Antiallergic effects of ethanol extract of Cnidium monnieri (L.) Cuss. on DNCB-induced atopic dermatitis in mice

Purpose: To study the anti-allergic effects of ethanol extract of Cnidium monnieri (L.) Cuss. on 2, 4-dinitrochlorobenzene (DNCB)-induced atopic dermatitis in mice.Method: Atopic dermatitis (AD) was induced by DNCB in Balb/c mice, and the mice randomly divided into normal group, negative control group, hydrocortisone group, and ethanol extract of Cnidium monnieri (L.) Cuss. (EECM) group. Ear swelling was determined by measuring the thicknesses of the left and right ears of each mouse. Spleen and thymus indices were calculated from spleen, thymus and body weight values. The levels of TNF-α and IgE in serum were determined by enzyme-linked immunosorbent assay (ELISA). Hematoxylin-eosin (H & E) staining and toluidine blue staining were used to evaluate pathological changes in ear tissue, while high performance liquid chromatography (HPLC) was performed to ascertain the bioactive compounds in EECM.Results: Compared with the negative control group, EECM significantly alleviated skin lesions, reduced thickness of ear swelling, and decreased spleen and thymus indexes of mice (p < 0.05). Moreover, EECM significantly reduced epidermal thickness (p < 0.01). However, EECM did not significantly alter the number of mast cells (p > 0.05). The expressions of TNF-α and IgE in serum were also significantly down-regulated (p < 0.01, p < 0.05). Results from HPLC revealed that the contents of bergapten, imperatorin and osthole in EECM were 0.73, 3.69 and 9.40 mg/g, respectively.Conclusion: EECM ameliorates AD in mice via inhibition of inflammation and by a mechanism that might be related to the regulation of TNF-α and IgE levels. The major bioactive constituents of EECM are osthole, imperatorin and bergapten. Thus, this plant extract has a potential to be developed for the treatment of of atopic dermatitis

dc-europe bulletin no. 1973.7

Published by Groupe democrate-chrétien du Parlement europée

Adiponectin protects against paraquat-induced lung injury by attenuating oxidative/nitrative stress.

The specific mechanisms underlying paraquat (PQ)-induced lung injury remain unknown, which limits understanding of its cytotoxic potential. Although oxidative stress has been established as an important mechanism underlying PQ toxicity, multiple antioxidants have proven ineffective in attenuating the deleterious effects of PQ. Adiponectin, which shows anti-oxidative and antinitrative effects, may have the potential to reduce PQ-mediated injury. The present study determined the protective action of globular domain adiponectin (gAd) on PQ-induced lung injury, and attempted to elucidate the underlying mechanism or mechanisms of action. BALB/c mice were administered PQ, with and without 12 or 36 h of gAd pre-treatment. The pulmonary oxidative/nitrative status was assessed by measuring pulmonary O2(•-), superoxide dismutase (SOD), malondialdehyde (MDA), nitric oxide (NO) and 8-hydroxy-2-dydeoxy guanosine (8-OHdG) production, and blood 3-Nitrotyrosine (3-NT). At a dose of 20 mg/kg, PQ markedly increased O2(•-), SOD, MDA, NO and 8-OHdG production 3 h post-administration, but did not significantly increase 3-NT levels until 12 h. gAd inhibited these changes in a dose-dependent manner, via transient activation of MDA, followed by attenuation of MDA formation from 6 h onwards. Histological analysis demonstrated that gAd decreased interstitial edema and inflammatory cell infiltration. These results suggest that gAd protects against PQ-induced lung injury by mitigating oxidative/nitrative stress. Furthermore, gAd may be a potential therapeutic agent for PQ-induced lung injury, and further pharmacological studies are therefore warranted

Linkage between surface energy balance non‐closure and horizontal asymmetric turbulent transport

A number of studies have reported that the traditional eddy covariance (EC) method generally underestimated vertical turbulent fluxes, leading to an outstanding non-closure problem of the surface energy balance (SEB). Although it is recognized that the enlarged surface energy imbalance frequently coincides with the increasing wind shear, the role of large eddies in affecting the SEB remains unclear. On analyzing data collected by an EC array, considerable horizontal inhomogeneity of kinematic heat flux is observed. The results show that the combined EC method that incorporates the spatial flux contribution increases the kinematic heat flux by 21% relative to the traditional EC method, improving the SEB closure. Additionally, spectral analysis indicates that large eddies with scales ranging from 0.0005 to 0.01 (in the normalized frequency) mainly account for the horizontal inhomogeneity of kinematic heat flux. Under unstable conditions, this process is operating upon large eddies characterized by enlarged asymmetric turbulent flux transport. With enhanced wind shear, the increment of flux contribution associated with sweeps and ejections becomes disproportionate, contributing to the horizontal inhomogeneity of kinematic heat flux, and thus may explain the increased SEB non-closure

DAppSCAN: Building Large-Scale Datasets for Smart Contract Weaknesses in DApp Projects

The Smart Contract Weakness Classification Registry (SWC Registry) is a widely recognized list of smart contract weaknesses specific to the Ethereum platform. Despite the SWC Registry not being updated with new entries since 2020, the sustained development of smart contract analysis tools for detecting SWC-listed weaknesses highlights their ongoing significance in the field. However, evaluating these tools has proven challenging due to the absence of a large, unbiased, real-world dataset. To address this problem, we aim to build a large-scale SWC weakness dataset from real-world DApp projects. We recruited 22 participants and spent 44 person-months analyzing 1,199 open source audit reports from 29 security teams. In total, we identified 9,154 weaknesses and developed two distinct datasets, i.e., DAPPSCAN-SOURCE and DAPPSCAN-BYTECODE. The DAPPSCAN-SOURCE dataset comprises 39,904 Solidity files, featuring 1,618 SWC weaknesses sourced from 682 real-world DApp projects. However, the Solidity files in this dataset may not be directly compilable for further analysis. To facilitate automated analysis, we developed a tool capable of automatically identifying dependency relationships within DApp projects and completing missing public libraries. Using this tool, we created DAPPSCAN-BYTECODE dataset, which consists of 6,665 compiled smart contract with 888 SWC weaknesses. Based on DAPPSCAN-BYTECODE, we conducted an empirical study to evaluate the performance of state-of-the-art smart contract weakness detection tools. The evaluation results revealed sub-par performance for these tools in terms of both effectiveness and success detection rate, indicating that future development should prioritize real-world datasets over simplistic toy contracts.Comment: Dataset available at https://github.com/InPlusLab/DAppSCA

Turn the Rudder: A Beacon of Reentrancy Detection for Smart Contracts on Ethereum

Smart contracts are programs deployed on a blockchain and are immutable once deployed. Reentrancy, one of the most important vulnerabilities in smart contracts, has caused millions of dollars in financial loss. Many reentrancy detection approaches have been proposed. It is necessary to investigate the performance of these approaches to provide useful guidelines for their application. In this work, we conduct a large-scale empirical study on the capability of five well-known or recent reentrancy detection tools such as Mythril and Sailfish. We collect 230,548 verified smart contracts from Etherscan and use detection tools to analyze 139,424 contracts after deduplication, which results in 21,212 contracts with reentrancy issues. Then, we manually examine the defective functions located by the tools in the contracts. From the examination results, we obtain 34 true positive contracts with reentrancy and 21,178 false positive contracts without reentrancy. We also analyze the causes of the true and false positives. Finally, we evaluate the tools based on the two kinds of contracts. The results show that more than 99.8% of the reentrant contracts detected by the tools are false positives with eight types of causes, and the tools can only detect the reentrancy issues caused by call.value(), 58.8% of which can be revealed by the Ethereum's official IDE, Remix. Furthermore, we collect real-world reentrancy attacks reported in the past two years and find that the tools fail to find any issues in the corresponding contracts. Based on the findings, existing works on reentrancy detection appear to have very limited capability, and researchers should turn the rudder to discover and detect new reentrancy patterns except those related to call.value().Comment: Accepted by ICSE 2023. Dataset available at https://github.com/InPlusLab/ReentrancyStudy-Dat

Immunological Aspects of Fulminant Type 1 Diabetes in Chinese

Background. Fulminant type 1 diabetes (FT1D) is a novel subtype of type 1 diabetes characterized by extremely rapid onset and complete deficiency of insulin due to the destruction of pancreatic β cells. However, the precise mechanisms underlying the etiology of this disease remain unclear. Methods. A total of 22 patients with FT1D and 10 healthy subjects were recruited. Serum antibodies to GAD, IA2, and ZnT8 in patients were tested. And peripheral T cell responses to GAD65, insulin B9–23 peptide, or C peptide were determined in 10 FT1D patients and 10 healthy controls. The mRNA levels of several related cytokines and molecules, such as IFN-γ, IL-4, RORC, and IL-17 in PBMCs from FT1D patients were analyzed by qRT-PCR. Result. We found that a certain proportion of Chinese FT1D patients actually have developed islet-related autoantibodies after onset of the disease. The GAD, insulin, or C peptide-reactive T cells were found in some FT1D patients. We also detected a significant increase for IFN-γ expression in FT1D PBMCs as compared with that of healthy controls. Conclusion. Autoimmune responses might be involved in the pathogenesis of Chinese FT1D