Stochastic Distributed Optimization under Average Second-order Similarity: Algorithms and Analysis

We study finite-sum distributed optimization problems involving a master node and $n-1$ local nodes under the popular $\delta$-similarity and $\mu$-strong convexity conditions. We propose two new algorithms, SVRS and AccSVRS, motivated by previous works. The non-accelerated SVRS method combines the techniques of gradient sliding and variance reduction and achieves a better communication complexity of $\tilde{\mathcal{O}}(n {+} \sqrt{n}\delta/\mu)$ compared to existing non-accelerated algorithms. Applying the framework proposed in Katyusha X, we also develop a directly accelerated version named AccSVRS with the $\tilde{\mathcal{O}}(n {+} n^{3/4}\sqrt{\delta/\mu})$ communication complexity. In contrast to existing results, our complexity bounds are entirely smoothness-free and exhibit superiority in ill-conditioned cases. Furthermore, we establish a nearly matched lower bound to verify the tightness of our AccSVRS method.Comment: Camera-ready version for NeurIPS 202

Active headrest combined with a depth camera-based ear-positioning system

Active headrests can reduce low-frequency noise around ears based on active noise control (ANC) system. Both the control system using fixed control filters and the remote microphone-based adaptive control system provide good noise reduction performance when the head is in the original position. However, their performance degrades significantly when the head is in motion. In this paper, a human ear-positioning system based on the depth camera is introduced to address this problem. The system uses RTMpose model to estimate the two-dimensional (2D) positions of the ears in the color frame, and then derives the corresponding three-dimensional (3D) coordinates in the depth frame with a depth camera. Experimental results show that the ear-positioning system can effectively track the movement of ears, and the broadband noise reduction performance of the active headrest combined with the system is significantly improved when the human head is translating or rotating

Annexin A2 Coordinates STAT3 to Regulate the Invasion and Migration of Colorectal Cancer Cells In Vitro

The present study aimed to reveal the expression of STAT3 and Anxa 2 in CRC specimens and to investigate the effects of STAT3 and Anxa 2 signaling on the proliferation, invasion, and migration in CRC Caco-2 cells. Results demonstrated that both Anxa 2 and STAT3 were highly expressed in CRC specimens in both mRNA and protein levels, with or without phosphorylation (Tyrosine 23 in Anxa 2 and Tyrosine 705 in STAT3). And the upregulated Anxa 2 promoted the phosphorylation of STAT3 (Tyrosine 705) in CRC Caco-2 cells. The upregulated Anxa 2 promoted the proliferation, migration, and invasion of Caco-2 cells in vitro. Moreover, the STAT3 knockdown also repressed the proliferation, migration, and invasion of Caco-2 cells. In conclusion, the overexpressed Annexin A2 regulated the proliferation, invasion, and migration in CRC cells in an association with STAT3

Downregulation of ITGβ3 in colon adenocarcinoma reveals poor prognosis by affecting genome stability, cell cycle, and the tumor immune microenvironment

IntroductionAbnormal expression of integrin subunit beta 3 (ITGβ3), a gene-encoding protein, is related to the occurrence and development of cancers; however, the biological role of ITGβ3 in colon adenocarcinoma (COAD) remains unclear.MethodsWe used the Cancer Genome Atlas database to obtain the clinical data of patients with COAD, analyzed the mRNA gene clusters related to ITGβ3, and analyzed the interaction signal pathway and interaction protein network of the differentially expressed gene clusters. The results showed that ITGβ3 expression in COAD tumor tissues was significantly downregulated compared with that in paracancerous tissues. Low ITGβ3 expression in tumor tissues is associated with poor overall survival of patients with COAD. In multivariate analysis, stage IV and ITGβ3 low expression were independent prognostic factors. Gene Ontology analysis showed that differentially expressed genes (DEGs) were significantly enriched in leukocyte migration, cell adhesion, and extracellular matrix (ECM) organization. Kyoto Encyclopedia of Genes and Genomes analysis revealed that the DEGs were mainly enriched in ECM-receptor interactions, focal adhesion, and the PI3K-Akt signaling pathway. Protein-protein interaction network analysis revealed the hub and seed genes of the key modules related to ITGβ3. Finally, we analyzed the correlation between TGβ3 and immune-related genes and found that ITGβ3 expression was significantly correlated with tumor purity and infiltration level of dominant immune cells.DiscussionThese findings indicate that ITGβ3 downregulation in COAD may profoundly affect genome stability and multiple steps of the cell cycle, alter the tumor immune microenvironment, and be related to the prognosis of patients with COAD

Clinicopathological Significance and Prognostic Value of DNA Methyltransferase 1, 3a, and 3b Expressions in Sporadic Epithelial Ovarian Cancer

Altered DNA methylation of tumor suppressor gene promoters plays a role in human carcinogenesis and DNA methyltransferases (DNMTs) are responsible for it. This study aimed to determine aberrant expression of DNMT1, DNMT3a, and DNMT3b in benign and malignant ovarian tumor tissues for their association with clinicopathological significance and prognostic value. A total of 142 ovarian cancers and 44 benign ovarian tumors were recruited for immunohistochemical analysis of their expression. The data showed that expression of DNMT1, DNMT3a, and DNMT3b was observed in 76 (53.5%), 92 (64.8%) and 79 (55.6%) of 142 cases of ovarian cancer tissues, respectively. Of the serious tumors, DNMT3a protein expression was significantly higher than that in benign tumor samples (P = 0.001); DNMT3b was marginally significant down regulated in ovarian cancers compared to that of the benign tumors (P = 0.054); DNMT1 expression has no statistical difference between ovarian cancers and benign tumor tissues (P = 0.837). Of the mucious tumors, the expression of DNMT3a, DNMT3b, and DNMT1 was not different between malignant and benign tumors. Moreover, DNMT1 expression was associated with DNMT3b expression (P = 0.020, r = 0.195). DNMT1 expression was associated with age of the patients, menopause status, and tumor localization, while DNMT3a expression was associated with histological types and serum CA125 levels and DNMT3b expression was associated with lymph node metastasis. In addition, patients with DNMT1 or DNMT3b expression had a trend of better survival than those with negative expression. Co-expression of DNMT1 and DNMT3b was significantly associated with better overall survival (P = 0.014). The data from this study provided the first evidence for differential expression of DNMTs proteins in ovarian cancer tissues and their associations with clinicopathological and survival data in sporadic ovarian cancer patients

Transcriptional regulation of the muscle-specific troponin I gene

The quail fast skeletal troponin I (TnI) gene is transcribed specifically in differentiated skeletal muscle cells. TnI gene expression is under the control of an internal regulatory element (IRE) in the first intron which functions as a muscle-specific enhancer. My studies have demonstrated that the muscle regulatory factors MyoD, myogenin, Myf-5, and MRF4, in the presence of the ubiquitous helix-loop-helix transcription factor E12, interact with identical nucleotides within the E-box sequence of the TnI IRE in vitro. Utilizing a novel analysis strategy involving protein cross-linking and two-dimensional gel electrophoresis, I found that the muscle regulatory factors must form heterodimers with E12 to bind efficiently to the TnI E-box. The TnI E-box-binding proteins in vivo are restricted to skeletal muscle cells and are antigenically related to MyoD and myogenin. The full enhancer activity of the IRE requires two additional cis-acting elements, Site I and Site II, which bind to nuclear proteins from both muscle and nonmuscle cells. Point mutations in either Site I or Site II abolish the respective protein binding abilities and greatly reduce the enhancer function of the TnI IRE. These results demonstrate that muscle-specific TnI gene transcription relies on interactions between muscle regulatory factors and ubiquitously expressed proteins. To isolate cDNA clones encoding Site I-binding proteins, $\lambda$gt11 expression libraries were screened using the TnI Site I DNA as a probe. Several cDNA clones obtained from the library screenings encode the human nonhistone chromosomal high mobility group protein (HMG)-I and its isoform HMG-Y. An additional human cDNA clone, referred to as clone E, encodes a ${\sim}60$ kDa protein which also binds to Site I. Sequence analyses suggest that the E cDNA clone encodes a novel DNA-binding protein. Taken together, these results suggest that muscle-specific regulation of TnI gene expression requires a mechanism in which the IRE cis-acting elements, including E-box, Site I, and Site II, each interact with multiple muscle-specific and/or ubiquitous proteins to form an active transcriptional complex