Invariant Feature Regularization for Fair Face Recognition

Fair face recognition is all about learning invariant feature that generalizes to unseen faces in any demographic group. Unfortunately, face datasets inevitably capture the imbalanced demographic attributes that are ubiquitous in real-world observations, and the model learns biased feature that generalizes poorly in the minority group. We point out that the bias arises due to the confounding demographic attributes, which mislead the model to capture the spurious demographic-specific feature. The confounding effect can only be removed by causal intervention, which requires the confounder annotations. However, such annotations can be prohibitively expensive due to the diversity of the demographic attributes. To tackle this, we propose to generate diverse data partitions iteratively in an unsupervised fashion. Each data partition acts as a self-annotated confounder, enabling our Invariant Feature Regularization (INV-REG) to deconfound. INV-REG is orthogonal to existing methods, and combining INV-REG with two strong baselines (Arcface and CIFP) leads to new state-of-the-art that improves face recognition on a variety of demographic groups. Code is available at https://github.com/PanasonicConnect/InvReg.Comment: Accepted by International Conference on Computer Vision (ICCV) 202

NMI inhibits cancer stem cell traits by downregulating hTERT in breast cancer.

N-myc and STAT interactor (NMI) has been proved to bind to different transcription factors to regulate a variety of signaling mechanisms including DNA damage, cell cycle and epithelial-mesenchymal transition. However, the role of NMI in the regulation of cancer stem cells (CSCs) remains poorly understood. In this study, we investigated the regulation of NMI on CSCs traits in breast cancer and uncovered the underlying molecular mechanisms. We found that NMI was lowly expressed in breast cancer stem cells (BCSCs)-enriched populations. Knockdown of NMI promoted CSCs traits while its overexpression inhibited CSCs traits, including the expression of CSC-related markers, the number of CD44+CD24- cell populations and the ability of mammospheres formation. We also found that NMI-mediated regulation of BCSCs traits was at least partially realized through the modulation of hTERT signaling. NMI knockdown upregulated hTERT expression while its overexpression downregulated hTERT in breast cancer cells, and the changes in CSCs traits and cell invasion ability mediated by NMI were rescued by hTERT. The in vivo study also validated that NMI knockdown promoted breast cancer growth by upregulating hTERT signaling in a mouse model. Moreover, further analyses for the clinical samples demonstrated that NMI expression was negatively correlated with hTERT expression and the low NMI/high hTERT expression was associated with the worse status of clinical TNM stages in breast cancer patients. Furthermore, we demonstrated that the interaction of YY1 protein with NMI and its involvement in NMI-mediated transcriptional regulation of hTERT in breast cancer cells. Collectively, our results provide new insights into understanding the regulatory mechanism of CSCs and suggest that the NMI-YY1-hTERT signaling axis may be a potential therapeutic target for breast cancers

Rapid Determination of Nine Acrylates in Food Contact Materials by Ultra Performance Convergence Chromatography

Ultra performance convergence chromatography (UPC2) was used to establish a rapid analytical method to determine nine acrylate compounds in plastic food contact materials simultaneously. The samples were extracted with methanol, filtered through an organic membrane, and separated on an ACQUITY UPC2 HSS C18 SB column with gradient elution using a mobile phase consisting of supercritical carbon dioxide and acetonitrile. The photodiode array (PDA) detector was set at 210 nm. Experimental results showed that under the optimal conditions (column temperature, 40 ℃; and back pressure, 13.79 MPa), qualitative and quantitative analysis of the nine acrylates was completed within 4 min. Linear ranges were 0.2–100 mg/L for phenyl methacrylate (PNMA), benzyl methacrylate (BZMA) and ethylene dimethacrylate (EDMA); 0.3–100 mg/L for methacrylic acid (MAA); 0.4–100 mg/L for butyl acrylate (BTA), hydroxyethyl methylacrylate (HEMA) and hydroxyethyl acrylate (HEA); and 0.5–100 mg/L for isobutylmeth acrylate (IBMA) and benzyl acrylate (BZA). The determination coefficients (R2) of the standard curves for all acrylates were higher than 0.998 5, and recoveries obtained at high (30 mg/kg), middle (6 mg/kg) and low (0.2, 0.3, 0.4 and 0.5 mg/kg) spiked concentrations ranged from 89.3% to 109.7%, with relative standard deviations of 0.62% to 3.86% (n = 6). The limits of detection (RSN ≥ 3) were 0.05–0.15 mg/kg, and the limits of quantification (RSN ≥ 10) were 0.2–0.5 mg/kg. The proposed method identified the risk of acrylate residues in 30 batches of actual samples

Real-time calcium uptake monitoring of a single renal cancer cell based on an all-solid-state potentiometric microsensor

Introduction: In addition to many cellular processes, Ca2+ is also involved in tumor initiation, progression, angiogenesis, and metastasis. The development of new tools for single-cell Ca2+ measurement could open a new avenue for cancer therapy.Methods: The all-solid-state calcium ion-selective microelectrode (Ca2+-ISμE) based on carbon fiber modified with PEDOT (PSS) as solid-contact was developed in this work, and the characteristics of the Ca2+-ISμE have also been investigated.Results: The Ca2+-ISμE exhibits a stable Nernstian response in CaCl2 solutions in the active range of 1.0 × 10−8 - 3.1 × 10−3 M with a low detection limit of 8.9 × 10−9 M. The Ca2+-ISμE can be connected to a patch clamp to fabricate a single-cell analysis platform for in vivo calcium monitoring of a single renal carcinoma cell. The calcium signal decreased significantly (8.6 ± 3.2 mV, n = 3) with severe fluctuations of 5.9 ± 1.8 mV when the concentration of K+ in the tumor microenvironment is up to 20 mM.Discussion: The results indicate a severe cell response of a single renal carcinoma cell under high K+ stimuli. The detection system could also be used for single-cell analysis of other ions by changing different ion-selective membranes with high temporal resolution

The First Data Release of the Beijing-Arizona Sky Survey

The Beijing-Arizona Sky Survey (BASS) is a new wide-field legacy imaging survey in the northern Galactic cap using the 2.3m Bok telescope. The survey will cover about 5400 deg$^2$ in the $g$ and $r$ bands, and the expected 5$\sigma$ depths (corrected for the Galactic extinction) in the two bands are 24.0 and 23.4 mag, respectively. BASS started observations in January 2015, and has completed about 41% of the whole area as of July 2016. The first data release contains both calibrated images and photometric catalogs obtained in 2015 and 2016. The depths of single-epoch images in the two bands are 23.4 and 22.9 mag, and the full depths of three epochs are about 24.1 and 23.5 mag, respectively.Comment: 16 pages, published by A

Jia-Wei-Kai-Xin-San treatment alleviated mild cognitive impairment through anti-inflammatory and antiapoptotic mechanisms in SAMP8 mice

Background. Alleviating mild cognitive impairment (MCI) is crucial to delay the progression of Alzheimer’s disease (AD). Jia-Wei-Kai-Xin-San (JWKXS) is applied for treating AD with MCI. However, the mechanism of JWKXS in the treatment of MCI is unclear. Thus, this study aimed to investigate the effect and mechanism of JWKXS in SAMP8 mice models of MCI. Methods. MCI models were established to examine learning and memory ability and explore the pathomechanisms in brain of SAMP8 mice at 4, 6, and 8 months. The mice were treated for 8 weeks and the effects of JWKXS on MCI were characterized through Morris water maze and HE/Nissl’s/immunohistochemical staining. Its mechanism was predicted by the combination of UPLC-Q-TOF/MS and system pharmacology analysis, further verified with SAMP8 mice, BV2 microglial cells, and PC12 cells. Results. It was found that 4-month-old SAMP8 mice exhibited MCI. Two months of JWKXS treatment improved the learning and memory ability, alleviated the hippocampal tissue and neuron damage. Through network pharmacology, four key signaling pathways were found to be involved in treatment of MCI by JWKXS, including TLR4/NF-κB pathway, NLRP3 inflammasome activation, and intrinsic and extrinsic apoptosis. In vitro and in vivo experiments demonstrated that JWKXS attenuated neuroinflammation by inhibiting microglia activation, suppressing TLR4/NF-κB and NLRP3 inflammasome pathways, and blocking the extrinsic and intrinsic apoptotic pathways leading to neuronal apoptosis suppression in the hippocampus. Conclusion. JWKXS treatment improved the learning and memory ability and conferred neuroprotective effects against MCI by inducing anti-inflammation and antiapoptosis. Limitations. The small sample size and short duration of the intervention limit in-depth investigation of the mechanisms. Future Prospects. This provides a direction for further clarification of the anti-AD mechanism, and provides certain data support for the formulation to move toward clinical practice

Efficacy and safety of low-dose IL-2 in the treatment of systemic lupus erythematosus: A randomised, double-blind, placebo-controlled trial

Objectives Open-labelled clinical trials suggested that low-dose IL-2 might be effective in treatment of systemic lupus erythematosus (SLE). A double-blind and placebocontrolled trial is required to formally evaluate the safety and efficacy of low-dose IL-2 therapy. Methods A randomised, double-blind and placebocontrolled clinical trial was designed to treat 60 patients with active SLE. These patients received either IL-2 (n=30) or placebo (n=30) with standard treatment for 12 weeks, and were followed up for additional 12 weeks. IL-2 at a dose of 1 million IU or placebo was administered subcutaneously every other day for 2 weeks and followed by a 2-week break as one treatment cycle. The primary endpoint was the SLE Responder Index-4 (SRI-4) at week 12. The secondary endpoints were other clinical responses, safety and dynamics of immune cell subsets. Results At week 12, the SRI-4 response rates were 55.17% and 30.00% for IL-2 and placebo, respectively (p=0.052). At week 24, the SRI-4 response rate of IL-2 group was 65.52%, compared with 36.67% of the placebo group (p=0.027). The primary endpoint was not met at week 12. Low-dose IL-2 treatment resulted in 53.85% (7/13) complete remission in patients with lupus nephritis, compared with 16.67% (2/12) in the placebo group (p=0.036). No serious infection was observed in the IL-2 group, but two in placebo group. Besides expansion of regulatory T cells, low-dose IL-2 may also sustain cellular immunity with enhanced natural killer cells. Conclusions Low-dose IL-2 might be effective and tolerated in treatment of SThe work was supported by the National Natural Science Foundation of China (31530020,31570880,81471601,81601417 and 81701598), Peking-Tsinghua Center for Life Sciences to ZG LI, Beijing Sci-Tech Committee Z171100000417007,Clinical Medicine Plus X-Young Scholars Project of Peking University (PKU2019LCXQ013) supported by the Fundamental Research Funds for the Central Universities, Beijing Nova Program Z171100001117025, National Key Research and Development Program of China (2017YFC0909003 to DY), BellberryViertel Senior Medical Research Fellowship to DY and Beijing SL PHARM

Data on functional characterization of LECT2 from Lampetra japonica

The data presented in this article are related to the research article entitled “Characterization of the LECT2 gene and its protective effects against microbial infection via large lymphocytes in Lampetra japonica” (Wang et al., 2017) [1]. Here, we presented new original data about the effect of rL-LECT2 on cancer cells migration and macrophages phagocytosis. Wound healing assay and transwell chemotaxis assays were used to measure rL-LECT2 inhibition rates on cancer cell migration. Additionally, fluospheres beads and Escherichia coli–FITC were used to measure whether the rL-LECT2 can affect the phagocytosis of RAW264.7 cells. Keywords: Lamprey, LECT2, Cell migration, Phagocytosi

Stock Price Prediction Based on XGBoost and LightGBM

Stock trading, as a kind of high frequency trading, generally seeks profits in extremely short market changes. And effective stock price forecasting can help investors obtain higher returns. Based on the data set provided by Jane Street, this paper makes use of XGBoost model and LightGBM model to realize the prediction of stock price. Since the given training set has a large amount of data and includes abnormal data such as missing value, we first carry out feature engineering processing on the original data and take the mean value of the missing value, so as to obtain the preprocessed data that can be used in modeling. The experimental results show that the combined model of XGBoost and LightGBM has better prediction performance than the single model and neural network

MMP-3-mediated cleavage of OPN is involved in copper oxide nanoparticle-induced activation of fibroblasts

Abstract Background Copper oxide nanoparticles (Nano-CuO) are one of the most produced and used nanomaterials. Previous studies have shown that exposure to Nano-CuO caused acute lung injury, inflammation, and fibrosis. However, the mechanisms underlying Nano-CuO-induced lung fibrosis are still unclear. Here, we hypothesized that exposure of human lung epithelial cells and macrophages to Nano-CuO would upregulate MMP-3, which cleaved osteopontin (OPN), resulting in fibroblast activation and lung fibrosis. Methods A triple co-culture model was established to explore the mechanisms underlying Nano-CuO-induced fibroblast activation. Cytotoxicity of Nano-CuO on BEAS-2B, U937* macrophages, and MRC-5 fibroblasts were determined by alamarBlue and MTS assays. The expression or activity of MMP-3, OPN, and fibrosis-associated proteins was determined by Western blot or zymography assay. Migration of MRC-5 fibroblasts was evaluated by wound healing assay. MMP-3 siRNA and an RGD-containing peptide, GRGDSP, were used to explore the role of MMP-3 and cleaved OPN in fibroblast activation. Results Exposure to non-cytotoxic doses of Nano-CuO (0.5 and 1 µg/mL) caused increased expression and activity of MMP-3 in the conditioned media of BEAS-2B and U937* cells, but not MRC-5 fibroblasts. Nano-CuO exposure also caused increased production of cleaved OPN fragments, which was abolished by MMP-3 siRNA transfection. Conditioned media from Nano-CuO-exposed BEAS-2B, U937*, or the co-culture of BEAS-2B and U937* caused activation of unexposed MRC-5 fibroblasts. However, direct exposure of MRC-5 fibroblasts to Nano-CuO did not induce their activation. In a triple co-culture system, exposure of BEAS-2B and U937* cells to Nano-CuO caused activation of unexposed MRC-5 fibroblasts, while transfection of MMP-3 siRNA in BEAS-2B and U937* cells significantly inhibited the activation and migration of MRC-5 fibroblasts. In addition, pretreatment with GRGDSP peptide inhibited Nano-CuO-induced activation and migration of MRC-5 fibroblasts in the triple co-culture system. Conclusions Our results demonstrated that Nano-CuO exposure caused increased production of MMP-3 from lung epithelial BEAS-2B cells and U937* macrophages, which cleaved OPN, resulting in the activation of lung fibroblasts MRC-5. These results suggest that MMP-3-cleaved OPN may play a key role in Nano-CuO-induced activation of lung fibroblasts. More investigations are needed to confirm whether these effects are due to the nanoparticles themselves and/or Cu ions