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Objective To analyze the literature on artificial intelligence in forensic research from 2012 to 2022 in the Web of Science Core Collection Database, to explore research hotspots and developmental trends. Methods A total of 736 articles on artificial intelligence in forensic medicine in the Web of Science Core Collection Database from 2012 to 2022 were visualized and analyzed through the literature measuring tool CiteSpace. The authors, institution, country （region）, title, journal, keywords, cited references and other information of relevant literatures were analyzed. Results A total of 736 articles published in 220 journals by 355 authors from 289 institutions in 69 countries （regions） were identified, with the number of articles published showing an increasing trend year by year. Among them, the United States had the highest number of publications and China ranked the second. Academy of Forensic Science had the highest number of publications among the institutions. Forensic Science International, Journal of Forensic Sciences, International Journal of Legal Medicine ranked high in publication and citation frequency. Through the analysis of keywords, it was found that the research hotspots of artificial intelligence in the forensic field mainly focused on the use of artificial intelligence technology for sex and age estimation, cause of death analysis, postmortem interval estimation, individual identification and so on. Conclusion It is necessary to pay attention to international and institutional cooperation and to strengthen the cross-disciplinary research. Exploring the combination of advanced artificial intelligence technologies with forensic research will be a hotspot and direction for future research.

Future HIV-1 curative therapies require a thorough understanding of the distribution of genetically-intact HIV-1 within T-cell subsets during antiretroviral therapy (ART) and the cellular mechanisms that maintain this reservoir. Therefore, we sequenced near-full-length HIV-1 genomes and identified genetically-intact and genetically-defective genomes from resting naive, stem-cell memory, central memory, transitional memory, effector memory, and terminally-differentiated CD4+ T-cells with known cellular half-lives from 11 participants on ART. We find that a higher infection frequency with any HIV-1 genome was significantly associated with a shorter cellular half-life, such as transitional and effector memory cells. A similar enrichment of genetically-intact provirus was observed in these cells with relatively shorter half-lives. We found that effector memory and terminally-differentiated cells also had significantly higher levels of expansions of genetically-identical sequences, while only transitional and effector memory cells contained genetically-intact proviruses that were part of a cluster of identical sequences. Expansions of identical sequences were used to infer cellular proliferation from clonal expansion. Altogether, this indicates that specific cellular mechanisms such as short half-life and proliferative potential contribute to the persistence of genetically-intact HIV-1. IMPORTANCE The design of future HIV-1 curative therapies requires a more thorough understanding of the distribution of genetically-intact HIV-1 within T-cell subsets as well as the cellular mechanisms that maintain this reservoir. These genetically-intact and presumably replication-competent proviruses make up the latent HIV-1 reservoir. Our investigations into the possible cellular mechanisms maintaining the HIV-1 reservoir in different T-cell subsets have revealed a link between the half-lives of T-cells and the level of proviruses they contain. Taken together, we believe our study shows that more differentiated and proliferative cells, such as transitional and effector memory T-cells, contain the highest levels of genetically-intact proviruses, and the rapid turnover rate of these cells contributes to the expansion of genetically-intact proviruses within them. Therefore, our study delivers an in-depth assessment of the cellular mechanisms, such as cellular proliferation and half-life, that contribute to and maintain the latent HIV-1 reservoir.

This study aimed to investigate the role of the MIR210 host gene (MIR210HG), a long noncoding RNA (lncRNA), in the proliferation of colon cancer cells and its potential mechanism involving the ferroptosis pathway. We assessed MIR210HG expression in colon cancer cell lines and tissues, and examined the effects of its overexpression and knockdown on cell proliferation. Proteomic analysis was conducted to explore the interaction between MIR210HG and ferroptosis pathway components. The binding of MIR210HG to poly(rC) binding protein 1 (PCBP1) was predicted using catRAPID and confirmed through RNA pull-down and RNA immunoprecipitation (RIP) experiments. MIR210HG was significantly upregulated in colon cancer cells and tissues. Its overexpression promoted, while its knockdown inhibited, colon cancer cell proliferation. MIR210HG was found to be associated with ferroptosis pathway components and to bind to PCBP1, which was experimentally validated. The inhibition of ferroptosis by MIR210HG through PCBP1 binding was confirmed, highlighting its role in promoting cell proliferation. MIR210HG promotes colon cancer cell proliferation by binding to PCBP1 and inhibiting ferroptosis. These findings suggest MIR210HG as a potential therapeutic target for colon cancer. [ABSTRACT FROM AUTHOR]

Graphene has exceptional properties with great promise for various applications. However, pristine graphene cannot be used in nano-electronics because it lacks a gap in energy dispersion at the Dirac point. Therefore, researchers have been developing methods to open the gap, which would open the door for the use of graphene in a wide range of electronic and photovoltaic devices. Through density functional theory calculations, we identified a specific range of electric field values that could potentially open the Dirac cones and separate the two π (VB) and two π* (CB) bands belonging to each graphene layer in FeCl3 intercalated bilayer graphene. To our knowledge, no such findings have been reported in the literature. These findings could aid in developing a better understanding of the electronic structure of materials and enable the design of more efficient electronic devices. [ABSTRACT FROM AUTHOR]

Objective To explore whether PM2.5 induces the secretion of IL-6 and TNF-α in 16HBE via the Wnt-5a/JNK signaling pathway. Methods The research was implemented by rats and 16HBE cells. Rats were divided into control group and motor vehicle exhaust(MVE) group(concentration 1.5 mg/m2,2 h/day); 16HBE cells were divided into control group,PM2.5(20 μg/mL)group,control siRNA+PM2.5 group,Wnt-5a siRNA+PM2.5 group,Wnt-5a siRNA+control group,JNK inhibitor SP600125+PM2.5 group and SP600125+control group. The expressions of p-JNK and p-c-Jun in lung tissues were examined by immune-histochemistry method. The expressions of Wnt-5a,JNK,c-Jun,p-JNK and p-c-Jun were measured by Western blot. The secretions of IL-6 and TNF-α were assessed by ELISA. Results Compared with the control rat group, MVE group exhibited significantly up-regulated the expression of p-JNK and p-c-Jun(P＜0.05); Compared with the 16HBE cell control group,PM2.5 group significantly up-regulated the expressions of Wnt-5a,p-JNK and p-c-Jun and the secretions of IL-6 and TNF-α(P＜0.05);Compared with the PM2.5 group, Wnt-5a siRNA+PM2.5 group blocked these effects(P＜0.05). Furthermore,SP600125+PM2.5 group showed a significantly decreased expression of p-c-Jun and the secretion of IL-6 and TNF-α by 16HBE cells(P＜0.05). Conclusions PM2.5 induces the secretions of IL-6 and TNF-α by 16HBE cells via Wnt-5a/JNK signaling pathway.

Under the background of global climate change, crop leaves usually experience fluctuating light (FL) under compound stresses of drought and heat in the field. However, photoinhibition and photosynthetic regulation in FL under these compound stresses are little known. To elucidate this, we measured gas exchange, chlorophyll fluorescence, P700 redox state and electrochromic shift signals for tomato (Solanum lycopersicum) leaves exposed to FL under individual and compound stresses of moderate drought and heat stresses. After treatment with short‐term FL, photosystem I (PSI) activity decreased slightly in all treatments. By comparison, photosystem II (PSII) activity was reduced slightly under individual stress but largely decreased by 46% under compound stresses. Therefore, PSI is more tolerant than PSII when exposed to FL under compound stresses of drought and heat. Under compound stresses, PSII photoinhibition largely downregulated linear electron flow and photorespiration became a major electron sink downstream. Concomitantly, cyclic electron flow (CEF) was highly enhanced to help the building up of trans‐thylakoid proton gradient. This study highlights the importance of PSII activity and CEF in crop tolerance under future compound climate extremes such as drought and heat. [ABSTRACT FROM AUTHOR]

Drought and heat stresses usually occur concomitantly in nature, with increasing frequency and intensity of both stresses expected due to climate change. The synergistic agricultural impacts of these compound climate extremes are much greater than those of the individual stresses. However, the mechanisms by which drought and heat stresses separately and concomitantly affect dynamic photosynthesis have not been thoroughly assessed. To elucidate this, we used tomato (Solanum lycopersicum) seedlings to measure dynamic photosynthesis under individual and compound stresses of drought and heat. Individual drought and heat stresses limited dynamic photosynthesis at the stages of diffusional conductance to CO2 and biochemistry, respectively. However, the primary limiting factor for photosynthesis shifted to mesophyll conductance under the compound stresses. Compared with the control, photosynthetic carbon gain in fluctuating light decreased by 38%, 73%, and 114% under the individual drought, heat, and compound stresses, respectively. Therefore, compound stresses caused a greater reduction in photosynthetic carbon gain in fluctuating light conditions than individual stress. These findings highlight the importance of mitigating the effects of compound climate extremes on crop productivity by targeting mesophyll conductance and improving dynamic photosynthesis. Compound stresses of drought and heat inhibit photosynthesis through restricting mesophyll conductance. [ABSTRACT FROM AUTHOR]