper, we present the transport design,
fabrication and packaging techniques, and finally a novel
fluorescence imaging technique to visualize the capillary
flow in these nanostructured wicks.United States. Defense Advanced Research Projects Agency (SSC SD Contract No. N66001-08-C-2008
Role of obesity in a randomized placebo-controlled trial of difluoromethylornithine (DFMO) + sulindac for the prevention of sporadic colorectal adenomas
BACKGROUND: Chemoprevention with the polyamine-inhibitory regimen difluoromethylornithine (DFMO) + sulindac markedly reduces risk of recurrent adenoma in colorectal adenoma patients. Obesity is associated with risk of colorectal adenoma and colorectal cancer. This study investigates how obesity influences risk of recurrent adenoma after prolonged treatment with DFMO + sulindac versus placebo. METHODS: Our analysis included subjects enrolled in the phase III colorectal adenoma prevention clinical trial investigating DFMO + sulindac versus placebo. Patients were classified by obesity (body mass index, BMI ≥ 30 kg/m(2)) status at baseline. Pearson χ(2) statistic and Mann–Whitney U test were used to compare baseline characteristics, including rectal tissue polyamine levels. Log-binomial regression analysis was used to determine the risk ratio (RR) of recurrent adenomas, adjusted for covariates and an interaction term for obesity and treatment. RESULTS: The final analytic cohort was comprised of 267 patients. In separate regression models, the risk of adenoma recurrence after treatment compared to placebo was similar for obese (RR = 0.32, 95 % CI 15–71) and non-obese patients (RR = 0.27, 95 % CI 15–49). No significant interaction was detected between obesity, treatment, and risk of colorectal adenoma in the full regression model (p(interaction) = 0.91). CONCLUSIONS: Obesity does not substantially modify the colorectal adenoma risk reduction ascribed to DFMO + sulindac versus placebo
International Spread of Multidrug-resistant Salmonella Schwarzengrund in Food Products
This serovar was isolated from persons, food, and food animals in Thailand, Denmark, and the United States
Congenital Diarrhea and Cholestatic Liver Disease: Phenotypic Spectrum Associated with MYO5B Mutations
Myosin Vb (MYO5B) is a motor protein that facilitates protein trafficking and recycling in polarized cells by RAB11- and RAB8-dependent mechanisms. Biallelic MYO5B mutations are identified in the majority of patients with microvillus inclusion disease (MVID). MVID is an intractable diarrhea of infantile onset with characteristic histopathologic findings that requires life-long parenteral nutrition or intestinal transplantation. A large number of such patients eventually develop cholestatic liver disease. Bi-allelic MYO5B mutations are also identified in a subset of patients with predominant early-onset cholestatic liver disease. We present here the compilation of 114 patients with disease-causing MYO5B genotypes, including 44 novel patients as well as 35 novel MYO5B mutations, and an analysis of MYO5B mutations with regard to functional consequences. Our data support the concept that (1) a complete lack of MYO5B protein or early MYO5B truncation causes predominant intestinal disease (MYO5B-MVID), (2) the expression of full-length mutant MYO5B proteins with residual function causes predominant cholestatic liver disease (MYO5B-PFIC), and (3) the expression of mutant MYO5B proteins without residual function causes both intestinal and hepatic disease (MYO5B-MIXED). Genotype-phenotype data are deposited in the existing open MYO5B database in order to improve disease diagnosis, prognosis, and genetic counseling.This research was funded by Jubiläumsfonds der Österreichischen Nationalbank, grant no.16678 (to A.R.J.), grant no. 18019 (to G.-F.V.) and Tiroler Wissenschaftsfonds, grant No. 0404/2386 (toG.-F.V.).info:eu-repo/semantics/publishedVersio
AXIAL JET-INDUCED MIXING IN LOW GRAVITY: RESULTS OF THE REDUCED-FILL TANK PRESSURE CONTROL EXPERIMENT
Mathematical Modeling of Novel Two-Phase Heat Transfer Device for Thermal Management of Light Emitting Diodes
Thermal Modeling and Experimental Validation for High Thermal Conductivity Heat Pipe Thermal Ground Planes
CaMKK2 facilitates Golgi-associated vesicle trafficking to sustain cancer cell proliferation
Abstract Calcium/calmodulin-dependent protein kinase kinase 2 (CaMKK2) regulates cell and whole-body metabolism and supports tumorigenesis. The cellular impacts of perturbing CAMKK2 expression are, however, not yet fully characterised. By knocking down CAMKK2 levels, we have identified a number of significant subcellular changes indicative of perturbations in vesicle trafficking within the endomembrane compartment. To determine how they might contribute to effects on cell proliferation, we have used proteomics to identify Gemin4 as a direct interactor, capable of binding CAMKK2 and COPI subunits. Prompted by this, we confirmed that CAMKK2 knockdown leads to concomitant and significant reductions in δ-COP protein. Using imaging, we show that CAMKK2 knockdown leads to Golgi expansion, the induction of ER stress, abortive autophagy and impaired lysosomal acidification. All are phenotypes of COPI depletion. Based on our findings, we hypothesise that CAMKK2 sustains cell proliferation in large part through effects on organelle integrity and membrane trafficking