Breaking 3-Factor Approximation for Correlation Clustering in Polylogarithmic Rounds

In this paper, we study parallel algorithms for the correlation clustering problem, where every pair of two different entities is labeled with similar or dissimilar. The goal is to partition the entities into clusters to minimize the number of disagreements with the labels. Currently, all efficient parallel algorithms have an approximation ratio of at least 3. In comparison with the $1.994+\epsilon$ ratio achieved by polynomial-time sequential algorithms [CLN22], a significant gap exists. We propose the first poly-logarithmic depth parallel algorithm that achieves a better approximation ratio than 3. Specifically, our algorithm computes a $(2.4+\epsilon)$-approximate solution and uses $\tilde{O}(m^{1.5})$ work. Additionally, it can be translated into a $\tilde{O}(m^{1.5})$-time sequential algorithm and a poly-logarithmic rounds sublinear-memory MPC algorithm with $\tilde{O}(m^{1.5})$ total memory. Our approach is inspired by Awerbuch, Khandekar, and Rao's [AKR12] length-constrained multi-commodity flow algorithm, where we develop an efficient parallel algorithm to solve a truncated correlation clustering linear program of Charikar, Guruswami, and Wirth [CGW05]. Then we show the solution of the truncated linear program can be rounded with a factor of at most 2.4 loss by using the framework of [CMSY15]. Such a rounding framework can then be implemented using parallel pivot-based approaches

Coordinate Ascent for Off-Policy RL with Global Convergence Guarantees

We revisit the domain of off-policy policy optimization in RL from the perspective of coordinate ascent. One commonly-used approach is to leverage the off-policy policy gradient to optimize a surrogate objective -- the total discounted in expectation return of the target policy with respect to the state distribution of the behavior policy. However, this approach has been shown to suffer from the distribution mismatch issue, and therefore significant efforts are needed for correcting this mismatch either via state distribution correction or a counterfactual method. In this paper, we rethink off-policy learning via Coordinate Ascent Policy Optimization (CAPO), an off-policy actor-critic algorithm that decouples policy improvement from the state distribution of the behavior policy without using the policy gradient. This design obviates the need for distribution correction or importance sampling in the policy improvement step of off-policy policy gradient. We establish the global convergence of CAPO with general coordinate selection and then further quantify the convergence rates of several instances of CAPO with popular coordinate selection rules, including the cyclic and the randomized variants of CAPO. We then extend CAPO to neural policies for a more practical implementation. Through experiments, we demonstrate that CAPO provides a competitive approach to RL in practice.Comment: 47 pages, 4 figure

The Affinity of Elongated Membrane-Tethered Ligands Determines Potency of T Cell Receptor Triggering

T lymphocytes are important mediators of adoptive immunity but the mechanism of T cell receptor (TCR) triggering remains uncertain. The interspatial distance between engaged T cells and antigen-presenting cells (APCs) is believed to be important for topological rearrangement of membrane tyrosine phosphatases and initiation of TCR signaling. We investigated the relationship between ligand topology and affinity by generating a series of artificial APCs that express membrane-tethered anti-CD3 scFv with different affinities (OKT3, BC3, and 2C11) in addition to recombinant class I and II pMHC molecules. The dimensions of membrane-tethered anti-CD3 and pMHC molecules were progressively increased by insertion of different extracellular domains. In agreement with previous studies, elongation of pMHC molecules or low-affinity anti-CD3 scFv caused progressive loss of T cell activation. However, elongation of high-affinity ligands (BC3 and OKT3 scFv) did not abolish TCR phosphorylation and T cell activation. Mutation of key amino acids in OKT3 to reduce binding affinity to CD3 resulted in restoration of topological dependence on T cell activation. Our results show that high-affinity TCR ligands can effectively induce TCR triggering even at large interspatial distances between T cells and APCs

(1−ϵ)(1-\epsilon)-Approximate Maximum Weighted Matching in Distributed, Parallel, and Semi-Streaming Settings

The maximum weighted matching (MWM) problem is one of the most well-studied combinatorial optimization problems in distributed graph algorithms. Despite a long development on the problem, and the recent progress of Fischer, Mitrovic, and Uitto [FMU22] who gave a $\text{poly}(1/\epsilon, \log n)$-round algorithm for obtaining a $(1-\epsilon)$-approximate solution for unweighted maximum matching, it had been an open problem whether a $(1-\epsilon)$-approximate MWM can be obtained in $\text{poly}(1/\epsilon, \log n)$ rounds in the CONGEST model. Algorithms with such running times were only known for special graph classes such as bipartite graphs [AKO18] and minor-free graphs [CS22]. For general graphs, the previously known algorithms require exponential in $(1/\epsilon)$ rounds for obtaining a $(1-\epsilon)$-approximate solution [FFK21] or achieve an approximation factor of at most 2/3 [AKO18]. In this work, we settle this open problem by giving a deterministic $\text{poly}(1/\epsilon, \log n)$-round algorithm for computing a $(1-\epsilon)$-approximate MWM for general graphs in the CONGEST model. Our proposed solution extends the algorithm of Fischer, Mitrovic, and Uitto [FMU22], blends in the sequential algorithm from Duan and Pettie [DP14] and the work of Faour, Fuchs, and Kuhn [FFK21]. Interestingly, this solution also implies a CREW PRAM algorithm with $\text{poly}(1/\epsilon, \log n)$ span using only $O(m)$ processors. In addition, with the reduction from Gupta and Peng [GP13], we further obtain a semi-streaming algorithm with $\text{poly}(1/\epsilon)$ passes. When $\epsilon$ is smaller than a constant $o(1)$ but at least $1/\log^{o(1)} n$, our algorithm is more efficient than both Ahn and Guha's $\text{poly}(1/\epsilon, \log n)$-passes algorithm [AG13] and Gamlath, Kale, Mitrovic, and Svensson's $(1/\epsilon)^{O(1/\epsilon^2)}$-passes algorithm [GKMS19].Comment: A preliminary version appears in PODC 202

Cytotoxic, Antibacterial, and Antioxidant Activities of the Leaf Extract of <i>Sinningia bullata</i>

Sinningia bullata is a tuberous member of the flowering plant family Gesneriaceae. Prior to this work, the antibacterial, antioxidant, and cytotoxic properties of S. bullata were undetermined. Here, we prepared different extracts from the leaf, stem, and tuber of S. bullata and investigated their pharmacological activities. The leaf extract of S. bullata, obtained by 100% acetone (Sb-L-A), had the highest total flavonoid content, antioxidation capacity, and cytotoxic and antibacterial activities. Sb-L-A displayed a broad range of antibacterial activities against Escherichia coli, Staphylococcus aureus, and Pseudomonas aeruginosa. The inhibition zones of Sb-L-A ranged from 8 to 30 mm and were in the following order: S. aureus > E. coli > P. aeruginosa. Incubation of B16F10 melanoma cells with Sb-L-A at a concentration of 80 μg/mL caused deaths at the rate of 96%, reduced migration by 100%, suppressed proliferation and colony formation by 99%, and induced apoptosis, which was observed in 96% of the B16F10 cells. In addition, the cytotoxic activities of Sb-L-A were synergistically enhanced when coacting with the antitumor drug epothilone B. Sb-L-A was also used to determine the cytotoxic effects against 4T1 mammary carcinoma cells. Sb-L-A of 60 μg/mL boosted the distribution of the G2 phase from 1.4% to 24.4% in the B16F10 cells. Accordingly, Sb-L-A might suppress melanoma cell proliferation by inducing G2 cell-cycle arrest. The most abundant compounds in Sb-L-A were identified using gas chromatography–mass spectrometry. The top two contents in this extract were adlupulone and villosin. Overall, the collective data in this study may indicate the pharmacological potentials of Sb-L-A for possible medical applications

Long-Term Prednisolone Treatments Increase Bioactive Vitamin B(6) Synthesis In Vivo

The etiology of vitamin B(6) depletion in inflammation remains unknown. Hepatic vitamin B(6) decreased in adrenalectomized rats, and such reductions were restored by an acute muscle injection of a very high dose of glucocorticoids. We tested the hypothesis that long-term prednisolone treatment for treating inflammation restores vitamin B(6) status by induction of tissue B6 metabolic enzymes. Two independent in vivo models were used. Lewis rats and C57BL/6J mice received prednisolone regimens that reflected clinical prednisolone uses in treating human inflammation. We found: 1) prednisolone increased circulating B6 vitamer pyridoxal 5'-phosphate (PLP; bioactive B6 vitamer), pyridoxal (PL), and 4-pyridoxic acid without altering vitamin B(6) excretion; 2) prednisolone simultaneously induced the hepatic PLP-synthesizing enzyme pyridoxine kinase (PDXK) and pyridoxamine-5'-phosphate oxidase (PMPO) and suppressed PLP catabolic enzyme pyridoxal-5'-phosphate phosphatase (PDXP); and 3) elevations in circulating PL were caused by its release from the liver, not by PLP dephosphorylation (PDXP was suppressed and alkaline phosphatase was unaltered). We conclude that long-term prednisolone treatments promoted hepatic bioactive vitamin B(6) synthesis by inducing the synthesizing enzymes PDXK and PMPO and simultaneously suppressing the catabolic enzyme PDXP. Prednisolone increased circulating B6 vitamer without altering urinary B6 excretion. As the major form of vitamin B(6) across cell membrane, elevated circulating PL may facilitate the cellular uptake and utilization of B6. The elevated plasma PLP may increase vitamin B(6) supply to tissues with a higher B6 demand during inflammation. Results from two independent in vivo models suggested a potential advantage of clinical prednisolone use in treating inflammation with respect to vitamin B(6) status

Cymbidium mosaic potexvirus isolate-dependent host movement systems reveal two movement control determinants and the coat protein is the dominant

AbstractLittle is known about how plant viruses of a single species exhibit different movement behavior in different host species. Two Cymbidium mosaic potexvirus (CymMV) isolates, M1 and M2, were studied. Both can infect Phalaenopsis orchids, but only M1 can systemically infect Nicotiana benthamiana plants. Protoplast inoculation and whole-mount in situ hybridization revealed that both isolates can replicate in N. benthamiana; however, M2 was restricted to the initially infected cells. Genome shuffling between M1 and M2 revealed that two control modes are involved in CymMV host dependent movement. The M1 coat protein (CP) plays a dominant role in controlling CymMV movement between cells, because all chimeric CymMV viruses containing the M1 CP systemically infected N. benthamiana plants. Without the M1 CP, one chimeric virus containing the combination of the M1 triple gene block proteins (TGBps), the M2 5′ RNA (1–4333), and the M2 CP effectively moved in N. benthamiana plants. Further complementation analysis revealed that M1 TGBp1 and TGBp3 are co-required to complement the movement of the chimeric viruses in N. benthamiana. The amino acids within the CP, TGBp1 and TGBp3 which are required or important for CymMV M2 movement in N. benthamiana plants were mapped. The required amino acids within the CP map to the predicted RNA binding domain. RNA–protein binding assays revealed that M1 CP has higher RNA binding affinity than does M2 CP. Yeast two-hybrid assays to detect all possible interactions of M1 TGBps and CP, and only TGBp1 and CP self-interactions were observed

USE OF PREDNISOLONE IN ELEVATING THE LEVEL OF ENDOGENOUS VITAMIN B6

本發明係關於去氫羥化腎上腺皮質素(prednisolone)用於增加內源性維生素B6之用途。基於本發明之發現，去氫羥化腎上腺皮質素可供做為須服用消炎劑或免疫抑制劑患者之維生素B6補充劑，以及可供用於治療或預防由於體內維生素B6缺乏所引起的疾病