Abbreviations D diotic dissonant DD dichotic dissonant GMD gray matter density IC inferior colliculus O original VBM voxel-based morphometry “
“Division of Diabetes, Endocrinology & Metabolism, Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN, USA Department of Neuroscience, University of Texas Southwestern Medical Center, Dallas, TX, USA The methamphetamine-sensitive circadian oscillator (MASCO) is an enigmatic circadian clock whose output is observed during continuous consumption

of low-dose methamphetamine. The MASCO rhythm persists when the light-entrainable pacemaker in the suprachiasmatic nucleus (SCN) is lesioned, but Romidepsin mouse the anatomical location of MASCO is unknown. We recently found that the period of the MASCO rhythm is unusually short (21 h) in mice with disruption of all three paralogs of the canonical clock Sorafenib cost gene, Period. In this study, we investigated the contribution of each Period paralog to timekeeping in MASCO. We measured wheel-running activity rhythms in intact and SCN-lesioned Per1-, 2- and 3-mutant mice administered methamphetamine, and found that none of the

mice displayed a short (21-h) period, demonstrating that no single Period gene is responsible for the short-period MASCO rhythm of Per1−/−/Per2−/−/Per3−/− mice. We also found that the periods of activity Thymidylate synthase rhythms in constant darkness were lengthened by methamphetamine treatment in intact wild-type, Per1−/− and Per3−/− mice but not Per2−/− mice, and Per2−/− mice had two distinct activity rhythms upon release to constant light. These data suggest that the SCN and MASCO are not coupled in Per2−/− mice. The

MASCO rhythm in Per1−/−/Per2−/− mice in constant darkness alternated between a short (22-h) and a long (27-h) period. This pattern could result from two coupled oscillators that are not synchronised to each other, or from a single oscillator displaying birhythmicity. Finally, we propose a working model of the in vivo relationship between MASCO and the SCN that poses testable hypotheses for future studies. “
“Cleavage of amyloid-β precursor protein (APP) at the Asp1 β-secretase site of the amyloid-β protein (Aβ) domain by β-site Aβ precursor protein-cleaving enzyme 1 (BACE1) is required for the generation of Aβ, a central component of neuritic plaques in the Alzheimer’s disease (AD) brain. In this study, we found that Aβ Glu11 is the major β-secretase site for cleavage of APP by BACE1 to generate soluble secreted APP (sAPPβ)606 and the C-terminal membrane-bound fragment (CTF)β product C89. Cleavage of C89 by γ-secretase resulted in truncated Aβ generation in a non-amyloidogenic pathway.

Biochemical as well as molecular tools were used to characterize the cultured actinomycetes. Mucus of four healthy individuals of the coral A. digitifera were collected from Hare Island (9°12′N latitude and 79°5′E longitude), the largest island in the Gulf of Mannar, Tamil Nadu, India. Coral mucus was collected using sterile cotton swabs (Guppy & Bythell, 2006). The coral surface mucus layer was swabbed using sterile cotton swabs. Mucus samples of c. 1 cm2 coral surface area were taken with these swabs. After swabbing, the swabs were immediately placed in sterile polypropylene tubes. Seawater samples were collected with 50-mL sterile tubes that were opened underwater adjacent to the

same corals. Sediment samples were collected from right below the corals. All samples were transported to the laboratory (in about 4-h time) in ice-cold condition and were plated for isolation of bacteria. selleck chemicals llc The mucus swab samples were transferred to sterile

tubes with 1 mL of autoclave-sterilized seawater, in a sterile hood. The cotton swabs were vigorously vortexed to suspend the bacteria in seawater (Guppy & Bythell, 2006). Actinomycetes were isolated using standard serial dilution and plating techniques in Volasertib molecular weight triplicate on starch casein agar supplemented with actidione (40 μg mL−1) (Himedia Laboratories, Mumbai, India) found to inhibit the growth of fungi (Goodfellow & Williams, 1988) and nalidixic acid (10 μg mL−1) (Himedia Laboratories), which inhibits the bacteria capable of swarming without affecting the growth of actinomycetes (Nonomura & Hayakawa, 1988). Actinomycetes colonies were recognized Sclareol on the basis of morphological and physiological characteristics following directions given by the International Streptomyces Project (Shirling & Gottlieb, 1966). Morphological characteristics were studied under a light microscope after

15 days of growth on oatmeal agar (ISP3) (Shirling & Gottlieb, 1966). Actinomycetes counts were recorded as CFUs and expressed as CFU per 1 cm2 of coral surface area for mucus and tissue. Culturable actinomycetes from seawater and sediment were recorded as CFU mL−1 (of seawater) and CFU g−1 (of sediment), respectively. The isolated actinomycetes were identified by performing various biochemical tests according to the Bergey’s manual and Lampert et al. (2006). Carbohydrate tests were performed using the HiCarbohydrate kit (Himedia Laboratories). The sensitivity of the actinomycetes to various antibiotics was determined after incubation for 24–48 h at 30 °C on ISP2 (International Streptomyces Project) agar (Himedia Laboratories). Total genomic DNA was extracted using a modified cetyltrimethylammonium bromide–NaCl protocol. For each isolate, a loopful of mycelium and spores was scraped from colonies grown on Starch Casein Agar (SCA) and resuspended in TE buffer as described previously (Zin et al., 2007). As suggested by Stach et al.

Less fortunate, poorly -resourced scientists and busy clinicians, especially in developing nations, are forced to carry out poorly designed retrospective studies.

The pressure is felt even more if research methodologies are not taught in medical curriculum to create scientific temper and zeal for research resulting in irrelevant and poorly designed studies. A research question should always include a clause “if the research will benefit the find more mankind in an economic manner? Practice of evidence-based medicine (EBM) is undergoing its own natural evolution. EBM has come a long way starting from large series and case control studies to observational and cohort studies, from randomized control trials to meta-analysis and still evolving. Technology driven basic science research has strengthened biological understanding of diseases. While genetic variation of an individual including pharmacogenetic factors may eventually be the deciding factors in choosing the right therapeutic agent, it remains

costly and elusive at PI3K inhibitor the moment and in its rudimentary phase too. Nevertheless, the concept of Personalised and individualized medicine has come to stay. Technological advancements are marching faster than ever before. Technologically sophisticated choices are expected to be within reach of all sections of society in the future. Any new venture of research in that direction should also keep the social commitments and economic considerations in mind, so that the benefits of advanced medicine do not become prerogatives of privileged few. In other words, such futuristic medicine, or if one can call it “Next generation EBM”, should be humanized and not just personalized or individualized. Prescribing TNF blocker or triple DMARD or IL-6 inhibitor or rituximab or any other agent singly or in combination to an RA patient then will not be a trial and error subjecting the patient to cost, toxicity and inefficacy. This reality is still evolving, but comparative

effectiveness trials (CET) with large sample size in populous nations may be good economic alternatives this website to RCT to generate evidence for resource limited set up. A landmark study of this kind is the 2012 CET with triple DMARD therapy in RA showing benefit comparable or superior to biological agents.[1] This year several RCTs have proven this point beyond doubt. Similarly, large series as observational, case control or cohort studies also contribute to evidence, though not as strong as RCTs or meta-analysis. Relevant research questions can be answered by sound methodology in economical and humane manner in large cohorts to benefit the less advantaged societies till next generation EBM is readily and economically available. Neither present day EBM or nor next Generation EBM will succeed, if not humanized. Happy 2014.

A small study from the Mayo Clinic of patients on stable doses of thiopurines showed a trend toward increased 6TGN levels and leucopenia after the addition of sulphasalazine and mesalazine, but not balsalazide[42]; however, elevations in 6TGN do not seem to be dose-dependent. A Dutch group subjected 17 patients on stable doses of thiopurines to 2 g of mesalazine for 4 weeks, dose escalation of the 5-ASA to 4 g for another 4 weeks, followed by cessation for DNA Damage inhibitor 4 weeks. Median 6TGN levels increased from 370 at baseline to 553 with 2 g mesalazine (P ≤ 0.05). Escalation to 4 g of mesalazine

did not lead to significant increases in 6TGN levels (median 553 to 572). After mesalazine washout, 6TGN levels decreased to 449 (P ≤ 0.05). Interestingly, 6MMP levels decreased significantly from a median of 1676 to 880 (P ≤ 0.05), but this required 4 g of mesalazine. There was also a favorable improvement (i.e., fall) in the 6MMP : 6TGN ratio.[43] Two Australian studies have highlighted the ability of thiopurine metabolite testing to improve outcomes with thiopurine therapy.[27, 28] Both clustered patient results into five

groups (see Table 1): underdosed/rapid metabolisers, non-adherent, refractory, ‘thiopurine shunters’ and overdosed patients. Haines et al. studied 63 consecutive IBD patients who, despite a stable dose of thiopurines for the last 3 months, had persistent clinically active disease.

Kennedy et al. ALK inhibitor reviewed the outcomes of 151 consecutive patients undergoing metabolite testing. 6TGN levels were subtherapeutic in 29% and 43% of patients with active disease and non-adherence was 9% and 1%, respectively in each study. The metabolite results led to the addition of allopurinol in 9% and 10% of patients, respectively, in each study. Metabolite testing revealed that 40% and 58% of patients Loperamide were truly refractory to thiopurine therapy, and 13% and 21% of patients were overdosed. In the study by Haines et al., 87% of patients improved with thiopurine optimization and 15 patients avoided a change of therapy, compared to only 18% of patients who were not optimised (P = 0.0001). Three patients with therapeutic levels whose doctors ignored the algorithm and dose-escalated showed no improvement. In the study by Kennedy et al., 74% of patients with subtherapeutic 6TGN levels improved with dose escalation, and across the entire cohort, optimization of thiopurines improved outcomes in 38% of patients. These two manuscripts make a compelling case for the application of thiopurine metabolite testing in order to optimise the dosage and use of thiopurines and achieve better outcomes. In some centres, metabolite testing is accepted as standard of care for IBD patients on thiopurines.

The instrument has a 100-µm multi-purpose large scanner and was operated in contact

mode with speeds ranging from 0.5 to 1.0 Hz and 512 pixels per line scan. A Veeco MLCT-E cantilever with a resonant frequency ranging from 26 to 50 kHz and a nominal spring constant of 0.5 N m−1 CH5424802 solubility dmso was used for imaging. Scans were acquired with sizes ranging from 10 to 75 µm for all samples. Sterile 55-mm glass bottom petri dishes (MatTek Corp., Columbia, MD) were prepared with lectin prior to inoculation. LcH and WGA lectins, diluted to a final concentration of 100 µg mL−1 in PBS, were added to the glass bottom dishes and incubated for 2 h at room temperature. Next, the liquid was removed and 3 mL of overnight cell cultures in TY, diluted to OD600 nm of 1.0 (approximately Rapamycin manufacturer 106 CFU mL−1) were immediately placed on the wet glass surface of the petri dish. Dishes were incubated statically at 28 °C for 24 h. SYTO 9 dye (1 µL) (Molecular Probes, Invitrogen Inc., Eugene, OR) was then added for 15 min in the dark to fluorescently label

the cells. Images were acquired with laser intensity and gain held constant using a Leica TCS SP2 scanning confocal microscope equipped with a Leica HCX PL APO 63×/1.40–0.60 oil objective lens and Leica LCS software (version 1537, Leica Microsystems Inc., Buffalo Grove, IL). The number of attached cells was assessed using the imagej software to convert the images to a binary format. The pixel area corresponding to the fluorescent cells was identified SPTLC1 and calculated as a percentage of the total image area (http://rsb.info.nih.gov/ij). Wheat seeds (Triticum aestivum cv. Jagger) were surface-sterilized and allowed to germinate as described (Greer-Phillips et al., 2004). For the wheat root attachment assay, A. brasilense strains were cultured in TY liquid overnight (28 °C, 200 rpm) and the cultures were normalized to an OD600 nm of 1.0 using sterile phosphate buffer. A volume of 200 μL of each strain prepared as described above was inoculated, in triplicate, into glass tubes containing 9.8 mL sterile phosphate buffer and 0.5 g of sterile roots isolated from 1-week-old

plantlets and allowed to incubate for 2 h with shaking. The excised roots were then collected and washed three times with 5 mL of buffer with gentle shaking. Root material was then homogenized in 5 mL of fresh buffer and aliquots of the homogenized slurry were serially diluted and inoculated in triplicate on MMAB plates to determine colony forming units. The fraction of root-attached cells was expressed as percent of total cells inoculated. Wheat colonization assays were performed as described previously (Greer-Phillips et al., 2004) with cultures inoculated at comparable levels (107 cells mL−1) into 15 mL molten semi-soft (0.4% agar) Fahraeus medium (Zamudio & Bastarrachea, 1994) modified with traces of sodium molybdate.

5). These results suggested that the cell death process may not be associated with activation of inflammasomes, but rather that IL-1β and ATP are released from damaged cells. Alternatively, oxidative stress may contribute to the cell death, because ROS inhibitor reduced the cell death of macrophages (Fig. 5). ROS generated from damaged mitochondoria are known to induce cell death in various ways (Ott et al.,

2007). In this regard, several oral streptococcal species including S. sanguinis are known to produce hydrogen peroxide (Chen et al., 2011). This bacterial product is a possible candidate for ubiquitin-Proteasome degradation the virulence factor that mediates cellular damage in macrophages, because Streptococcus gordonii, another oral streptococcus, is reported to induce cell death of endothelial cells by peroxidogenesis (Stinson

et al., 2003). Our preliminary study suggested that the concentrations of hydrogen peroxide in the culture supernatants of S. sanguinis were <5 μM under the conditions of the infection assay, although its effect on macrophages was unknown. The involvement of hydrogen peroxide produced by S. sanguinis in the cell death of infected macrophages should be investigated further. To evaluate the molecular mechanisms underlying S. sanguinis-induced cell death, further study on the mitochondorial dysfunction induced by this microorganism will be required. This work was supported in part by Grants-in-Aid for Scientific Research (A) (#19209063), (B) (#20390465, #20390531) and (C) (#20592398), and Grants-in-Aid for Young Scientists (B) (#21792069,

#21791786) from the Japan MG-132 manufacturer Society for the Promotion of Science. We thank Dr M. Killian for providing PFKL S. sanguinis strain SK36. “
“Ophiobolins are sesterterpene-type phytotoxins produced by fungi belonging mainly to the genus Bipolaris. In this study, the antifungal effect of ophiobolins A and B on different zygomycetes has been examined. Depending on the zygomycete tested, MIC values of 3.175–50 μg mL–1 were found for ophiobolin A and 25–50 μg mL–1 for ophiobolin B. Ophiobolin A inhibited sporangiospore germination of Mucor circinelloides and caused morphological changes; the fungus formed degenerated, thick or swollen cells with septa. Cytoplasm effusions from the damaged cells were also observed. Fluorescence microscopy after annexin and propidium iodide staining of the treated cells suggested that the drug induced an apoptosis-like cell death process in the fungus. Ophiobolins are secondary metabolites of certain fungi belonging to the genera Bipolaris, Drechslera, Cephalosporium and Aspergillus (Au et al., 2000a). These sesterterpene-type compounds (C25) are characterized by a unique tricyclic chemical structure (Fig. 1). More than 25 ophiobolin analogues have been described (Au et al., 2000a; Wei et al., 2004; Evidente et al., 2006) and various biological actions have been attributed to them, such as phytotoxic (Au et al.

5). These results suggested that the cell death process may not be associated with activation of inflammasomes, but rather that IL-1β and ATP are released from damaged cells. Alternatively, oxidative stress may contribute to the cell death, because ROS inhibitor reduced the cell death of macrophages (Fig. 5). ROS generated from damaged mitochondoria are known to induce cell death in various ways (Ott et al.,

2007). In this regard, several oral streptococcal species including S. sanguinis are known to produce hydrogen peroxide (Chen et al., 2011). This bacterial product is a possible candidate for Selleck Panobinostat the virulence factor that mediates cellular damage in macrophages, because Streptococcus gordonii, another oral streptococcus, is reported to induce cell death of endothelial cells by peroxidogenesis (Stinson

et al., 2003). Our preliminary study suggested that the concentrations of hydrogen peroxide in the culture supernatants of S. sanguinis were <5 μM under the conditions of the infection assay, although its effect on macrophages was unknown. The involvement of hydrogen peroxide produced by S. sanguinis in the cell death of infected macrophages should be investigated further. To evaluate the molecular mechanisms underlying S. sanguinis-induced cell death, further study on the mitochondorial dysfunction induced by this microorganism will be required. This work was supported in part by Grants-in-Aid for Scientific Research (A) (#19209063), (B) (#20390465, #20390531) and (C) (#20592398), and Grants-in-Aid for Young Scientists (B) (#21792069,

#21791786) from the Japan ALK mutation Society for the Promotion of Science. We thank Dr M. Killian for providing why S. sanguinis strain SK36. “
“Ophiobolins are sesterterpene-type phytotoxins produced by fungi belonging mainly to the genus Bipolaris. In this study, the antifungal effect of ophiobolins A and B on different zygomycetes has been examined. Depending on the zygomycete tested, MIC values of 3.175–50 μg mL–1 were found for ophiobolin A and 25–50 μg mL–1 for ophiobolin B. Ophiobolin A inhibited sporangiospore germination of Mucor circinelloides and caused morphological changes; the fungus formed degenerated, thick or swollen cells with septa. Cytoplasm effusions from the damaged cells were also observed. Fluorescence microscopy after annexin and propidium iodide staining of the treated cells suggested that the drug induced an apoptosis-like cell death process in the fungus. Ophiobolins are secondary metabolites of certain fungi belonging to the genera Bipolaris, Drechslera, Cephalosporium and Aspergillus (Au et al., 2000a). These sesterterpene-type compounds (C25) are characterized by a unique tricyclic chemical structure (Fig. 1). More than 25 ophiobolin analogues have been described (Au et al., 2000a; Wei et al., 2004; Evidente et al., 2006) and various biological actions have been attributed to them, such as phytotoxic (Au et al.

5). These results suggested that the cell death process may not be associated with activation of inflammasomes, but rather that IL-1β and ATP are released from damaged cells. Alternatively, oxidative stress may contribute to the cell death, because ROS inhibitor reduced the cell death of macrophages (Fig. 5). ROS generated from damaged mitochondoria are known to induce cell death in various ways (Ott et al.,

2007). In this regard, several oral streptococcal species including S. sanguinis are known to produce hydrogen peroxide (Chen et al., 2011). This bacterial product is a possible candidate for Enzalutamide price the virulence factor that mediates cellular damage in macrophages, because Streptococcus gordonii, another oral streptococcus, is reported to induce cell death of endothelial cells by peroxidogenesis (Stinson

et al., 2003). Our preliminary study suggested that the concentrations of hydrogen peroxide in the culture supernatants of S. sanguinis were <5 μM under the conditions of the infection assay, although its effect on macrophages was unknown. The involvement of hydrogen peroxide produced by S. sanguinis in the cell death of infected macrophages should be investigated further. To evaluate the molecular mechanisms underlying S. sanguinis-induced cell death, further study on the mitochondorial dysfunction induced by this microorganism will be required. This work was supported in part by Grants-in-Aid for Scientific Research (A) (#19209063), (B) (#20390465, #20390531) and (C) (#20592398), and Grants-in-Aid for Young Scientists (B) (#21792069,

#21791786) from the Japan Selleck Erismodegib Society for the Promotion of Science. We thank Dr M. Killian for providing heptaminol S. sanguinis strain SK36. “
“Ophiobolins are sesterterpene-type phytotoxins produced by fungi belonging mainly to the genus Bipolaris. In this study, the antifungal effect of ophiobolins A and B on different zygomycetes has been examined. Depending on the zygomycete tested, MIC values of 3.175–50 μg mL–1 were found for ophiobolin A and 25–50 μg mL–1 for ophiobolin B. Ophiobolin A inhibited sporangiospore germination of Mucor circinelloides and caused morphological changes; the fungus formed degenerated, thick or swollen cells with septa. Cytoplasm effusions from the damaged cells were also observed. Fluorescence microscopy after annexin and propidium iodide staining of the treated cells suggested that the drug induced an apoptosis-like cell death process in the fungus. Ophiobolins are secondary metabolites of certain fungi belonging to the genera Bipolaris, Drechslera, Cephalosporium and Aspergillus (Au et al., 2000a). These sesterterpene-type compounds (C25) are characterized by a unique tricyclic chemical structure (Fig. 1). More than 25 ophiobolin analogues have been described (Au et al., 2000a; Wei et al., 2004; Evidente et al., 2006) and various biological actions have been attributed to them, such as phytotoxic (Au et al.

However, common issues such as access to care and cultural perspective arise across different ethnic minority groups. Identifying studies and key words on MRPs experienced by ethnic minority

populations in the UK were challenging. Thus, there is a possibility that some relevant studies were not included despite a thorough investigation. Secondly, to ensure a scientific evidence base this review includes only peer-reviewed journal articles. Thirdly, as discussed above, some of the studies included in this review were either small with numbers of ethnic minority participants (ranging from 17–44, with a median of 32 patients),[14, 20, 23, 32, 35, 36] or did not report find more the sample size (n = 3).[15, 30, 32]

The results are also limited by the short length of follow-up for problem identification.[14, 15, 20, 23, 33, 35, 36] A further limitation is that different terms and definitions were used to describe MRPs among the selected studies. For example, some studies used a wide holistic definition to identify MRPs[14, 15, 36] others used a narrow definition such as ADR,[28, 29] ADE[30] or adherence[23, 35] or used no universally accepted definition.[20-22, 31, 33, 34] Finally, this review focused on ethnic click here minority groups in the UK. Whilst some similarities and differences might be expected elsewhere, the extent to which findings are relevant to population groups in other countries, societies, settings and contexts is unclear. There has been no holistic approach Ureohydrolase or systematic investigation of MRPs among ethnic minorities in the UK. This review

highlights that ethnic minority patients have their own problems and needs with both medicine use and service access and also that some ethnic minority groups may be at higher risk of MRPs than the majority ethnic group.[21, 22, 28, 29, 34, 35] This is possibly because ethnic minority patients may experience more difficulties in accessing healthcare services, getting the correct diagnosis and medicine, being supported with the use of medicines and getting regular monitoring or review. The full body of evidence on the extent to which ethnic minorities have more or less MRPs than the majority ethnic group is lacking. However, we can anticipate that ethnic minorities have their own perspectives and needs because of cultural and religious issues, language and communication barriers, previous experiences and different expectations. Recommendations made in the literature to support ethnic minorities in the effective use of medicines have not been evaluated. The recommendations need to be addressed for all stages including diagnosis of disease, safe and effective use of medicines, monitoring or review of their chronic disease and medication regimens.

, 2005), invasive growth and pseudohyphal formation (Lambrechts et al., 1996; Lo & Dranginis, 1996), flor formation (Ishigami et al., 2004; Zara et al., 2005; Fidalgo et al., 2006) and adhesion to biotic Cytoskeletal Signaling inhibitor and

abiotic surfaces (Verstrepen et al., 2004; Verstrepen & Klis, 2006). In addition, the flocculent phenotype displayed by both BM45-F11H and VIN13-F11H transgenic strains was not inhibited in the presence of either glucose or mannose. Because NewFlo-type flocculation is inhibited by both mannose and glucose, while Flo1-type flocculation is exclusively inhibited by mannose (Stratford & Assinder, 1991), this result clearly demonstrates that FLO11 transgenic wine yeast-encoded flocculins exhibit neither Flo1-type nor NewFlo-type flocculation mechanisms. It can be suggested that the flocculent phenotype of BM45-F11H and VIN13-F11H

transformants may at least in part belong to a third group named MI, which is insensitive to mannose (and glucose), and independent of Ca2+ ions (Masy et al., 1992). Masy and colleagues postulated that flocculation in such strains could be produced by hydrophobic interactions or other specific interactions not involving mannans. While Stratford (1992) suggested that MI probably results from very low specificity to monosaccharides because lectins may have much greater affinity for tri- or polysaccharides than for simple sugars. Therefore, it is most likely that the flocculation mechanism of these FLO11-based transgenic wine

yeast strains would deviate from the widely accepted lectin selleckchem hypothesis that was originally proposed by Miki et al. (1982). Importantly, this industrially relevant FLO11-mediated flocculation phenotype that was observed in Merlot fermentations does not appear to be red grape varietal dependent as it was also evident in fermentations using Cabernet Sauvignon and Petit Verdot red grape varietals. This study clearly demonstrates for the first time that it is indeed possible to harness the innate Urease dominant FLO11 gene ORF of nonflocculent commercial wine yeast strains using of self-cloning promoter replacement cassettes to yield conditionally flocculent wine yeast strains with oenological properties that are superior to their parental wild-type strains. From the data generated thus far, further investigation is required to have a complete and detailed understanding of flocculation mechanism that underpins this biotechnologically important and interesting FLO11-mediated adhesion phenotype. This work was financially supported by the National Research Foundation (NRF) and the South African Wine Industry (Winetech). Table S1. Volatile components in wines produced from Merlot grape must. Table S2. FT-IR analysis of oenological factors of Merlot red wines. Please note: Wiley-Blackwell is not responsible for the content or functionality of any supporting materials supplied by the authors.