Oilseed rape straw (ORS) is a kind of biorefractory waste widely existing in the rural area of China, which is highly suitable to mix with kitchen waste (KW) and duck droppings (DD) in two-phase anaerobic digestion (AD). This research introduced the importance of KW and DD addition to improve the biogas production and biodegradation of ORS. A set of comparative experiments were conducted on two-phase mono- and co-digestion with organic load of 60 g VS/L. The total methane yield (TMY) and the biodegradation of ORS of co-digestions were obviously improving, and the synergistic effect found in the two-phase co-digestions. The optimum mixing ratio of ORS, KW and DD was 50:40:10, and the corresponding TMY and VS degradation rate of ORS were 374.5 mL/g VS and 49.7%, respectively. Addition of KW and DD maintained the pH within the optimal range for the hydrolyzing-acidification, improved the phase separation and buffering capacity of AD system.

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Chronic stress causes duodenal damage, in which iron death is likely to play an important role. Chlorogenic acid (CGA), one of the most widely consumed dietary polyphenols, has been shown to protect the intestine. However, it is unclear whether CGA exerts a duodenoprotective effect in chronic stress by inhibiting ferroptosis. In this work, rats were daily exposed to restraint stress for 6 h over 21 consecutive days, with/without CGA (100 mg/kg, gavage). CGA reduced blood hepcidin, iron, reactive oxygen species (ROS), and ferroportin 1 (FPN1) levels and upregulated the levels of ferroptosis-related biomarkers (GPX4, GSH, NADPH, etc.). These results confirmed that CGA inhibited ferroptosis in the duodenum. Furthermore, the use of S3I-201 (STAT3 inhibitor) helped to further clarify the mechanism of action of CGA. Overall, CGA could reduce hepcidin production by inhibiting the IL-6/JAK2/STAT3 pathway in the liver to increase the expression of FPN1 in the duodenum, which restored iron homeostasis and inhibited ferroptosis, alleviating chronic stress-induced duodenal injury.

Highly active antiretroviral therapy (HAART) is very effective in suppressing human immunodeficiency virus type 1 (HIV‑1) replication. However, the treatment is required to be administered for the remainder of an individual's lifetime due to latent HIV‑1 reservoirs. The 'shock‑and‑kill' strategy, which involves using agents to reactivate latent HIV‑1 and subsequently killing latently infected cells in the presence of HAART, was recently proposed. Unfortunately, no agents have currently demonstrated an ability to reactivate latent HIV‑1 in vivo in the absence of toxicity. Therefore, the identification of novel latency activators is required. In order to identify a potential novel agent, the present study investigated the effect of quercetin on latent HIV‑1 reactivation using an established model of HIV‑1 latency. As a marker for reactivation of HIV‑1 in C11 Jurkat cells, the expression of green fluorescent protein, controlled by HIV‑1 long terminal repeat, was observed by fluorescence microscopy. The results of the present study demonstrated that quercetin effectively reactivated latent HIV‑1 gene expression alone, and led to synergistic reactivation when combined with prostratin or valproic acid. In addition, the present study provides evidence that quercetin may reactivate HIV‑1 expression by inducing nuclear factor‑κB nuclear translocation, and that the toxicity of quercetin is lower when compared with various additional activators of HIV‑1. Combined, the results of the present study indicate that quercetin may be an effective agent to disrupt HIV‑1 latency and may be useful in future eradication strategies.

Sepsis, an infection-induced systemic inflammatory disorder, is often accompanied by multiple organ dysfunction syndromes with high incidence and mortality rates, and those who survive are often left with long-term sequelae, bringing great burden to social economy. Therefore, novel approaches to solve this puzzle are urgently needed. Previous studies revealed that long non-coding RNAs (lncRNAs) have exerted significant influences on the process of sepsis. The aim of this review is to summarize our understanding of lncRNAs as potential sepsis-related diagnostic markers and therapeutic targets, and provide new insights into the diagnosis and treatment for sepsis. In this study, we also introduced the current diagnostic markers of sepsis and discussed their limitations, while review the research advances in lncRNAs as promising biomarkers for diagnosis and prognosis of sepsis. Furthermore, the roles of lncRNAs in sepsis-induced organ dysfunction were illustrated in terms of different organ systems. Nevertheless, further studies should be carried out to elucidate underlying molecular mechanisms and pathological process of sepsis.

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Despite the remarkable success of immunotherapy in the treatment of melanoma, resistance to these agents still affects patient prognosis and response to therapies. Beta-2-microglobulin (β2M), an important subunit of major histocompatibility complex (MHC) class I, has important biological functions and roles in tumor immunity. In recent years, increasing studies have shown that B2M gene deficiency can inhibit MHC class I antigen presentation and lead to cancer immune evasion by affecting β2M expression. Based on this, B2M gene defect and T cell-based immunotherapy can interact to affect the efficacy of melanoma treatment. Taking into account the many recent advances in B2M-related melanoma immunity, here we discuss the immune function of the B2M gene in tumors, its common genetic alteration in melanoma, and its impact on and related improvements in melanoma immunotherapy. Our comprehensive review of β2M biology and its role in tumor immunotherapy contributes to understanding the potential of B2M gene as a promising melanoma therapeutic target.