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Copyright of Mycosystema is the property of Mycosystema Editorial Board and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Food Research & Development is the property of Food Research & Development Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

As an essential trace element, copper has major effects on cell metabolism. Therefore, interfering with the balance of copper metabolism in such a way that leads to copper deficiency or excess causes disease. It has been reported that copper metabolic imbalance, or cuproptosis, affects the development of cardiovascular diseases by mediating cellular oxidative stress and vascular remodeling and by interfering with mitochondrial functions. Importantly, copper chelators, copper ion carriers, small molecule inhibitors of copper chaperones, and dietary copper can alleviate cardiovascular diseases caused by copper metabolic imbalance or cuproptosis. In this review, we comprehensively considered the molecular mechanisms of copper metabolic homeostasis and cuproptosis, as well as their significance and therapeutic advances in cardiovascular diseases, aiming to provide insights on therapeutically targeting copper metabolic homeostasis and cupro-ptosis as a novel strategy for managing cardiovascular diseases. [ABSTRACT FROM AUTHOR]

Copyright of Shipin Kexue/ Food Science is the property of Food Science Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Food Research & Development is the property of Food Research & Development Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Shipin Kexue/ Food Science is the property of Food Science Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The formation mechanism of antibiotics resistance genes (ARGs) in the environment was de-scribed from the perspective of DNA damage and error repair, and the relevant core functional gene fragments involved in DNA damage and error repair were summarized. Three main mechanisms of horizontal transfer of ARGs in the environment, including pili bridging, signal transduction and type IV cell secretion system were discussed from the perspective of cell metabolism. The existing studies further strengthen the understanding of the formation and transfer mechanism of ARGs in the environment, and provide a theoretical basis for future research on the reduction of ARGs. At present, the internal mechanism of antibiotic induced ARGs formation and transfer was still relatively lacking, and further studies could be conducted from the biological toxicity and molecular biology levels. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Chinese Institute of Food Science & Technology / Zhongguo Shipin Xuebao is the property of Journal of Chinese Institute of Food Science & Technology Periodical Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Science & Technology of Food Industry is the property of Science & Technology of Food Industry Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective: To investigate the lipidomics differences of CD4+T immune cells in diabetic kidney disease (DKD) mice, and screen out the differential metabolites with biological significance. Methods: CD4 (L3T4) MicroBeads immunomagnetic beads were used to isolate CD4+T immune cells from spleen of BKS. Cg-Dock7m+/+ Leprdb/J mice with spontaneous DKD; the purity of CD4+T cells were identified by flow cytometry. The non-targeted lipidomics of CD4+T cells were detected by LC-MS/MS, and the differential metabolites were analyzed. Results: A total of 463 metabolites were detected by LC-MS. PCA and OPLS-DA analysis showed that the metabolic components were significantly separated; twenty-four differential metabolites were screened out. KEGG and enrichment analysis showed that the differential metabolites involved in the disorder of glycerol phospholipid metabolism. Conclusion: Phospholipid metabolism of CD4+T cells is closely related to the occurrence of DKD. Phospholipid metabolism targeting DKD CD4+T cells in DKD may be a new direction of DKD treatment. [ABSTRACT FROM AUTHOR]

Copyright of Science & Technology of Food Industry is the property of Science & Technology of Food Industry Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Food Research & Development is the property of Food Research & Development Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

BACKGROUND: Spinal cord injury is a serious disease of the central nervous system, characterized by weak regeneration of neurons and complex pathological processes. Mitochondrial autophagy is a highly selective autophagy that can degrade damaged mitochondria and plays an important role in energy supply, cell metabolism and neuronal survival. OBJECTIVE: To explore the mechanism of mitochondrial autophagy and the effects of drugs on mitochondrial autophagy, and provide a new target for the treatment of spinal cord injury. METHODS: In CNKI, Wanfang and PubMed databases, “spinal cord injury, mitophagy, autophagy, mitochondria” were used as search terms. We searched for articles on the role and mechanism of mitophagy and spinal cord injury. RESULTS AND CONCLUSION: (1) The regulation of mitochondrial autophagy level plays a key role in the treatment of spinal cord injury, and its regulatory mechanism is complex, mainly including PINK1/Parkin, Nix/BNIP3L, FUNDC1, and Atg proteins. In addition, GIT1 regulatory pathway and down-regulated miRNA-124 induction pathway were also found. (2) In terms of treatment, rapamycin, acetyl-L-carnitine, salidroside, betulinic acid, and maltol can inhibit apoptosis and improve spinal cord injury by appropriately activating mitochondrial autophagy. In contrast, rosiglitazone ameliorates spinal cord injury by inhibiting mitochondrial autophagy. This suggests that activation or inhibition of mitochondrial autophagy may improve spinal cord injury, which is related to the different mechanisms of drug action. The specific mechanism of action of the drugs remains to be further studied. [ABSTRACT FROM AUTHOR]

Copyright of Food Research & Development is the property of Food Research & Development Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Chinese Institute of Food Science & Technology / Zhongguo Shipin Xuebao is the property of Journal of Chinese Institute of Food Science & Technology Periodical Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Stroke is one of the leading causes of death and disability worldwide, but its mechanism remains unclear. Forkhead box protein O3a （FoxO3a） is an important transcription factor protein involved in a variety of cellular processes. Recent studies have shown that the transcriptional modification of FoxO3a regulates oxidative stress, autophagy, apoptosis, inflammatory reaction and energy metabolism of cells and is involved in the initiation and progression of stroke. Clarifying the signal transduction and action mechanism of FoxO3a in stroke can bring further enlightenment for the identification of targeted drugs. In this paper, we will review the research progress of FoxO3a in the effects and targeted intervention on ischemic stroke. [ABSTRACT FROM AUTHOR]

Objective To evaluate the effect of nitric oxide (NO) on the proliferative function of airway club progenitor cells and underlying metabolic mechanisms. Methods The mouse airway progenitor club cells were sorted using flow sorting technique, then treated with 25 µmol/L DEA NONOate (diethylaminononanoate) for transcriptomic sequencing analysis. Mouse club cells were cultured using organoid culture technique. The cells were cultured in normal medium, 40 nmol/L simvastain (Hmgcr inhibitor), 0.2 µmol/L DON (Gmps inhibitor) or 1 mmol/L AOA (Gpt2 inhibitor) respectively. Microscopic photographs were taken with an inverted microscope on the day 8 of culture to observe the growth of club cellderived organoids and to measure the organoid diameter and formation efficiency. Results DEA NONOate treatment of club cells resulted in significant changes in transcriptome expression (2 894 up-regulated genes and 3 270 down-regulated genes, fold ≥ 1.2), with significant decrease in expression levels of metabolism-related genes Hmgcr, Gmps and Gpt2 (P＜ 0.01). Compared with the control group, the organoid diameter was significantly reduced (P＜0.01), but the organoid forming efficiency was unchanged in the simvastain-treated group. Both organoid diameter and forming efficiency were significantly reduced in the DON-treated group (P＜0.01) and the AOA-treated group (P＜0.01). Conclusion NO inhibits the proliferative function of mouse airway club progenitor cells probably through its negative regulation of three metabolismrelated pathways, Hmgcr, Gmps and Gpt2. [ABSTRACT FROM AUTHOR]

Copyright of Shipin Kexue/ Food Science is the property of Food Science Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Chinese Institute of Food Science & Technology / Zhongguo Shipin Xuebao is the property of Journal of Chinese Institute of Food Science & Technology Periodical Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Northwest A & F University - Natural Science Edition is the property of Editorial Department of Journal of Northwest A&F University (Natural Science Edition) and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Environmental Science & Technology (10036504) is the property of Editorial Board of Environmental Science & Technology and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

BACKGROUND: Increasing studies have shown that autophagy plays an important role in myocardial ischemia-reperfusion injury and moderate autophagy help maintain the normal and metabolic function of the heart. Non-coding RNAs, including long non-coding RNAs, circular RNAs, and microRNAs, can maintain cardiomyocyte homeostasis and protect cardiomyocytes by regulating autophagy. OBJECTIVE: To review the role and molecular mechanism of non-coding RNAs in regulating autophagy in myocardial ischemia-reperfusion injury, in order to lay a foundation for the treatment of myocardial ischemia-reperfusion injury and other related cardiovascular diseases. METHODS: PubMed, Web of Science, WanFang and CNKI databases were searched for relevant literature published from January 2011 to January 2021 using the keywords of “noncoding RNAs, non-coding RNAs, long non-coding RNA, circRNA, microRNA, miRNA, autophagy, myocardial ischemia-reperfusion injury” in full-text contents. RESULTS AND CONCLUSION: Autophagy plays a dual role in the pathology of myocardial ischemia-reperfusion injury. Under physiological conditions, moderate autophagy can maintain the balance of cell metabolism and promote the survival of cardiomyocytes by degrading and recovering damaged organelles and proteins, but excessive autophagy will aggravate the damage of cardiomyocytes. Non-coding RNA regulating autophagy may become a new target for the development of diagnosis and therapeutic drugs. In addition, it is reasonable to think that the study on the mechanism of autophagy and non-coding RNAs can provide a new strategy for the prevention and treatment of myocardial ischemia-reperfusion injury. [ABSTRACT FROM AUTHOR]

BACKGROUND: As a ligand of Na+ /K+ -ATPase, ouabain can be combined with it to regulate cell proliferation and metabolism. Studying the effect of ouabain on the osteogenic differentiation of bone marrow mesenchymal stem cells can provide ideas for the treatment of bone defects and bone diseases. OBJECTIVE: To explore the effects of different concentrations of Na+ /K+ -ATPase ligand ouabain on the osteogenic differentiation of human bone marrow mesenchymal stem cells.METHODS: Human bone marrow mesenchymal stem cells were isolated from fresh bone marrow samples from patients that experienced hip replacement, using the whole bone marrow direct adherence method, as experimental cells for inducing osteogenic differentiation. Before osteoinduction, human bone marrow mesenchymal stem cells were treated in different concentrations of ouabain (10, 100, and 1 000 nmol/L) for 24 hours. The untreated human bone marrow mesenchymal stem cells were used as the control group to induce directly. At 21 days after osteoinduction, alizarin red staining was performed. The proportion area was measured using Image Pro Plus software to compare the differences in the amount of calcified nodules produced in each group. RESULTS AND CONCLUSION: Compared with the control group, as human bone marrow mesenchymal stem cells in vitro treated with ouabain in low concentration (10 nmol/L), the number of calcified nodules increased after alizarin red staining and the staining areas were higher than that in the control group (P < 0.05). The number of calcified nodules observed after treatment in the high concentration group (100, 1 000 nmol/L) was reduced, and the measured stained area was smaller than that in the control group (P < 0.05). The higher the concentration, the fewer the calcifiednodules were. It is concluded that the fresh bone marrow form hip arthroplasty can be used as a test material for isolating human bone marrow mesenchymal stem cells. Low concentrations of ouabain promote differentiation of human bone marrow mesenchymal stem cells into osteoblasts, while a high concentration of ouabain showed an inhibitory effect. [ABSTRACT FROM AUTHOR]

Copyright of Food Research & Development is the property of Food Research & Development Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Shipin Kexue/ Food Science is the property of Food Science Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of East China University of Science & Technology is the property of Journal of East China University of Science & Technology Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Practical Oncology Journal is the property of Journal of Practical Oncology Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Different varieties have different resistances. In order to further explore the resistance differences in different varieties of pitaya and to provide a reference for further study on breeding of pitaya resistance, we used Illumina HiSeq 2000 sequence platform to sequence the transcriptomes of ‘Putongbairou'(BR)and ‘Ecuador Yellow'(EY). Functional classification and enrichment analysis of differentially expressed genes(DEGs)were performed by reference to GO Ontology, KEGG and others databases. The results were as follows:(1)There were 14 248 DEGs between BR and EY, of which 5 446 genes were up-regulated and 8 802 genes were down-regulated.(2)GO functional analysis showed that these DEGs were mainly involved in enzyme catalytic activity, cell components, metabolic processes, etc. Among them, there were 349 differential genes involved in oxidoreductase activity.(3)KEGG pathway analysis showed that most of the DEGs were enriched in metabolism, biosynthesis, etc., and 12 key genes such as CYP86 and CER1 involving in cutin, suberine and wax biosynthesis. We found that the expressions of DEGs involved in oxidoreductase activity were higher in BR than those in EY, which significantly enriched, indicating that may be significant differences in growth and cell metabolism between BR and EY. DEGs involved in the cutin, suberine and wax biosynthesis were up-regulated in BR, and such genes had higher expressions in BR, and were significantly enriched, which suggest that BR may be superior drought and disease resistance than EY. [ABSTRACT FROM AUTHOR]

Copyright of Asian Journals of Ecotoxicology is the property of Gai Kan Bian Wei Hui and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

BACKGROUND: Although the tension band technique can stimulate skin regeneration to repair skin defects, it has been successfully applied in clinical practice and has achieved satisfactory results, but the most suitable tension intensity for skin regeneration is still inconclusive. OBJECTIVE: To discuss the effect of different tension intensities on skin regeneration in rat models of skin defect. METHODS: Male SD rats aged 3 months old were selected as experimental animals. The back skin of SD rats was fixed by the 3D printed oval skin fixing device to establish rat models of skin defect wound on the back, and the 3D printed tension band device was fixed on the edge of the skin. The silicone loop was installed on the principle of tying shoelaces, and different tension parameters (0, 0.2, 1 N) of the silicone loop were adjusted by the tension detector. The changes in the area of the skin defect were observed immediately, 3, and 7 days after model establishment. At 7 days after the surgical procedure, histological sections of the skin at the edge of the wound were taken for immunohistochemical staining of CD31 and vascular endothelial growth factor to observe the effect of different tension stimulation on skin regeneration. RESULTS AND CONCLUSION: (1) Appropriate tension stimulation could effectively stimulate skin proliferation and healing; skin defect wounds without tension stimulation could expand with the contracture of the skin edge and increase the area of the skin defect, which was not conducive to the treatment of skin defects. (2) Tension stimulation was not the bigger the better. Simultaneously, the wound shrinkage speed of 0.2 N tension group was faster than that of 1 N tension group. In 1 N tension group, the skin around the wound was sclerotic and the elasticity was decreased. It was considered that the larger tension led to skin ischemia. (3) The number of microvessels in the 0.2 N tension group was significantly increased, and the expression of vascular endothelial growth factor was significantly higher than that of the 0 N tension and 1 N tension groups, indicating that tension stimulation could promote the formation of microvessels and increase the expression of vascular endothelial growth factor, but high tension stimulation (1 N in this study) is not conducive to the formation of skin capillaries around the skin defect and is not conducive to wound healing. (4) It is concluded that appropriate tension can cause extensive reconstruction of extracellular matrix in local skin. By inducing angiogenesis, it can improve the supply of nutrients for local cell metabolism and promote the reorganization of cytoskeleton. This process has strict requirements on the size of tension. [ABSTRACT FROM AUTHOR]

[ Objective ] The present paper aimied to study the effects of cadmium stress on the physiological response of hydroponic seedlings of Cichorium endivia L. and the changes of leaf ultrastructure, so as to provide reference for the study of heavy metal stress in the cultivation process of C. endivia L. . [ Method ] Hydroponics method was used in plant factory, adding cadmium chloride concentration of O (CK), 0. 5 (low concentration), 1, 5, 10 mg/L ( high concentration) for culture. Total cadmium content, chlorophyll and carotenoid content, stress physiological indexes and ultrastructure of C. endivia L. were determined at 3 days of treatment. The growth indexes of C. endivia L. were measured at day 30. [ Results ] High concentrations of Cd significantly decreased fresh weight and plant height of C. endivia L seed lings, and increased seedling mortality. With the increase of cadmium ion concentration, the contents of malondialdehyde and free proline both showed a trend of first increase and then decrease, but they were always higher than that of the control. SOD enzyme activity decreased with the increase of total cadmium content in C. endivia L. seedlings. The activity of POD enzyme was firstly decreased and then increased, and reached the highest when cadmium chloride was added at the concentration of 10 mg/L. The structure and function of chloroplasts were destroyed after cadmium chloride was added. [ Conclusion ] C. endivia L. seedlings had certain tolerance to Cd through a series of self-regu lation, but high concentration of Cd significantly affects the physiological metabolism of C. endivia L. seedlings, causing dysregulation and metabolic abnormalities, and destroying the structure and function of chloroplasts. In the future, we could funher study the physiological re sponse of plants to heavy metal stress from the perspective of cell metabolism pathway. [ABSTRACT FROM AUTHOR]

[Objectives] This study aimed to verify the correlation between the c.-751 A>C in ACSF2(encoded by acyl-CoA synthetase family member 2) promoter and laying performance of Yangzhou goose, and analyze the effect of the SNP on ACSF2 expression. [Methods] We used allele specific PCR(AS-PCR) to analyze the genotype of SNP c.-751 A>C in a 343 Yangzhou geese population, and performed the correlation analysis between genotype and laying performance of Yangzhou goose. Quantitative real-time PCR(qPCR) and luciferase reporter gene vector were used to detect the difference between AA and CC promoter activity. ACSF2 over-expression was performed to analyze its role in the energy metabolism of granulosa cells and laying performance. [Results] Genotyping and association analysis results showed that the egg numbers of geese with AA genotype were significantly higher than those CC ones. Quantitative real-time PCR analysis indicated that AA individuals showed lower ACSF2 expression level in ovary tissues. Moreover, the overexpression experiment indicated that ACSF2 was involved in the energy metabolism of granulosa cells. [Conclusions] We identified a functional mutation in the promoter region of ACSF2 affecting gene expression in Yangzhou goose, and indicated the role of ACSF2 in laying performance by regulating energy metabolism of granulosa cells. Our results provide insight into the improvement of goose laying performance by ACSF2 genetic variation selection. [ABSTRACT FROM AUTHOR]

Copyright of China Brewing is the property of China Brewing Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

BACKGROUND: The key pathological characteristics of osteoarthritis are manifested in the degeneration of the cartilage caused by inflammation, and chondrocytes are the only cells in cartilage tissues. Studies have shown that Chemerin can stimulate the migration of leukocytes to the inflammation site and increase the inflammation signal of chondrocytes, suggesting that Chemerin can play a role in arthritis. Our previous research indicated that the serum Chemerin level in patients with osteoarthritis was significantly increased, and the Chemerin level in the synovial fluid was related to the severity of osteoarthritis based on the Kellgren-Lawrence classification. Chemerin may be used as an inflammatory factor in osteoarthritis. OBJECTIVE: To investigate the effect of Chemerin on the proliferation and metabolism of chondrocytes. METHODS: The chondrocytes from neonatal mice were isolated by collagenase type II digestion, and then cultured. Cell growth curves were established and the range of concentrations of Chemerin that exhibited toxicity to normal chondrocytes was screened using an MTT assay. Subsequently, 10 μg/L interleukin-1β was used to stimulate the chondrocytes in order to establish an in vitro model of osteoarthritis induction. After the chondrocytes had been cultured in the presence of the drug for 2 days, cell morphology, proliferation and metabolism were evaluated by hematoxylin-eosin staining and diacetate fluorescein/propidium iodide staining. In addition, the expression of inducible nitric oxide polymerase was analyzed by measuring the secretion of nitric oxide. Furthermore, qRT-PCR was used to quantify mRNA expression of proteoglycan, type II collagen α1, matrix metalloprotease-13 and nitric oxide synthase 2. RESULTS AND CONCLUSION: The chondrocytes cultured in vitro exhibited healthy activity and morphology. Furthermore, chemerin (50 μg/L) and interleukin-1β (10 μg/L) were able to reduce the synthesis of extracellular matrix, enhance the secretion of nitric oxide and increase chondrocyte apoptosis. More importantly, the qRT-PCR results indicated that Chemerin and interleukin-1β caused similar effects, by which the expression of cartilage-specific genes was downregulated and catabolism-related genes upregulated. As a pro-inflammatory factor, Chemerin can increase the generation of nitric oxide in chondrocytes, regulate cell metabolism, stimulate cell apoptosis and act synergistically with interleukin-1β. [ABSTRACT FROM AUTHOR]

The main purpose of organ preservation in organ transplantation is to maintain tissue and cell activity of donor organs so as to gain time for allocation and transportation of the organ, preparation of the recipient and organization of staff and facilities. The main principles of organ preservation can be divided into normothermic mechanical perfusion and cryopreservation. Cryopreservation is the favourite organ preservation method in clinical practice currently. However, the metabolic activity still exists in donor organs preserved with current cryopreservation technique, which makes the long-term preservation of organs extremely difficult. The supercooling organ preservation is a new type of cryopreservation technology, which greatly prolongs the preservation time of organs. It is expected to become an important organ preservation technique in the future, and it will provide technical support for the establishment of "organ bank". [ABSTRACT FROM AUTHOR]

Copyright of Journal of Modern Laboratory Medicine is the property of Journal of Modern Laboratory Medicine Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Mycosystema is the property of Mycosystema Editorial Board and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The prediction of the three-dimensional spatial structure of chromosomes by chromosome interaction frequency data (Hi-e) has been a hot topic in epigenetic studies in recent years. It has been shown that the three-dimensional spatial structure of chromosome plays an important role in gene expression and regulation. Three-dimensional reconstruction is the basic way to study the process of cell metabolism. According to the statistical characteristics of yeast Hi-e data on different chromosomes, the mathematical model of the distribution of the cross-frequency data of each chromosome was fitted, and then the gradient ascending iterative algorithm was used to predict and reconstruct its three-dimensional structure. The evaluation index of the model was established. Experimental results showed that the model has high repeatability and prediction accuracy. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Food Safety & Quality is the property of Journal of Food Safety & Quality Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Ｗｅ ｓｔｕｄｉｅｄ ｔｈｅ ｄｅｈｙｄｒａｔｉｏｎ ｓｅｎｓｉｔｉｖｉｔｙ ａｎｄ ｓｔｏｒａｇｅ ｃｈａｒａｃｔｅｒｉｓｔｉｃｓ ｏｆ Ｇ. ｐａｕｃｉｎｅｒｖｉｓ ｓｅｅｄｓ ｂｙ ｍｅａｓｕｒｉｎｇ ｔｈｅ ｇｅｒｍｉｎａｔｉｏｎ ｏｆ ｓｅｅｄｓ ｗｉｔｈ ｄｉｆｆｅｒｅｎｔ ｄｅｈｙｄｒａｔｉｏｎ ｅｘｔｅｎｔｓ ａｎｄ ｔｈｅ ｗａｔｅｒ ａｂｓｏｒｐｔｉｏｎ ａｆｔｅｒ ｒｅｈｙｄｒａｔｉｏｎ, ｔｈｅ ｃｈａｎｇｅ ｏｆ ｐｈｙｓｉｏｌｏｇｉｃａｌ ｉｎｄｉｃｅｓ ｏｆ ｒｅｓｉｓｔａｎｃｅ ｉｎ ｔｈｅ ｐｒｏｃｅｓｓ ｏｆ ｄｅｈｙｄｒａｔｉｏｎ ａｓ ｗｅｌｌ ａｓ ｔｈｅ ｓｅｅｄ ｇｅｒｍｉｎａｔｉｏｎ ｕｎｄｅｒ ｄｉｆｆｅｒｅｎｔ ｓｔｏｒａｇｅ ｍｅｔｈｏｄｓ. Ｔｈｅ ｒｅｓｕｌｔｓ ｗｅｒｅ ａｓ ｆｏｌｌｏｗｓ: (１) Ｔｈｅ ｉｎｉｔｉａｌ ｍｏｉｓｔｕｒｅ ｃｏｎｔｅｎｔ ｏｆ Ｇ. ｐａｕｃｉｎｅｒｖｉｓ ｓｅｅｄｓ ｗａｓ ４５.２９％. Ｔｈｅ ｄｅｈｙｄｒａｔｉｏｎ ｒａｔｅ ｗａｓ ｕｐ ｔｏ ４５％ ｗｈｅｎ ｐｌａｃｅｄ ａｆｔｅｒ ３５ ｄ ｉｎ ｔｈｅ ｉｎｄｏｏｒ ｖｅｎｔｉｌａｔｅｄ ｐｌａｃｅ. (２) Ｗｈｅｎ ｔｈｅ ｄｅｈｙｄｒａｔｉｏｎ ｒａｔｅ ｗａｓ ｌｅｓｓ ｔｈａｎ １８％, ｇｅｒｍｉｎａｔｉｏｎ ｐｅｒｃｅｎｔａｇｅ(ＧＰ) ａｎｄ ｔｈｅ ｗａｔｅｒ ａｂｓｏｒｐｔｉｏｎ ｒａｔｅ ａｆｔｅｒ ｒｅｗａｔｅｒｉｎｇ ｗｅｒｅ ｎｏｔ ｓｉｇｎｉｆｉｃａｎｔｌｙ ｄｉｆｆｅｒｅｎｔ ｆｒｏｍ ｔｈｏｓｅ ｏｆ ｆｒｅｓｈ ｓｅｅｄｓ. Ｈｏｗｅｖｅｒ, ｗｈｅｎ ｔｈｅ ｄｅｈｙｄｒａｔｉｏｎ ｒａｔｅ ｅｘｃｅｅｄｅｄ １８％, ＧＰ ａｎｄ ｔｈｅ ｗａｔｅｒ ａｂｓｏｒｐｔｉｏｎ ｒａｔｅ ａｆｔｅｒ ｒｅｗａｔｅｒｉｎｇ ｗｅｒｅ ｓｉｇｎｉｆｉｃａｎｔｌｙ ｄｅｃｒｅａｓｅｄ, ａｎｄ ＧＰ ｗａｓ ０ ａｔ ｄｅｈｙｄｒａｔｉｏｎ ｒａｔｅ ４２％. Ｔｈｅ ｃｒｉｔｉｃａｌ ｍｏｉｓｔｕｒｅ ｃｏｎｔｅｎｔ ｏｆ ｓｅｅｄｓ ｗａｓ ２７.２９％, ａｎｄ ｔｈｅ ｌｅｔｈａｌ ｍｏｉｓｔｕｒｅ ｃｏｎｔｅｎｔ ｏｆ ５０％ ｗａｓ １２.７２％. (３) Ｔｈｅ ｒｅｌａｔｉｖｅ ｃｏｎｄｕｃｔｉｖｉｔｙ, ｔｈｅ ｃｏｎｔｅｎｔｓ ｏｆ ｓｏｌｕｂｌｅ ｓｕｇａｒ ａｎｄ ｐｒｏｌｉｎｅ ｗｅｒｅ ｉｎｃｒｅａｓｅｄ ｇｒａｄｕａｌｌｙ ｗｉｔｈ ｔｈｅ ｄｅｅｐｅｎｉｎｇ ｏｆ ｓｅｅｄ ｄｅｈｙｄｒａｔｉｏｎ. Ｔｈｅ ｃｏｎｔｅｎｔ ｏｆ ｍａｌｏｎｄｉａｌｄｅｈｙｄｅ (ＭＤＡ) ｃｈａｎｇｅｄ ｌｉｔｔｌｅ ｗｈｅｎ ｔｈｅ ｄｅｈｙｄｒａｔｉｏｎ ｒａｔｅ ｗａｓ ｌｅｓｓ ｔｈａｎ ２４％, ａｎｄ ｉｎｃｒｅａｓｅｄ ｓｉｇｎｉｆｉｃａｎｔｌｙ ｗｈｅｎ ｅｘｃｅｅｄｉｎｇ ２４％. Ｂｏｔｈ ａｃｔｉｖｉｔｉｅｓ ｏｆ ｓｕｐｅｒｏｘｉｄｅ ｄｉｓｍｕｔａｓｅ (ＳＯＤ) ａｎｄ ｐｅｒｏｘｉｄａｓｅ (ＰＯＤ) ｓｈｏｗｅｄ ａ ｔｒｅｎｄ ｏｆ ｆｌｕｃｔｕａｔｉｏｎ ａｎｄ ｐｅａｋｅｄ ａｔ ｄｅｈｙｄｒａｔｉｏｎ ｒａｔｅ １８％. (４) Ｓｅｅｄｓ ｗｉｔｈ ｄｅｓｉｃｃａｔｉｏｎ ｓｔｏｒａｇｅ ｆｏｒ ｏｎｅ ｍｏｎｔｈ ａｔ ｒｏｏｍ ｔｅｍｐｅｒａｔｕｒｅ, ａｎｄ ａｌｌ ｔｈｅ ｓｅｅｄｓ ｗｉｔｈ ｓｔｏｒａｇｅ ｉｎ ｄａｍｐ ｓａｎｄ ａｔ －１ ℃ ａｎｄ －２０ ℃ ｆｏｒ ｏｎｅ ｍｏｎｔｈ ｃｏｕｌｄ ｎｏｔ ｇｅｒｍｉｎａｔｅ. ＧＰ ｏｆ ｓｅｅｄｓ ｗｉｔｈ ｗａｔｅｒ ｉｍｍｅｒｓｉｏｎ ｆｏｒ ｏｎｅ ｍｏｎｔｈ ｄｒｏｐｐｅｄ ｓｉｇｎｉｆｉｃａｎｔｌｙ. Ｇｅｒｍｉｎａｔｉｏｎ ｐｒｏｃｅｓｓｅｓ ｏｆ ｓｅｅｄｓ ｗｉｔｈ ｓｔｏｒａｇｅ ｉｎ ｄａｍｐ ｓａｎｄ ｆｏｒ ｏｎｅ ｍｏｎｔｈ, ｔｈｒｅｅ ｍｏｎｔｈｓ ｏｒ ｓｉｘ ｍｏｎｔｈｓ ａｔ ４ ℃ ｗｅｒｅ ｄｅｌａｙｅｄ, ｂｕｔ ｔｈｅｒｅ ｗａｓ ｎｏ ｓｉｇｎｉｆｉｃａｎｔ ｅｆｆｅｃｔ ｏｎ ＧＰ. Ｉｔ ｉｎｄｉｃａｔｅｓ ｔｈａｔ ｗｈｅｎ ｔｈｅ ｄｅｈｙｄｒａｔｉｏｎ ｒａｔｅ ｏｆ Ｇ. ｐａｕｃｉｎｅｒｖｉｓ ｉｓ ｌｅｓｓ ｔｈａｎ １８％, ｓｅｅｄｓ ｃａｎ ｒｅｇｕｌａｔｅ ｒｅｓｉｓｔａｎｃｅ ｔｏ ｍａｉｎｔａｉｎ ｎｏｒｍａｌ ｍｅｔａｂｏｌｉｓｍ ｏｆ ｃｅｌｌｓ. Ｔｈｅ ｓｅｅｄｓ ｃａｎ ｅｎｄｕｒｅ ａ ｃｅｒｔａｉｎ ｄｅｇｒｅｅ ｏｆ ｄｅｈｙｄｒａｔｉｏｎ ａｎｄ ｌｏｗ ｔｅｍｐｅｒａｔｕｒｅ. Ｗｈｅｎ ｔｈｅ ｄｅｈｙｄｒａｔｉｏｎ ｒａｔｅ ｅｘｃｅｅｄｓ １８％, ｔｈｅ ｍｅｔａｂｏｌｉｓｍ ｏｆ ｓｅｅｄｓ ｉｓ ｕｎｂａｌａｎｃｅｄ, ａｎｄ ｔｈｅｎ ｄｅｔｅｒｉｏｒａｔｅｄ ｕｎｔｉｌ ｄｅａｔｈ, ｗｈｉｃｈ ｂｅｌｏｎｇ ｔｏ ｍｉｎｉｍａｌｌｙ ｒｅｃａｌｃｉｔｒａｎｔ ｓｅｅｄｓ. Ｉｔ ａｌｓｏ ｉｎｄｉｃａｔｅｓ ｔｈａｔ ｓｔｏｒａｇｅ ｉｎ ｄａｍｐ ｓａｎｄ ａｔ ４ ℃ (ｍｏｉｓｔｕｒｅ ｃｏｎｔｅｎｔ ７.５％) ｉｓ ａ ｇｏｏｄ ｍｅｔｈｏｄ ｆｏｒ ｓｈｏｒｔ￣ｔｅｒｍ ｓｔｏｒａｇｅ ｏｆ Ｇ. ｐａｕｃｉｎｅｒｖｉｓ ｓｅｅｄｓ. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Agricultural Science & Technology (1008-0864) is the property of Journal of Agricultural Science & Technology and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective To explore the relationship of phosphatase and tensin homolog (PTEN) with cell proliferation in cervical cancer cells so as to further analyze the role of PTEN and its underlying mechanisms in the pathogenesis and progression of cervical cancer cells. Methods The expression of PTEN was detected in different cervical cancer cell lines by Western blotting. Then the overexpression vector of PTEN was constructed and transfected into cervical cancer cells with Lipofectemine 2000. The proliferative index was estimated by cell counting and MTT. The contents of glucose, glutamine and lactic acid were detected by the BioProfile FLEX analyzer to evaluate the effect of PTEN on the cell metabolism. The proteins related to cell metabolism were measured by Western blotting. Results The expression of PTEN was down-regulated in cervical cancer cell lines compared to that of normal cervical epithelium cells. The overexpression PTEN vector was transfected into HeLa and C33A cells, resulting in the up-regulation of PTEN. Enforced expression of PTEN inhibited the proliferation of cervical cancer cells, which was confirmed by cell counting and MTT (P<0.05). We also found that glucose and glutamine contents in the medium with PTEN-overexpressing cells were increased, but lactic acid content was decreased. Moreover, PTEN suppressed the expression of pAKT, PFKFB3, PKM2 and GLS in these cells. Conclusion PTEN regulates the proliferation of cervical cancer cells by AKT mediated cell metabolism, providing new insights into novel molecular target for the diagnosis and therapy of cervical cancer. [ABSTRACT FROM AUTHOR]

In this study, gas chromatography coupled with mass spectrometry(GC-MS) was used to analyze the changes of 12 kinds of cancer cells treated by curcumin. The related differential metabolites were screened and the metabolic pathways were analyzed to explore the anti-tumor mechanism of curcumin. Methyl thiazol tetrazolium(MTT) assay was used to detect the 50% inhibiting concentration(IC&#95;(50)) of curcumin on 12 human tumor cells. After treatment with curcumin for 48 h, the cells were collected and analyzed by GC-MS, followed by pathway analysis and multivariate data analysis including principal component analysis(PCA), orthogonal partial least squares discriminant analysis(OPLS-DA) and One-way analysis of variance(ANOVA),etc. Overall, 34 metabolites showed significant concentration changes after intervention for 48 h, mainly involving multiple metabolic pathways, including lysine degradation, glycine, serine and threonine metabolism, arginine and proline metabolism, cysteine and methionine metabolism, aminoacyl-tRNA biosynthesis, primary bile acid biosynthesis, lysine biosynthesis. In this study, the anti-tumor mechanisms of curcumin interfering with energy metabolism, amino acid metabolism, microtubule system, protein synthesis and oxidative stress response of tumor cells were analyzed from the perspective of metabolism, providing a new reference for further tumor pharmacology study.

As a member of the Sirtuins family in mammals, SIRT7 locates in nucleus and is a highly specific H3K18Ac (acetylated lysine 18 of histone H3) deacetylase. Recent studies showed that SIRT7 could participate in the ribosomal RNA transcription, cell metabolism, cell stress and DNA damage repair through various signaling pathways. In addition, SIRT7 is also closely related with aging, heart disease and fatty liver. In particular, SIRT7 plays important roles in the regulation of initiation and development of various tumors, such as liver cancer, gastric cancer, breast cancer, bladder cancer, colorectal cancer, and head/neck squamous cell carcinoma. This review describes the cellular and molecular functions of SIRT7, and systematically summarizes recent progress of SIRT7 in human disease.