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Inflammation is a beneficial and physiological process, but there are a number of inflammatory diseases which have detrimental effects on the body. In addition, the drugs used to treat inflammation have toxic side effects when used over a long period of time. Mesenchymal stem cells (MSCs) are pluripotent stem cells that can be isolated from a variety of tissues and can be differentiate into diverse cell types under appropriate conditions. They also exhibit noteworthy anti-inflammatory properties, providing new options for the treatment of inflammatory diseases. The therapeutic potential of MSCs is currently being investigated for various inflammatory diseases, such as kidney injury, lung injury, osteoarthritis (OA), rheumatoid arthritis (RA), and inflammatory bowel disease (IBD). MSCs can perform multiple functions, including immunomodulation, homing, and differentiation, to enable damaged tissues to form a balanced inflammatory and regenerative microenvironment under severe inflammatory conditions. In addition, accumulated evidence indicates that exosomes from extracellular vesicles of MSCs (MSC-Exos) play an extraordinary role, mainly by transferring their components to recipient cells. In this review, we summarize the mechanism and clinical trials of MSCs and MSC-Exos in various inflammatory diseases in detail, with a view to contributing to the treatment of MSCs and MSC-Exos in inflammatory diseases.

Background The evidence of sarcopenia based on CT-scan as an important prognostic factor for critically ill patients has not seen consistent results. To determine the impact of sarcopenia on mortality in critically ill patients, we performed a systematic review and meta-analysis to quantify the association between sarcopenia and mortality. Methods We searched studies from the literature of PubMed, EMBASE, and Cochrane Library from database inception to June 15, 2020. All observational studies exploring the relationship between sarcopenia based on CT-scan and mortality in critically ill patients were included. The search and data analysis were independently conducted by two investigators. A meta-analysis was performed using STATA Version 14.0 software using a fixed-effects model. Results Fourteen studies with a total of 3,249 participants were included in our meta-analysis. The pooled prevalence of sarcopenia among critically ill patients was 41 % (95 % CI:33-49 %). Critically ill patients with sarcopenia in the intensive care unit have an increased risk of mortality compared to critically ill patients without sarcopenia (OR = 2.28, 95 %CI: 1.83–2.83; P < 0.001; I 2  = 22.1 %). In addition, a subgroup analysis found that sarcopenia was associated with high risk of mortality when defining sarcopenia by total psoas muscle area (TPA, OR = 3.12,95 %CI:1.71–5.70), skeletal muscle index (SMI, OR = 2.16,95 %CI:1.60–2.90), skeletal muscle area (SMA, OR = 2.29, 95 %CI:1.37–3.83), and masseter muscle(OR = 2.08, 95 %CI:1.15–3.77). Furthermore, critically ill patients with sarcopenia have an increased risk of mortality regardless of mortality types such as in-hospital mortality (OR = 1.99, 95 %CI:1.45–2.73), 30-day mortality(OR = 2.08, 95 %CI:1.36–3.19), and 1-year mortality (OR = 3.23, 95 %CI:2.08 -5.00). Conclusions Sarcopenia increases the risk of mortality in critical illness. Identifying the risk factors of sarcopenia should be routine in clinical assessments and offering corresponding interventions may help medical staff achieve good patient outcomes in ICU departments.

The Pellino family is a novel and well-conserved E3 ubiquitin ligase family and consists of Pellino1, Pellino2, and Pellino3. Each family member exhibits a highly conserved structure providing ubiquitin ligase activity without abrogating cell and structure-specific function. In this review, we mainly summarized the crucial roles of the Pellino family in pattern recognition receptor-related signaling pathways: IL-1R signaling, Toll-like signaling, NOD-like signaling, T-cell and B-cell signaling, and cell death-related TNFR signaling. We also summarized the current information of the Pellino family in tumorigenesis, microRNAs, and other phenotypes. Finally, we discussed the outstanding questions of the Pellino family in immunity.

Compared to wide-field telescopes, small-field detection systems have higher spatial resolution, resulting in stronger detection capabilities and higher positioning accuracy. When detecting by small fields in synchronous orbit, both space debris and fixed stars are imaged as point targets, making it difficult to distinguish them. In addition, with the improvement in detection capabilities, the number of stars in the background rapidly increases, which puts higher requirements on recognition algorithms. Therefore, star detection is indispensable for identifying and locating space debris in complex backgrounds. To address these difficulties, this paper proposes a real-time star extraction method based on adaptive filtering and multi-frame projection. We use bad point repair and background suppression algorithms to preprocess star images. Afterwards, we analyze and enhance the target signal-to-noise ratio (SNR). Then, we use multi-frame projection to fuse information. Subsequently, adaptive filtering, adaptive morphology, and adaptive median filtering algorithms are proposed to detect trajectories. Finally, the projection is released to locate the target. Our recognition algorithm has been verified by real star images, and the images were captured using small-field telescopes. The experimental results demonstrate the effectiveness of the algorithm proposed in this paper. We successfully extracted hip-27066 star, which has a magnitude of about 12 and an SNR of about 1.5. Compared with existing methods, our algorithm has advantages in both recognition rate and false-alarm rate, and can be used as a real-time target recognition algorithm for space-based synchronous orbit detection payloads.

Background Despite having been extensively studied, it remains largely unclear why humans bear a particularly high risk of cancer. The antagonistic pleiotropy hypothesis predicts that primate-specific genes (PSGs) tend to promote tumorigenesis, while the molecular atavism hypothesis predicts that PSGs involved in tumors may represent recently derived duplicates of unicellular genes. However, these predictions have not been tested. Results By taking advantage of pan-cancer genomic data, we find the upregulation of PSGs across 13 cancer types, which is facilitated by copy-number gain and promoter hypomethylation. Meta-analyses indicate that upregulated PSGs (uPSGs) tend to promote tumorigenesis and to play cell cycle-related roles. The cell cycle-related uPSGs predominantly represent derived duplicates of unicellular genes. We prioritize 15 uPSGs and perform an in-depth analysis of one unicellular gene-derived duplicate involved in the cell cycle, DDX11 . Genome-wide screening data and knockdown experiments demonstrate that DDX11 is broadly essential across cancer cell lines. Importantly, non-neutral amino acid substitution patterns and increased expression indicate that DDX11 has been under positive selection. Finally, we find that cell cycle-related uPSGs are also preferentially upregulated in the highly proliferative embryonic cerebrum. Conclusions Consistent with the predictions of the atavism and antagonistic pleiotropy hypotheses, primate-specific genes, especially those PSGs derived from cell cycle-related genes that emerged in unicellular ancestors, contribute to the early proliferation of the human cerebrum at the cost of hitchhiking by similarly highly proliferative cancer cells.

The prevalence of chronic kidney disease is high in developing countries. However, no national survey of chronic kidney disease has been done incorporating both estimated glomerular filtration rate (eGFR) and albuminuria in a developing country with the economic diversity of China. We aimed to measure the prevalence of chronic kidney disease in China with such a survey. We did a cross-sectional survey of a nationally representative sample of Chinese adults. Chronic kidney disease was defined as eGFR less than 60 mL/min per 1·73 m2 or the presence of albuminuria. Participants completed a lifestyle and medical history questionnaire and had their blood pressure measured, and blood and urine samples taken. Serum creatinine was measured and used to estimate glomerular filtration rate. Urinary albumin and creatinine were tested to assess albuminuria. The crude and adjusted prevalence of indicators of kidney damage were calculated and factors associated with the presence of chronic kidney disease analysed by logistic regression. 50 550 people were invited to participate, of whom 47 204 agreed. The adjusted prevalence of eGFR less than 60 mL/min per 1·73 m2 was 1·7% (95% CI 1·5–1·9) and of albuminuria was 9·4% (8·9–10·0). The overall prevalence of chronic kidney disease was 10·8% (10·2–11·3); therefore the number of patients with chronic kidney disease in China is estimated to be about 119·5 million (112·9–125·0 million). In rural areas, economic development was independently associated with the presence of albuminuria. The prevalence of chronic kidney disease was high in north (16·9% [15·1–18·7]) and southwest (18·3% [16·4–20·4]) regions compared with other regions. Other factors independently associated with kidney damage were age, sex, hypertension, diabetes, history of cardiovascular disease, hyperuricaemia, area of residence, and economic status. Chronic kidney disease has become an important public health problem in China. Special attention should be paid to residents in economically improving rural areas and specific geographical regions in China. The Ministry of Science and Technology (China); the Science and Technology Commission of Shanghai; the National Natural Science Foundation of China; the Department of Health, Jiangsu Province; the Sichuan Science and Technology Department; the Ministry of Education (China); the International Society of Nephrology Research Committee; and the China Health and Medical Development Foundation.

Peptide-drug conjugates (PDCs) represent an emerging class of targeted therapeutic agents that consist of small molecular drugs coupled to multifunctional peptides through cleavable or non-cleavable linkers. The principal advantage of PDCs lies in their capacity to deliver drugs to diseased tissues at increased local concentrations, thereby reducing toxicity and mitigating adverse effects by limiting damage to non-diseased tissues. Despite the increasing number of PDCs being developed for various diseases, their advancements remain relatively slow due to several development constraints, which include limited available peptides and linkers, narrow therapeutic applications, and incomplete evaluation and information platforms for PDCs. Marked by the recent Nobel Prize awarded to artificial intelligence (AI) and de novo protein design for “protein design and structure prediction,” AI is playing an increasingly important role in drug discovery and development. In this review, we summarize the recent developments and limitations of PDCs, highlights the potential of AI in revolutionizing the design and evaluation of PDC.

Fucoidan exhibits several pharmacological activities and is characterized by high safety and the absence of toxic side effects. However, the absorption of fucoidan is not well-characterized. In the present study, fucoidan were labeled with fluorescein isothiocyanate (FITC) and their ability to traverse a monolayer of Caco-2 cells was examined. The apparent permeability coefficients (Papp × 10−6) of FITC-labeled fucoidan (FITC-fucoidan) were 26.23, 20.15, 17.93, 16.11 cm/sec, respectively, at the concentration of 10 μg/mL at 0.5, 1, 1.5 and 2 h. The absorption of FITC-fucoidan was suppressed by inhibitors of clathrin-mediated endocytosis, chlorpromazine, NH4Cl, and Dynasore; the inhibition rates were 84.24%, 74.61%, and 63.94%, respectively. This finding suggested that clathrin-mediated endocytosis was involved in fucoidan transport. Finally, tissue distribution of FITC-fucoidan was studied in vivo after injection of 50 mg/kg body weight into the tail vein of mice. The results showed that FITC-fucoidan targeted kidney and liver, reaching concentrations of 1092.31 and 284.27 μg/g respectively after 0.5 h. In summary, the present work identified the mechanism of absorption of fucoidan and documented its tissue distribution, providing a theoretical basis for the future development of fucoidan applications.

Tinkering with pre-existing genes has long been known as a major way to create new genes. Recently, however, motherless protein-coding genes have been found to have emerged de novo from ancestral non-coding DNAs. How these genes originated is not well addressed to date. Here we identified 24 hominoid-specific de novo protein-coding genes with precise origination timing in vertebrate phylogeny. Strand-specific RNA-Seq analyses were performed in five rhesus macaque tissues (liver, prefrontal cortex, skeletal muscle, adipose, and testis), which were then integrated with public transcriptome data from human, chimpanzee, and rhesus macaque. On the basis of comparing the RNA expression profiles in the three species, we found that most of the hominoid-specific de novo protein-coding genes encoded polyadenylated non-coding RNAs in rhesus macaque or chimpanzee with a similar transcript structure and correlated tissue expression profile. According to the rule of parsimony, the majority of these hominoid-specific de novo protein-coding genes appear to have acquired a regulated transcript structure and expression profile before acquiring coding potential. Interestingly, although the expression profile was largely correlated, the coding genes in human often showed higher transcriptional abundance than their non-coding counterparts in rhesus macaque. The major findings we report in this manuscript are robust and insensitive to the parameters used in the identification and analysis of de novo genes. Our results suggest that at least a portion of long non-coding RNAs, especially those with active and regulated transcription, may serve as a birth pool for protein-coding genes, which are then further optimized at the transcriptional level.