Intrinsic thermal interfacial resistance measurement in bonded metal-polymer foils.

Heat conduction through bonded metal-polymer interfaces often limits the overall heat transfer in electronic packaging, batteries, and heat recovery systems. To design the thermal circuit in such systems, it is essential to measure the thermal interfacial resistance (TIR) across ∼1 µm to 100 µm junctions. Previously reported TIR of metal-polymer junctions utilize ASTM E1530-based two-block systems that measure the TIR by applying pressure across the interface through external heating and cooling blocks. Here, we report a novel modification of the ASTM-E1530 technique that employs integrated heaters and sensors to provide an intrinsic TIR measurement of an adhesively bonded metal-polymer junction. We design the measurement technique using finite element simulations to either passively suppress or actively compensate the lateral heat diffusion through the polymer, which can minimize the systematic error to ≲5%. Through proof-of-concept experiments, we report the TIR of metal-polymer interfaces made from DuPont's Pyralux double-side copper-clad laminates, commonly used in flexible printed circuit boards. Our TIR measurement errors are <10%. We highlight additional sources of errors due to non-idealities in the experiment and discuss possible ways to overcome them. Our measurement technique is also applicable to interfaces that are electrically insulating such as adhesively joined metal-metal junctions and sputter-coated or welded metal-polymer junctions. Overall, the technique is capable of measuring TIR ≳10-5 m2 KW-1 in bonded metal-polymer foils and can be tailored for in situ measurements in flexible electronics, circuit packaging, and other hybrid metal-polymer systems.

The Effects of Forced Exhalation and Inhalation, Grunting, and Valsalva Maneuver on Forehand Force in Collegiate Tennis Players.

To examine the effects of forced expiration (FE), forced inspiration (FI), grunting (GR), and valsalva maneuver (VM), on air volume, maximum force production, and muscle recruitment during a simulated forehand stroke in collegiate tennis players. Superficial electrodes were placed over the anterior deltoid, pectoralis major, rectus abdominis, lumbar and thoracic erector spinae, and external and internal obliques. Subjects stood in a simulated forehand stroke stance with their dominant hand positioned on a force plate. Subjects performed 3 repetitions of maximal 2- to 3-second isometric forehands with randomly assigned breathing conditions (FE, FI, VM, and GR) and 30-seconds rest between contractions. Air volumes were also collected during each trial. A repeated-measures multivariate analysis of variance compared normalized peak electromyographic activity across the 7 muscle groups. Separate repeated measures ANOVAs compared the effect of breathing conditions on peak force production and air volume. Statistical significance was set at p ≤ 0.05 for all analyses. Overall muscle activity differed significantly by breathing condition (p = 0.031) with greater anterior deltoid activity was seen in FE and GR vs. VM. Internal oblique activity was significantly greater in GR than FI or VM, and thoracic erector spinae activity was significantly greater during FE and VM than FI. Force production did not differ significantly among breathing conditions (p = 0.74); however, GR forces were greater than FI and VM forces (p ≤ 0.05). Forced expiration air volume was significantly greater (p < 0.001) than FI, GR, or VM. These findings suggest that either GR or a more quiescent FE can be used to enhance force production. Forced expiration is a potentially safer alternative to VM and more aurally pleasing than GR.

Matrix-metalloproteinase-14 deficiency in bone-marrow-derived cells promotes collagen accumulation in mouse atherosclerotic plaques.

BACKGROUND: Interstitial collagen plays a crucial structural role in arteries. Although in vitro results suggest collagenase activity for membrane-bound matrix metalloproteinase type 1 (MMP-14), in vivo evidence for such a function in atherosclerosis remains scant. METHODS AND RESULTS: Because Mmp14-/- mice die by 3 weeks of age, this study used lethally irradiated low-density lipoprotein receptor-deficient mice reconstituted with syngeneic bone marrow cells of Mmp14-/- or Mmp14+/+ mice. In both groups, histological analyses of the aortic root revealed similar plaque size and macrophage and smooth muscle cell content after 8 or 16 weeks of atherogenic diet. By 16 weeks, however, the plaques of low-density lipoprotein receptor-deficient mice engrafted with Mmp14-/- bone marrow (n=12) contained significantly more interstitial collagen than those receiving Mmp14+/+ bone marrow (n=14; P<0.05). In vitro, bone marrow-derived macrophages from Mmp14-/- mice had significantly less interstitial collagenase activity than those from Mmp14+/+ mice both basally (P<0.01) and on tumor necrosis factor-alpha stimulation (P<0.05). Western blot analysis and gelatin zymography of aortic extracts revealed that MMP-14 deficiency yielded decreased activation of pro-MMP-13 but not of pro-MMP-2 or pro-MMP-8. CONCLUSIONS: MMP-14 from bone marrow-derived cells can influence the collagen content of mouse atheroma, a critical component of plaque stability.

Delta-like 4 induces notch signaling in macrophages: implications for inflammation.

BACKGROUND: Activated macrophages contribute to the pathogenesis of inflammatory diseases such as atherosclerosis. Although Notch signaling participates in various aspects of immunity, its role in macrophage activation remains undetermined. METHODS AND RESULTS: To explore the role of Notch signaling in inflammation, we examined the expression and activity of Notch pathway components in human primary macrophages in vitro and in atherosclerotic plaques. Macrophages in culture express various Notch pathway components including all 4 receptors (Notch1 to Notch4). Notch3 selectively increased during macrophage differentiation; however, silencing by RNA interference demonstrated that all receptors are functional. The ligand Delta-like 4 (Dll4) increased in macrophages exposed to proinflammatory stimuli such as lipopolysaccharide, interleukin-1beta, or minimally-modified low-density lipoprotein in a Toll-like receptor 4- and nuclear factor-kappaB-dependent fashion. Soluble Dll4 bound to human macrophages. Coincubation of macrophages with cells that expressed Dll4 triggered Notch proteolysis and activation; increased the transcription of proinflammatory genes such as inducible nitric oxide synthase, pentraxin 3 and Id1; resulted in activation of mitogen-activated protein kinase, Akt, and nuclear factor-kappaB pathways; and increased the expression of Dll4 in macrophages. Notch3 knockdown during macrophage differentiation decreased the transcription of genes that promote inflammation, such as inducible nitric oxide synthase, pentraxin 3, Id1, and scavenger receptor-A. These in vitro findings correlate with results of quantitative immunohistochemistry, which demonstrated the presence of Dll4 and other Notch components within macrophages in atherosclerotic plaques. CONCLUSION: Dll4-triggered Notch signaling may mediate inflammatory responses in macrophages and promote inflammation.