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Extensive research into green technologies is driven by the worldwide push for eco‐friendly materials and energy solutions. The focus is on synergies that prioritize sustainability and environmental benefits. This study explores the potential of abundant, non‐toxic, and sustainable resources such as paper, lignin‐enriched paper, and cork for producing laser‐induced graphene (LIG) supercapacitor electrodes with improved capacitance. A single‐step methodology using a CO2 laser system is developed for fabricating these electrodes under ambient conditions, providing an environmentally friendly alternative to conventional carbon sources. The resulting green micro‐supercapacitors (MSCs) achieve impressive areal capacitance (≈7–10 mF cm−2) and power and energy densities (≈4 μW cm‐2 and ≈0.77 µWh cm−2 at 0.01 mA cm−2). Stability tests conducted over 5000 charge–discharge cycles demonstrate a capacitance retention of ≈80–85%, highlighting the device durability. These LIG‐based devices offer versatility, allowing voltage output adjustment through stacked and sandwich MSCs configurations (parallel or series), suitable for various large‐scale applications. This study demonstrates that it is possible to create high‐quality energy storage devices based on biodegradable materials. This development can lead to progress in renewable energy and off‐grid technology, as well as a reduction in electronic waste. [ABSTRACT FROM AUTHOR]

Costa C, Soares R, Schmitt F. Angiogenesis: now and then. APMIS 2004;112:402–12.Angiogenesis or new blood vessel formation plays an essential role during embryogenesis, adult vascular remodeling and in several pathological disorders, as in tumor development. Although sprouting of blood vessels is the principal angiogenic mechanism, additional ones, such as the recruitment of bone marrow-derived cells, have recently been described. These processes are controlled by several molecules, although members of the VEGF family of angiogenic factors and its receptors seem to be the main mediators. Initially, VEGF receptors were described as endothelial specific; however, further studies have reported their presence in several types of cells of non-endothelial origin, such as tumor cells. This VEGF receptor altered expression has suggested an angiogenesis-independent growth advantage mechanism on certain types of cancers by the generation of autocrine loops. A possible role in tumorigenesis and a potential novel target in cancer therapy have been hypothesized. Detection of other receptors and molecules considered to be angiogenic players has also been observed on tumor cells. Currently, their clinical significance as well as their potential as therapeutic targets for the treatment of certain cancers is being evaluated, having in mind the future development of promising mechanism-based therapies. The aspects mentioned above are the main focus of this review, which aims to throw light on recent findings respecting angiogenesis and novel therapeutic approaches. [ABSTRACT FROM AUTHOR]

Schistosoma haematobium, a parasitic flatworm that infects more than 100 million people, mostly in the developing world, is the causative agent of urogenital schistosomiasis, and is associated with a high incidence of squamous cell carcinoma (SCC) of the bladder. During infection, eggs are deposited in the bladder causing an intense inflammatory reaction. Angiogenesis is defined as the formation of new blood vessels from preexisting ones and is recognized as a key event in cell proliferation and carcinogenesis and spread of malignant lesions. A growing amount of evidence points to angiogenesis playing a key role in schistosomiasis-associated bladder cancer. Thus, identifying biomarkers of this process plays an important role in the study of cancer. Here, we review recent findings on the role of angiogenesis in bladder cancer and the growth factors that induce and assist in their development, particularly SCC of the bladder associated to urogenital schistosomiasis. [ABSTRACT FROM AUTHOR]

Presents a letter to the editor concerning triggering transcription growth factor-beta and notch signalling cross-talk.

Cylindrospermopsin (CYN) is a cyanotoxin that has raised serious concerns about public health in many parts of the world. It can bioaccumulate and affect the health of aquatic organisms, but despite this, few studies have been conducted on CYN uptake and clearance in fish. In this paper, the authors evaluate the uptake and clearance of CYN in the muscle tissue and viscera of juvenile tilapia (Oreochromis niloticus) after exposure to aqueous extracts and whole cells of Cylindrospermopsis raciborskii (CYN‐producer). CYN blended with commercial fish food, and three experiments were conducted. In the first trial, fish food, and aqueous extracts containing 0.31 μg CYN g−1 of food per day, was administered to tilapia for 15 days. In the second trial, fish were provided food and intact cells (5.4 μg CYN g−1 of food per day) for 15 days. In the last trial, they were provided fish food and aqueous extracts (0.8 μg CYN g−1 of food per day) for 12 days, and for the next 10 days, the animals were fed food without toxic cell extracts (to simulate a clearance period). The concentration of CYN in muscle tissue and viscera was analysed using ELISA. In the case of juvenile tilapia, the presence of CYN was higher in viscera than in muscle tissue, and the toxin remained in the tissues even after 10 days without the addition of contaminated food. The results suggest that tilapia represents a potential source of CYN transfer through the food web, and this shows the need for a continuous monitoring of this compound in organisms that are used for human and animal consumption. [ABSTRACT FROM AUTHOR]

Angiogenesis and inflammation are becoming distinguished players in the pathogenesis of many heterogeneous diseases, such as diabetes, cardiovascular disease, and cancer. Therefore, it is crucial to study new compounds that are able to modulate these events. Isoxanthohumol (IXN) is a polyphenol with antioxidant, anti-inflammatory, and antiangiogenic properties. The aim of this study was to evaluate the effects of IXN on blood vessel proliferation and maturation and describe underlying molecular mechanisms in endothelial cells (ECs) and vascular smooth muscle cells (VSMCs). Angiogenic profile of IXN was analyzed by retinal angiogenesis at different time points. IXN modulation of angiogenic and inflammatory signaling pathways was evaluated by Western blotting on EC and VSMC cultures. IXN inhibited by 20% sprouting angiogenesis and decreased vascular coverage by mural cells up to 39%. IXN of 10 µM also decreased inflammatory signals, namely tumor necrosis factor alpha (TNF-α) (26 and 40%) and factor nuclear kappa B (24 and 42%) in human aortic smooth muscle cells (HASMCs) and human umbilical vein endothelial cells (HUVECs). Angiogenic regulators, including vascular endothelial growth factor receptor 2 (HUVEC, 55%), angiopoietins 1 (HUVEC, 39%; HASMC, 35%), angiopoietin 2 (HUVEC, 38%), and Tie2 (HUVEC, 56%) were also inhibited by 10 µM of IXN treatments. Akt activation was reduced by 47% in HUVEC-treated cells and Erk activation was also reduced by 52 and 69% upon IXN treatment of HUVEC and HASMC. IXN seems to regulate in vivo vascular proliferation and stabilization and the EC-VSMC-inflammatory crosstalk, leaving this molecule as an interesting nutritional player for angiogenesis and inflammation-related diseases. © 2013 BioFactors, 39(6):608-622, 2013 [ABSTRACT FROM AUTHOR]

. Purpose: To evaluate the changes of vascular endothelial growth factor (VEGF) plasma levels after intravitreal injections of ranibizumab or bevacizumab in patients with exudative age-related macular degeneration (AMD). Methods: Forty-three patients with exudative AMD and 19 age- and sex-matched control patients without chorioretinal diseases were studied. Nineteen patients were treated with intravitreal ranibizumab 0.5 mg, 24 with intravitreal bevacizumab 1.25 mg. Blood samples were collected just before the first injection, and 28 days after three initial consecutive injections performed in 4-weekly intervals (loading dose). Concentration of VEGF in the plasma was measured by ELISA. Results: At baseline, the median VEGF concentrations in controls were 180.97 pg/ml, in the bevacizumab group 189.72 pg/ml and in the ranibizumab group 191.36 pg/ml. VEGF plasma concentrations in patients with wet AMD were comparable to controls (p = 0.225). Twenty-eight days after the third injection, a significant reduction of 42% in the median VEGF plasma levels was found in bevacizumab-treated patients (109.97 pg/ml; p = 0.0002) but not in ranibizumab-treated patients (189.97 pg/ml; p = 0.198) where a reduction of 0.7% in the median value was found. Conclusions: Intravitreal bevacizumab significantly reduced VEGF plasma levels until 28 days after intravitreal injection in patients with exudative AMD. Ranibizumab did not achieve a significant plasma VEGF reduction at the same time-point. These findings alert to the potential systemic safety differences between the two drugs after intravitreal administration. [ABSTRACT FROM AUTHOR]

When human breast cancer MCF7 cells were treated with progesterone, our group found high expression of genes involved in Platelet-derived Growth Factor (PDGF) signalling pathway. PDGF expression in turnout cells is associated with increased angiogenic levels and its role in vessel stabilization is well established. The aim is to investigate whether blocking PDGF might be an antitumourigenic way in hormone-dependent breast cancer. Imatinib is a drug which interacts with specific Tyrosine-Kinase receptors such as c-KIT and PDGFR. Cultures of MCF7 cells, incubated with Progesterone or Progesterone+Imatinib were evaluated for viability, by MTT assay, apoptosis, by TUNEL assay, and migration, by Injury and Double-Chamber assays. Imunoexpression for PDGFR-α was accomplished by Western-blotting. Experiences using the same conditions in Endothelial Cells and Smooth Muscle Cells were addressed in our laboratory to investigate the interplay between progesterone and the role of PDGF in angiogenesis. Results seem to indicate that Imatinib-treated cells have higher apoptosis levels, poorer viability and less migration ability when compared to non-treated cell cultures. The findings obtained in this study, focusing the role of Imatinib in tumour angiogenesis can drive us to new therapeutic strategies against hormone-dependent cancers, which maintain a high incidence in our population. [ABSTRACT FROM AUTHOR]

Purpose: This study aimed to elucidate the precise effects of bevacizumab in all steps in the neovascularization process in endothelial cells. Methods: Human umbilical vein endothelial cells (HUVECs) were incubated with bevacizumab at concentrations within the clinically established range or with identical amounts of excipient. Cell cytotoxicity (evaluated by MTT assay), proliferation (by BrdU incorporation assay), apoptosis (by TUNEL assay), migration (by double-chamber assay) and vessel assembly in matrigel-coated plates were assessed in vitro. Mouse plug matrigel assays were performed to confirm in vitro results. Results: Incubation of HUVECs with bevacizumab did not present cytotoxicity. Concentrations comparable with those after intravitreal doses of bevacizumab significantly reduced proliferation and migration capacity, and increased apoptotic rates in these cells. In addition, bevacizumab led to a significant decrease in the assembly of capillary-like structures on matrigel assay in comparison with excipient-treated cells. Further substantiating these in vitro findings, bevacizumab also inhibited angiogenesis in a mouse plug matrigel assay, as evaluated by haemoglobin content levels. Conclusions: These results demonstrate that clinical doses of bevacizumab are able to prevent several steps of the angiogenic process. Bevacizumab is thus currently recommended for treating disorders that present augmented angiogenesis. [ABSTRACT FROM AUTHOR]

Naringenin (NGEN) is a flavanone especially abundant in the Mediterranean diet (citrus fruits and tomato), which is reported to present anti-proliferative effects in many cancer cell lines and to induce apoptosis via activation of NF-KB. Previous studies reported that NGEN has estrogen agonistic and antagonistic activities in distinct types of cells. Knowing that estrogens are cell growth promoters, the aim of this study was to examine the effects of NGEN (at concentrations ranging from 1 µM to 100 µM) using a human breast cancer oestrogen receptor-dependent (ERα+/ERβ+) cell line (MCF-7).and an ER-independent ERα-/ERβ-) cell line (SKBR-3). Although cell viability was not affected by NGEN alone at any concentration used in either cell line, incubation of cells with NGEN together with InM 17β-estradiol resulted in decreased cell viability in MCF-7 cells but not in SKBR-3. These findings are in agreement with the literature, suggesting that NGEN effects depend on the presence or absence of ER. Apoptosis was further evaluated after incubation of both types of cells with 10 µM NGEN. Cell migration was also affected by incubation with 10 µM NGEN as analyzed by injury assay and by double-chamber assay. These ongoing studies suggest that dietary flavanone NGEN exerts inhibitory effects on cancer cell growth and migration, and emphasize that these effects might be mediated by the presence of ER. [ABSTRACT FROM AUTHOR]