Thermal performance of phase change wallboard for residential cooling application

Cooling of residential California buildings contributes significantly to electrical consumption and peak power demand mainly due to very poor load factors in milder climates. Thermal mass can be utilized to reduce the peak-power demand, downsize the cooling systems, and/or switch to low-energy cooling sources. Large thermal storage devices have been used in the past to overcome the shortcomings of alternative cooling sources, or to avoid high demand charges. The manufacturing of phase change material (PCM) implemented in gypsum board, plaster or other wall-covering material, would permit the thermal storage to become part of the building structure. PCMs have two important advantages as storage media: they can offer an order-of-magnitude increase in thermal storage capacity, and their discharge is almost isothermal. This allows the storage of high amounts of energy without significantly changing the temperature of the room envelope. As heat storage takes place inside the building, where the loads occur, rather than externally, additional transport energy is not required. RADCOOL, a thermal building simulation program based on the finite difference approach, was used to numerically evaluate the latent storage performance of treated wallboard. Extended storage capacity obtained by using double PCM-wallboard is able to keep the room temperatures close to the upper comfort limits without using mechanical cooling. Simulation results for a living room with high internal loads and weather data for Sunnyvale, California, show significant reduction of room air temperature when heat can be stored in PCM-treated wallboards

Is elevated creatinine level a contraindication to endovascular aneurysm repair?

AbstractPurposeIt is widely believed that chronic renal insufficiency (CRI) greatly increases the risk associated with endovascular abdominal aortic aneurysm repair (EVAR) and is a relative contraindication to the procedure and to the use of intra-arterial contrast agents (IACA). We reviewed a 5-year EVAR experience to determine whether the procedure and use of IACA have an important deleterious effect on renal function in patients with and without pre-existing CRI.MethodsEndovascular aneurysm repair (EVAR) was performed in 200 patients with a variety of endografts, with intra-arterial contrast agents. The patients were retrospectively assigned to three groups on the basis of preoperative serum creatinine concentration (Cr): group 1 (n = 108), Cr less than 1.5 mg/dL (normal range); group 2 (n = 65), Cr 1.5 to 2.0 mg/dL; group 3 (n = 27), Cr 2.1 to 3.5 mg/dL. No patients had undergone hemodialysis. In groups 2 and 3, patients received hydration perioperatively, and received mannitol intraoperatively; no nephrotoxic drugs were administered during the procedure, other than nonionic contrast agent (Omnipaque 350).ResultsThe incidence of postoperative complications between the three study groups was not statistically different. In group 1 a transient increase in serum Cr (>30% over baseline and >1.4 mg/dL) was noted in three patients (2.7%), two of whom (1.9%) required temporary hemodialysis and one (0.9%) who died of renal failure. In group 2 a transient increase in serum Cr was noted in two patients (3.1%); both patients (3.1%) required temporary hemodialysis, and one patient (1.5%) died of renal failure. In group 3 a transient increase in serum Cr was noted in two patients (7.4%); one patient (3.7%) required temporary hemodialysis, and one patient (3.7%) died of renal failure. Perioperative hypotension significantly increased the risk for elevated serum Cr and death (P < .05), and larger contrast volume was associated with an increase in serum Cr (P < .05) during the postoperative period.ConclusionsEVAR with intra-arterial contrast agents can be accomplished in patients with chronic renal insufficiency who do not require dialysis, with limited and acceptable morbidity and mortality, similar to that observed with open aneurysm repair. Contrary to other reports in which perioperative precautions were not used, our study shows that with EVAR the risk for worsening renal failure, dialysis, and death is only slightly, and not significantly, greater in patients with preoperative chronic renal insufficiency compared with patients with normal renal function. Perioperative hypotension and increased contrast volume are significant risk factors for postoperative increase in serum Cr and death. With appropriate precautions such as averting perioperative hypotension and limiting the volume of nonionic contrast agents, elevated Cr need not be a contraindication to EVAR with intra-arterial contrast agents

Ligation of Macrophage Fcγ Receptors Recapitulates the Gene Expression Pattern of Vulnerable Human Carotid Plaques

Stroke is a leading cause of death in the United States. As ∼60% of strokes result from carotid plaque rupture, elucidating the mechanisms that underlie vulnerability is critical for therapeutic intervention. We tested the hypothesis that stable and vulnerable human plaques differentially express genes associated with matrix degradation. Examination established that femoral, and the distal region of carotid, plaques were histologically stable while the proximal carotid plaque regions were vulnerable. Quantitative RT-PCR was used to compare expression of 22 genes among these tissues. Distal carotid and femoral gene expression was not significantly different, permitting the distal carotid segments to be used as a paired control for their corresponding proximal regions. Analysis of the paired plaques revealed differences in 16 genes that impact plaque stability: matrix metalloproteinases (MMP, higher in vulnerable), MMP modulators (inhibitors: lower, activators: higher in vulnerable), activating Fc receptors (FcγR, higher in vulnerable) and FcγR signaling molecules (higher in vulnerable). Surprisingly, the relative expression of smooth muscle cell and macrophage markers in the three plaque types was not significantly different, suggesting that macrophage distribution and/or activation state correlates with (in)stability. Immunohistochemistry revealed that macrophages and smooth muscle cells localize to distinct and non-overlapping regions in all plaques. MMP protein localized to macrophage-rich regions. In vitro, treatment of macrophages with immune complexes, but not oxidized low density lipoprotein, C-reactive protein, or TNF-α, induced a gene expression profile similar to that of the vulnerable plaques. That ligation of FcγR recapitulates the pattern of gene expression in vulnerable plaques suggests that the FcγR → macrophage activation pathway may play a greater role in human plaque vulnerability than previously appreciated

Current opinion on the role of testosterone in the development of prostate cancer: a dynamic model

Background: Since the landmark study conducted by Huggins and Hodges in 1941, a failure to distinguish between the role of testosterone in prostate cancer development and progression has led to the prevailing opinion that high levels of testosterone increase the risk of prostate cancer. To date, this claim remains unproven. Presentation of the Hypothesis: We present a novel dynamic mode of the relationship between testosterone and prostate cancer by hypothesizing that the magnitude of age-related declines in testosterone, rather than a static level of testosterone measured at a single point, may trigger and promote the development of prostate cancer. Testing of the Hypothesis: Although not easily testable currently, prospective cohort studies with population-representative samples and repeated measurements of testosterone or retrospective cohorts with stored blood samples from different ages are warranted in future to test the hypothesis. Implications of the Hypothesis: Our dynamic model can satisfactorily explain the observed age patterns of prostate cancer incidence, the apparent conflicts in epidemiological findings on testosterone and risk of prostate cancer, racial disparities in prostate cancer incidence, risk factors associated with prostate cancer, and the role of testosterone in prostate cancer progression. Our dynamic model may also have implications for testosterone replacement therapy

The Epistemic Status of Processing Fluency as Source for Judgments of Truth

This article combines findings from cognitive psychology on the role of processing fluency in truth judgments with epistemological theory on justification of belief. We first review evidence that repeated exposure to a statement increases the subjective ease with which that statement is processed. This increased processing fluency, in turn, increases the probability that the statement is judged to be true. The basic question discussed here is whether the use of processing fluency as a cue to truth is epistemically justified. In the present analysis, based on Bayes’ Theorem, we adopt the reliable-process account of justification presented by Goldman (1986) and show that fluency is a reliable cue to truth, under the assumption that the majority of statements one has been exposed to are true. In the final section, we broaden the scope of this analysis and discuss how processing fluency as a potentially universal cue to judged truth may contribute to cultural differences in commonsense beliefs

Two Distinct Modes of Hypoosmotic Medium-Induced Release of Excitatory Amino Acids and Taurine in the Rat Brain In Vivo

A variety of physiological and pathological factors induce cellular swelling in the brain. Changes in cell volume activate several types of ion channels, which mediate the release of inorganic and organic osmolytes and allow for compensatory cell volume decrease. Volume-regulated anion channels (VRAC) are thought to be responsible for the release of some of organic osmolytes, including the excitatory neurotransmitters glutamate and aspartate. In the present study, we compared the in vivo properties of the swelling-activated release of glutamate, aspartate, and another major brain osmolyte taurine. Cell swelling was induced by perfusion of hypoosmotic (low [NaCl]) medium via a microdialysis probe placed in the rat cortex. The hypoosmotic medium produced several-fold increases in the extracellular levels of glutamate, aspartate and taurine. However, the release of the excitatory amino acids differed from the release of taurine in several respects including: (i) kinetic properties, (ii) sensitivity to isoosmotic changes in [NaCl], and (iii) sensitivity to hydrogen peroxide, which is known to modulate VRAC. Consistent with the involvement of VRAC, hypoosmotic medium-induced release of the excitatory amino acids was inhibited by the anion channel blocker DNDS, but not by the glutamate transporter inhibitor TBOA or Cd2+, which inhibits exocytosis. In order to elucidate the mechanisms contributing to taurine release, we studied its release properties in cultured astrocytes and cortical synaptosomes. Similarities between the results obtained in vivo and in synaptosomes suggest that the swelling-activated release of taurine in vivo may be of neuronal origin. Taken together, our findings indicate that different transport mechanisms and/or distinct cellular sources mediate hypoosmotic medium-induced release of the excitatory amino acids and taurine in vivo