Impact of Additive Manufacturing Materials on Thermal Performance of Silicon Reference Cells.

Additive manufacturing, or 3D printing, is quickly becoming a widespread manufacturing method offering timely and cost-effective build times for unique part geometries with an increasing range of material offerings. One unique use for additive manufacturing is constructing the housing for reference solar cells, which are crucial instruments for evaluating the electrical performance of photovoltaic solar cells and modules. These instruments, which require good thermal conduction, are costly to manufacture because they are usually machined from aluminum using precision milling machines. In this work, we set out to evaluate several presently available additive manufacturing materials for their thermal properties when used to house reference solar cells. We fabricated several types of reference cell instruments with a tabletop, filament-based 3D printer using polylactic acid (PLA) and composite PLA/metal materials with different infill percentages. Furthermore, we fabricated several all-metal 3D printed reference cells using a binder jet printed stainless steel-bronze material blend and compared the thermal properties of all 3D printed instruments against a standard aluminum housing reference cell. Measurements included temperature monitoring of an embedded thermocouple sensor on an isothermal plate under the ambient environment and when exposed to high irradiation under a solar simulator. Current vs voltage measurements were also taken under the solar simulator and the open circuit voltage results were used to verify the actual silicon cell temperature. Our findings indicate that the stainless steel-bronze option can function well as an alternative to traditional aluminum-based housings, while the lower-cost metal-PLA composite can only be used under indoor light spectra or when used in a flash-type solar simulator when the instrument is not exposed to excessive radiation and heat.

Large-area irradiance-mode spectral response measurements of solar cells by a light-emitting, diode-based integrating sphere source.

An irradiance-mode absolute differential spectral response (SR) measurement system based on a light emitting diode (LED) array is described. The LEDs are coupled to an integrating sphere whose output irradiance is uniform to better than 2% over an area of 160 mm by 160 mm. SR measurements of solar cells when subject to diffuse irradiation, as provided by the integrating sphere, are compared with collimated irradiance SR measurements. Issues originating from the differences in angular response of the reference versus the test cells are also investigated. The SR curves of large-area cells with dimensions of up to 155 mm are measured and then used to calculate the cell's short circuit current (I(sc)), if illuminated by a defined solar spectrum. The resulting values of I(sc) agree well with the values obtained from secondary measurements.

Cold-induced changes in gene expression in brown adipose tissue, white adipose tissue and liver.

Cold exposure imposes a metabolic challenge to mammals that is met by a coordinated response in different tissues to prevent hypothermia. This study reports a transcriptomic analysis in brown adipose tissue (BAT), white adipose (WAT) and liver of mice in response to 24 h cold exposure at 8°C. Expression of 1895 genes were significantly (P<0.05) up- or down-regulated more than two fold by cold exposure in all tissues but only 5 of these genes were shared by all three tissues, and only 19, 14 and 134 genes were common between WAT and BAT, WAT and liver, and BAT and liver, respectively. We confirmed using qRT-PCR, the increased expression of a number of characteristic BAT genes during cold exposure. In both BAT and the liver, the most common direction of change in gene expression was suppression (496 genes in BAT and 590 genes in liver). Gene ontology analysis revealed for the first time significant (P<0.05) down regulation in response to cold, of genes involved in oxidoreductase activity, lipid metabolic processes and protease inhibitor activity, in both BAT and liver, but not WAT. The results reveal an unexpected importance of down regulation of cytochrome P450 gene expression and apolipoprotein, in both BAT and liver, but not WAT, in response to cold exposure. Pathway analysis suggests a model in which down regulation of the nuclear transcription factors HNF4α and PPARα in both BAT and liver may orchestrate the down regulation of genes involved in lipoprotein and steroid metabolism as well as Phase I enzymes belonging to the cytochrome P450 group in response to cold stress in mice. We propose that the response to cold stress involves decreased gene expression in a range of cellular processes in order to maximise pathways involved in heat production.

Combinatorial transcription factor regulation of the cyclic AMP-response element on the Pgc-1alpha promoter in white 3T3-L1 and brown HIB-1B preadipocytes.

Cold stress in rodents increases the expression of UCP1 and PGC-1alpha in brown and white adipose tissue. We have previously reported that C/EBPbeta specifically binds to the CRE on the proximal Pgc-1alpha promoter and increases forskolin-sensitive Pgc-1alpha and Ucp1 expression in white 3T3-L1 preadipocytes. Here we show that in mice exposed to a cold environment for 24 h, Pgc-1alpha, Ucp1, and C/ebpbeta but not C/ebpalpha or C/ebpdelta expression were increased in BAT. Conversely, expression of the C/EBP dominant negative Chop10 was increased in WAT but not BAT during cold exposure. Reacclimatization of cold-exposed mice to a warm environment for 24 h completely reversed these changes in gene expression. In HIB-1B, brown preadipocytes, forskolin increased expression of Pgc-1alpha, Ucp1, and C/ebpbeta early in differentiation and inhibited Chop10 expression. Employing chromatin immunoprecipitation, we demonstrate that C/EBPbeta, CREB, ATF-2, and CHOP10 are bound to the Pgc-1alpha proximal CRE, but CHOP10 does not bind in HIB-1B cell lysates. Forskolin stimulation and C/EBPbeta overexpression in 3T3-L1 cells increased C/EBPbeta and CREB but displaced ATF-2 and CHOP10 binding to the Pgc-1alpha proximal CRE. Overexpression of ATF-2 and CHOP10 in 3T3-L1 cells decreased Pgc-1alpha transcription. Knockdown of Chop10 in 3T3-L1 cells using siRNA increased Pgc-1alpha transcription, whereas siRNA against C/ebpbeta in HIB-1B cells decreased Pgc-1alpha and Ucp1 expression. We conclude that the increased cAMP stimulation of Pgc-1alpha expression is regulated by the combinatorial effect of transcription factors acting at the CRE on the proximal Pgc-1alpha promoter.