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Edible insects are a highly nutritious source of protein and are enjoyed by people all over the world. Insects contain various other nutrients and beneficial compounds, such as lipids, vitamins and minerals, chitin, phenolic compounds, and antimicrobial peptides, which contribute to good health. The practice of insect farming is far more resource-efficient compared to traditional agriculture and animal husbandry, requiring less land, energy, and water, and resulting in a significantly lower carbon footprint. In fact, insects are 12 to 25 times more efficient than animals in converting low-protein feed into protein. When it comes to protein production per unit area, insect farming only requires about one-eighth of the land needed for beef production. Moreover, insect farming generates minimal waste, as insects can consume food and biomass that would otherwise go to waste, contributing to a circular economy that promotes resource recycling and reuse. Insects can be fed with agricultural waste, such as unused plant stems and food scraps. Additionally, the excrement produced by insects can be used as fertilizer for crops, completing the circular chain. Despite the undeniable sustainability and nutritional benefits of consuming insects, widespread acceptance of incorporating insects into our daily diets still has a long way to go. This paper provides a comprehensive overview of the nutritional value of edible insects, the development of farming and processing technologies, and the problems faced in the marketing of edible insect products and insect foods to improve the reference for how people choose edible insects.

Background Sexual dysfunction and cervical cancer are genetically and molecularly two complex health problems. Here, we integrate genetic inference and single-cell expression analysis to identify potential genetic targets for sexual dysfunction and cervical cancer, and assess causality of these targets utilizing Mendelian randomization approaches. Methods We performed a genome-wide association study (GWAS) to identify genetic variants associated with sexual dysfunction and cervical cancer. Next, we examined the cellular landscape of these variation regions based on scRNAseq data. Results The study identified several genetic variants that are correlated with sexual dysfunction and cervical cancer, respectively, and these differentially expressed in reproductive and cervical cells. Two-Gene Combination Panel Increased expression of the WISP1 gene was detected in cervical cancer tissues. Twas most highly expressed in T cells, and least well- when cells were proliferating. Conclusions The study integrates genetics with single-cell expression to nominate genetic targets for sexual dysfunction and cervical cancer and establishes causal support from Mendelian randomization approach.

This study focuses on optimizing the flow field uniformity within a vertical honeycomb wet electrostatic precipitator (WESP), which is a critical prerequisite for achieving high particulate removal efficiency. For a vertical honeycomb WESP with an air capacity of 25,000 m3/h, the internal flow field is optimized by adjusting the opening ratio and aperture ratio of the airflow equalizing plate, installing additional deflector plates, and adding additional airflow equalizing plates at strategic locations. The optimization reduces the velocity relative standard deviation at the anode inlet section to 0.14. Through 1:1-scale equipment construction and testing, the particle concentration at the outlet is stabilized below 10 mg/Nm3, with an average removal efficiency of 95.88%—a 5.7% improvement over the original model. This study solves the design dependency on empirical guidance for vertical honeycomb WESP in the food industry, providing a green technology paradigm for low-carbon industrial emissions.

Anion exchange membranes (AEMs) with high ionic conductivity and excellent stability are critical for long-life AEM fuel cells. In this paper, a novel double crosslinked AEM was prepared successfully based on polybenzimidazole (PBI) and poly(vinylbenzyl chloride) (PVBC) with N , N , N ″, N ′-tetramethyl-1,6-hexanediamine as a homogeneous quaternization reagent. As the mass ratios of PBI and PVBC increased from 1:1 to 3:1, the water uptake and swelling ratio of AEM decreased by half, while the ionic exchange capacity had a small reduction. Moreover, little change occurred in water uptake and swelling ratio under elevated temperature, as well as the ionic exchange capacity after soaking in KOH for 500 h. When the mass ratios of PBI and PVBC was 1:1, the AEM showed the minimum tensile strength of 45.8 MPa and highest conductivity of 31.5 mS cm −1 at 20 °C and 68.8 mS cm −1 at 80 °C. In addition, excellent alkali resistance and oxidative stability were reflected in durability studies and the maximum power density of an H 2 /O 2 single fuel cell using the AEM reached 244.93 mW cm −2 at 0.54 V.

Gadolinium (Gd) compounds have important applications as MRI contrast and potential anticancer agents. The present study investigated the mechanisms of the proapoptotic effect of gadolinium chloride (GdCl₃) on hepatoblastoma cell line (Hep G2) tumor cells. The experimental results indicated that GdCl₃ induced apoptosis of Hep G2 at high concentration and with long time incubation; however, unlike the actions on normal cell lines, GdCl₃ did not cause any oxidative stress on tumor cells. Cytochrome c (Cyt c) and apoptosis inducing factor release, Bax translocation, collapse of mitochondria membrane potential, caspase 3 and 8 activation, and Bid cleavage were observed along with a sustained activation of extracellular signal-regulated kinase (ERK) and c-Jun NH2 terminal kinase (JNK). Addition of ERK and JNK inhibitor attenuated the effect of GdCl₃ induced apoptosis and Cyt c release. All the results suggested a novel mechanism that GdCl₃ induced Hep G2 cell death through intrinsic and external death pathways without significant elevation of reactive oxygen species generation. The present work provided new insight to understand the mechanisms of the biological effects of GdCl₃ and implications for the development of anticancer Gd agents.

In order to explore the role of mitochondria in proliferation promotion and/or apoptosis induction of lanthanum, the mutual influences between La³⁺ and Ca²⁺ on mitochondrial permeability transition pore (PTP) opening were investigated with isolated mitochondria from rat liver. The experimental results revealed that La³⁺ influence the state of mitochondria in a concentration-dependent biphasic manner. La³⁺ in nanomolar concentrations, acting as a Ca²⁺ analog, entered mitochondrial matrix via the RuR sensitive Ca²⁺ channel and elevated ROS level, leading to opening of PTP indicated by mitochondrial swelling, reduction of ΔΨm and cytochrome c release. Inhibition of PTP with 10 μM CsA attenuated the effects of La³⁺. However, micromolar concentrations La³⁺ acted mainly as a Ca²⁺ antagonist, inhibiting PTP opening induced by Ca²⁺. We postulated that this action of La³⁺ on mitochondria through interaction with Ca²⁺ might be involved in the proliferation-promoting and apoptosis induction by La³⁺.

In order to explore the role of mitochondria in proliferation promotion and/or apoptosis induction of lanthanum, the mutual influences between La(3+) and Ca(2+) on mitochondrial permeability transition pore (PTP) opening were investigated with isolated mitochondria from rat liver. The experimental results revealed that La(3+) influence the state of mitochondria in a concentration-dependent biphasic manner. La(3+) in nanomolar concentrations, acting as a Ca(2+) analog, entered mitochondrial matrix via the RuR sensitive Ca(2+) channel and elevated ROS level, leading to opening of PTP indicated by mitochondrial swelling, reduction of q(m) and cytochrome c release. Inhibition of PTP with 10kM CsA attenuated the effects of La(3+). However, micromolar concentrations La(3+) acted mainly as a Ca(2+) antagonist, inhibiting PTP opening induced by Ca(2+). We postulated that this action of La(3+) on mitochondria through interaction with Ca(2+) might be involved in the proliferation-promoting and apoptosis induction by La(3+).

Gadolinium (Gd) compounds have important applications as MRI contrast and potential anticancer agents. The present study investigated the mechanisms of the proapoptotic effect of gadolinium chloride (GdCl^sub 3^) on hepatoblastoma cell line (Hep G2) tumor cells. The experimental results indicated that GdCl^sub 3^ induced apoptosis of Hep G2 at high concentration and with long time incubation; however, unlike the actions on normal cell lines, GdCl^sub 3^ did not cause any oxidative stress on tumor cells. Cytochrome c (Cyt c) and apoptosis inducing factor release, Bax translocation, collapse of mitochondria membrane potential, caspase 3 and 8 activation, and Bid cleavage were observed along with a sustained activation of extracellular signal-regulated kinase (ERK) and c-Jun NH2 terminal kinase (JNK). Addition of ERK and JNK inhibitor attenuated the effect of GdCl^sub 3^ induced apoptosis and Cyt c release. All the results suggested a novel mechanism that GdCl^sub 3^ induced Hep G2 cell death through intrinsic and external death pathways without significant elevation of reactive oxygen species generation. The present work provided new insight to understand the mechanisms of the biological effects of GdCl^sub 3^ and implications for the development of anticancer Gd agents.[PUBLICATION ABSTRACT]

Gadolinium (Gd) compounds have important applications as MRI contrast and potential anticancer agents. The present study investigated the mechanisms of the proapoptotic effect of gadolinium chloride (GdCl sub(3) ) on hepatoblastoma cell line (Hep G2) tumor cells. The experimental results indicated that GdCl sub(3) induced apoptosis of Hep G2 at high concentration and with long time incubation; however, unlike the actions on normal cell lines, GdCl sub(3) did not cause any oxidative stress on tumor cells. Cytochrome c (Cyt c) and apoptosis inducing factor release, Bax translocation, collapse of mitochondria membrane potential, caspase 3 and 8 activation, and Bid cleavage were observed along with a sustained activation of extracellular signal-regulated kinase (ERK) and c-Jun NH2 terminal kinase (JNK). Addition of ERK and JNK inhibitor attenuated the effect of GdCl sub(3) induced apoptosis and Cyt c release. All the results suggested a novel mechanism that GdCl sub(3) induced Hep G2 cell death through intrinsic and external death pathways without significant elevation of reactive oxygen species generation. The present work provided new insight to understand the mechanisms of the biological effects of GdCl sub(3) and implications for the development of anticancer Gd agents.

Detachment is the initial and critical step for cancer metastasis. Only the cells that survive from detachment can develop metastases. Following the disruption of cell–extracellular matrix (ECM) interactions, cells are exposed to a totally different chemical and mechanical environment. During which, cells inevitably suffer from multiple stresses, including loss of growth stimuli from ECM, altered mechanical force, cytoskeletal reorganization, reduced nutrient uptake, and increased reactive oxygen species generation. Here we review the impact of these stresses on the anchorage-independent survival and the underlying molecular signaling pathways. Furthermore, its implications in cancer metastasis and treatment are also discussed.