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Follicular thyroid carcinoma (FTC) is the second most common form of thyroid malignancy, and it is associated with more aggressive growth and worse long-term survival outcomes relative to papillary thyroid carcinoma (PTC). Reliable approaches to preoperative FTC detection, however, remain to be established. Herein, a targeted Affibody-Au-Tripod nanoprobe was developed and successfully utilized to facilitate the targeted photoacoustic imaging (PAI) of epidermal growth factor receptor (EGFR)-positive cells and tumors. These Affibody-Au-Tripods were found to be highly sensitive and specific for cells expressing EGFR when used as a PA contrast agent in vitro, and studies conducted in an FTC-133 subcutaneous tumor model system in mice further revealed that these Affibody-Au-Tripods were able to specifically target these EGFR-expressing tumors while providing a strong photoacoustic signal in vivo. Importantly, these nanoprobes exhibited negligible cytotoxicity and robust chemical and physical stability, making Affibody-Au-Tripods promising candidates for targeted PAI-based FTC diagnosis. In addition, these nanoprobes have the potential to facilitate the individualized treatment of patients harboring EGFR-positive tumors.

Providing high-quality medical services is of great importance in the imaging department, as there is a growing focus on personal health, and high-quality services can lead to improved patient outcomes. Many quality improvement (QI) programs with good guidance and fine measurement for improvement have been reported to be effective. In order to improve the quality of ultrasound departments in China, we conducted this study of a national quality improvement program. A total of 1297 public hospitals were included in this QI program on ultrasound departments in China from 2017 to 2019. The effect of this QI program was investigated, and potential factors, including hospital level and local economic development, were considered. The outcome indicators, the positive rate and diagnostic accuracy, were improved significantly between the two phases (positive rate, 2017 vs. 2019: 66.21% vs. 73.91%, p < 0.001; diagnostic accuracy, 2017 vs. 2019: 85.37% vs. 89.74%; p < 0.001). Additionally, they were improved in secondary and tertiary hospitals, with the improvement in secondary hospitals being greater. Notably, the enhancement of diagnostic accuracy in low-GDP provinces was almost 20%, which was more significant than the enhancement in high-GDP provinces. However, the important structural indicator, the doctor-to-patient ratio, decreased from 1.05:10,000 to 0.96:10,000 (p = 0.026). This study suggests that the national ultrasound QI program improved the outcome indicators, with secondary-level hospitals improving more than tertiary hospitals and low-GDP provinces improving more than high-GDP regions. Additionally, as there is a growing need for ultrasound examinations, more ultrasound doctors are needed in China.

Effective therapies for renal fibrosis, the common endpoint for most kidney diseases, are lacking. We previously reported that alternative polyadenylation (APA) drives transition from acute kidney injury to chronic kidney disease, suggesting a potential role for APA in renal fibrogenesis. Here, we found that among canonical APA writers, CSTF2 expression was upregulated in tubular epithelial cells (TEC) of fibrotic kidneys. CSTF2 was also identified as a TGF-β-inducible pro-fibrotic gene. Further analysis revealed that CSTF2 promoted epithelial-mesenchymal transition (EMT) and extracellular matrix (ECM) overproduction in TEC by inducing 3'UTR shortening and upregulation of the expression of basic fibroblast growth factor 2 (FGF2). Additionally, 3'UTR shortening stabilised FGF2 mRNA through miRNA evasion. Interestingly, FGF2 enhanced CSTF2 expression, leading to the forming of a CSTF2-FGF2 positive loop in TEC. Furthermore, CSTF2 knockdown alleviated unilateral ureteral obstruction-induced renal fibrosis in vivo. Finally, we developed a CSTF2-targeted antisense oligonucleotide (ASO) and validated its effectiveness in vitro. These results indicate that the expression of the APA writer, CSTF2, is upregulated by TGF-β and CSTF2 facilitates TGF-β-induced FGF2 overexpression, forming a TGF-β-CSTF2-FGF2 pro-fibrotic axis in TEC. CSTF2 is a potentially promising target for renal fibrosis that does not directly disrupt TGF-β.

Renal ischemia-reperfusion injury (IRI) is an inevitable process in kidney transplantation, leading to acute kidney injury, delayed graft function (DGF), and even graft loss. Ferroptosis is an iron-dependent regulated cell death in various diseases including IRI. We aimed to identify subtypes of renal IRI and construct a robust DGF predictive signature based on ferroptosis-related genes (FRGs). A consensus clustering analysis was applied to identify ferroptosis-associated subtypes of 203 renal IRI samples in the GSE43974 dataset. The FRG-associated DGF predictive signature was constructed using the Least Absolute Shrinkage and Selection Operator (LASSO), and its robustness was further verified in the validation set GSE37838. The present study revealed two ferroptosis-related patient clusters (pBECN1 and pNF2 cluster) in renal IRI samples based on distinct expression patterns of BECN1 and NF2 gene clusters. Cluster pBECN1 was metabolically active and closely correlated with less DGF, while pNF2 was regarded as the metabolic exhausted subtype with higher incidence of DGF. Additionally, a six-gene (ATF3, SLC2A3, CXCL2, DDIT3, and ZFP36) ferroptosis-associated signature was constructed to predict occurrence of DGF in renal IRI patients and exhibited robust efficacy in both the training and validation sets. High-risk patients tended to have more infiltration of dendritic cells, macrophages, and T cells, and they had significantly enriched chemokine-related pathway, WNT/β-catenin signaling pathway, and allograft rejection. Patients with low risks of DGF were associated with ferroptosis-related pathways such as glutathione and fatty acid metabolism pathways. In conclusion, patient stratification with distinct metabolic activities based on ferroptosis may help distinguish patients who may respond to metabolic therapeutics. Moreover, the DGF predictive signature based on FRGs may guide advanced strategies toward prevention of DGF in the early stage.

Multiple objective assessments have been used to assess the activity of keloids to compare different therapeutic regimens and facilitate the best individual treatment choice for patients, but none of them are standardized. A multimodal photoacoustic/ultrasonic (PA/US) imaging system, including photoacoustic imaging, elastography, ultra-micro-angiography, and conventional US technologies (gray scale US, color Doppler US, and power Doppler US), was applied to evaluate keloids by a radiologist. Growing stages were defined by patients, and Vancouver Scar Scale (VSS) was assessed by a plastic surgeon. A comprehensive model based on multimodal ultrasound parameters (poor-echo pattern, high vascular density, decreased elasticity, and low SO2 within the keloid) and VSS might be a potential indicator of active keloids, comparing with VSS alone. The multimodal PA/US imaging system could be a promising technique for keloids assessment.

Well-described evidence has demonstrated the critical roles of aerobic glycolysis in triple-negative breast cancer (TNBC) oncotherapy. Moreover, next-generation high-throughput sequencing indicates the potential regulation of energy metabolism by circular RNAs (circRNAs) in TNBC. However, circRNA modulation of TNBC aerobic glycolysis is still unclear. Here, the present research aimed to investigate the function and underlying mechanisms of novel circPDCD11 (hsa_circ_0019853) in TNBC aerobic glycolysis. The results revealed that circPDCD11 expression was significantly upregulated in TNBC tissues and cells. Clinical data demonstrated that the high expression of circPDCD11 was closely correlated with a poor prognosis and acted as an independent risk factor for TNBC prognosis. Functionally, in vitro gain- and loss-of-function experiments revealed that circPDCD11 accelerated glucose uptake, lactate production, ATP generation, and the extracellular acidification rate in TNBC cells. In vivo, circPDCD11 silencing repressed tumor growth. Mechanistically, circPDCD11 acted as a miRNA sponge to enhance LDHA expression by sponging miR-432-5p. In conclusion, these combined results demonstrated that circPDCD11 acts as an oncogene for TNBC, providing a promising prognostic biomarker for TNBC.

Background: The number of publications on SMAD7 in the field of oncology is increasing rapidly with an upward tendency. In most cases, the mechanisms of carcinogenesis usually relate to disorders of signaling activity. Considering the crucial role of SMAD7 in the crosstalk of multiple signaling pathways, it is necessary to clarify and define the dominant research topics, core authors, and their cumulative research contributions, as well as the cooperative relationships among documents or researchers.Methods: Altogether, 3477 documents were retrieved from the Web of Science Core Collection with the following criteria: TS= (SMAD7 OR SMAD7-protein OR Small-Mothers-Against-Decapentaplegic-7) refined by WEB OF SCIENCE CATEGORY (ONCOLOGY) AND [excluding] PUBLICATION YEARS (2021) AND DOCUMENT TYPES (ARTICLE OR REVIEW) AND LANGUAGES (ENGLISH) AND WEB OF SCIENCE INDEX (Web of Science Core Collection, SCI), and the timespan of 2011–2020. Bibliometric visualization analysis was conducted with CiteSpace and VOSviewer.Results: The number of documents grew each year. A total of 2703 articles and 774 reviews were identified from 86 countries/regions, 3524 organizations, 928 journals, and 19,745 authors. China was the most prolific country, with 1881 documents. Contributions from China, the United States, and Germany were the most substantial. The most influential author was Lan Huiyao at The Chinese University of Hong Kong, with 24 publications and 2348 total citations. The bibliometric analysis showed that multilateral cooperation among diverse institutions or investigators was beneficial to high-quality outputs. The keyword “PPAR-gamma” exhibited the strongest burst in recent years, suggesting a potent research focus in the future.Conclusion: Research on SMAD7 in oncology is continuously developing. Bibliometrics is an interesting tool to present the characteristics of publication years, main authors, and productive organizations in a visualized way. It is worth mentioning that a prospective focus might be the specific mechanism of the interaction of PPAR-gamma with SMAD7 in oncology. In all, bibliometric analysis provides an overview and identifies potential research trends for further studies in this academic field.

We examined 14 benign and 26 malignant breast nodules by a handheld dual-modal PA/US imaging system and analyzed the data using the quantitative and semi-quantitative method. The PA signal spatial density and PA scores of different regions of the benign and malignant nodules were compared, and the diagnostic performances of two diagnostic methods based on PA parameters were evaluated. For both quantitative and semi-quantitative results, significant differences in the distributions of PA signals in different regions of benign and malignant breast lesions were identified. The PA parameters showed good performance in diagnosing breast cancer, indicating the potential of PAI in clinical utilization.

Silver nitrate (AgNO3) was used to prepare Silver nanoparticles (Ag NPs), where polyphenols obtained from leaf extract of Cocos nucifera were used as capping and reducing agents. Furthermore, Characterization techniques like HRTEM, UV–Vis, XRD and FT-IR were used to study the as-prepared Ag NPs. With the help of various spectroscopic and microscopic techniques, the as-synthesized silver nanoparticles were characterized. Various analyses like HRTEM, EDS, FT-IR, XRD and UV–Vis have confirmed the synthesis of silver nanoparticles. Images from HRTEM microscope confirmed the formation of small, spherical and poly dispersive AgNPs having 10 nm average size. In the current paper, the possible synergistic impact of silver nanoparticles and ultrasound waves was examined as a potential route to cancer therapy. Eventually, AgNPs were produced, characterized and then exposed to MCF-7 cell lines in various concentrations. Cells were administrated with ultrasonic waves after 24 h, and the viability of cells after treatment was recorded at 72, 48 and 24 h. Ultrasound was noticed to have the potential to promote ROS development in the cells causing to cell death. In addition, although the results of current study revealed that Ag NPs at higher concentrations (100 μg/mL) function as sonosensitizer, and reinforce the production of ROS, yet, further research and study in vitro and particularly in vivo are required to prove the assumption.

Keratinocyte growth factor receptor (KGFR), also known as fibroblast growth factor receptor (FGFR)2 IIIb, is located in many types of epithelial cells and is activated by four known ligands (FGF-1, FGF-3, FGF-7 (also known as KGF) and FGF-10) that are predominantly synthesized by mesenchymal cells. In the early stage of atherosclerosis, vascular smooth muscle cells (VSMC) transform from a contractile to a synthetic phenotype, proliferate and migrate into the intima. Previously, FGF-7 mRNA expression was reported in VSMC, but KGFR mRNA was not detected. In the present study, we attempted to determine whether KGFR is localized in VSMC cultured from rat aorta and VSMC in human normal and atherosclerotic coronary arteries. Expression of KGFR mRNA and its protein was detected in cultured rat VSMC by reverse transcription-polymerase chain reaction and western blot analysis, respectively. Immunohistochemically, KGFR was localized in the VSMC of the outer layer of the media in normal human coronary arteries. Furthermore, it was localized in the VSMC of the media and thickened intima of atherosclerotic arteries. Recombinant FGF-7 and/or FGF-10 proteins stimulated the growth of cultured rat VSMC. These findings indicate that KGFR localized in VSMC may contribute to the proliferation of VSMC in normal and atherosclerotic arteries.

Lumican is a member of a small leucine-rich proteoglycan family. Members of this family play an important role in cell migration and proliferation during embryonic development, tissue repair, and tumor growth. Lumican is reported to be overexpressed during the wound-healing process in the cornea and ischemic and reperfused heart. Recently, we found that lumican mRNA and its protein are expressed in cultured vascular smooth muscle cells (VSMCs) from the rat aorta. However, the expression and role of lumican in human atherosclerotic tissues are not clearly elucidated. In the present study, we aimed to clarify whether lumican is expressed in VSMCs and its localization in human coronary atherosclerotic tissues. The lumican protein and its mRNA were expressed in a small number of VSMCs in the media of normal coronary artery, but the lumican protein was not localized in the medial stroma. In contrast, the lumican protein and its mRNA were expressed in most of VSMCs that migrated into the thickened intima, but not in infiltrating foamy macrophages. The lumican protein was prominently localized in the thickened intimal stroma. The lumican protein and its mRNA were also expressed in VSMCs in the inner layer of the media and its protein was localized in medial stromal tissues. These findings indicate that the lumican protein is mainly synthesized by intimal and medial VSMCs in coronary atherosclerosis and that lumican contributes to collagen fibrillogenesis of coronary atherosclerosis.

This study was undertaken to biochemically and immunohistochemically clarify the expression of basic fibroblast growth factor (bFGF), insulin-like growth factor-I (IGF-I), fibroblast growth factor receptor (bFGFR), insulin-like growth factor-I receptor (IGF-IR) and vascular smooth muscle cell (VSMC) growth by using Streptozotocin (STZ) treated rat serum. At 12, 16, 24 weeks after STZ administration, blood sera were collected from STZ treated rats. STZ treated rat sera promoted much more vascular smooth muscle cel proliferation than control sera. IGF-I was increased in the sera of STZ treated rats. Also according to western blot analysis, the protein synthesis of bFGFR and IGF-IR in the VSMCs was increased in STZ treated rat sera. Immunohistochemically, bFGF, IGF-I and their receptors were much more localized in VSMCs in STZ treated rat sera than in control sera. These results suggest that the growth factors and their receptors produced in VSMCs in STZ treated rat serum may contribute to the proliferation of VSMCs in autocrine and paracrine patterns.

Proliferation of vascular smooth muscle cells (VSMC) represents an essential event in the developement of diabetic atherosclerosis. Previous studies suggest that several cytokines and growth factors mediate the proliferation capability in VSMC from diabetic animals. In addition, advanced glycation end products (AGE) and receptor for AGE (RAGE) are important for pathologic features of diabetic complications. In the present study, we attempted to clarify the roles of AGE and RAGE in the proliferation of VSMC using streptozotocin (STZ)-treated rat sera and aortic SMC prepared from non-diabetic rats. AGE levels increased in the diabetic sera, which enhanced the growth of VSMC in proportion to their diabetic periods. AGE-bovine serum albumin (BSA) prepared in vitro also exhibited a stimulatory effect on VSMC growth. The endocytic uptake of AGE and enhanced RAGE expression in VSMC after culture with diabetic sera were observed. In addition, anti-AGE and anti-RAGE antibodies inhibited these stimulatory effects on VSMC growth. These findings suggest that AGE in diabetic rat sera may cause an enhanced effect on VSMC proliferation. However, the concentrations of AGE in diabetic sera were much lower than that of AGE-BSA which demonstrated a significant stimulatory effect on VSMC growth. The magnitude of the VSMC growth-enhancement by the diabetic sera was markedly greater than that by the AGE-BSA solution. In conclusion, the AGE-RAGE interaction in VSMC, in addition to growth factors induced by AGE, contributes to the stimulatory effect of diabetic sera on VSMC proliferation which can accelerate atherosclerosis.

1-3 . Atherosclerosis is a major cause of the morbidity and mortality associated with myocardial infarction and cerebral bleeding 4 . Intimal thickening with lipid depo‑ sition affects the elastic properties and contributes to the hydrophobic changes that occur in the intima of arteries. The anisotropic elasticity induced by micro‑ elastic changes is associated with functional distur‑ bances of the vascular wall 5 . In the atheromatous lesion infiltrated macrophages lymphocytes and platelets produce various kinds of cytokines and growth factors 6 . These cytokines and growth factors are synthesized by vascular cells such as the endothelial and smooth muscle cells and induce the inflammatory‑fibroproliferative response that is associated with cell proliferation and the production of extracellular matrix( ECM ) 7 . Proliferated smooth muscle cells induce local changes in the production of extracellular matrix components and may contribute to local weakening of the fibrous cap 8 . In the review presented here we discuss the mechanisms underly‑ ing the devolopment and fragility of atherosclerosis. 1.The role of endothelial dysfunction in athero‑ sclerosis Normal endothelial cells synthesize prostacyclin plasminogen activator factor VIII including the von Willebrand factor and various other components 1 .