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Hybrid PEDOT:PSS-silicon heterojunction solar cells have the advantages of low temperature, low cost and solution process. However, as a low-quality native oxide layer can easily form on the surface of silicon substrates, the hybrid solar cells still suffer from charged carrier recombination at the defective interface, hence affecting the device characteristics. In this work, we employ a thermally induced silicon hydrosilylation technique to form a self-assembled monolayer(SAM) on the hydrogen-terminated silicon substrate, in order to prevent the oxidation and passivate the surface of silicon. The quality of this monolayer passivation is characterized by the contact angle, X-ray photoelectron spectroscopy (XPS) analyses. We have found that the SAM passivation can effectively reduce the contact resistance between silicon and the aluminum electrode, leading to an improved open-circuit voltage and fill-factor. However, as the silicon surface with the SAM passivation becomes hydrophobic, it is difficult to apply aqueous PEDOT:PSS solution onto silicon. Therefore, we further apply a low-damage oxygen plasma treatment to modify the terminal functional group of the monolayer to form a hydrophilic surface. The power conversion efficiency of the modified devices is between 10–12%. Although the PCE does not surpass the reference device due to possible chemical reactions between the PEDOT:PSS and SAM, the proposed low- damage oxygen-plasma treatment provide a viable solution for modifying the functional passivation of hybrid PEDOT:PSS silicon solar cells using SAMs.

The dopant-free carrier selective contacts (CSC) to replace the complex diffusion manufacturing are increasingly explored using a variety of different materials. In this work, we investigate various organic materials, including conductive polymer PEDOT: PSS, fluorescent polymers PFO and Green B, and small molecules DMFL-NPB, to serve as the hole selective con-tact (HSC). By analyzing the lifetime and implied open-circuit voltage, assessing of contact resistivity and band alignment, as well as the device efficiency, we evaluate the potential of soluble organic materials acting as the HSC. The results have shown that PEDOT: PSS could effectively passivate the silicon surface to increases the open-circuit voltage by 31 mV and the short-circuit current density by 2.9 mA/cm2. Overall, the power conversion efficiency increases from 12.36% to 14.55%.

In this work, we use the metal-assisted chemical etching (MACE) to produce our multi-scale surface textures, namely “Hierarchical structure”, which is combined with micropyramid and nanowires. The templates are modulated through controlling the morphology of silver cluster on the randomly distributed micro-pyramidal surface with rapid thermal annealing (RTA) and the ratio of hydrogen fluoride (HF) and hydrogen peroxide (H 2 O 2 ) during metal-assisted chemical etching. The power conversion efficiency (PCE) of new multi-structure on a hybrid solar cell can achieve 14.07 % by reducing reflectance to 3.61 % and enhancing J SC to 33.43 mA/cm2 with a 1x1 cm2 active area.

In this work, we demonstrate the packaging of hybrid organic - silicon solar cell mini-modules employing flexible and ultrathin transparent conductive films. The unique engineering plastic substrates are printed with high-resolution, micrometer-scaled silver meshes to achieve superior optical transmittance and low sheet resistance, offering the efficient collection of charged carriers through distributed metallic grids. The width of silver grid can be as low as 3 μm, which is a 10 to 15 fold reduction compared to the conventional grid width used in screen printing. By systematically comparing various substrate materials and process conditions, we achieve a power conversion efficiency of 9.5% on 2x2 cm2 mini-modules.

OBJECTIVE: Polynuclear aromatic hydrocarbons are important components of cigarette smoke. The toxicity of polynuclear hydrocarbons depends on their metabolic biotransformation by tissues. This study was performed to assess the effects of cigarette smoke exposure on polynuclear aromatic hydrocarbon metabolism in the human placental tissues of first-trimester pregnancy. STUDY DESIGN: The expression of essential enzymes that metabolize polynuclear aromatic hydrocarbons and regulate toxic metabolism, aryl hydrocarbon hydroxylase, epoxide hydrolase, and glutathione S-transferase, were determined by immunocytochemical staining of the specific enzymes in first-trimester placental samples from both smoker and nonsmoker donors. The overall polynuclear aromatic hydrocarbon metabolism by such tissues was quantitated by a radiometric assay with benzo[a]pyrene substrate in placental villi tissues and also in isolated trophoblast cells or in cultured trophoblast cells in the presence of polynuclear aromatic hydrocarbon agent. RESULTS: Immunocytochemical staining revealed that aryl hydrocarbon hydroxylase was localized on trophoblast cells of first-trimester placentas from smoker donors. Epoxide hydrolase was present in stromal and trophoblast cells, and glutathione S-transferase (π) was present in trophoblast cells of both nonsmoker and smoker subjects. In addition, the overall metabolism of polynuclear aromatic hydrocarbon xenobiotics in such tissues (8 to 11 weeks) of donors who smoked cigarettes was observed to be increased compared with that of nonsmokers by radiometric assay of metabolic products. The increased polynuclear aromatic hydrocarbon metabolism from such exposure was also shown in isolated and purified trophoblast cells of first-trimester placental villi and in culture of such trophoblast cells of nonsmoker donors with polynuclear aromatic hydrocarbon by the same assay procedure. CONCLUSIONS: Therefore, contrary to previous assumptions, these data demonstrate that cigarette smoke exposure increases the polynuclear aromatic hydrocarbon metabolism of placentas even during the early stages of pregnancy. Augmented polynuclear aromatic hydrocarbon metabolism may produce genotoxic metabolites deleterious to conceptus development.

BACKGROUND: Polynuclear aromatic hydrocarbons (PAH), benzo[α]pyrene (B[α]P) and 7,12-dimethylbenz[α]anthracene (DMBA) are toxic environmental agents distributed widely. The relative deleterious effects of these agents on growth and blood vasculature of fetus and placental tissues of the rat were studied. METHODS: Pregnant rats (Day 1 sperm positive) with implantation sites confirmed by laparotomy were treated intraperitoneally (i.p.) on Pregnancy Days 10, 12, and 14 with these agents dissolved in corn oil at cumulated total doses 50, 100, and 200 mg/kg/rat, and control with corn oil only (3–20 dams/group). Fetal growth, tissue hemorrhage, and placental pathology were evaluated by different parameters on Pregnancy Day (PD) 20 in treated and control rats. RESULTS: DMBA was relatively more deleterious compared to B[α]P indicated by increased lethality and progressive reduction of body weight of the mother with increasing doses. At 200 mg/kg/rat doses of these agents, maternal survival was 45% and 100% and body weight reduced 24% and 52% of controls, respectively. The fetal survival rates in live mothers were similar to that of controls. They induced marked fetal growth retardation and necrosis of placental tissues. B[α]P and DMBA produced significant toxicity to differentiating fetal blood vascular system as exhibited by rupture of blood vessels and hemorrhage, especially in the skin, cranial, and brain tissues. CONCLUSIONS: Maternal PAH exposure induced placental toxicity and associated adverse fetal development and hemorrhage in different parts of the fetal body, in particular, marked intradermal and cranial hemorrhage, showing that developing fetal blood vasculature is a target of PAH toxicity. Birth Defects Res (PartB), 2007. © 2007 Wiley-Liss, Inc.

OBJECTIVES: Generation of different metabolites and DNA-adduct(s) of metabolites of benzo[α]pyrene (B[α]P) in vitro by placental tissues (microsomes) of mothers who actively smoked cigarettes (tobacco) and those who did not smoke were analyzed to determine the variability in metabolism of the B[α]P substrate among individual placental samples. METHODS: Overall B[α]P metabolism was assayed by alkaline aqueous extraction of metabolites, and reactive metabolites by DNA adducts of B[α]P-metabolites produced by salmon sperm DNA added to the incubation mixtures of the substrate and microsomes of exposed- and unexposed-placentas to maternal cigarette smoke. Array of B[α]P-metabolites produced by the same incubations were identified by high pressure liquid chromatography of the aqueous extracts. RESULTS: Subsets of smoke-exposed placentas assessed by cluster analysis had augmented metabolic activity, others did not respond to smoke exposure. CYP1A1 expression in trophoblast cells analyzed by immunohistochemistry did not correlate with smoke exposure. The DNA-adducts generated was variable, regardless of verbally reported levels of maternal exposure. The amounts of different B[α]P-metabolites produced by individual samples matched for similar levels of exposure during pregnancy by self-reported smoking (1 pack/day) were also not comparable. Metabolism of B[α]P into different metabolites, and production of toxic DNA adducts from metabolites in vitro by human placenta were variable and unrelated to the extent of smoke exposure. CONCLUSIONS: The metabolic characteristic of human placenta for xenobiotic exposure substrates is based on the expression and function of diverse enzymes, and such metabolism exhibited inter-individual variation for toxic metabolite production or detoxification of the substrates in response to maternal smoke exposure. Birth Defects Res (Part B) 80:49–56, 2007. © 2007 Wiley-Liss, Inc.

We have previously found that myocyte-specific enhancer binding factor 2C (MEF2C) is expressed in the brain, where it is found at high levels in the developing cerebral cortex. We have now examined MEF2C expression in fetal mouse brain by in situ hybridization and by immunohistochemistry from E11 to E17, the period when most cortical neurons are born. The distribution of MEF2C mRNA detected by in situ hybridization closely resembles that of MEF2C immunoreactivity. MEF2C is not present in proliferative zones in the brain. It is present at high levels in cells that have migrated to the subplate and cortical plate. MEF2C is also found in the olfactory blub at high levels and at lower levels in hippocampus, basal forebrain, striatum, cerebellum, and inferior colliculus, and in some nuclei of the hypothalamus, thalamus and brainstem. The pattern of expression suggests that MEF2C is expressed in a subset of postmitotic neurons in the brain and that it may therefore function to promote terminal differentiation of the cells that express it.