Green roof development knowledge map: A review of visual analysis using CiteSpace and VOSviewer.

Green roofs are generally acknowledged as environmentally sustainable roof systems with several environmental, economic, and social benefits, as well as an effective and practical strategy for mitigating the negative consequences of urbanization. In this paper, we used CiteSpace and VOSviewer bibliometric software for visual analysis, citation analysis, co-authorship network, co-citation analysis, and keyword analysis for descriptive statistics on 3986 articles on "green roofs" published in the Web of Science core database since 2000. Descriptive statistics were used for citation analysis, co-authorship network, co-citation analysis, and keyword analysis. According to a review of green roofing-related research literature, (1) Through analysis from three dimensions of country, institution, and author, it was found that China, the United States, and Italy ranked among the top three countries in terms of green roof publication volume; All but three of the top 10 institutions in terms of publications are from China and all are from developed countries; A large-scale collaborative network has not yet formed among authors. (2) Through keyword clustering analysis, it was found that "green roof," "performance," and "UHI" were the three keywords with the highest frequency. The research direction of this theme mainly includes five primary themes: rainwater management, urban biodiversity, building energy efficiency, alleviating urban heat islands and improving air quality, sustainable development, and public health. Through keyword hot words, it is found that the frequency of occurrence is relatively high, mainly involving energy conservation, alleviating urban heat islands, biodiversity, and sustainable development. The research on sustainable development, its impact on urban microclimate, and air quality remains a hot topic through keyword highlighting. (3) Co-citation analysis was used to identify the most influential journals, highly cited publications, and authors. (4) Three potential study objectives have been identified: synergistic development with other green infrastructures from an urban planning standpoint, localized research on green roofs, and photovoltaic green roofs.

Downregulation of miR-100-5p in cancer-associated fibroblast-derived exosomes facilitates lymphangiogenesis in esophageal squamous cell carcinoma.

BACKGROUND: Esophageal squamous cell carcinoma (ESCC), an aggressive gastrointestinal tumor, often has high early lymphatic metastatic potential. Cancer-associated fibroblasts (CAFs) are primary components in tumor microenvironment (TME), and the impact of CAFs and its derived exosomes on lymphangiogenesis remains elusive. MATERIALS AND METHODS: CAFs and the microlymphatic vessel density (MLVD) in ESCC was examined. Exosomes were extracted from primary normal fibroblast (NFs) and CAFs. Subsequently, tumor-associated lymphatic endothelial cells (TLECs) were treated with these exosomes, and the effect on their biological behavior was examined. miR-100-5p was selected as the target miRNA, and its effect on TLECs was examined. The target of miR-100-5p was predicted and confirmed. Subsequently, IGF1R, PI3K, AKT, and p-AKT expression in TLECs and tumors treated with exosomes and miR-100-5p were examined. RESULTS: A large number of CAFs and microlymphatic vessels were present in ESCC, leading to a poor prognosis. CAF-derived exosomes promoted proliferation, migration, invasion, and tube formation in TLECs. Further, they also enhanced lymphangiogenesis in ESCC xenografts. miR-100-5p levels were significantly lower in CAF-derived exosomes than in NF-derived exosomes. miR-100-5p inhibited proliferation, migration, invasion, and tube formation in TLECs. Further, miR-100-5p inhibited lymphangiogenesis in ESCC xenografts. Mechanistic studies revealed that this inhibition was mediated by the miR-100-5p-induced inhibition of IGF1R/PI3K/AKT axis. CONCLUSION: Taken together, our study demonstrates that CAF-derived exosomes with decreased miR-100-5p levels exhibit pro-lymphangiogenesis capacity, suggesting a possibility of targeting IGF1R/PI3K/AKT axis as a strategy to inhibit lymphatic metastasis in ESCC.

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With the development of high-density and high-rise buildings on both sides of the street, widespread attention has been paid to the applicability of the traditional greening model of 'the more trees, the better atmospheric environment' in dealing with air pollution in urban street canyons. Clarifying the characteristics of street canyons greening and its planting design pattern on the reduction of emission pollutants by vehicles is an important prerequisite for the improvement of air quality in the street canyons. Based on literature review, we compared the applicability and limitations of the three methods, including field observation, wind tunnel test, and numerical simulation. We further analyzed the effects of roadside trees and hedges on the dispersion and deposition of air pollutants, and put forward a framework of adaptive greening design for air quality improvement. Finally, we proposed that future studies should address the creation of graphic languages for roadside greening design, the development of technical guidelines for evaluating the exposure of air pollution, and the optimization of parameterization schemes for the physical processes of greening effect in computational fluid dynamics models. Overall, our review could provide ideas and reference for the subsequent research.

Exosomal miR-301a-3p from esophageal squamous cell carcinoma cells promotes angiogenesis by inducing M2 polarization of macrophages via the PTEN/PI3K/AKT signaling pathway.

BACKGROUND: Growing evidence has indicated that tumor-associated macrophages (TAMs) promote tumor angiogenesis. However, the mechanisms underlying the pro-angiogenic switch of TAMs remains unclear. Here, we examined how exosomal miR-301a-3p secreted by esophageal squamous cell carcinoma (ESCC) cells triggers the pro-angiogenic switch of TAMs. METHODS: We quantified miR-301a-3p levels in ESCC tumors using qRT-PCR. Macrophage phenotypes were identified using flow cytometry and qRT-PCR. The pro-angiogenic ability of TAMs was measured using the CCK-8 assay, scratch assay, Transwell migration and invasion assay, and tube formation assay. The mechanism by which exosomal miR-301a-3p secreted by ESCC cells triggers the pro-angiogenic switch of TAMs was elucidated using western blots, qRT-PCR, and a dual-luciferase reporter assay. RESULTS: We observed anomalous miR-301a-3p overexpression in ESCC tumor tissues and cell lines. Then, we verified that ESCC-derived exosomes promoted angiogenesis by inducing macrophage polarization into M2 type, and exosomal miR-301a-3p secreted by ESCC cells was responsible for this effect. Finally, we discovered that exosomal miR-301a-3p promoted M2 macrophage polarization via the inhibition of PTEN and activation of the PI3K/AKT signaling pathway, subsequently promoting angiogenesis via the secretion of VEGFA and MMP9. CONCLUSION: The pro-angiogenic switch of TAMs is triggered by exosomal miR-301a-3p secreted from ESCC cells via the PTEN/PI3K/AKT signaling pathway. Although tumor angiogenesis can be regulated by a wide range of factors, exosomal miR-301a-3p could hold promise as a novel anti-angiogenesis target for ESCC treatment.

Relationship Between PTEN and Angiogenesis of Esophageal Squamous Cell Carcinoma and the Underlying Mechanism.

Esophageal squamous cell carcinoma (ESCC) has high morbidity and mortality rates owing to its ability to infiltrate and metastasize. Microvessels formed in early-stage ESCC promote metastasis. Phosphatase and tensin homolog (PTEN) mediates macrophage polarization, but its effect and mechanism on early ESCC angiogenesis are unclear. To explore the molecular mechanism underlying early ESCC metastasis through blood vessels, we investigated the relationship between PTEN/phosphoinositide 3-kinase (PI3K)/p-AKT protein levels, number of infiltrated macrophages, and angiogenesis in ESCC and ESCC-adjacent normal esophageal mucosa tissues from 49 patients. Additionally, PTEN was overexpressed or silenced in the esophageal cancer cell line EC9706, and its supernatant served as conditioning medium for M1 tumor-associated macrophages (TAMs). The culture medium of macrophages served as conditioning medium for esophageal tumor-associated vascular endothelial cells (TECs) to study the biological behavior of PTEN-plasmid, PTEN-siRNA, and control TECs. We found that M1 TAM infiltration in ESCC tissues was low, whereas M2 TAM infiltration was high. Microvessel density was large, PTEN was down-regulated, and the PI3K/AKT pathway was activated in ESCC specimens. These parameters significantly related to the depth of tumor invasion, lymph node metastasis, and pathological staging of ESCC. Silencing of PTEN in EC9706 cells significantly activated the PI3K/AKT signaling pathway in macrophages, promoting M1-to-M2 TAM polarization and enhancing TECs' ability to proliferate, migrate, invade, form tubes, and secrete vascular endothelial growth factor. We believe that PTEN silencing in esophageal cancer cells activates the PI3K/AKT signaling pathway in macrophages via the tumor microenvironment, induces M2 TAM polarization, and enhances the malignant behavior of TECs, thereby promoting ESCC angiogenesis. Our findings lay an empirical foundation for the development of novel diagnostic and therapeutic strategies for ESCC.

Tumor-associated macrophages modulate angiogenesis and tumor growth in a xenograft mouse model of multiple myeloma.

Tumor-associated macrophages (TAMs) are closely associated with poor multiple myeloma (MM) prognosis. Therefore, in-depth understanding of the mechanism by which TAM supports MM progression may lead to its effective treatment. We used the MM nude mouse subcutaneous xenograft model to evaluate the efficacy of the macrophage-depleting agent clodronate liposome (Clo) against MM and elucidate the mode of action of this therapy. At the same time, observe whether the elimination of TAM in vivo while silencing the expression of VEGFA has the same effect as in vitro experiments. We also used Clo to eliminate macrophages and reinjected M1 or M2 TAM through mouse tail veins to investigate the effects of various macrophage subtypes on MM xenograft tumor growth. We applied qRT-PCR, immunohistochemistry, and enzyme-linked immunosorbent assay to quantify VEGFA, CD31, and CD163 expression in tumor tissues and sera. Removal of TAMs from the tumor microenvironment impeded tumor growth. The combination of Clo plus VEGFA siRNA had a stronger inhibitory effect on tumor growth than Clo alone, and M2 and M1 macrophages promoted and inhibited tumor growth, respectively. Macrophage depletion combined with cytokine blocking is a promising MM treatment. Targeted M2 macrophage elimination together with cytokine block may be more effective at inhibiting MM growth than either treatment alone. The results of the present study lay an empirical foundation for the development of novel therapeutic strategies for MM.

Exosome-derived miR-let-7c promotes angiogenesis in multiple myeloma by polarizing M2 macrophages in the bone marrow microenvironment.

Angiogenesis is an integral part of the multiple myeloma (MM) microenvironment, and affects tumorigenesis, progression, invasion, and metastasis. Exosomes are essential for cell-cell communication and help in regulating the bone marrow microenvironment. Herein, we investigated macrophage polarization and angiogenesis in MM in vitro via exosome-derived miR-let-7c. We observed that exosomal miR-let-7c secreted by mesenchymal stem cells promoted M2 macrophage polarization, thereby enhancing angiogenesis in the bone marrow microenvironment. Suppressing miR-let-7c expression significantly inhibited vascular endothelial cell function in myeloma. Thus, exosomal miR-let-7c may be a reliable biomarker for early prediction of tumor progression and a promising therapeutic target for MM.

Synergistic effects of multiple myeloma cells and tumor-associated macrophages on vascular endothelial cells in vitro.

Angiogenesis is a prerequisite for multiple myeloma development. Tumor cells can stimulate angiogenesis by secreting vascular endothelial growth factor A (VEGFA), but we previously reported that tumor angiogenesis was not significantly reduced when VEGFA expression was inhibited in myeloma cells. Tumor-associated macrophages (TAMs) are important components of the tumor microenvironment and have been reported to be involved in the regulation of angiogenesis. In this study, we performed in vitro macrophage coculture studies and studies with RPMI 8226 and TAMs cell-conditioned media to explore their effects on the proliferation, migration, and tube formation of human umbilical vein endothelial cells (HUVECs). Our results showed that M2 macrophages and RPMI 8226 cells could synergistically promote HUVEC proliferation, migration, and tube formation, and that VEGFA depletion in both cell types suppressed HUVEC tube formation ability. Conversely, M1 macrophages inhibited the tube formation in HUVECs. Mechanistically, M2 macrophage secretion of VEGFA may affect vascular endothelial growth factor receptor 1 signaling to regulate angiogenesis. In summary, our results suggest that macrophage clearance or inducing of transformation of M2 macrophages into M1 macrophages are potential treatment strategies for multiple myeloma.

ciRS-7 Promotes the Proliferation and Migration of Papillary Thyroid Cancer by Negatively Regulating the miR-7/Epidermal Growth Factor Receptor Axis.

PURPOSE: The incidence of papillary thyroid cancer (PTC) is increasing, and traditional diagnostic methods are unsatisfactory. Therefore, identifying novel prognostic markers is very important. ciRS-7 has been found to play an important role in many cancers, but its role in PTC has not been reported. This study was performed to evaluate the biological role and mechanism of ciRS-7 in PTC. Material and Methods. The expression of ciRS-7 in PTC tissues and the matched adjacent tissues was determined by quantitative reverse transcription polymerase chain reaction (qRT-PCR). The PTC cell lines (TPC-1 and BCPAP) were used to evaluate the role of ciRS-7. ciRS-7-siRNA and overexpression plasmid were constructed and transfected into PTC cells. A CCK-8 assay and colony formation assay were performed to explore the effects of ciRS-7 on cell proliferation. Annexin V/PI staining and FACS detection were used to detect cell apoptosis. Wound healing assay was performed to detect cell migration. A transwell assay was conducted to explore the effects of ciRS-7 on invasion and migration. Western blotting was performed to evaluate protein expression. The luciferase reporter system was used to determine the underlying mechanism of miR-7. RESULT: ciRS-7 was highly expressed in PTC tissues and cell lines compared with the corresponding controls. In vitro study showed that ciRS-7 silencing suppressed proliferation, migration, and invasion of TPC-1 and BCPAP. Mechanistically, the effects of ciRS-7 on invasion and migration may be related to epithelial-mesenchymal transition (EMT). ciRS-7 silencing could attenuate effects on PTC cells induced by miR-7 knockdown. Epidermal growth factor receptor (EGFR), which was demonstrated to be a target of miR-7, decreased significantly in ciRS-7-siRNA PTC cells. Overexpression of EGFR also attenuated effects of PTC cells induced by silencing ciRS-7. CONCLUSION: ciRS-7 was significantly upregulated in PTC tissues, and it promoted the progression of PTC by regulating the miR-7/EGFR axis. ciRS-7 is a promising prognostic biomarker and therapeutic target in PTC.

Terminal osseous dysplasia with pigmentary defects in a Chinese girl with the FLNA mutation: A case report and published work review.

Terminal osseous dysplasia with pigmentary defects (TODPD) is an extremely rare X-linked dominant syndrome characterized by pigmentary skin defects, cutaneous digital fibromas and skeletal anomalies. Recent studies have identified that TODPD is caused by a unique variant, c.5217G>A (p.Val1724_Thr1739del), in the FLNA gene, which could in turn lead to the elastic fiber abnormality in TODPD. We herein present a rare case of TODPD in a Chinese girl due to an FLNA c.5217G>A heterozygous mutation, but the skin lesion biopsy showed that the elastic fibers were within normal limits in the dermis. A published work review of TODPD with the FLNA mutation from various origins is also included in this paper. To the best of our knowledge, this is the first report on TODPD with the FLNA mutation in China.

Association of dietary intake of folate, vitamin B6 and B12 and MTHFR genotype with breast cancer risk.

AIM: We aimed to investigate the associations of dietary intake of folate, vitamin B6 and B12 and MTHFR genotype with breast cancer in a Chinese population. METHODS: A matched case-control study was conducted, and 435 patients with newly diagnosed and histologically confirmed breast cancer and 435 controls were collected. The folate intake, vitamin B6 and vitamin B12 were calculated, and MTHFR C665T, C677T and A1298C were analyzed by PCR-RFLP. RESULTS: We found vitamin B12 was likely to reduce the risk of breast cancer, and MTHFR 665TT was associated with increased risk of breast cancer. Folate intake, vitamin B12 intake and variants of MTHFR C677T and MTHFR A1298C demonstrated no association with risk of breast cancer. However, we found patients with low intake of vitamin B6 and MTHFR 665TT genotype had a higher risk of breast cancer (OR=1.87, 95% CI=1.29-2.77), the association being less pronounced among subjects with a moderate intake of vitamin B6 and MTHFR 665TT genotype (OR=1.58, 95% CI=1.03-2.49, P=0.03). CONCLUSION: Our study indicated that the MTHFR C665T polymorphism and vitamin B6 are associated with risk of breast cancer, which indicated roles for nutrients in developing breast cancer.