Machine learning reduces soft costs for residential solar photovoltaics.

Further deployment of rooftop solar photovoltaics (PV) hinges on the reduction of soft (non-hardware) costs-now larger and more resistant to reductions than hardware costs. The largest portion of these soft costs is the expenses solar companies incur to acquire new customers. In this study, we demonstrate the value of a shift from significance-based methodologies to prediction-oriented models to better identify PV adopters and reduce soft costs. We employ machine learning to predict PV adopters and non-adopters, and compare its prediction performance with logistic regression, the dominant significance-based method in technology adoption studies. Our results show that machine learning substantially enhances adoption prediction performance: The true positive rate of predicting adopters increased from 66 to 87%, and the true negative rate of predicting non-adopters increased from 75 to 88%. We attribute the enhanced performance to complex variable interactions and nonlinear effects incorporated by machine learning. With more accurate predictions, machine learning is able to reduce customer acquisition costs by 15% ($0.07/Watt) and identify new market opportunities for solar companies to expand and diversify their customer bases. Our research methods and findings provide broader implications for the adoption of similar clean energy technologies and related policy challenges such as market growth and energy inequality.

Quantifying the importance of feed-in tariffs to wind power development in China.

Governments worldwide often provide subsidies to renewable energy for reasons such as climate change mitigation and environmental pollution reduction. However, the importance of such subsides is not well understood and much debated. In this study, 109 monthly observations of the installed wind power capacity at the provincial level were used to assess the most important wind power subsidy policy in China-feed-in tariffs, while controlling for other confounding factors, such as technological change, local energy mix, and wind curtailment. The long panel regression results indicate that with other factors unchanged, an increase of 0.1 yuan/kWh in feed-in tariffs added 7.4-9.6 GW of wind capacity to China's national wind power market annually, higher than most of the estimates in the literature, but more consistent with the fast wind capacity development in China. Without the FIT subsidy, China's current wind power market size would likely be approximately 80% smaller. Our findings can be used to predict the impact of future cost reduction of wind technologies, and examine the interconnected relationships between wind capacity development, subsidy burden, and wind curtailment issues.

Decomposing PM2.5 air pollution rebounds in Northern China before COVID-19.

China's efforts to curb air pollution have drastically reduced its concentrations of fine particulate matter (PM2.5) from 2013 to 2018 nationwide. However, few studies examined the most recent changes in PM2.5 concentrations and questioned if the previous PM2.5 declining trend was sustained or not. This study took a deep dive into the PM2.5 trend for 136 northern cities of China from 2015 to early 2020 before the coronavirus disease 2019 (the COVID-19 hereafter) crisis, using ground-based PM2.5 data notably adjusted for a key measurement method change. We find that mean PM2.5 concentrations in northern China increased by 5.16 µg/m3 in 2019, offsetting 80% of the large reduction achieved in 2018. The rebound was more significant during the heating seasons (HS; Nov to next Mar) over the 2 years: 10.49 µg/m3 from the 2017 HS to the 2019 HS. A multiple linear regression analysis further revealed that anthropogenic factors contributed to around 50% of the PM2.5 rebound in northern cities of China. Such a significant role of anthropogenic factors in driving the rebound was tightly linked to deep cuts in PM2.5 concentrations in the previous year, systemic adjustment of policy targets and mitigation measures by the government, and the rising marginal cost of these measures. These findings suggest the need to chart a more sustainable path for future PM2.5 emission reductions, with an emphasis on key regions during key pollution periods.

Lentiviral Delivery of Small Hairpin RNA Targeting Connective Tissue Growth Factor Blocks Profibrotic Signaling in Tenon's Capsule Fibroblasts.

PURPOSES: Trabeculectomy is a surgical procedure for lowering intraocular pressure in glaucoma patients, in which excessive scarring leading to failure of the filtering bleb adversely affects the surgical outcome. Heightened Tenon's capsule fibroblast (TCF) proliferation and extracellular matrix (ECM) deposition are implicated in this process but endogenous factors that regulate TCF functions remain largely elusive. This study sought to elucidate the role of connective tissue growth factor (CTGF) in the regulation of TCF phenotypes and signaling. METHODS: Expression of CTGF in scarring and nonscarring Tenon's capsules was measured by real-time PCR and immunofluorescence. Knockdown of CTGC was achieved by lentivirus delivery of small-hairpin RNA. Cell proliferation was measured by CCK8, cell cycle progression, and apoptosis by flow cytometry, adhesion, migration, and invasion of TCF by functional assays in vitro. Proteins and cytokines related to fibrosis were measured by Western blot and ELISA, respectively. RESULTS: Expression of CTGF was significantly upregulated in scarring Tenon's capsules and their isolated fibroblasts when compared with the nonfibrotic counterparts. Functionally, targeting CTGF with lentivirus-delivered small-hairpin RNA inhibited the proliferation, adhesion, migration, and invasion of TCFs, accompanied by downregulation of p38 and nuclear factor-κB as well as matrix metalloproteinase-2, cyclin D1, and collagen I. In addition, lentiviral targeting of CTGF reduced the release of fibrosis-related cytokines from TCFs and inhibited TCF-conditioned, medium-induced macrophage chemotaxis. CONCLUSIONS: Our study supports a crucial role of CTGF in the regulation of TCF proliferation and ECM deposition. Targeting CTGF using lentiviral vector may be a promising approach for preventing excessive scarring after trabeculectomy.

MicroRNA-145 targets TRIM2 and exerts tumor-suppressing functions in epithelial ovarian cancer.

OBJECTIVE: Epithelial ovarian cancer (EOC) is one of the most common cancers in women worldwide but relatively little is known about its molecular pathogenesis. MicroRNAs, which regulate gene expression post-transcriptionally, have emerged as key players in tumorigenesis. The present study aims to investigate the dysregulation of miR-145 in EOC. METHODS: miRNA expression was assessed in EOC tissues and cell lines by quantitative reverse transcription (RT)-PCR. Xenograft mouse model was used for evaluation of the effect of miR-145 on tumor growth. Cell proliferation, colony formation assays, invasion assay, flow cytometry, Western blot and gene expression analysis were used for identification of the functional role of miR-145 in EOC cells. Luciferase reporter assay was used to confirm the interaction between miR-145 and its target mRNA 3'-UTR. RESULTS: miR-145 expression was downregulated in EOC tissues and cell lines as compared with normal ovarian tissues. Transfection of miR-145 agomiR significantly inhibited the proliferation, colony forming ability, invasiveness and in vivo tumorigenicity of EOC cells. Transfection of agomiR-145 into EOC cells also markedly induced apoptosis. Furthermore, computational algorithm combined with luciferase reporter assays identified TRIM2 as the direct target of miR-145 in EOC cells. To this end, agomiR-145 downregulated TRIM2 to derepress Bim (a pro-apoptotic Bcl-2 family member degraded by TRIM2). CONCLUSIONS: These data confirmed the tumor-suppressing function of miR-145 in EOC and identified TRIM2 as a new miR-145 target. In vivo delivery of agomiR-145 might be a feasible approach for miRNA-directed cancer therapy.

MicroRNA-10b downregulation mediates acute rejection of renal allografts by derepressing BCL2L11.

Kidney transplantation is the major therapeutic option for end-stage kidney diseases. However, acute rejection could cause allograft loss in some of these patients. Emerging evidence supports that microRNA (miRNA) dysregulation is implicated in acute allograft rejection. In this study, we used next-generation sequencing to profile miRNA expression in normal and acutely rejected kidney allografts. Among 75 identified dysregulated miRNAs, miR-10b was the most significantly downregulated miRNAs in rejected allografts. Transfecting miR-10b inhibitor into human renal glomerular endothelial cells recapitulated key features of acute allograft rejection, including endothelial cell apoptosis, release of pro-inflammatory cytokines (interleukin-6, tumor necrosis factor α, interferon-γ, and chemokine (C-C motif) ligand 2) and chemotaxis of macrophages whereas transfection of miR-10b mimics had opposite effects. Downregulation of miR-10b directly derepressed the expression of BCL2L11 (an apoptosis inducer) as revealed by luciferase reporter assay. Taken together, miR-10b downregulation mediates many aspects of disease pathogenicity of acute kidney allograft rejection. Restoring miR-10b expression in glomerular endothelial cells could be a novel therapeutic approach to reduce acute renal allograft loss.

Oxygen free radical involvement in acute lung injury induced by H5N1 virus in mice.

BACKGROUND: Acute lung injury is an important cause of death in humans infected with H5N1. It has been found that oxygen free radicals (OFRs) are elevated in lung tissue during influenza virus infections. In this study, we used a mouse model to explore the role of OFRs in acute lung injury caused by H5N1 viral infection. METHODS: Four- to six-week-old male specific pathogen-free BALB/c mice were inoculated intranasally with 10(5) 50% tissue culture infective doses (TCID50) of highly pathogenic A/Chicken/Hebei/108/2002 (H5N1) viruses and were then given 1000 IU of lauric acid modified superoxide dismutase (LA-SOD) by intraperitoneal injection, starting 2 days post-infection and continuing for 6 days. RESULTS: The extent of lung injury and the concentration of OFRs were higher, and the SOD activity was lower in H5N1 virus-infected mice than that in uninfected control mice on days 3, 6, and 7 post-inoculation. Weak amelioration of clinical signs, a minor decrease in the total mortality and the extent of lung injury, and the lower OFRs concentration were seen in the LA-SOD treatment group, but a reduction in lung virus titers was not observed in the LA-SOD treatment at all time points. CONCLUSIONS: The LA-SOD treatment has a mild inhibitory effect on H5N1 influenza virus infection in mice. OFRs, therefore, might play an important role in the pathogenesis of acute lung injury induced by H5N1 virus.

Positive selection and functional divergence after melanopsin gene duplication.

A newly discovered melanopsin gene (Opn4) encodes a member of the opsins, melanopsin. Two melanopsin genes, mammalian-like Opn4m and Xenopus-like Opn4x, have been described in nonmammalian vertebrates, but the underlying evolutionary mechanisms behind the duplication of melanopsin genes remain unclear. We conducted a comprehensive evolutionary analysis within a phylogenetic framework. In our phylogenetic tree, the duplication of Opn4m and Opn4x probably occurred prior to the emergence of vertebrates, and subsequently Opn4x disappeared in the lineages leading to mammalian species. Evolutionary analyses show strong purifying selection during melanopsin evolution. We also provide evidence that Opn4x underwent positive selection after the early gene duplication events. It has been indicated that functional divergence and altered functional constraints occurred between Opn4m and Opn4x duplicates with the identification of positively selected amino acids. Our findings highlight the evolutionary malleability in vertebrate melanopsin genes and provide a genetic basis for comparative studies of functional properties of these two melanopsins.

Amantadine-resistance among H5N1 avian influenza viruses isolated in Northern China.

We tested the amantadine-resistance among avian influenza A (H5N1) viruses isolated from chicken in Hebei Province of Northern China from 2001 to 2005, and investigated the amantadine use in this area. Plague reduction assay in MDCK cells showed that 83.3% isolates (5/6) were amantadine-resistant strains. The M2 sequence analysis revealed that four of five resistant isolates contained the point mutations (Ser to Asn) at position 31 that could confer resistance to amantadine. These results indicated that the incidence of amantadine-resistant viruses isolated in Northern China was particularly high. In the investigation of amantadine use, we found that amantadine was used extensively in poultry farms in this area, which maybe was one of reasons of the high amantadine-resistance incidence.

Acute respiratory distress syndrome induced by avian influenza A (H5N1) virus in mice.

RATIONALE AND OBJECTIVE: The acute respiratory distress syndrome (ARDS) caused by avian influenza H5N1 viral infection has been reported in many humans since this virus was found to infect humans in Hong Kong in 1997, but no studies regarding an animal model of ARDS with H5N1 viral infection have been found in the literature. Here we present a mouse model of ARDS induced by H5N1 virus. METHODS: Six- to 8-wk-old BALB/c mice were inoculated intranasally (50 micro l) with 1 x 10(2) 50% mouse infectious doses of A/Chicken/Hebei/108/2002 (H5N1) virus. Lung injury was assessed by observation of lung water content and histopathology. Arterial blood gas, white blood cell count in bronchial alveolar lavage fluid, and tumor necrosis factor-alpha and interleukin-6 in bronchoalveolar lavage fluid and serum were measured at the indicated time points. RESULTS: Our data showed that H5N1 viral infection in mice resulted in typical ARDS, which was characterized by the following features: (1) about 80% of mice (13 of 16) dead on Days 6 to 8 postinoculation; (2) highly edematous lungs and dramatically increased lung wet:dry weight ratios and lung wet weight:body weight ratios; (3) inflammatory cellular infiltration, alveolar and interstitial edema, and hemorrhage in lungs; (4) progressive and severe hypoxemia; and (5) significant increase in neutrophils, tumor necrosis factor-alpha, and interleukin-6 in BALF. CONCLUSION: These results suggested that we successfully established a mouse model of ARDS with H5N1 viral infection, which may benefit further investigation into the pathogenesis of human ARDS induced by H5N1 virus.