Impacts of COVID-19 related stay-at-home restrictions on residential electricity use and implications for future grid stability.

"Stay-at-home" orders and other health precautions enacted during the COVID-19 pandemic have led to substantial changes in residential electricity usage. We conduct a case study to analyze data from 390 apartments in New York City (NYC) to examine the impacts of two key drivers of residential electricity usage: COVID-19 case-loads and the outdoor temperature. We develop a series of regression models to predict two characteristics of residential electricity usage on weekdays: The average occupied apartment's consumption (kWh) over a 9am-5pm window and the hourly peak demand (Watt) over a 12pm-5pm window. Via a Monte Carlo simulation, we forecast the two usage characteristics under a possible scenario in which stay-at-home orders in NYC, or a similar metropolitan region, coincide with warm summer weather. Under the scenario, the 9am-5pm residential electricity usage on weekdays is predicted to be 15% - 24% higher than under prior, pre-pandemic conditions. This could lead to substantially higher utility costs for residents. Additionally, we predict that the residential hourly peak demand between 12pm and 5pm on weekdays could be 35% - 53% higher than that under pre-pandemic conditions. We conclude that the projected increase in peak demand - which might arise if stay-at-home guidelines coincided with hot weather conditions - could pose grid management challenges, especially for residential feeders. We also note that, if there is a longer lasting shift towards work and study-from-home, utilities will have to rethink load profile considerations. The applications of our predictive models to managing future smart-grid technology are also highlighted.

GbCYP86A1-1 from Gossypium barbadense positively regulates defence against Verticillium dahliae by cell wall modification and activation of immune pathways.

Suberin acts as stress-induced antipathogen barrier in the root cell wall. CYP86A1 encodes cytochrome P450 fatty acid ω-hydroxylase, which has been reported to be a key enzyme for suberin biosynthesis; however, its role in resistance to fungi and the mechanisms related to immune responses remain unknown. Here, we identified a disease resistance-related gene, GbCYP86A1-1, from Gossypium barbadense cv. Hai7124. There were three homologs of GbCYP86A1 in cotton, which are specifically expressed in roots and induced by Verticillium dahliae. Among them, GbCYP86A1-1 contributed the most significantly to resistance. Silencing of GbCYP86A1-1 in Hai7124 resulted in severely compromised resistance to V. dahliae, while heterologous overexpression of GbCYP86A1-1 in Arabidopsis improved tolerance. Tissue sections showed that the roots of GbCYP86A1-1 transgenic Arabidopsis had more suberin accumulation and significantly higher C16-C18 fatty acid content than control. Transcriptome analysis revealed that overexpression of GbCYP86A1-1 not only affected lipid biosynthesis in roots, but also activated the disease-resistant immune pathway; genes encoding the receptor-like kinases (RLKs), receptor-like proteins (RLPs), hormone-related transcription factors, and pathogenesis-related protein genes (PRs) were more highly expressed in the GbCYP86A1-1 transgenic line than control. Furthermore, we found that when comparing V. dahliae -inoculated and noninoculated plants, few differential genes related to disease immunity were detected in the GbCYP86A1-1 transgenic line; however, a large number of resistance genes were activated in the control. This study highlights the role of GbCYP86A1-1 in the defence against fungi and its underlying molecular immune mechanisms in this process.

Comparative Transcriptome Analysis of Two Aegilops tauschii with Contrasting Drought Tolerance by RNA-Seq.

As the diploid progenitor of common wheat, Aegilops tauschii is considered to be a valuable resistance source to various biotic and abiotic stresses. However, little has been reported concerning the molecular mechanism of drought tolerance in Ae. tauschii. In this work, the drought tolerance of 155 Ae. tauschii accessions was firstly screened on the basis of their coleoptile lengths under simulated drought stress. Subsequently, two accessions (XJ002 and XJ098) with contrasting coleoptile lengths were selected and intensively analyzed on rate of water loss (RWL) as well as physiological characters, confirming the difference in drought tolerance at the seedling stage. Further, RNA-seq was utilized for global transcriptome profiling of the two accessions seedling leaves under drought stress conditions. A total of 6969 differentially expressed genes (DEGs) associated with drought tolerance were identified, and their functional annotations demonstrated that the stress response was mediated by pathways involving alpha-linolenic acid metabolism, starch and sucrose metabolism, peroxisome, mitogen-activated protein kinase (MAPK) signaling, carbon fixation in photosynthetic organisms, and glycerophospholipid metabolism. In addition, DEGs with obvious differences between the two accessions were intensively analyzed, indicating that the expression level of DEGs was basically in alignment with the physiological changes of Ae. tauschii under drought stress. The results not only shed fundamental light on the regulatory process of drought tolerance in Ae. tauschii, but also provide a new gene resource for improving the drought tolerance of common wheat.

Endoplasmic reticulum stress is involved in the connection between inflammation and autophagy in type 2 diabetes.

Type 2 diabetes is a chronic inflammatory disease. A number of studies have clearly demonstrated that cytokines such as interleukin 1ß (IL1ß) contribute to pancreatic inflammation, leading to impaired glucose homeostasis and diabetic disease. There are findings which suggest that islet ß-cells can secrete cytokines and cause inflammatory responses. In this process, thioredoxin-interacting protein (TXNIP) is induced by endoplasmic reticulum (ER) stress, which further demonstrates a potential role for ER stress in innate immunity via activation of the NOD-like receptor (NLRP) 3/caspase1 inflammasome and in diabetes pathogenesis via the release of cytokines. Recent developments have also revealed a crucial role for the autophagy pathway during ER stress and inflammation. Autophagy is an intracellular catabolic system that not only plays a crucial role in maintaining the normal islet architecture and intracellular insulin content but also represents a form of programmed cell death. In this review, we focus on the roles of autophagy, inflammation, and ER stress in type 2 diabetes but, above all, on the connections among these factors.

Genetic Basis of Fiber Improvement and Decreased Stress Tolerance in Cultivated Versus Semi-Domesticated Upland Cotton.

Crop domestication from wild ancestors has resulted in the wide adaptation coupled with improved yield and quality traits. However, the genetic basis of many domesticated characteristics remains to be explored. Upland cotton (Gossypium hirsutum) is the most important tetraploid cotton species, accounting for about 90% of world cotton commerce. Here, we reveal the effects of domestication on fiber and stress traits through comprehensive analyses of semi-domesticated races and cultivated cotton accessions. A total of 416 cotton accessions were genotyped, and a decrease in genetic diversity from races to landraces and modern cultivars was detected. Furthermore, 71 domestication selective sweeps (DSS) and 14 improvement selective sweeps (ISS) were identified, with the Dt sub-genome experiencing stronger selection than the At sub-genome during the both selection types. The more expressed genes and a delay in the expression peak of genes related to secondary cell wall (SCW) development in modern cultivars compared to semi-domesticated cotton races, may have contributed to long fibers in these plants. However, down-regulation of genes related to stress response was responsible for decreasing stress tolerance in modern cultivars. We further experimentally confirmed that silencing of PR1 and WRKY20, genes that showed higher expression in the semi-domesticated races, drastically compromised cotton resistance to V. dahliae. Our results reveal fiber improvement and decreased stress tolerance as a result of the domestication of modern upland cotton cultivars.

EGR1 regulates angiogenic and osteoclastogenic factors in prostate cancer and promotes metastasis.

Early growth response-1 (EGR1) is a transcription factor correlated with prostate cancer (PC) progression in a variety of contexts. For example, EGR1 levels increase in response to suppressed androgen receptor signaling or loss of the tumor suppressor, PTEN. EGR1 has been shown to regulate genes influencing proliferation, apoptosis, immune cell activation, and matrix degradation, among others. Despite this, the impact of EGR1 on PC metastatic colonization is unclear. We demonstrate using a PC model (DU145/RasB1) of bone and brain metastasis that EGR1 expression regulates angiogenic and osteoclastogenic properties of metastases. We have shown previously that FN14 (TNFRSF12A) and downstream NF-κB signaling is required for metastasis in this model. Here we demonstrate that FN14 ligation also leads to NF-κB-independent, MEK-dependent EGR1 expression. EGR1-depletion in DU145/RasB1 cells reduced both the number and size of metastases but did not affect primary tumor growth. Decreased EGR1 expression led to reduced blood vessel density in brain and bone metastases as well as decreased osteolytic bone lesion area and reduced numbers of osteoclasts at the bone-tumor interface. TWEAK (TNFSF12) induced several EGR1-dependent angiogenic and osteoclastogenic factors (e.g., PDGFA, TGFB1, SPP1, IL6, IL8, and TGFA, among others). Consistent with this, in clinical samples of PC, the level of several genes encoding angiogenic/osteoclastogenic pathway effectors correlated with EGR1 levels. Thus, we show here that EGR1 has a direct effect on prostate cancer metastases. EGR1 regulates angiogenic and osteoclastogenic factors, informing the underlying signaling networks that impact autonomous and microenvironmental mechanisms of cancer metastases.

Genome-Wide Association Studies Reveal Genetic Variation and Candidate Genes of Drought Stress Related Traits in Cotton (Gossypium hirsutum L.).

Cotton is an important industrial crop worldwide and upland cotton (Gossypium hirsutum L.) is most widely cultivated in the world. Due to ever-increasing water deficit, drought stress brings a major threat to cotton production. Thus, it is important to reveal the genetic basis under drought stress and develop drought tolerant cotton cultivars. To address this issue, in present study, 319 upland cotton accessions were genotyped by 55,060 single nucleotide polymorphisms (SNPs) from high-density CottonSNP80K array and phenotyped nine drought tolerance related traits. The two datasets were used to identify quantitative trait nucleotides (QTNs) for the above nine traits using multi-locus random-SNP-effect mixed linear model method. As a result, a total of 20 QTNs distributed on 16 chromosomes were found to be significantly associated with six drought tolerance related traits. Of the 1,326 genes around the 20 QTNs, 205 were induced after drought stress treatment, and 46 were further mapped to Gene ontology (GO) term "response to stress." Taken genome-wide association study (GWAS) analysis, RNA-seq data and qRT-PCR verification, four genes, RD2 encoding a response to desiccation 2 protein, HAT22 encoding a homeobox-leucine zipper protein, PIP2 encoding a plasma membrane intrinsic protein 2, and PP2C encoding a protein phosphatase 2C, were proposed to be potentially important for drought tolerance in cotton. These results will deepen our understanding of the genetic basis of drought stress tolerance in cotton and provide candidate markers to accelerate the development of drought-tolerant cotton cultivars.

MicroRNA-195 targets VEGFR2 and has a tumor suppressive role in ACHN cells via PI3K/Akt and Raf/MEK/ERK signaling pathways.

Increasing evidence indicates that dysregulation of miR-195 may contribute to the occurrence and development of multiple types of human malignancies. However, the function and the mechanism of miR-195 in clear cell renal cell carcinoma (ccRCC) are still not fully understood. In the present study, we used qRT-PCR to detect the expression of miR-195 in ccRCC tissues and normal kidney tissues. MTT assay was performed to detect the cell viability of miR-195. Migration and invasion were evaluated by Transwell migration and Matrigel invasion assays, respectively. Additionally, apoptosis levels were evaluated using TUNEL assays, and signaling pathway changes were determined by western blot analysis. We observed that miR-195 was downregulated in clear cell renal cell carcinoma samples compared with normal renal samples. We identified that overexpression of miR-195 inhibited ACHN cell viability, migration, invasion, and it also induced cell apoptosis by targeting VEGFR2 via PI3K/Akt and Raf/MEK/ERK signaling pathways. These findings indicate that miR-195 has a tumor suppressive role in ACHN cells and miR-195 may be a promising candidate target for prevention and treatment of renal cell carcinoma.

Study of autophagy-related protein light chain 3 (LC3)-II expression levels in thyroid diseases.

Thyroid cancers are the most common malignant tumors of the endocrine system. The survival-promoting role of autophagy in tumor cells has been received universally. This study aimed to explore autophagy-related protein light chain 3 (LC3)-II expression levels in thyroid diseases including papillary thyroid cancer. A total of 45 thyroid samples, including 19 samples of papillary thyroid cancer, 7 samples of nodular goiter, 8 samples of Hashimoto thyroiditis and 11 samples of normal thyroid tissue resected during surgery, were selected and divided into pathological groups using light microscope. Levels of autophagy-related protein LC3-II in four different types of thyroid tissue were tested through Western blot. SPSS19 software was utilized to analyze the research data statistically. LC3-II protein levels in papillary thyroid cancer tissues were lower than that in normal thyroid tissues significantly (P<0.05). Compared with normal thyroid tissue, expression levels of LC3-II protein were higher in samples of Hashimoto thyroiditis and nodular goiter (P<0.05). Multi-factor analysis of variance showed that there was no significant correlation between LC3-II protein levels and patients' gender of thyroid cancer, while there was significant variation between patients with and without lymph node metastasis. Compared with patients of thyroid cancer without lymph node metastasis, the level of LC3-II protein was lower in patients of thyroid cancer with lymph node metastasis (P<0.05). Detection of LC3-II protein expression levels in thyroid diseases may contribute to the clinical diagnosis and provide theoretic basis for the therapy.

Autophagy, a novel target for chemotherapeutic intervention of thyroid cancer.

PURPOSE: Thyroid cancers with unsatisfactory curative effect nowadays are the most common malignant tumors of the endocrine system. Apoptosis evasion, a hallmark of cancer, has driven the search of stimulating novel cell death way in cancer therapy. This review aims to explore the relationship between autophagy and thyroid cancer, especially the chemotherapy agents which are based on autophagy in treating thyroid cancers. METHODS: A computerized literature search of MEDLINE was performed using the following search terms: autophagy and thyroid cancer. RESULTS: Recent studies have found that several chemotherapeutic agents and knockdown of specific microRNA may contribute to autophagic tumor cell death in most thyroid cancer types. CONCLUSIONS: Stimulating autophagy may be an effective alternative treatment to most types of thyroid cancer.