Research note: The influence of micro-oxygenation on the long-term ageing ability of Pinot noir wine

In this study, Pinot noir wines were bottle aged for 12 and 18 months after micro-oxygenation (MOX) applied before or after malolactic fermentation (MLF) at two doses (10.8 and 52.4 mg/L/month). After ageing, a greater decrease in the total SO₂ concentration was found in wines with the higher MOX dosage, demonstrating a long-term impact of higher oxygen exposure on wines’ SO₂ requirement. Meanwhile, a negative impact of MOX on wine colour development occurred over time, resulting in a large loss of colour measures (i.e., 420 nm for brown hues, 520 nm for red colour, SO₂ resistant pigments, and colour intensity), which was greater with the early oxygen exposure. This was linked to a significantly lower content of large polymeric pigments in MOX treatments. Tannin concentration was, in the end, not affected by the MOX treatments. However, regarding tannin composition, considerably higher (-)-epicatechin extension units but much lower (-)-epicatechin terminal units were found with MOX treatments. In addition, a significant reduction of tannin trihydroxylation (%Tri-OH) but a higher galloylation (%Galloyl) and mean degree of tannin polymerisation (mDP) remained in wines with MOX, indicating a long-term negative influence on astringency intensity

Impact of microoxygenation on Pinot noir wines with different initial phenolic content

Microoxygenation (MOX) is used to improve wine colour and sensory quality; however, limited information is available for Pinot noir wines and wines with different initial phenolic content. In this study, MOX was applied to two Pinot noir wines, with either a low or a high phenolic content, at two doses (0.50 and 2.11 mg/L/day) for 14 days. With the sterile filtration applied, acetaldehyde formation during MOX was very low, supporting the influence of yeast on acetaldehyde production during MOX. The MOX dosage rate did not significantly affect colour development, while the Pinot noir wine with higher phenolics benefited more from MOX, significantly increasing colour intensity and SO₂ resistant (polymeric) pigments. However, these changes did not guarantee colour stability, as a final SO₂ addition (100 mg/L) largely erased the improvement to colour in all wines. This could be due to the lower acetaldehyde formation, thus less ethyl-bridged stable pigments resistant to SO₂ bleaching. MOX also decreased the flavan-3-ols and anthocyanin monomers, which differed between the two Pinot noir wines, reflecting the initial phenolic content. Lastly, MOX generally increased the measured tannin concentration and affected the proportion of tannin subunits, with a decrease in tannin mass conversion and proportion of (-)-epigallocatechin extension units. Some of these changes in phenolic compounds could potentially increase astringency, suggesting that MOX should be applied to Pinot noir and other low phenolic wines with caution

Characterization of an antioxidant and antimicrobial extract from cool climate, white grape marc

Valorization of agricultural waste has become increasingly important. Wastes generated by wineries are high in phenolic compounds with antioxidant and antibacterial properties, which contribute to phytotoxicity, making their immediate use for agricultural means limited. Utilizing a water-based extraction method, the phenolic compounds from winery waste were extracted and purified. The resulting extract was characterized for phenolic composition using high-pressure liquid chromatography-ultraviolet/visible and electrochemical detectors (HPLC-UV/Vis, ECD) for monomers, and spectral assessment of the tannins present using attenuated total reflectance-Fourier transform infrared (ATR-FTIR), FT-Raman, and solid-state nuclear magnetic resonance (SSNMR) spectroscopies. The extract’s antioxidant activity was assessed by the scavenging of the 2,2-diphenyl-1–picrylhydrazyl (DPPH) radical and Folin-Ciocalteu total phenolic assay, and was found to be as effective as a commercially obtained grape extract. The extract’s antimicrobial efficacy was tested for minimum bactericidal concentration using Candida albicans, Escherichia coli 25922, and Staphylococcus aureus 6538, which resulted in greater efficacy against gram-positive bacteria as shown over gram-negative bacteria, which can be linked to both monomeric and tannin polyphenols, which have multiple modes of bactericidal action

Synergistic Effect of Functionalized Nickel Nanoparticles and Quercetin on Inhibition of the SMMC-7721 Cells Proliferation

The effect of functionalized nickel (Ni) nanoparticles capped with positively charged tetraheptylammonium on cellular uptake of drug quercetin into hepatocellular carcinoma cells (SMMC-7721) has been explored in this study via microscopy and electrochemical characterization as well as MTT assay. Meanwhile, the influence of Ni nanoparticles and/or quercetin on cell proliferation has been further evaluated by the real-time cell electronic sensing (RT-CES) study. Our observations indicate that Ni nanoparticles could efficiently improve the permeability of cancer cell membrane, and remarkably enhance the accumulation of quercetin in SMMC-7721 cells, suggesting that Ni nanoparticles and quercetin would facilitate the synergistic effect on inhibiting proliferation of cancer cells

Autoimmune and autoinflammatory mechanisms in uveitis

The eye, as currently viewed, is neither immunologically ignorant nor sequestered from the systemic environment. The eye utilises distinct immunoregulatory mechanisms to preserve tissue and cellular function in the face of immune-mediated insult; clinically, inflammation following such an insult is termed uveitis. The intra-ocular inflammation in uveitis may be clinically obvious as a result of infection (e.g. toxoplasma, herpes), but in the main infection, if any, remains covert. We now recognise that healthy tissues including the retina have regulatory mechanisms imparted by control of myeloid cells through receptors (e.g. CD200R) and soluble inhibitory factors (e.g. alpha-MSH), regulation of the blood retinal barrier, and active immune surveillance. Once homoeostasis has been disrupted and inflammation ensues, the mechanisms to regulate inflammation, including T cell apoptosis, generation of Treg cells, and myeloid cell suppression in situ, are less successful. Why inflammation becomes persistent remains unknown, but extrapolating from animal models, possibilities include differential trafficking of T cells from the retina, residency of CD8(+) T cells, and alterations of myeloid cell phenotype and function. Translating lessons learned from animal models to humans has been helped by system biology approaches and informatics, which suggest that diseased animals and people share similar changes in T cell phenotypes and monocyte function to date. Together the data infer a possible cryptic infectious drive in uveitis that unlocks and drives persistent autoimmune responses, or promotes further innate immune responses. Thus there may be many mechanisms in common with those observed in autoinflammatory disorders

The Temperature-Sensitive Role of Cryptococcus neoformans ROM2 in Cell Morphogenesis

ROM2 is associated with Cryptococcus neoformans virulence. We examined additional roles of ROM2 in C. neoformans and found that ROM2 plays a role in several cell functions specifically at high temperature conditions. Morphologically rom2 mutant cells demonstrated a “tear”-like shape and clustered together. A sub-population of cells had a hyperelongated phenotype at restrictive growth conditions. Altered morphology was associated with defects in actin that was concentrated at the cell periphery and with abnormalities in microtubule organization. Interestingly, the ROM2 associated defects in cell morphology, location of nuclei, and actin and microtubule organization were not observed in cells grown at temperatures below 37°C. These results indicate that in C. neoformans, ROM2 is important at restrictive temperature conditions and is involved in several cell maintenance functions

A Mycobacterium leprae Hsp65 Mutant as a Candidate for Mitigating Lupus Aggravation in Mice

Hsp60 is an abundant and highly conserved family of intracellular molecules. Increased levels of this family of proteins have been observed in the extracellular compartment in chronic inflammation. Administration of M. leprae Hsp65 [WT] in [NZBxNZW]F1 mice accelerates the Systemic Lupus Erythematosus [SLE] progression whereas the point mutated K409A Hsp65 protein delays the disease. Here, the biological effects of M. leprae Hsp65 Leader pep and K409A pep synthetic peptides, which cover residues 352–371, are presented. Peptides had immunomodulatory effects similar to that observed with their respective proteins on survival and the combined administration of K409A+Leader pep or K409A pep+WT showed that the mutant forms were able to inhibit the deleterious effect of WT on mortality, indicating the neutralizing potential of the mutant molecules in SLE progression. Molecular modeling showed that replacing Lysine by Alanine affects the electrostatic potential of the 352–371 region. The number of interactions observed for WT is much higher than for Hsp65 K409A and mouse Hsp60. The immunomodulatory effects of the point-mutated protein and peptide occurred regardless of the catalytic activity. These findings may be related to the lack of effect on survival when F1 mice were inoculated with Hsp60 or K409A pep. Our findings indicate the use of point-mutated Hsp65 molecules, such as the K409A protein and its corresponding peptide, that may minimize or delay the onset of SLE, representing a new approach to the treatment of autoimmune diseases

Regulation of the Actin Cytoskeleton by an Interaction of IQGAP Related Protein GAPA with Filamin and Cortexillin I

Filamin and Cortexillin are F-actin crosslinking proteins in Dictyostelium discoideum allowing actin filaments to form three-dimensional networks. GAPA, an IQGAP related protein, is required for cytokinesis and localizes to the cleavage furrow during cytokinesis. Here we describe a novel interaction with Filamin which is required for cytokinesis and regulation of the F-actin content. The interaction occurs through the actin binding domain of Filamin and the GRD domain of GAPA. A similar interaction takes place with Cortexillin I. We further report that Filamin associates with Rac1a implying that filamin might act as a scaffold for small GTPases. Filamin and activated Rac associate with GAPA to regulate actin remodelling. Overexpression of filamin and GAPA in the various strains suggests that GAPA regulates the actin cytoskeleton through interaction with Filamin and that it controls cytokinesis through association with Filamin and Cortexillin

Doyne lecture 2016:intraocular health and the many faces of inflammation

Dogma for reasons of immune privilege including sequestration (sic) of ocular antigen, lack of lymphatic and immune competent cells in the vital tissues of the eye has long evaporated. Maintaining tissue and cellular health to preserve vision requires active immune responses to prevent damage and respond to danger. A priori the eye must contain immune competent cells, undergo immune surveillance to ensure homoeostasis as well as an ability to promote inflammation. By interrogating immune responses in non-infectious uveitis and compare with age-related macular degeneration (AMD), new concepts of intraocular immune health emerge. The role of macrophage polarisation in the two disorders is a tractable start. TNF-alpha regulation of macrophage responses in uveitis has a pivotal role, supported via experimental evidence and validated by recent trial data. Contrast this with the slow, insidious degeneration in atrophic AMD or in neovasular AMD, with the compelling genetic association with innate immunity and complement, highlights an ability to attenuate pathogenic immune responses and despite known inflammasome activation. Yolk sac-derived microglia maintains tissue immune health. The result of immune cell activation is environmentally dependent, for example, on retinal cell bioenergetics status, autophagy and oxidative stress, and alterations that skew interaction between macrophages and retinal pigment epithelium (RPE). For example, dead RPE eliciting macrophage VEGF secretion but exogenous IL-4 liberates an anti-angiogenic macrophage sFLT-1 response. Impaired autophagy or oxidative stress drives inflammasome activation, increases cytotoxicity, and accentuation of neovascular responses, yet exogenous inflammasome-derived cytokines, such as IL-18 and IL-33, attenuate responses

A horticultural medium established from the rapid removal of phytotoxins from winery grape marc

Grape (Vitis vinifera L.) marc has long been utilized as a compost feedstock. However, this process takes an extended period of time due to the phytotoxic chemical composition of the marc. Removal of these compounds presents an opportunity to utilize the grape marc as a growing medium. Following a water-based extraction procedure to remove polyphenolic compounds of interest, analysis of the depleted marc showed a decrease in the content of these compounds, and in nutrient and trace element levels. Carrot (Daucus carota L.) and corn (Zea mays L.) seedling emergence in the depleted marc and blends with compost were not adversely affected, demonstrating its effectiveness for growing plants at all ratios. A 50:50 blend of compost and depleted grape marc resulted in plant growth equivalent to the compost alone. This combined with the observed water holding capacity suggests that depleted grape marc, when blended with compost, can be a suitable alternative to peat or coconut coir for seedlings