Optimal Clustering of Discrete Mixtures: Binomial, Poisson, Block Models, and Multi-layer Networks

In this paper, we first study the fundamental limit of clustering networks when a multi-layer network is present. Under the mixture multi-layer stochastic block model (MMSBM), we show that the minimax optimal network clustering error rate, which takes an exponential form and is characterized by the Renyi divergence between the edge probability distributions of the component networks. We propose a novel two-stage network clustering method including a tensor-based initialization algorithm involving both node and sample splitting and a refinement procedure by likelihood-based Lloyd algorithm. Network clustering must be accompanied by node community detection. Our proposed algorithm achieves the minimax optimal network clustering error rate and allows extreme network sparsity under MMSBM. Numerical simulations and real data experiments both validate that our method outperforms existing methods. Oftentimes, the edges of networks carry count-type weights. We then extend our methodology and analysis framework to study the minimax optimal clustering error rate for mixture of discrete distributions including Binomial, Poisson, and multi-layer Poisson networks. The minimax optimal clustering error rates in these discrete mixtures all take the same exponential form characterized by the Renyi divergences. These optimal clustering error rates in discrete mixtures can also be achieved by our proposed two-stage clustering algorithm

Research progress on denervation in cardiovascular diseases

Denervation is closely related to many cardiovascular diseases, such as myocardial infarction, myocardial ischemia-reperfusion injury, hypertension, arrhythmia, heart failure, atherosclerosis and ventricular remodeling. Denervation affects the patients resting heart rate and responsiveness to exercise in the early stages of heart transplantation. Therefore, this article reviews the research progress of denervation in the field of cardiovascular diseases and elaborates on the mechanism of denervation in the treatment of cardiovascular disease, intending to provide new complementary treatment methods for the treatment of cardiovascular diseases

Effectiveness of external Sanjierupi Gao on mastalgia caused by mammary gland hyperplasia: a placebo controlled trial

AbstractObjectiveTo evaluate the curative effect of external application of the Chinese drug, Sanjierupi Gao, on mastalgia caused by mammary gland hyperplasia.MethodsThis randomized, double-blinded, and placebo controlled study enrolled 260 patients with mammary gland hyperplasia from five hospitals. Patients were randomly and equally divided into a Sanjierupi Gao treatment group and a placebo control group. An adhesive plaster was applied to the most painful area on either breast for 7 h a day. Treatment lasted for two menstrual cycles without application during menstruation. Mastalgia was used as the main index of curative effect. The change before and after treatment in days of mastalgia, the time to alleviate pain, pain extent, and severe pain scores were observed.ResultsCompared to the control group, the treatment group had significantly fewer days of mastalgia (P<0.01), a significantly lower severe pain score (P<0.01), and significantly less subjective pain and tenderness (P<0.05 and P<0.01, respectively). Three days before the follow-up visit, the pain score in the treatment group was significantly lower than that in the control group (P<0.05). A non-parametric test was used to compare the time to alleviate mastalgia between the two groups and found no statistical difference (Z=−0.313, P=0.754).ConclusionApplication of Sanjierupi Gao can decrease mastalgia duration in patients with mammary gland hyperplasia during menstruation and alleviate the extent of mastalgia. The time to alleviate pain is psychologically influenced

Tumor promoter TPA activates Wnt/β-catenin signaling in a casein kinase 1-dependent manner.

The tumor promoter 12-O-tetra-decanoylphorbol-13-acetate (TPA) has been defined by its ability to promote tumorigenesis on carcinogen-initiated mouse skin. Activation of Wnt/β-catenin signaling has a decisive role in mouse skin carcinogenesis, but it remains unclear how TPA activates Wnt/β-catenin signaling in mouse skin carcinogenesis. Here, we found that TPA could enhance Wnt/β-catenin signaling in a casein kinase 1 (CK1) ε/δ-dependent manner. TPA stabilized CK1ε and enhanced its kinase activity. TPA further induced the phosphorylation of LRP6 at Thr1479 and Ser1490 and the formation of a CK1ε-LRP6-axin1 complex, leading to an increase in cytosolic β-catenin. Moreover, TPA increased the association of β-catenin with TCF4E in a CK1ε/δ-dependent way, resulting in the activation of Wnt target genes. Consistently, treatment with a selective CK1ε/δ inhibitor SR3029 suppressed TPA-induced skin tumor formation in vivo, probably through blocking Wnt/β-catenin signaling. Taken together, our study has identified a pathway by which TPA activates Wnt/β-catenin signaling

Research Progress in Molecular Biology of Fish Immunoglobulin M (IgM)

Immunoglobulin (Ig) is a type of globulin produced by B lymphocytes during pathogenic infection of vertebrates. It has immune functions and can realize specific recognition and neutralization of corresponding antigens. As IgM is reported first in fish, IgM is the first antibody produced during immune responses and plays a vital role in systemic and mucosal immune tissues. IgM molecules have two forms: membrane-bound IgM (mIgM) and secreted IgM (sIgM). The latter is produced by plasmacytes and secreted into body fluid, existing as immunological effect molecules. The former embeds into B cytomembrane and exists as an antigen receptor. It binds with assistant molecules to form cell receptor compounds. This study reviews research progress on the structures and production processes of IgM genes in different fish species and the distribution characteristics of IgM on B cells, mediated signal pathways, and functions. It aims to enrich basic theoretical knowledge of fish immunology and provide some scientific references for disease control in fishes

Research Progress on the Fish Complement C3 Gene

Complement (C) is a serum protein with immunity-related functions and enzymatic activities. It can induce inflammatory responses and antibody formation following activation by substances such as pathogens. Moreover, it is a crucial molecule in the congenital immune defense system. Complement manifests earlier than immunoglobulin in the evolutionary process of fish's immune system. Therefore, the complement system of fish is vital for congenital and acquired immunities. A complement system is a polymolecule system comprising more than 30 soluble proteins, membrane-bound proteins, and complement receptors. It can be activated through three pathways for immunoregulation, the clearance of the immune complex, etc. The liver primarily produces the fish complement C3, which is a significant component of the complement system of fishes. C3 is the hub of three activation pathways. Research works concerning the structure, generation process, expression, and functions of C3 in fishes are reviewed in this study

Suppression of Excessive Histone Deacetylases Activity in Diabetic Hearts Attenuates Myocardial Ischemia/Reperfusion Injury via Mitochondria Apoptosis Pathway

Background. Histone deacetylases (HDACs) play a pivotal role in signaling modification and gene transcriptional regulation that are essential for cardiovascular pathophysiology. Diabetic hearts with higher HDACs activity were more vulnerable to myocardial ischemia/reperfusion (MI/R) injury compared with nondiabetic hearts. We are curious about whether suppression of excessive HDACs activity in diabetic heart protects against MI/R injury. Methods. Diabetic rats were subjected to 45 min of ischemia, followed by 3 h of reperfusion. H9C2 cardiomyocytes were exposed to high glucose for 24 h, followed by 4 h of hypoxia and 2 h of reoxygenation (H/R). Results. Both MI/R injury and diabetes mellitus elevated myocardium HDACs activity. MI/R induced apoptotic cell death was significantly decreased in diabetic rats treated with HDACs inhibitor trichostatin A (TSA). TSA administration markedly moderated dissipation of mitochondrial membrane potential, protected the integrity of mitochondrial permeability transition pore (mPTP), and decreased cell apoptosis. Notably, cotreatment with Akt inhibitor partly or absolutely inhibited the protective effect of TSA in vivo and in vitro. Furthermore, TSA administration activated Akt/Foxo3a pathway, leading to Foxo3a cytoplasm translocation and attenuation proapoptosis protein Bim expression. Conclusions. Both diabetes mellitus and MI/R injury increased cardiac HDACs activity. Suppression of HDACs activity triggered protective effects against MI/R and H/R injury under hyperglycemia conditions through Akt-modulated mitochondrial apoptotic pathways via Foxo3a/Bim