Glyphosate is a non-selective herbicide that inhibits the shikimate pathway’s enzyme EPSPS (5-enolpyruvylshikimate-3-phosphate synthase) preventing the production of aromatic amino acids. This herbicide is largely used and appreciated because it controls a wide range of annual and perennial weeds but it has a minimal environmental impact when compared with other herbicides. Initially it was thought that resistance to glyphosate was not easy to evolve but the continuous applications, as it happened for other herbicides, have induced the development of several glyphosate-resistant weeds.

Glyphosate resistance can be developed as target-site and non-target-site mechanisms. In the target-site mechanism of resistance, either a mutation on the EPSPS enzyme (enzyme modification) or the overexpression of the EPSPS enzyme have been found to confer resistance. In the non-target-site mechanism of glyphosate resistance, the herbicide translocation and neutralization is observed. Pumping glyphosate into vacuoles via membrane transporters has been suggested as a possible process involved in the restricted glyphosate translocation. As a consequence, a different vacuolar organization or plasticity could be an interesting character or marker to correlate to glyphosate resistance.

Vacuolar markers AleuGFP (Sar1 dependent sorting) or GFPChi (Sar1 independent sorting) respectively can be used to monitor independent vacuolar sorting mechanisms during glyphosate induced stress. We observed that the adaptive reaction of tobacco protoplasts vacuolar system to the treatment with glyphosate, can be mimicked by the overexpression of a Triticum durum TdGST gene. Previous analysis evidenced that the herbicide glyphosate increased TdGST expression, confirming the role of GST in the protection against xenobiotics. Non-target-site glyphosate resistance mechanisms may correlate with an independent regulation of cell compartmentalization and herbicide induced genes may have a direct effect on it.

Acetylcholine and its receptors are not only essential for the nervous system but also act as mediators of cell communication between non-neuronal cells. Signal transduction after cholinergic stimulation is mediated by two types of receptors. The nicotinic acetylcholine receptors are ion channels, whereas the muscarinic receptors belong to the group of G protein coupled receptors (GPCR). Their activation can lead to initiation of the mitogen-activated protein (MAP) kinase cascade which contributes to cell survival, differentiation and other important cellular responses. The non-neuronal acetylcholine plays a substantial role in the human skin and regulates cell adhesion and migration, as well as proliferation and differentiation of keratinocytes. We here show that in the human keratinocyte cell line HaCaT, the muscarinic acetylcholine receptors are mediators of mitogenic signaling. Stimulation with the cholinergic agonist carbachol leads to an extensive activation of the MAP kinase ERK, together with an activation of the protein kinase Akt. These signaling pathways are dependent on the transactivation of the epidermal growth factor receptor (EGFR), and EGFR transactivation even appears to be the only pathway through which muscarinic receptors facilitate ERK activation in these cells. The transactivation pathway involves a triple-membrane-passing process, proceeding through the activation of matrix metalloproteases and an extracellular EGF-like ligand release.

The photodynamic therapy (PDT) is a combination of using a photosensitizer agent, light and oxygen that can cause oxidative cellular damage. This technique is applied in several cases, including microbial control. Various porphyrin and metalloporphyrin compounds are used as photosensitizer agents. In this study, the effect of a tetra-cationic porphyrin and its zinc compound was investigated on Bacillus subtilis under irradiation with a tungsten lamp as a visible light and the illumination time varied from 0 min to 30 min. Increasing the illumination time reduced the colony number, through the disorganisation of the bacterial cell wall. 

Introduction: Fabrication of three-dimensional (3D) liver tissue is limited by many factors, one of them is the lack of vascularization in the tissue-engineered constructs. To overcome these limitations, an in vivo engineered liver pocket-scaffold's ability to increase neo-angiogenesis was considered in the present study. Methods: Hyaluronan-besed scaffolds enriched with human Mesenchymal Stem Cells (hMSCs) and hepatocytes were implanted into rats. Angiogenesis and hepatocyte function were monitored. Results: The formation of de novo vascular networks within scaffolding matrices was noted as well as a better albumin production by the implanted hepatocytes. Conclusions: Our results emphasized that the presence in culture of hMSC increased tissue concentrations of growth factors and may promote angiogenesis resulting in a higher density of blood vessels coupled with a better metabolic support of hepatocytes.

Quercetin (3,3′,4′,5,6-Pentahydroxyflavone) is one of well-known antioxidants and a flavonol found in many fruits, leaves, and vegetables. Quercetin is also well-known to have anti-inflammatory effects on lipopolysaccharide-induced macrophages. However, the effects of quercetin on virus-induced macrophages are not fully reported. In this study, the anti-inflammatory effect of quercetin on double-stranded RNA (dsRNA)-induced macrophages was examined. Quercetin at concentrations of up to 50 μM significantly inhibited the production of nitric oxide (NO), IL-6, MCP-1, IP-10, RANTES, GM-CSF, G-CSF, TNF-α, LIX,VEGF, and MIP-1α as well as calcium release in dsRNA [50 µg/mL of polyinosinic-polycytidylic acid]-induced RAW 264.7 mouse macrophages (P < 0.05). Quercetin at concentrations of up to 50 μM also significantly inhibited mRNA expression of signal transducer and activated transcription 1 (STAT1) and STAT3 in dsRNA-induced RAW 264.7 (P < 0.05). In conclusion, quercetin has alleviating effects on viral inflammation concerned with its inhibition of NO, cytokines, chemokines, and growth factors in dsRNA-induced macrophages via the calcium-STAT pathway.