PELI1 overexpression contributes to pancreatic cancer progression through upregulating ubiquitination-mediated INPP5J degradation.

Inositol Polyphosphate-5-Phosphatase J (INPP5J), a 5-phosphatase, has been identified as a tumor suppressor in several types of cancer. However, its role in pancreatic cancer (PC) is unknown. We found that the INPP5J expression was markedly lower in PC tissues (n = 50) compared to paired adjacent non-tumor tissues, and the lower INPP5J expression was relevant to a worse prognosis of PC patients. We thus proposed that INPP5J might inhibit PC progression and conducted gain-of- and loss-of-function experiments to test our hypothesis. Our results showed that overexpression of INPP5J inhibited cell proliferation, invasion, migration, and xenografted tumor of PC cells. INPP5J silencing showed the opposite effect. Pellino E3 Ubiquitin Protein Ligase 1 (PELI1) is one of the ubiquitin ligases known to promote ubiquitination of its downstream targets. We found that PELI1 could interact with INPP5J and promote the ubiquitination and degradation of INPP5J. PELI1 overexpression enhanced malignant behaviors of PC cells. However, INPP5J overexpression restored the alterations caused by PELI1 overexpression. In conclusion, the results suggest that the decreased INPP5J expression, caused by PELI1 through ubiquitination, may promote PC progression. The PELI1-INPP5J axis represents a potential therapeutic targetable node for PC.

Biosynthesis and function of 7-deazaguanine derivatives in bacteria and phages.

SUMMARYDeazaguanine modifications play multifaceted roles in the molecular biology of DNA and tRNA, shaping diverse yet essential biological processes, including the nuanced fine-tuning of translation efficiency and the intricate modulation of codon-anticodon interactions. Beyond their roles in translation, deazaguanine modifications contribute to cellular stress resistance, self-nonself discrimination mechanisms, and host evasion defenses, directly modulating the adaptability of living organisms. Deazaguanine moieties extend beyond nucleic acid modifications, manifesting in the structural diversity of biologically active natural products. Their roles in fundamental cellular processes and their presence in biologically active natural products underscore their versatility and pivotal contributions to the intricate web of molecular interactions within living organisms. Here, we discuss the current understanding of the biosynthesis and multifaceted functions of deazaguanines, shedding light on their diverse and dynamic roles in the molecular landscape of life.

The Evolution and Future Trends of Stromal Vascular Fraction: A Bibliometric Analysis.

The heterogeneous population of cells obtained from processed adipose tissue, known as stromal vascular fraction (SVF), exhibits immunomodulatory and angiogenic properties. The therapeutic efficacy of SVF has been substantiated in numerous diseases, instilling hope for its clinical application as a cellular therapy. This study aims to provide a comprehensive analysis of the scholarly literature on SVF, including its worldwide progression, highlighting significant literatures, temporal development, research clusters, current active topics, and emerging trends. The combination of CiteSpace, HistCite Pro, and VOS Viewer tools was used to analyze the SVF literature. The overall panorama of the field is elucidated in terms of publication count, timeline, institutional distribution, journal coverage, and authors' contributions. In addition, this analysis explores the literature and keywords through the lens of co-occurrence, citation, and co-citation frequencies. Clustering algorithms are used to track the trajectory of the literature further, providing insight into its development. The findings offer a comprehensive overview of the progress made in the SVF field, highlighting distinct phases of development: the "Seedling period" from 1980 to 2010, the "Panicle period" from 2011 to 2016, and the "Flowering period" from 2017 to 2023. Within these periods, the evolution of 10 clusters is unraveled, encompassing topics such as vascular disease, CD34 expression, adipose tissue macrophage in 2013, cell-assisted lipotransfer, and knee osteoarthritis. In summary, this bibliometric study, conducting a quantitative analysis of publications in SVF research, encompasses a global overview of research, an analysis of pivotal literature in the field, research hotspots, and emerging frontiers.

Queuosine Salvage in Bartonella henselae Houston 1: A Unique Evolutionary Path.

Queuosine (Q) stands out as the sole tRNA modification that can be synthesized via salvage pathways. Comparative genomic analyses identified specific bacteria that showed a discrepancy between the projected Q salvage route and the predicted substrate specificities of the two identified salvage proteins: 1) the distinctive enzyme tRNA guanine-34 transglycosylase (bacterial TGT, or bTGT), responsible for inserting precursor bases into target tRNAs; and 2) Queuosine Precursor Transporter (QPTR), a transporter protein that imports Q precursors. Organisms like the facultative intracellular pathogen Bartonella henselae, which possess only bTGT and QPTR but lack predicted enzymes for converting preQ1 to Q, would be expected to salvage the queuine (q) base, mirroring the scenario for the obligate intracellular pathogen Chlamydia trachomatis. However, sequence analyses indicate that the substrate-specificity residues of their bTGTs resemble those of enzymes inserting preQ1 rather than q. Intriguingly, mass spectrometry analyses of tRNA modification profiles in B. henselae reveal trace amounts of preQ1, previously not observed in a natural context. Complementation analysis demonstrates that B. henselae bTGT and QPTR not only utilize preQ1, akin to their Escherichia coli counterparts, but can also process q when provided at elevated concentrations. The experimental and phylogenomic analyses suggest that the Q pathway in B. henselae could represent an evolutionary transition among intracellular pathogens-from ancestors that synthesized Q de novo to a state prioritizing the salvage of q. Another possibility that will require further investigations is that the insertion of preQ1 has fitness advantages when B. henselae is growing outside a mammalian host.

FTO Knockdown-Mediated Maturation of miR-383-5p Inhibits Malignant Advancement of Pancreatic Cancer by Targeting ITGA3.

m6A demethylase FTO is confirmed to be involved in pancreatic cancer progression. FTO regulates miRNA processing. To investigate the regulatory effect of FTO on miR-383-5p and its role in pancreatic cancer. The expression of miR-383-5p, ITGA3, and FTO was predicted using bioinformatic analysis in tissues and was measured using qPCR in cells. Cell biological functions were investigated using MTT assay, Transwell assay, sphere formation assay, and qPCR. The targeting relationship between miR-383-5p and ITGA3 was evaluated using the dual-luciferase reporter assay. The effect of FTO on miR-383-5p processing was evaluated using RIP and MeRIP assay. FTO expression was upregulated in pancreatic cancer and silencing of FTO promoted the processing of miR-383-5p in an m6A-dependent manner. m6A-modified miRNA processing was recognized by IGF2BP1. Downregulation of miR-383-5p reversed FTO knockdown-induced inhibition of cellular processes. The FTO/miR-383-5p/ITGA3 axis facilitated cell viability, metastasis, and stemness in pancreatic cancer.

Sequential embryo transfer versus double cleavage-stage embryo or double blastocyst transfer in patients with recurrent implantation failure with frozen-thawed embryo transfer cycles: a cohort study.

Background: Recurrent implantation failure (RIF) is more common among patients receiving assisted reproductive treatment. Many efforts have been made to increase the incidence of clinical pregnancy among patients with RIF. The effect of the sequential transfer procedure, a two-step interval transfer of a cleavage-stage embryo followed by a blastocyst in one transfer cycle, on the clinical outcomes of RIF patients remains controversial. Methods: In total, 1774 frozen-thawed embryo transfer (FET) cycles in RIF patients were included. Of these cycles, 302 were sequential embryo transfer (ET) cycles, 979 were double day 3 cleavage-stage ET cycles, and 493 were double blastocyst ET cycles. The primary outcomes were the rates of implantation, clinical pregnancy and multiple pregnancy, and the secondary outcomes were the rates of hCG positive, early miscarriage and ectopic pregnancy. Results: The implantation, hCG positive, and clinical pregnancy rates in the sequential ET group (32.1%, 58.9%, 50.7%) were significantly higher than those in the day 3 cleavage-stage ET group (24.9%, 46.5%, 40.4%) and were similar to those in the blastocyst transfer group (30.1%, 56.4%, 47.1%). The early miscarriage rate in the blastocyst transfer group was significantly higher than that in the cleavage-stage ET group (17.2% vs. 8.1%, P <0.05), while the ectopic pregnancy rate in the blastocyst transfer group was significantly lower than that in the cleavage-stage ET group (0.4% vs. 3.0%, P <0.05). The multiple pregnancy rate in the sequential ET group was significantly lower than that in the cleavage-stage ET group (17.0% vs. 25.5%, P <0.05) and the blastocyst transfer group (17.0% vs. 27.6%, P <0.05). When cycles of blastocyst culture failure were excluded, the clinical pregnancy rate was significantly higher (55.7% vs. 47.1%, P <0.05), and the early miscarriage rate and multiple pregnancy rate were significantly lower (8.5% vs. 17.2%, 17.7% vs. 27.6%; P <0.05, respectively) in the sequential ET group than in the double blastocyst ET group. Conclusions: Sequential embryo transfer in FET cycles could improve the clinical outcomes of patients with RIF.

PSMD12 interacts with CDKN3 and facilitates pancreatic cancer progression.

Proteasome 26S subunit, non-ATPase 12 (PSMD12) genes have been implicated in several types of malignancies but the role of PSMD12 in pancreatic cancer (PC) remains elusive. Bioinformatics analysis showed that PSMD12 was highly expressed in PC patients and was associated with shorter overall survival. PSMD12 was also shown to be highly expressed in PC tissues and cell lines. Upregulated PSMD12 showed enhanced cell viability, increased colony formation rate and upregulated levels of PCNA and c-Myc, while the inhibition of PSMD12 abated these levels. PSMD12 knockdown promoted cell apoptosis. The results of xenografts in nude mice confirmed that PSMD12 promoted PC tumor growth in vivo. Protein‒protein interaction network and functional enrichment analyses implied that PSMD12 may have a connection with cyclin-dependent kinase inhibitor 3 (CDKN3). Co­immunoprecipitation and western blot results confirmed that PSMD12 could interact with and abate the ubiquitination level of CDKN3, thus stabilizing the CDKN3 protein. Rescue assays showed that PSMD12 overexpression caused cell proliferation and that knockdown-induced cell apoptosis could be reversed by CDKN3 regulation. This work reveals the essential roles of PSMD12 in the proliferation and apoptosis of PC development. PSMD12 may regulate CDKN3 expression by interacting with and abating the ubiquitination level of CDKN3, thereby participating in the malignant behavior of PC.

GID2 Interacts With CDKN3 and Regulates Pancreatic Cancer Growth and Apoptosis.

Dysregulation of deubiquitinase or ubiquitinase-mediated protein expression contributes to various diseases, including cancer. In the present study, we identified GID2, a subunit of the glucose-induced degradation-deficient (GID) complex that functions as an E3 ubiquitin ligase, as a potential key candidate gene in pancreatic cancer (PC) progression. The functional role and potential mechanism of GID2 in PC progression were investigated. Integrated bioinformatics analysis was performed to identify differentially expressed genes in PC based on the Gene Expression Profiling Interactive Analysis data sets. We found that GID2 was upregulated in PC tissues and that a high level of GID2 expression in clinical PC samples was positively associated with tumor stage and poor survival. Functional assays elucidated that GID2 expression promoted cell growth in vitro and accelerated tumor growth in vivo. GID2 knockdown effectively attenuated the malignant behaviors of PC cells and tumor formation. Furthermore, the protein network that interacted with the GID2 protein was constructed based on the GeneMANIA website. Cyclin-dependent kinase inhibitor 3 (CDKN3), a cell cycle regulator, was identified as a potential target of the GID2 protein. We revealed that GID2 positively regulated CDKN3 expression and inhibited CDKN3 ubiquitination. Furthermore, CDKN3 downregulation reversed the promoting effects of GID2 on PC progression. Therefore, the present study demonstrated that GID2 might regulate PC progression by maintaining the stability of the CDKN3 protein. These findings highlight the potential roles of the GID2/CDKN3 axis as a potential therapeutic target in PC.

Exploratory study of sea buckthorn enhancing QiangGuYin efficacy by inhibiting CKIP-1 and Notum activating the Wnt/ß-catenin signaling pathway and analysis of active ingredients by molecular docking.

Background: Sea buckthorn (SBT) is a traditional Chinese medicine (TCM), rich in calcium, phosphorus, and vitamins, which can potentially prevent and treat osteoporosis. However, no research has been conducted to confirm these hypotheses. QiangGuYin (QGY) is a TCM compound used to treat osteoporosis. There is a need to investigate whether SBT enhances QGY efficacy. Objectives: The aim of this study was to explore whether SBT enhances QGY efficacy by inhibiting CKIP-1 and Notum expression through the Wnt/ß-catenin pathway. The study also aimed to explore the active components of SBT. Methods: Experimental animals were divided into control, model, QGY, SBT, SBT + Eucommia ulmoides (EU), and SBT + QGY groups. After treatment, bone morphometric parameters, such as estrogen, PINP, and S-CTX levels, and Notum, CKIP-1, and ß-catenin expression were examined. Screening of SBT active components was conducted by molecular docking to obtain small molecules that bind Notum and CKIP-1. Results: The results showed that all the drug groups could elevate the estrogen, PINP, and S-CTX levels, improve femoral bone morphometric parameters, inhibit Notum and CKIP-1 expression, and promote ß-catenin expression. The effect of SBT + EU and SBT + QGY was superior to the others. Molecular docking identified that SBT contains seven small molecules (folic acid, rhein, quercetin, kaempferol, mandenol, isorhamnetin, and ent-epicatechin) with potential effects on CKIP-1 and Notum. Conclusion: SBT improves bone morphometric performance in PMOP rats by inhibiting CKIP-1 and Notum expression, increasing estrogen levels, and activating the Wnt/ß-catenin signaling pathway. Furthermore, SBT enhances the properties of QGY. Folic acid, rhein, quercetin, kaempferol, mandenol, isorhamnetin, and ent-epicatechin are the most likely active ingredients of SBT. These results provide insight into the pharmacological mechanisms of SBT in treating osteoporosis.

The absence of the queuosine tRNA modification leads to pleiotropic phenotypes revealing perturbations of metal and oxidative stress homeostasis in Escherichia coli K12.

Queuosine (Q) is a conserved hypermodification of the wobble base of tRNA containing GUN anticodons but the physiological consequences of Q deficiency are poorly understood in bacteria. This work combines transcriptomic, proteomic and physiological studies to characterize a Q-deficient Escherichia coli K12 MG1655 mutant. The absence of Q led to an increased resistance to nickel and cobalt, and to an increased sensitivity to cadmium, compared to the wild-type (WT) strain. Transcriptomic analysis of the WT and Q-deficient strains, grown in the presence and absence of nickel, revealed that the nickel transporter genes (nikABCDE) are downregulated in the Q- mutant, even when nickel is not added. This mutant is therefore primed to resist to high nickel levels. Downstream analysis of the transcriptomic data suggested that the absence of Q triggers an atypical oxidative stress response, confirmed by the detection of slightly elevated reactive oxygen species (ROS) levels in the mutant, increased sensitivity to hydrogen peroxide and paraquat, and a subtle growth phenotype in a strain prone to accumulation of ROS.

Antiosteoporosis effect of tanshinol in osteoporosis animal models: A systematic review and meta-analysis.

Background: Osteoporosis (OP) is an age-related bone disease that has emerged as a worldwide public health concern due to its increasing incidence and high disability rate. Tanshinol [D (+) ß-3,4-dihydroxyphenyl lactic acid, TS], a water-soluble component extracted from Salvia miltiorrhiza, has proven to be effective in attenuating OP in vitro and in vivo. However, there is insufficient evidence to support its clinical application. Objective: This meta-analysis aimed to investigate available OP animal model studies to demonstrate the antiosteoporosis effects of TS in a systematic manner. Methods: Electronic searches of related studies were conducted in the following databases: EMBASE, PubMed, Web of Science, Cochrane Library, Chinese National Knowledge Infrastructure, Chinese VIP Database, Chinese Biomedical Literature Database, and Wanfang. The retrieval date was January 2022, and there were no time or language restrictions. The CAMARADES 10-item quality checklist was utilized to test the risk of potential bias for each study, and modifications were performed accordingly. The primary outcome was bone mineral density (BMD, which included the femur and lumbar spine); and secondary outcomes were parameters for trabecular bone such as bone volume over total volume (BV/TV), trabecular number (Tb.N), trabecular thickness (Tb.Th), trabecular separation (Tb.Sp), conditions of the femur (including bone maximum load and bone elastic load), and markers of bone metabolism (serum osteocalcin, S-OCN). Results: A total of nine studies including 176 rats were chosen for this analysis. Egger's test revealed the presence of publication bias in various studies regarding the primary outcome. According to this systematic review, TS significantly increased the BMD of the femur (BMD-femur) (SMD = 4.40; 95% CI = 1.61 to 7.19; p = 0.002, I 2 = 94.6%), BMD of the lumbar spine (BMD-lumbar) (SMD = 6.390; 95% CI = 2.036 to 10.744; p = 0.004, I2 = 95.9%), BV/TV (SMD = 0.790; 95% CI = 0.376 to 1.204; p = 0.000, I2 = 10.8), Tb.N (SMD = 0.690; 95% CI = 0.309 to 1.071; p = 0.000, I2 = 12%), Tb.Th (SMD = 0.772; 95% CI = 0.410 to 1.134; p = 0.000, I2 = 32.2%), and S-OCN (SMD = 3.13; 95% CI = 0.617 to 5.65; p = 0.015, I2 = 92.3%), while the Tb.Sp level was markedly decreased in OP models in comparison to the controls (SMD = -0.822; 95% CI = -1.207 to -0.437; p = 0.000, I2 = 0%). Moreover, TS treatment was associated with a significant improvement of the bone biomechanical indicators, including bone maximum load (SMD = 0.912; 95% CI = 0.370 to 1.455; p = 0.001, I2 = 40%) and elasticity load (SMD = 0.821; 95% CI = 0.290 to 1.351; p = 0.002, I 2 = 0%). Conclusion: Collectively, our findings suggest that TS can improve BMD, bone microarchitecture, bone biomechanics, and S-OCN expression in rats, implying that it could be used clinically in the future. Systematic Review Registration: https://inplasy.com/inplasy-2022-3-0053/, identifier [INPLASY202230053].

Injectable and Self-Healing Polysaccharide Hydrogel Loading Molybdenum Disulfide Nanoflakes for Synergistic Photothermal-Photodynamic Therapy of Breast Cancer.

In order to overcome the limitation of traditional therapies for cancer and improve the accuracy of treatment, more advantageous cancer treatment methods need to be explored and studied. As a result, photothermal photodynamic therapy of breast cancer using bovine serum albumin (BSA) modifies molybdenum disulfide nanoflakes. Then the well-dispersed BSA-MoS2 NFs are loaded in the injectable and self-healing polysaccharide hydrogel which is prepared by the reaction of oxidized sodium alginate (OSA) and hydroxypropyl chitosan (HPCS) through the formation of Schiff base bonds. The injection and self-healing properties of the nanocomposite hydrogel are investigated. In vitro photothermal and photodynamic investigations demonstrate that BSA-MoS2 NFs possess obvious photothermal conversion and production of reactive oxygen species (ROS) under the irradiation of near infrared (NIR) laser (808 nm). In vivo anticancer investigation indicates that the nanocomposite hydrogel can be directly injected and remain in the tumor sites and achieve the synergistic photothermal-photodynamic therapy of cancer.

GAS41 mediates proliferation and GEM chemoresistance via H2A.Z.2 and Notch1 in pancreatic cancer.

PURPOSE: GAS41 is a YEATS domain protein that binds to acetylated histone H3 to promote the chromatin deposition of H2A.Z in non-small cell lung cancer. The role of GAS41 in pancreatic cancer is still unknown. Here, we aimed to reveal this role. METHODS: GAS41 expression in pancreatic cancer tissues and cell lines was examined using qRT-PCR, Western blotting and immunohistochemistry. MTT, colony formation, spheroid formation and in vivo tumorigenesis assays were performed to assess the proliferation, tumorigenesis, stemness and gemcitabine (GEM) resistance of pancreatic cancer cells. Mechanistically, co-immunoprecipitation (co-IP) and chromatin immunoprecipitation (ChIP) assays were used to evaluate the roles of GAS41, H2A.Z.2 and Notch1 in pancreatic cancer. RESULTS: We found that GAS41 is overexpressed in human pancreatic cancer tissues and cell lines, and that its expression increases following the acquisition of GEM resistance. We also found that GAS41 up-regulates Notch, as well as pancreatic cancer cell stemness and GEM resistance in vitro and in vivo. We show that GAS41 binds to H2A.Z.2 and activates Notch and its downstream mediators, thereby regulating stemness and drug resistance. Depletion of GAS41 or H2A.Z.2 was found to down-regulate Notch and to sensitize pancreatic cancer cells to GEM. CONCLUSION: Our data indicate that GAS41 mediates proliferation and GEM resistance in pancreatic cancer cells via H2A.Z.2 and Notch1.

The Effect of Online Health Information Seeking on Physician-Patient Relationships: Systematic Review.

BACKGROUND: The internet has now become part of human life and is constantly changing people's way of life. With the increasing popularity of online health information (OHI), it has been found that OHI can affect the physician-patient relationship by influencing patient behaviors. OBJECTIVE: This study aims to systematically investigate the impact of OHI-seeking behavior on the physician-patient relationship. METHODS: Literature retrieval was conducted on 4 databases (Web of Science, PubMed, China National Knowledge Infrastructure, SinoMed), and the time limit for literature publication was before August 1, 2021. RESULTS: We selected 53 target papers (42 [79%] English papers and 11 [21%] Chinese papers) that met the inclusion criteria. Of these, 31 (58%) papers believe that patients' OHI behavior can enable them to participate in their own medical care, improve patient compliance, and improve the physician-patient relationship. In addition, 14 (26%) papers maintain a neutral attitude, some believing that OHI behavior has no significant effect on doctors and patients and others believing that due to changes in the factors affecting OHI behavior, they will have a negative or a positive impact. Furthermore, 8 (15%) papers believe that OHI search behavior has a negative impact on doctors and patients, while 6 (11%) papers show that OHI reduces Chinese patients' trust in doctors. CONCLUSIONS: Our main findings showed that (1) OHI-seeking behavior has an impact on patients' psychology, behavior, and evaluation of doctors; (2) whether patients choose to discuss OHI with doctors has different effects on the physician-patient relationship; and (3) the negative impact of OHI on China's internet users is worthy of attention. Due to the low quality of OHI, poor health information literacy, short physician-patient communication time, and various types of negative news, patients' trust in doctors has declined, thus affecting the physician-patient relationship. Improvement of people's health information literacy and the quality of OHI are important factors that promote the positive impact of OHI on the physician-patient relationship.

The effect of QiangGuYin on osteoporosis through the AKT/mTOR/autophagy signaling pathway mediated by CKIP-1.

Osteoporosis is a systemic bone disease characterized by decreased bone mass and deterioration of bone microstructure, which leads to increased bone fragility and increased risk of fractures. Casein kinase 2 interacting protein 1 (CKIP-1, also known as PLEKHO1) is involved in the biological process of bone formation, differentiation and apoptosis, and is a negative regulator of bone formation. QiangGuYin (QGY) is a famous TCM formula that has been widely used in China for the clinical treatment of postmenopausal osteoporosis for decades, but the effect in regulating CKIP-1 on osteoporosis is not fully understood. This study aimed to explore the potential mechanism of CKIP-1 participating in autophagy in bone cells through the AKT/mTOR signaling pathway and the regulatory effect of QGY. The results in vivo showed that QGY treatment can significantly improve the bone quality of osteoporotic rats, down-regulate the expression of CKIP-1, LC3II/I and RANKL, and up-regulated the expression of p62, p-AKT/AKT, p-mTOR/mTOR, RUNX2 and OPG. It is worth noting that the results in vitro confirmed that CKIP-1 interacts with AKT. By up-regulating the expression of Atg5 and down-regulating the p62, the level of LC3 (autophagosome) is increased, and the cells osteogenesis and differentiation are inhibited. QGY inhibits the combination of CKIP-1 and AKT in osteoblasts, activates the AKT/mTOR signaling pathway, inhibits autophagy, and promotes cell differentiation, thereby exerting an anti-osteoporosis effect. Therefore, QGY targeting CKIP-1 to regulate the AKT/mTOR-autophagy signaling pathway may represent a promising drug candidate for the treatment of osteoporosis.

Evolutionary Overview of Consumer Health Informatics: Bibliometric Study on the Web of Science from 1999 to 2019.

BACKGROUND: Consumer health informatics (CHI) originated in the 1990s. With the rapid development of computer and information technology for health decision making, an increasing number of consumers have obtained health-related information through the internet, and CHI has also attracted the attention of an increasing number of scholars. OBJECTIVE: The aim of this study was to analyze the research themes and evolution characteristics of different study periods and to discuss the dynamic evolution path and research theme rules in a time-series framework from the perspective of a strategy map and a data flow in CHI. METHODS: The Web of Science core collection database of the Institute for Scientific Information was used as the data source to retrieve relevant articles in the field of CHI. SciMAT was used to preprocess the literature data and construct the overlapping map, evolution map, strategic diagram, and cluster network characterized by keywords. Besides, a bibliometric analysis of the general characteristics, the evolutionary characteristics of the theme, and the evolutionary path of the theme was conducted. RESULTS: A total of 986 articles were obtained after the retrieval, and 931 articles met the document-type requirement. In the past 21 years, the number of articles increased every year, with a remarkable growth after 2015. The research content in 4 different study periods formed the following 38 themes: patient education, medicine, needs, and bibliographic database in the 1999-2003 study period; world wide web, patient education, eHealth, patients, medication, terminology, behavior, technology, and disease in the 2004-2008 study period; websites, information seeking, physicians, attitudes, technology, risk, food labeling, patient, strategies, patient education, and eHealth in the 2009-2014 study period; and electronic medical records, health information seeking, attitudes, health communication, breast cancer, health literacy, technology, natural language processing, user-centered design, pharmacy, academic libraries, costs, internet utilization, and online health information in the 2015-2019 study period. Besides, these themes formed 10 evolution paths in 3 research directions: patient education and intervention, consumer demand attitude and behavior, and internet information technology application. CONCLUSIONS: Averaging 93 publications every year since 2015, CHI research is in a rapid growth period. The research themes mainly focus on patient education, health information needs, health information search behavior, health behavior intervention, health literacy, health information technology, eHealth, and other aspects. Patient education and intervention research, consumer demand, attitude, and behavior research comprise the main theme evolution path, whose evolution process has been relatively stable. This evolution path will continue to become the research hotspot in this field. Research on the internet and information technology application is a secondary theme evolution path with development potential.

Nomogram to predict pregnancy outcomes of emergency oocyte freeze-thaw cycles.

BACKGROUND: Existing clinical prediction models for in vitro fertilization are based on the fresh oocyte cycle, and there is no prediction model to evaluate the probability of successful thawing of cryopreserved mature oocytes. This research aims to identify and study the characteristics of pre-oocyte-retrieval patients that can affect the pregnancy outcomes of emergency oocyte freeze-thaw cycles. METHODS: Data were collected from the Reproductive Center, Peking University Third Hospital of China. Multivariable logistic regression model was used to derive the nomogram. Nomogram model performance was assessed by examining the discrimination and calibration in the development and validation cohorts. Discriminatory ability was assessed using the area under the receiver operating characteristic curve (AUC), and calibration was assessed using the Hosmer-Lemeshow goodness-of-fit test and calibration plots. RESULTS: The predictors in the model of "no transferable embryo cycles" are female age (odds ratio [OR] = 1.099, 95% confidence interval [CI] = 1.003-1.205, P = 0.0440), duration of infertility (OR = 1.140, 95% CI = 1.018-1.276, P = 0.0240), basal follicle-stimulating hormone (FSH) level (OR = 1.205, 95% CI = 1.051-1.382, P = 0.0084), basal estradiol (E2) level (OR = 1.006, 95% CI = 1.001-1.010, P = 0.0120), and sperm from microdissection testicular sperm extraction (MESA) (OR = 7.741, 95% CI = 2.905-20.632, P < 0.0010). Upon assessing predictive ability, the AUC for the "no transferable embryo cycles" model was 0.799 (95% CI: 0.722-0.875, P < 0.0010). The Hosmer-Lemeshow test (P = 0.7210) and calibration curve showed good calibration for the prediction of no transferable embryo cycles. The predictors in the cumulative live birth were the number of follicles on the day of human chorionic gonadotropin (hCG) administration (OR = 1.088, 95% CI = 1.030-1.149, P = 0.0020) and endometriosis (OR = 0.172, 95% CI = 0.035-0.853, P = 0.0310). The AUC for the "cumulative live birth" model was 0.724 (95% CI: 0.647-0.801, P < 0.0010). The Hosmer-Lemeshow test (P = 0.5620) and calibration curve showed good calibration for the prediction of cumulative live birth. CONCLUSIONS: The predictors in the final multivariate logistic regression models found to be significantly associated with poor pregnancy outcomes were increasing female age, duration of infertility, high basal FSH and E2 level, endometriosis, sperm from MESA, and low number of follicles with a diameter >10 mm on the day of hCG administration.

Transcatheter Arterial Infusion Combined With Radioactive Particles in the Treatment of Advanced Body/Tail Pancreatic Cancer: A Retrospective Cohort Study.

OBJECTIVES: This retrospective cohort study investigated the efficacy of routine intravenous chemotherapy (the control group), transcatheter arterial infusion (TAI) chemotherapy, and TAI combined with radioactive particles as therapeutic methods for advanced body/tail pancreatic cancer by assessing the short-term and overall survival rates. METHODS: We screened our prospective database for patients with advanced body/tail pancreatic cancer, which tumor deemed unresectable, and no other confirmed malignant tumors, patients were assigned into 3 groups according to their treatment: routine intravenous chemotherapy, TAI, and TAI combined with radioactive particles. RESULTS: The median survival time was 6 months in the control group, 10 months in the TAI group, and 13 months in the TAI combined group. The Kaplan-Meier estimates of the overall survival among the 3 groups, indicating that there is significant difference among 3 groups (P < 0.000). The clinical remission rates were 17.5% in the control group, 41.5% in the TAI group, and 48.0% in the TAI combined group. Covariates analyzed showed that different treatment methods and times affected the results significantly (P < 0.002). CONCLUSIONS: In the treatment of advanced body/tail pancreatic cancer, TAI and TAI combined with radioactive particles significantly improved the clinical outcomes in patients compared with routine intravenous chemotherapy.

RBM14 Modulates Tubulin Acetylation and Regulates Spindle Morphology During Meiotic Maturation in Mouse Oocytes.

RBM14 is an RNA-binding protein that regulates spindle integrity in mitosis; however, its functions during meiosis are still unclear. In this study, we discovered that RBM14 expression was down-regulated in oocytes from old mice. The RBM14 distribution at different stages of meiosis was explored, while it presents overlapped localization patterns with α-tubulin in MI- and MII-stage oocytes. Treatment of MI-stage oocytes with spindle-perturbing agents revealed that RBM14 was co-localized with microtubules. RBM14 knockdown with RBM14-specific morpholino showed that RBM14-depleted oocytes underwent symmetric division compared to the controls. RBM14 knockdown also resulted in spindle defects and chromosome abnormalities during oocyte maturation, presumably due to α-tubulin hyperacetylation. Co-immunoprecipitation analysis demonstrated that RBM14 is interacted with endogenous α-tubulin in mammalian cells. These findings indicate that RBM14 is an essential modulator of oocyte meiotic maturation by regulating α-tubulin acetylation to affect spindle morphology and chromosome alignment. Consequently, RBM14 represents a potential biomarker of oocyte quality and a novel therapeutic target in women with oocyte maturation failure.