Catalogue Search | MBRL
Are you sure you want to remove the book from the shelf?
{{itemTitle}}
9,459
result(s) for
"Lin, Zhen"
Sort by:
Knockdown of otubain 2 inhibits liver cancer cell growth by suppressing NF‐κB signaling
The deubiquitinase otubain 2 (OTUB2) has been reported to play significant roles in the tumorigenesis of several cancers, but the role of OTUB2 in liver cancer is not investigated yet. In the present study, OTUB2 was found significantly upregulated in liver cancer tumor tissues and cell lines, and elevated OTUB2 indicated as a negative index for the overall survival of liver cancer patients. At the cellular level, knockdown of OTUB2 markedly inhibited liver cancer cell growth. Our further investigations revealed that knockdown of OTUB2 significantly suppressed NF‐κB‐driving luciferase activity, and markedly inhibited the phosphorylation of NF‐κB p65 in liver cancer cells, which indicated that OTUB2 mediated liver cancer cell growth by regulating NF‐κB signaling. Additionally, we found that liver cancer cell lines harboring higher OTUB2 expression were more sensitive to NF‐κB inhibitors, and overexpression of OTUB2 could significantly reduce the antitumor effects of NF‐κB inhibitors in liver cancer cells. This study indicated that OTUB2 could be a promising target for the treatment of liver cancer in the future.
Journal Article
A high-speed search engine pLink 2 with systematic evaluation for proteome-scale identification of cross-linked peptides
We describe pLink 2, a search engine with higher speed and reliability for proteome-scale identification of cross-linked peptides. With a two-stage open search strategy facilitated by fragment indexing, pLink 2 is ~40 times faster than pLink 1 and 3~10 times faster than Kojak. Furthermore, using simulated datasets, synthetic datasets,
15
N metabolically labeled datasets, and entrapment databases, four analysis methods were designed to evaluate the credibility of ten state-of-the-art search engines. This systematic evaluation shows that pLink 2 outperforms these methods in precision and sensitivity, especially at proteome scales. Lastly, re-analysis of four published proteome-scale cross-linking datasets with pLink 2 required only a fraction of the time used by pLink 1, with up to 27% more cross-linked residue pairs identified. pLink 2 is therefore an efficient and reliable tool for cross-linking mass spectrometry analysis, and the systematic evaluation methods described here will be useful for future software development.
The identification of cross-linked peptides at a proteome scale for interactome analyses represents a complex challenge. Here the authors report an efficient and reliable search engine pLink 2 for proteome-scale cross-linking mass spectrometry analyses, and demonstrate how to systematically evaluate the credibility of search engines.
Journal Article
Aberrant lipid metabolism in hepatocellular carcinoma cells as well as immune microenvironment: A review
Hepatocellular carcinoma (HCC) is a primary malignancy of the liver with a high worldwide prevalence and poor prognosis. Researches are urgently needed on its molecular pathogenesis and biological characteristics. Metabolic reprogramming for adaptation to the tumour microenvironment (TME) has been recognized as a hallmark of cancer. Dysregulation of lipid metabolism especially fatty acid (FA) metabolism, which involved in the alternations of the expression and activity of lipid‐metabolizing enzymes, is a hotspot in recent study, and it may be involved in HCC development and progression. Meanwhile, immune cells are also known as key players in the HCC microenvironment and show complicated crosstalk with cancer cells. Emerging evidence has shown that the functions of immune cells in TME are closely related to abnormal lipid metabolism. In this review, we summarize the recent findings of lipid metabolic reprogramming in TME and relate these findings to HCC progression. Our understanding of dysregulated lipid metabolism and associated signalling pathways may suggest a novel strategy to treat HCC by reprogramming cell lipid metabolism or modulating TME.
Journal Article
Interrupted time series analysis using the ARIMA model of the impact of COVID-19 on the incidence rate of notifiable communicable diseases in China
Background
The coronavirus disease 2019 (COVID-19) pandemic in China is ongoing. Some studies have shown that the incidence of respiratory and intestinal infectious diseases in 2020 decreased significantly compared with previous years. Interrupted time series (ITS) is a time series analysis method that evaluates the impact of intervention measures on outcomes and can control the original regression trend of outcomes before and after the intervention. This study aimed to analyse the impact of COVID-19 on the incidence rate of notifiable communicable diseases using ITS in China.
Methods
National data on the incidence rate of communicable diseases in 2009–2021 were obtained from the National Health Commission website. Interrupted time series analysis using autoregressive integrated moving average (ARIMA) models was used to analyse the changes in the incidence rate of infectious diseases before and after the COVID-19 epidemic.
Results
There was a significant short-term decline in the incidence rates of respiratory infectious diseases and enteric infectious diseases (step values of -29.828 and − 8.237, respectively), which remained at a low level for a long time after the decline. There was a short-term decline in the incidence rates of blood-borne and sexually transmitted infectious diseases (step = -3.638), which tended to recover to previous levels in the long term (ramp = 0.172). There was no significant change in the incidence rate of natural focus diseases or arboviral diseases before and after the epidemic.
Conclusion
The COVID-19 epidemic had strong short-term and long-term effects on respiratory and intestinal infectious diseases and short-term control effects on blood-borne and sexually transmitted infectious diseases. Our methods for the prevention and control of COVID-19 can be used for the prevention and control of other notifiable communicable diseases, especially respiratory and intestinal infectious diseases.
Journal Article
From inflammation to bone formation: the intricate role of neutrophils in skeletal muscle injury and traumatic heterotopic ossification
Neutrophils are emerging as an important player in skeletal muscle injury and repair. Neutrophils accumulate in injured tissue, thus releasing inflammatory factors, proteases and neutrophil extracellular traps (NETs) to clear muscle debris and pathogens when skeletal muscle is damaged. During the process of muscle repair, neutrophils can promote self-renewal and angiogenesis in satellite cells. When neutrophils are abnormally overactivated, neutrophils cause collagen deposition, functional impairment of satellite cells, and damage to the skeletal muscle vascular endothelium. Heterotopic ossification (HO) refers to abnormal bone formation in soft tissue. Skeletal muscle injury is one of the main causes of traumatic HO (tHO). Neutrophils play a pivotal role in activating BMPs and TGF-β signals, thus promoting the differentiation of mesenchymal stem cells and progenitor cells into osteoblasts or osteoclasts to facilitate HO. Furthermore, NETs are specifically localized at the site of HO, thereby accelerating the formation of HO. Additionally, the overactivation of neutrophils contributes to the disruption of immune homeostasis to trigger HO. An understanding of the diverse roles of neutrophils will not only provide more information on the pathogenesis of skeletal muscle injury for repair and HO but also provides a foundation for the development of more efficacious treatment modalities for HO.
Neutrophils in Muscle Injury: Implications for Heterotopic Ossification
Skeletal muscle, the body’s most common tissue, often gets injured and lacks highly effective treatments. This review investigates the complex relationship between skeletal muscle and neutrophils during injury and healing. Researchers study how neutrophils can both worsen muscle damage and assist in tissue repair. It looks at how neutrophil activity affects muscle repair, explaining the processes of inflammation, tissue regeneration, and the factors causing heterotopic ossification. It also emphasizes the significance of controlling neutrophil activity for effective muscle healing and avoiding complications. Key findings show that neutrophils are crucial in both harming and repairing skeletal muscle. Overactive neutrophils can cause extended inflammation, hindering the healing process, while controlled activity aids tissue regeneration. The researchers suggest that focusing on neutrophil activity could be a promising method for treating muscle injuries and preventing heterotopic ossification.
This summary was initially drafted using artificial intelligence, then revised and fact-checked by the author.
Journal Article
Assessment of Land-Use and Land-Cover Change in Guangxi, China
It is increasingly acknowledged that land-use and land-cover change has become a key subject that urgently needs to be addressed in the study of global environmental change. In the present study, supported by the long-time-series of land-use and land-cover data from 1990, 2000, and 2017, we used the land-use transition matrix, Markov chain model and Moran’s I to derive detailed information of the spatial patterns and temporal variation of the land-use and land-cover change; additionally, we highlight the deforestation/afforestation conversion process during the period of 1990–2017. The results show that a total of 4708 km
2
(i.e., 2.0% of the total area) changed in Guangxi from 1990 to 2017, while 418 km
2
of woodland has been lost in this region. The woodland lost (deforestation) and woodland gained (afforestation) were collocated with intensive forest practices in the past 27 years. The conversions from woodland to cropland and from woodland to grassland were the dominant processes of deforestation and afforestation, respectively. Steep slope cropland was one of the major conversion patterns of afforestation after 2000. This result is mainly explained by the implementation of the “Grain for Green Program” policy and the large-scale development of eucalyptus plantations. Further efforts should be made to control deforestation in this area. These findings can also be used as a reference in the formulation and implementation of sustainable woodland management policies.
Journal Article
SLC25A46 is required for mitochondrial lipid homeostasis and cristae maintenance and is responsible for Leigh syndrome
Mitochondria form a dynamic network that responds to physiological signals and metabolic stresses by altering the balance between fusion and fission. Mitochondrial fusion is orchestrated by conserved GTPases MFN1/2 and OPA1, a process coordinated in yeast by Ugo1, a mitochondrial metabolite carrier family protein. We uncovered a homozygous missense mutation in
SLC25A46
, the mammalian orthologue of
Ugo1
, in a subject with Leigh syndrome. SLC25A46 is an integral outer membrane protein that interacts with MFN2, OPA1, and the mitochondrial contact site and cristae organizing system (MICOS) complex. The subject mutation destabilizes the protein, leading to mitochondrial hyperfusion, alterations in endoplasmic reticulum (ER) morphology, impaired cellular respiration, and premature cellular senescence. The MICOS complex is disrupted in subject fibroblasts, resulting in strikingly abnormal mitochondrial architecture, with markedly shortened cristae. SLC25A46 also interacts with the ER membrane protein complex EMC, and phospholipid composition is altered in subject mitochondria. These results show that SLC25A46 plays a role in a mitochondrial/ER pathway that facilitates lipid transfer, and link altered mitochondrial dynamics to early‐onset neurodegenerative disease and cell fate decisions.
Synopsis
Whole‐exome sequencing in a Leigh syndrome patient identified mutations in SLC25A46, a degenerate member of the mitochondrial metabolite transport family, linking altered mitochondrial dynamics to early‐onset neurodegenerative disease.
Loss of SLC25A46 results in mitochondrial hyperfusion and striking changes in mitochondrial architecture.
SLC25A46 is an outer membrane protein that interacts with MFN2, OPA1, the MICOS complex, and the EMC complex in the ER.
Loss of SLC25A46 results in altered ER morphology and marked changes in the phospholipid composition of the mitochondrial membranes.
Loss of SLC25A46 results in premature cellular senescence in dividing cells.
Graphical Abstract
Whole‐exome sequencing in a Leigh syndrome patient identified mutations in SLC25A46, a degenerate member of the mitochondrial metabolite transport family, linking altered mitochondrial dynamics to early‐onset neurodegenerative disease.
Journal Article
Household perceptions of factors that affect food consumption in grassland areas: a case study in the Xilin Gol Grassland, China
Food consumption acts as an intermediary that connects ecosystems with human systems in grassland areas. In this study, we used fuzzy cognitive mapping to quantitatively assess the factors that affect food consumption in the Xilin Gol Grassland, China, from the perspective of local rural households. We found that household perceptions of the factors that affect food consumption differed among parts of the grassland transects in both the number and the strength of these factors. Livestock numbers, household income, regional economic development, consumption habits, age, and infrastructure were the most important factors mentioned by the farmers and herders, but herders were more sensitive to ecological and economic factors, whereas farmers focused more on personal and social factors. The differences in the main factors between study areas revealed the key economic, social, and ecological dimensions. Our results provide a reference for policymakers to develop improved policies to encourage regional sustainable development.
Journal Article
Global, regional and national burden of injuries caused by fire, heat, and hot substances from 1990 to 2021
Burn injuries, which are caused by fire, heat, and hot substances, are considered a chronic condition due to their long-term effects on the health of affected individuals. Moreover, burn injuries constitute a significant public health issue that cannot be overlooked within the global healthcare system.
This study comprehensively analyzed the burden of burn injuries, focusing on variations by Socio-Demographic Index (SDI) levels and Global Burden of Disease (GBD) regions, sex-based disparities, Frontier analysis, and future trend forecasting using the Bayesian Age-Period-Cohort (BAPC) model.
Compared to 1990, the global burden of burn injuries decreased in most regions worldwide in 2021. The majority of regions showed a negative Estimated Annual Percentage Change (EAPC), indicating a continuous decline in Age-Standardized Rate (ASR) annually. And the ASR decreased with the increasing SDI. Moreover, the forecasted trend from 2021 to 2030, indicates a continued decline with a well-fitted projection model.
Despite the observed and projected decline in global ASR of burn, the burden of burn remains a significant concern that should not be underestimated.
Journal Article