Large Language Models are reasoners with Self-Verification

When a large language model (LLM) performs complex reasoning by chain of thought (CoT), it can be highly sensitive to individual mistakes. We have had to train verifiers to address this issue. As we all know, after human inferring a conclusion, they often check it by re-verifying it, which can avoid some mistakes. We propose a new method called self-verification that uses the conclusion of the CoT as a condition to build a new sample and asks the LLM to re-predict the original conditions which be masked. We calculate an explainable verification score based on the accuracy. This method can improve the accuracy of multiple arithmetics and logical reasoning datasets when using few-shot learning. we have demonstrated that LLMs can conduct explainable self-verification of their own conclusions and achieve competitive reasoning performance. Extensive experimentals have demonstrated that our method can help multiple large language models with self-verification can avoid interference from incorrect CoT. Code is available at \url{https://github.com/WENGSYX/Self-Verification

Mycoplasma genitalium Lipoproteins Induce Human Monocytic Cell Expression of Proinflammatory Cytokines and Apoptosis by Activating Nuclear Factor κB

This study was designed to investigate the molecular mechanisms responsible for the induction of proinflammatory cytokines gene expression and apoptosis in human monocytic cell line THP-1 stimulated by lipoproteins (LPs) prepared from Mycoplasma genitalium. Cultured cells were stimulated with M. genitalium LP to analyze the production of proinflammatory cytokines and expression of their mRNA by ELISA and RT-PCR, respectively. Cell apoptosis was also detected by Annexin V-FITC-propidium iodide (PI) staining and acridine orange (AO)-ethidium bromide (EB) staining. The DNA-binding activity of nuclear factor-κB (NF-κB) was assessed by electrophoretic mobility shift assay (EMSA). Results showed that LP stimulated THP-1 cells to produce tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and IL-6 in a dose-dependent manner. The mRNA levels were also upregulated in response to LP stimulation. LPs were also found to increase the DNA-binding activity of NF-κB, a possible mechanism for the induction of cytokine mRNA expression and the cell apoptosis. These effects were abrogated by PDTC, an inhibitor of NF-κB. Our results indicate that M. genitalium-derived LP may be an important etiological factor of certain diseases due to the ability of LP to produce proinflammatory cytokines and induction of apoptosis, which is probably mediated through the activation of NF-κB

ZYZ-168 alleviates cardiac fibrosis after myocardial infarction through inhibition of ERK1/2-dependent ROCK1 activation

Selective treatments for myocardial infarction (MI) induced cardiac fibrosis are lacking. In this study, we focus on the therapeutic potential of a synthetic cardio-protective agent named ZYZ-168 towards MI-induced cardiac fibrosis and try to reveal the underlying mechanism. ZYZ-168 was administered to rats with coronary artery ligation over a period of six weeks. Ecocardiography and Masson staining showed that ZYZ-168 substantially improved cardiac function and reduced interstitial fibrosis. The expression of α–smooth muscle actin (α-SMA) and Collagen I were reduced as was the activity of matrix metalloproteinase 9 (MMP-9). These were related with decreased phosphorylation of ERK1/2 and expression of Rho-associated coiled-coil containing protein kinase 1 (ROCK1). In cardiac fibroblasts stimulated with TGF-β1, phenotypic switches of cardiac fibroblasts to myofibroblasts were observed. Inhibition of ERK1/2 phosphorylation or knockdown of ROCK1 expectedly reduced TGF-β1 induced fibrotic responses. ZYZ-168 appeared to inhibit the fibrotic responses in a concentration dependent manner, in part via a decrease in ROCK 1 expression through inhibition of the phosphorylation status of ERK1/2. For inhibition of ERK1/2 phosphorylation with a specific inhibitor reduced the activation of ROCK1. Considering its anti-apoptosis activity in MI, ZYZ-168 may be a potential drug candidate for treatment of MI-induced cardiac fibrosis

An Update on AMPK in Hydrogen Sulfide Pharmacology

Hydrogen sulfide (H2S), the third bio-active gasotransmitter, is produced endogenously and tightly involved in the pathogenesis and treatment for various diseases. Adenosine 5′-monophosphate-activated protein kinase (AMPK) plays a paramount role in maintaining cellular energetic balance. Increasing evidences have also suggested AMPK as a novel modulator in multiple pathological conditions. In this paper, we will review the biological principles of H2S and AMPK, and most importantly, the recent discoveries regarding AMPK-mediated pharmacological actions of H2S. Emphasis will be laid on AMPK/H2S interactions in the cardiovascular system, autophagy, diabetic complications, and inflammation. In most cases described in this article, by promoting AMPK activation, H2S exerts cytoprotective effects or therapeutic potentials, though there remain some controversies before we can fully understand the involved mechanisms. Further researches are in need to investigate more closely any relationship between H2S and AMPK, and to put forward the development of H2S donors for clinical application