Ultrasonic-assisted extraction of luteolin from peanut shells using ionic liquid and its molecular mechanism.

This study investigates the potential of ionic liquids (ILs) as sustainable solvents in ultrasonic-assisted extraction (UAE) to efficiently recover luteolin from peanut shells. Among the range of ILs tested, 1-butyl-3-methylimidazolium tetrafluoroborate stood out as the most effective solvent, achieving the highest extraction yield. Single-factor experiments were conducted to analyze the effects of ultrasonic power, extraction time, extraction temperature, IL concentration, and solid-to-liquid ratio on extraction efficiency.

Physiological and transcriptomic analyses of response of walnuts () to infection.

Introduction: Walnut blight is a serious bacterial disease that affects the yield and quality of walnuts. is one of the main causative agents of walnut blight. However, there have been few studies on the response of walnuts to infection.

Environment and natural resources degradation under COVID-19 crises: Recovery post pandemic.

Environmental stability improved during the covid 19 pandemic when production and industrial activities, and natural resources depletion processes stopped during the lockdown environment worldwide; however, based on the judgment of COP26 and the recent COP27, environmental degradation increased in the world in post-pandemic; therefore, policymakers and researchers re-focused their attention on the determinants of CO2 in economies. Hence, this study investigates the nexus of natural resource rents, including oil rents, mineral rents, and coal rents, on the carbon emissions of upper-middle-income economies from 1984 to 2021. The study included economic growth and renewable energy as additional determinants.

Loss of p21 promoted tumorigenesis in the background of telomere dysfunctions induced by TRF2 and Wrn deficiency.

Werner syndrome (WS) is a rare autosomal recessive progeria disease with genetic instability/cancer predisposition, thus a good model in understanding aging related carcinogenesis. Telomere dysfunction induced cellular senescence is essential in the manifestation of the WS phenotype. Our previous data has shown that p21 (encoded by gene) could induce cellular senescence and suppress cellular growth of ALT (alternative lengthening of telomere) tumors derived from WS, suggested that p21 might play a key role in maintaining senescence of WS cells.

[The regulation of anoikis in tumor invasion and metastasis].

As a barrier to metastasis of cancer, cells that lost contact with the neighbouring cells or extracellular matrix(Extracellular matrix, ECM) will be subjected to apoptosis. This cell death process has been termed "anoikis". When normal epithelial cells or solid tumor cells without metastatic potential detach from the primary site, and then enter into the circulatory system, the anoikis mechanism will be activated.

Association between the CTLA-4 +49A/G polymorphism and Graves' disease: A meta-analysis.

The +49A/G polymorphism of the cytotoxic T-lymphocyte-associated antigen-4 gene (CTLA-4) has been associated with Graves' disease (GD). However, results have been inconsistent. The aim of this study was to quantitatively summarize the evidence for CTLA-4 +49A/G polymorphism and GD.

Association between the CTLA-4 +49A/G polymorphism and type 1 diabetes: a meta-analysis.

Background: +49A/G polymorphism of the cytotoxic T-lymphocyte-associated antigen-4 gene (CTLA-4) has been associated with type 1 diabetes (T1D). However, results were inconsistent. The aim of this study was to quantitatively summarize the evidence for CTLA-4 +49A/G polymorphism and T1D.

Association between the CTGF -945C/G polymorphism and systemic sclerosis: a meta-analysis.

Background: The -945C/G polymorphism of the connective tissue growth factor (CTGF) has been associated with systemic sclerosis, however, results were conflicted. The aim of this study was to validate the evidence for the CTGF -945C/G polymorphism and systemic sclerosis risk.

Methods: Electronic search of PubMed was conducted to select studies.

Two mechanisms underlying the loss of p16(Ink4a) function are associated with distinct tumorigenic consequences for WS MEFs escaping from senescence.

Werner syndrome (WS) mouse embryonic fibroblasts (MEFs) can spontaneously escape from senescence and become immortalized, either tumorigenic or non-tumorigenic. Our data revealed a single p53(N236S) point mutation in the tumorigenic cell lines, which was correlated with the down-regulation of p21(Waf1/Cip1). p16(Ink4a) expression was significantly decreased in all immortalized cell lines.