Predicting S&P 500 Index ETF (SPY) During COVID-19 via K-Nearest Neighbors (KNN) Algorithm

In this paper, the daily adjusted closing price of SPY (SPDR S&P 500 ETF Trust) is predicted by using the High-Low prices of SPY, DIA (SPDR Dow Jones Industrial Average ETF Trust), and QQQ (Invesco NASDAQ-100 ETF Trust) via the KNN method during the COVID-19 pandemic period. Results show that applying the KNN method, a simple, intuitive, and explainable machine learning method, is feasible and effective in SPY price prediction and corresponding trade decisions during the COVID-19 pandemic. Experiments also indicate that adding information on High-Low prices from DIA (a value tilt ETF) and QQQ (a growth tilt ETF) cannot improve the accuracy of both SPY price prediction and trading decisions. Results are consistent with previous findings based on the portfolio approach that value spread does not help predict stock market returns

Une caméra pour ouvrir les portes de la mémoire

Ce texte est une introduction au Folk Memory Project, une initiative pluridisciplinaire visant à produire des archives écrites et visuelles de l’expérience historique des populations rurales, en particulier durant la famine du Grand bond en avant. Rédigé par son fondateur, le réalisateur de documentaires indépendant Wu Wenguang, cet article présente le projet et les travaux des réalisateurs participants, quatre ans après son lancement. Il fournit une description de la méthode de travail et des objectifs de ce projet non-officiel sur la mémoire, traité dans l’article « Performances, films documentaires et transmission de la mémoire de la famine du Grand Bond en avant dans le Folk Memory Project » à la page 17

On a divisor problem related to the Epstein Zeta-Function, IV

International audienceIn this paper we study several divisor problems related to the Epstein zeta-function. We are able to improve previous results and establish some new results by applying some classical techniques

Iron-binding activity of human iron-sulfur cluster assembly protein hIscA1

A human homologue of the iron-sulfur cluster assembly protein IscA (hIscA1) has been cloned and expressed in Escherichia coli cells. The UV-visible absorption and EPR (electron paramagnetic resonance) measurements reveal that hIscA1 purified from E. coli cells contains a mononuclear iron centre and that the iron binding in hIscA1 expressed in E. coli cells can be furthermodulated by the iron content in the cell growth medium. Additional studies show that purified hIscA1 binds iron with an iron association constant of approx. 2×1019 M-1, and that the iron-bound hIscA1 is able to provide the iron for the iron-sulfur cluster assembly in a proposed scaffold protein, IscU of E. coli, in vitro. The complementation experiments indicate that hIscA1 can partially substitute for IscA in restoring the cell growth of E. coli in the M9 minimal medium under aerobic conditions. The results suggest that hIscA1, like E. coli IscA, is an iron-binding protein that may act as an iron chaperone for biogenesis of iron-sulfur clusters. © The Authors

The footprint of gut microbiota in gallbladder cancer: a mechanistic review

Gallbladder cancer (GBC) is the most common malignant tumor of the biliary system with the worst prognosis. Even after radical surgery, the majority of patients with GBC have difficulty achieving a clinical cure. The risk of tumor recurrence remains more than 65%, and the overall 5-year survival rate is less than 5%. The gut microbiota refers to a variety of microorganisms living in the human intestine, including bacteria, viruses and fungi, which profoundly affect the host state of general health, disease and even cancer. Over the past few decades, substantial evidence has supported that gut microbiota plays a critical role in promoting the progression of GBC. In this review, we summarize the functions, molecular mechanisms and recent advances of the intestinal microbiota in GBC. We focus on the driving role of bacteria in pivotal pathways, such as virulence factors, metabolites derived from intestinal bacteria, chronic inflammatory responses and ecological niche remodeling. Additionally, we emphasize the high level of correlation between viruses and fungi, especially EBV and Candida spp., with GBC. In general, this review not only provides a solid theoretical basis for the close relationship between gut microbiota and GBC but also highlights more potential research directions for further research in the future

The Role of SPARC Protein Expression in the Progress of Gastric Cancer

We aimed to investigate the expression of SPARC (secreted protein, acidic and rich in cysteine) in gastric cancer and its relationship with tumor angiogenesis and cancer cells proliferation. Protein expression of SPARC, VEGF, CD34 and Ki-67 in 80 cases of gastric cancer and 30 cases of normal gastric tissue was evaluated by immunohistochemistry. CD34 staining was used as an indicator of microvessel density (MVD). Ki-67 labeling Index (LI) indicated cancer cells proliferation. Statistical analysis was used to investigate its relationship with clinical characteristics, tumor angiogenesis and cancer cells proliferation. SPARC expression was mainly in the stromal cells surrounding the gastric cancer cells, and was statistically significant differences between gastric cancer and normal gastric tissue (P < 0.05). Both the expression of SPARC and VEGF were related to differentiation degree, clinical stage, Lauren classification and lymph node metastasis (P < 0.05). Expression of SPARC was significantly negatively correlated with the expression of VEGF and MVD in gastric cancer tissues. Expression of SPARC was also negatively correlated with Ki-67-LI. Our findings suggest that both the expression of SPARC and VEGF are closed to tumor angiogenesis in gastric cancer, SPARC inhibited tumor angiogenesis but VEGF promoted tumor angiogenesis. SPARC also inhibited cells proliferation of gastric cancer

PUMA: Secure Inference of LLaMA-7B in Five Minutes

With ChatGPT as a representative, tons of companies have began to provide services based on large Transformers models. However, using such a service inevitably leak users' prompts to the model provider. Previous studies have studied secure inference for Transformer models using secure multiparty computation (MPC), where model parameters and clients' prompts are kept secret. Despite this, these frameworks are still limited in terms of model performance, efficiency, and deployment. To address these limitations, we propose framework PUMA to enable fast and secure Transformer model inference. Our framework designs high quality approximations for expensive functions, such as GeLU and Softmax, which significantly reduce the cost of secure inference while preserving the model performance. Additionally, we design secure Embedding and LayerNorm procedures that faithfully implement the desired functionality without undermining the Transformer architecture. PUMA is about 2x faster than the state-of-the-art MPC framework MPCFORMER(ICLR 2023) and has similar accuracy as plaintext models without fine-tuning (which the previous works failed to achieve). One more thing, PUMA can evaluate LLaMA-7B in around 5 minutes to generate 1 token. To our best knowledge, this is the first time that a model with such a parameter size is able to be evaluated under MPC. PUMA has been open-sourced in the Github repository of SecretFlow-SPU

Effect of BRCA1 R1325K mutation on proliferation and apoptosis of gallbladder cancer cells

Objective·To investigate the effects of breast cancer susceptibility gene 1 (BRCA1) R1325K mutation [arginine (R) to lysine (K) mutation at amino acid 1325] on the proliferation and apoptosis of gallbladder cancer cell lines GBC-SD and NOZ.Methods·BRCA1 wild-type overexpression lentivirus, BRCA1 R1325K mutation overexpression lentivirus, and negative control lentivirus were used to construct the stable transgenic strains of gallbladder carcinoma, cell lines GBC-SD and NOZ. The cells were divided into the control group without the target gene, the BRCA1 wild-type group, and the BRCA1 R1325K mutation group. The expression of target protein was verified by Western blotting. The BRCA1 R1325K mutant gallbladder cancer cells were treated with 20 μmol/L Olaparib, a BRCA1 mutation inhibitor. Gallbladder cancer cell lines were divided into the control group, the BRCA1 wild-type group, the BRCA1 R1325K mutation group, and the BRCA1 R1325K mutation+Olaparib group according to the target gene expression and whether or not the inhibitor was added. The effect of BRCA1 R1325K mutation on proliferation and clonogenesis ability of gallbladder cancer cell lines GBC-SD and NOZ was observed by CCK8 assay and clonogenesis assay, respectively. The effect of BRCA1 R1325K mutation on apoptosis of gallbladder cancer cell lines GBC-SD and NOZ was observed by TUNEL assay. The expressions of apoptosis-related proteins, cleaved PARP, Bcl-2 and Bax, were detected by Western blotting. The inhibitor Olaparib was used to treat the BRCA1 R1325K mutant gallbladder cancer cell lines GBC-SD and NOZ. The phenotypic changes (promoting proliferation, enhancing clonogenesis and inhibiting apoptosis) induced by BRCA1 R1325K mutation were tested in the presence of Olaparib to determine whether the changes could be reversed by the inhibitor.Results·The results of CCK8 assay and clonogenesis assay showed that BRCA1 R1325K mutation could promote the proliferation of gallbladder cancer cell lines GBC-SD and NOZ, and improve their clonal formation ability, compared with the control group and the BRCA1 wild-type group. Olaparib inhibited the proliferation of gallbladder cancer cell lines overexpressing BRCA1 R1325K mutation (P<0.05). Through TUNEL and Western blotting, it was found that overexpression of wild-type BRCA1 could induce the apoptosis of gallbladder cancer cell lines GBC-SD and NOZ, compared with the control group. Compared with the control group and the BRCA1 wild-type group, the BRCA1 R1325K mutation group had anti-apoptotic effect, in which the expression of apoptosis-inhibiting protein Bcl-2 increased and the expression of pro-apoptotic protein Bax decreased (P<0.05).Conclusion·BRCA1 R1325K mutation can promote the proliferation of GBC-SD and NOZ cell lines and inhibit their apoptosis