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Figure 4 illustrates that bench throw power also significantly im

Figure 4 illustrates that bench throw power also significantly improved following 14 days of B supplementation on both D1 and D2 testing. Figure 4 Individual (n = 12) and mean responses for bench throw Barasertib chemical structure power (W, Watts) on the two days before (PreDay) and after (PostDay, 14 days) placebo and betaine supplementation. * = p < 0.05 from corresponding betaine PreDay value, # = p < 0.05 from corresponding placebo PostDay value. Similar to the back squat, there were no significant differences between the P and B trials in the total number of bench press repetitions performed at 85% of 1 RM until fatigue. These values are presented in Table 2. Table 2 Total number of

repetitions to fatigue in the bench press during the two days before and after supplementation (n = 12)   Placebo Betaine Pre-Testing 12 ± 1 10 ± 1 Day 1     Pre-Testing 12 ± 2 12 ± 1 Day 2     Post-Testing 13 ± 1 11 ± 1 Day 1     Post-Testing 13 ± 1 11 ± 1 Day 2     Hematocrit (%), hemoglobin (g/dL), and plasma osmolality (mOsm/kg) were significantly greater at post-squat (49 ± 1, 15.7 ± 1.0, 303 ± 4, respectively) and immediately after REC (48 ± 1, 16.0 ± 1.0, 303 ± 3, respectively)

compared to pre-exercise values (43 ± 1, 14.3 ± 0.8, 289 ± 3, respectively) during D1 and D2 testing, but these values were not significantly click here different between the P and B trials. Plasma glucose was not different before P or B supplementation (5.1 ± 0.6 and 5.0 ± 0.7 mmol/L, respectively) or at any time in response to the REC protocol (averaging 5.1 ± 0.5 and 5.1 ± 0.8 mmol/L, respectively) after P or B supplementation. As expected, plasma lactate showed significant increases above average pre exercise (1.4 ± 0.4 mmol/L) values throughout the REC protocol on both D1 and D2 testing days, and this increase (8.7 ± 2.2 and 8.8 ± 1.8 mmol/L, respectively) was the same for P and B exercise testing sessions. Discussion There is an increased interest in the study Carbachol of betaine as an ergogenic supplement for the neuromuscular system. In the current study, the primary effect of the betaine supplement was observed in the upper body, with enhanced bench press force and power

production, but no change in the dynamic squat exercise performances. Additionally, the improvements in the bench press performances were observed on D2, demonstrating the efficacy of betaine as a potential aid to recovery. This is in contrast to the recent findings by Hoffman et al. [6] who demonstrated improvements in squat exercise endurance (i.e., number of repetitions to failure at 90% of the 1 RM yet not at 75% of the 1RM), but no changes in these measures in the bench press or for the lower body Wingate test. This disparity in results is likely due to a host of differences in the study design and dependent variables. Firstly, we utilized a within versus between group experimental design allowing greater control of statistical variance.

For the quantum transport, we use the non-equilibrium Green’s fun

For the quantum transport, we use the non-equilibrium Green’s function formalism [14]. We consider the coherent limit where it is equivalent to the Landaüer’s approach, and the current can be evaluated from the transmission as below: (2) where transmission is T(E) = tr(Γ s GΓ d G +). The Green’s function for the channel is (3) where I is an identity matrix and U L is the Laplace’s potential drop. Self-energies click here and broadening functions are and Γ s,d

= i[Σ s,d − Σ s,d +], respectively. are the contact Fermi functions. μ s,d are source/drain chemical potentials. μ d is shifted due to drain bias as μ d = μ o − qV d and μ s = μ o, where μ o is the equilibrium chemical potential. Results and discussion We next discuss the numerical results for a transistor with α = 0.4 and BWo = 0.1 eV. The transfer characteristics with V d = 0.16, 0.18 and 0.2 V are shown in Figure 2a. A steep subthreshold slope is obtained with a high on/off current ratio. The threshold voltage depends on the drain voltage V d, and it increases with the drain bias – a trend opposite to the drain-induced barrier

lowering of a FET. The subthreshold current much below the threshold voltage, which is due to the reflections from the barrier of the near-midgap state, decreases exponentially. Figure 2 Transport characteristics. (a) Transfer characteristics show steep subthreshold characteristics with drain-voltage dependent threshold voltage shift. (b) Output characteristics show a saturating behavior followed by a negative ACP-196 differential resistance. (c) With increasing drain bias, the C1GALT1 transmission window shrinks due to a spectral misalignment (Addition file 1). (d) The increasing Fermi function difference between the two

contacts and the decreasing transmission lead to an increasing and then decreasing T(E)[f s − f d] function. We further report the output characteristics in Figure 2b for V g = 0.04, 0.08, 0.12, 0.16, and 0.2 V, which show a negative differential resistance (NDR) behavior that is crucial for the low-power inverter operation (Additional file 1). The current cut-off mechanism is similar to the Bloch condition through minibands in superlattices, giving rise to an NDR event, when the drain voltage exceeds the miniband width [15, 16]. The miniband in superlattices is formed by the overlap of quantized states through tunnel barriers, inherently leading to small miniband widths and large effective masses [17]. The NDR events mediated by minibands have been reported in III-V heterostructures [18] and graphene superlattices [19]. However, the peak-to-valley ratio in such structures is limited to about 1.1 to 1.2. In comparison, the NDR feature reported for near-midgap state in this work shows a peak-to-valley ratio of greater than 103, which is important for the low-power operation.

In the perforated group, Sixty two (71%) patients had high WBC wi

In the perforated group, Sixty two (71%) patients had high WBC with 94% shift to the left compared to 72 (57%) patients with 61% shift to the left in the non perforated

group (Table 3). Clinical Assessment (CA), Ultrasonography (US) and Computerized Tomography (CT) scan were used in that order for diagnosis. Of all patients 31% were diagnosed by CA alone, US detected another 40% and the remaining 29% were diagnosed by CT scan (Table 4). Although we couldn’t calculate the sensitivity and specificity of each diagnostic test as we studied the positive cases only, we found that there were no false positive results Sorafenib research buy when CT scan was used. Table 4 Number and percentage of patients diagnosed with appendicitis Variable Total Perforated Nonperforated n=214 (100%) n= 87 (41%) n= 127 (59%) Diagnostic tools:       Clinical assessment 66 (31) 27 (31) 39 ( 31) Ultrasonography 85 (40) 29 (33) 56 (44) Computerized scan 63 (29) 31 (36) 32 (25) Mc Burney’s incision was used in 168 and lower midline incision in 46 patients. Post operative complications were seen in 44 (21%) patients. Complications were three times more frequent

in the perforated as compared to the nonperforated group of patients, 33 (75%) and 11 (25%) respectively (Table 1). Four patients developed wound dehiscence and other eight had intra abdominal Selleck BAY 80-6946 sepsis and collections, all in the perforated group except one. Other 22 patients in both groups had wound infection but all, except one, responded to antimicrobial treatment, debridement and dressings. Other complication as Edoxaban renal failure, chest infection, and respiratory failure, cardiovascular accidents were noted in both groups. There were 6 (3%) deaths in both groups, four in the perforated and two in the nonperforated group. In the perforated group, two patients developed multiple intra abdominal abscess collections and died due to uncontrollable sepsis. Of the other two, one was already on chemotherapy treatment for lymphoma and died due to uncontrollable atypical pneumonia while the other had an advanced cardiovascular

disease and died due to congestive heart failure. In the nonperforated group, one patient died due to uncontrolled intra abdominal sepsis and the other due to massive myocardial infarction. As expected, the hospital stay was longer for patients in the perforated group (7.4 ± 6.3 and 4.2 ±3.1 days in perforated and nonperforated groups respectively) (Table 2). Discussion Acute appendicitis continues to be the commonest cause of surgical abdominal emergency. It was often thought to be the disease of the young but as a result of recent increases in lifetime expectancy, the incidence of acute appendicitis also increased in the elderly [1–11]. The incidence of appendiceal perforation in acute appendicitis is estimated to be in the range of 20-30% which increases to 32-72% in patients above 60 years of age [3–9, 12–14].

Likewise, our data are in opposition to the work of Jacobs and co

Likewise, our data are in opposition to the work of Jacobs and colleagues [12] who recently Ibrutinib manufacturer reported an improvement of 2.6-15% in high intensity cycle sprint performance with 4.5 grams of GlycoCarn® compared to a placebo. In this same study these investigators also noted an approximate 16% decrease in post-exercise blood HLa with GlycoCarn® compared to placebo. Differences in the exercise protocol likely contributed to the discrepancy in findings between the two studies. Finally, we have noted previously that GlycoCarn® results in lower resting MDA following chronic intake [14]. The present study extends those findings by noting a decrease, albeit statistically insignificant, in MDA from

pre- to post-exercise, indicating a potential antioxidant effect. Interesting to note, this favorable effect of GlycoCarn® on MDA reduction was associated with the highest StO2 at the start of exercise, indicating a possible association between increased blood flow and decreased lipid peroxidation. The converse was also true, as SUPP1 demonstrated the greatest increase in MDA from pre- to post-exercise, while displaying

the lowest StO2 at the start of exercise and the greatest drop in StO2 from the start to the end of exercise. These findings support the idea that exercise-induced hypoxia is associated with increased lipid peroxidation, likely due Deforolimus to increased free radical production [24]. It is possible that chronic treatment of GlycoCarn® may result in more robust changes in MDA or other markers of oxidative stress. Using a different stress protocol (handgrip dynamometry vs. resistance exercise), we have reported recently that four weeks of GlycoCarn® treatment at a daily dosage of 4.5 grams in resistance trained men results in a 45% decrease in oxidized to total glutathione ratio [40]. Additional work is needed to determine the antioxidant effect of chronic GlycoCarn®

administration following resistance exercise, and to determine whether or not such an effect translates into improved post-exercise recovery. One explanation for our lack of a performance effect for the chosen supplements, in addition to GlycoCarn®, could be our specific sample of BCKDHB subjects. That is, they may have been non-responders to treatment, as has been reported previously for a variety of sport supplements including caffeine [41], creatine [42], and GlycoCarn®, in terms of nitrate/nitrite [13]. If this were true, it is possible that a different group of subjects may have responded positively to treatment. This should be considered when athletes are contemplating the use of such products. For example, of our 19 subjects, 11 responded positively to GlycoCarn® in terms of total volume load, with a mean improvement above placebo of 12.6%. This is in opposition to the 3.3% improvement above placebo when including all 19 subjects in the analysis.

While the opaque-transparent switch is reversible, the rough phen

While the opaque-transparent switch is reversible, the rough phenotype results from irreversible deletion of cell envelope glycopeptidolipid genes and is irreversible [24, 51]. TLC (Thin Layer Chromatography) analysis of the different morphotypes from strain 104 has been performed by Torelles [21]. They also analysed the sugar composition of the glycopeptidolipids (GPL) by gas chromatography–mass spectrometry (GC–MS) analysis. They found that the smooth opaque and smooth transparent colonies formed similar GPL and both expressed besides the nsGPL (ns: non-specific) the ssGPL (ss:serovar specific) of serovar 1. However, the ssGPL was absent Palbociclib in vitro in the rough morphotype, which had a strong band of the nsGPL. A band in the lipopeptid

region devoid of sugars was present in the smooth transparent morphotype and the rough morphotype but lacking in the smooth opaque morphotype. ALK inhibitor The sugar composition of all morphotypes showed the typical profiles related to ns and ssGPL of serovar 1,

only in the rough morphotype 6-deoxytalose and 3-O-methyl-6-deoxytalose were missing. The transparent colony variant grows better in macrophages and animals compared to the opaque variant. Moreover, white transparent colonies survived better in macrophages than red transparent colonies [19, 24, 50, 51, 56]. These differences in intracellular survival may be caused by variations in the cytokine response towards infection by different Tolmetin morphotypes. The smooth opaque morphotype has been shown to induce higher levels of secretion of IL-1α, IL-1β and TNF-α by human blood-derived monocytes compared to the smooth-transparent morphotype [57]. Variation in cytokine response upon infection with either smooth-opaque

or smooth-transparent M. avium was also reported upon infection of human microglia cultures [58]. The colony morphology of the WT and the mutants upon plating on Congo Red Agar is shown in Figure  3. The WT (Figure  3 A) mainly formed smooth-domed-opaque (sdo) colonies along with smooth-transparent (st) colonies. Mutant MAV_2555 showed the same morphologies, but additionally smooth-flat-red (sfr) colonies were visible (Figure  3 B). Relatively few smooth-transparent and rough colonies occurred in mutant MAV_1888 (Figure  3 C), MAV_4334 (Figure  3 D) and MAV_5106 (Figure  3 E). Mutant MAV_4334 (Figure  3 D) showed a higher variation with respect to the intensity of red color of smooth-domed-opaque colonies. Mutant MAV_1778 showed a very high degree of variability displaying red-rough (rr) and smooth-flat-red colonies additionally to the smooth-domed-opaque, smooth-transparent and rough-white (rw) colonies (Figure  3 F). The colonies generated by mutant MAV_3128 (Figure  3 G) were in average larger in size and the smooth-opaque colonies appeared paler than in the WT. Also, the edges of these colonies were more irregular. Some red-rough colonies were also visible. The most multifaceted image was displayed by mutant MAV_3625.

HSV is intermittently shed from the genital mucosa in the absence

HSV is intermittently shed from the genital mucosa in the absence of symptoms causing subconscious transmission of disease [11]. Vertical transmission of HSV to neonates is associated with a high mortality rate and a high incidence of neurological sequelae in survivors [12]. In addition, genital herpes has been linked to an increased risk of sexually acquiring and transmitting human immunodeficiency virus (HIV), which can be strongly reduced by HSV antiviral therapy [13, 14]. To date, the treatment and prevention of primary and recurrent disease is limited [15]. Experimental vaccine approaches against genital herpes have included

peptides, proteins, killed virus, DNA vaccines, heterologous replicating viral vectors, replication-defective viruses, and attenuated replication-competent viruses [16, 17]. Considering the general Crizotinib impact of HSV-1 diseases and rising importance of primary genital herpes caused by HSV-1, a desirable vaccine should be capable of offering effective protective immunity against both HSV subtypes. A main

target for subunit vaccine development has been HSV glycoprotein D (gD), a major antigen on the viral envelope [17]. Subunit vaccines containing gD in combination with an adjuvant appeared to be safe and effective against genital herpes in guinea pigs [18–20], but failed to provide general protection in clinical trials [21, 22]. Replication-defective viruses lacking functions essential for viral replication or assembly of progeny virus particles have a broad antigenic spectrum and are more efficient than subunit vaccines in eliciting protective immune selleck responses against genital HSV in mice and guinea pigs [23]. However,

the use of replication-defective viruses, particularly when used in latently infected individuals, imposes certain risks, as they might regain replication competence in the presence of wild-type Tyrosine-protein kinase BLK virus or reactivate latent wild-type virus infections [24]. To minimize these safety concerns, using the T-REx™ gene switch technology (Invitrogen, Carlsbad, CA) developed in our laboratory and the dominant-negative mutant polypeptide UL9-C535C of HSV-1 origin binding protein UL9, we generated a novel class of replication-defective HSV-1 recombinant, CJ83193, which can prevent its own viral DNA replication as well as that of wild-type HSV-1 and HSV-2 in co-infected cells [25, 26]. To increase its safety and vaccine efficacy against HSV infections, we recently constructed a CJ83193-derived HSV-1 recombinant CJ9-gD by replacing the essential UL9 gene with an extra copy of the HSV-1 gD (gD1) gene under the control of the tetO-bearing hCMV major immediate-early promoter [27]. We demonstrated that unlike the gD gene controlled by the endogenous promoter whose expression is dependent on viral replication [28], CJ9-gD expresses high-levels of gD at the immediate-early phase of HSV infection.

Cell Mol Life Sci 2003, 60:904–918 PubMed 5 Vazquez-Boland JA, K

Cell Mol Life Sci 2003, 60:904–918.PubMed 5. Vazquez-Boland JA, Kuhn M, Berche P, Chakraborty T, Dominguez-Bernal G, Goebel W, Gonzalez-Zorn B, Wehland J, Kreft J: Listeria pathogenesis and molecular virulence determinants. Clin Microbiol Rev 2001, 14:584–640.PubMedCentralPubMedCrossRef 6. Orsi RH, den Bakker HC, Wiedmann M: Listeria monocytogenes lineages: genomics, evolution, ecology, and phenotypic characteristics. Int J Med Microbiol

2011, 301:79–96.PubMedCrossRef Lapatinib cell line 7. Clayton EM, Hill C, Cotter PD, Ross RP: Real-time PCR assay to differentiate listeriolysin S-positive and -negative strains of Listeria monocytogenes . Appl Environ Microbiol 2011, 77:163–171.PubMedCentralPubMedCrossRef 8. Cotter PD, Draper LA, Lawton EM, Daly KM, Groeger DS, Casey PG, Ross RP, Hill C: Listeriolysin S, a novel peptide haemolysin associated with a subset of lineage I Listeria monocytogenes . PLoS

Pathog 2008, 4:e1000144.PubMedCentralPubMedCrossRef 9. Molloy EM, Cotter PD, Hill C, Mitchell DA, Ross RP: Streptolysin S-like virulence factors: the continuing sagA. Nature reviews. Microbiology 2011, 9:670–681.PubMedCentralPubMed 10. den Bakker HC, Bundrant BN, Fortes ED, Orsi RH, Wiedmann M: A population genetics-based and phylogenetic approach to understanding the evolution of virulence in the genus Listeria . Appl Environ Microbiol 2010, 76:6085–6100.PubMedCentralPubMedCrossRef selleck chemicals llc 11. den Bakker HC, Cummings CA, Ferreira V, Vatta P, Orsi RH, Degoricija L, Barker M, Petrauskene O, Furtado MR, Wiedmann M: Comparative genomics of the bacterial genus Listeria : genome evolution is characterized by limited gene acquisition and limited gene loss. BMC Genomics 2010, 11:688.PubMedCentralPubMedCrossRef 12. Johnson J, Jinneman K, Stelma G, Smith BG, Lye D, Messer J, Ulaszek J, Evsen L, Gendel Urease S, Bennett RW, Swaminathan B, Pruckler J, Steigerwalt A, Kathariou S, Yildirim S, Volokhov D, Rasooly A, Chizhikov V, Wiedmann M, Fortes E, Duvall RE, Hitchins AD: Natural atypical Listeria innocua strains with Listeria monocytogenes pathogenicity island 1 genes. Appl Environ Microbiol 2004,

70:4256–4266.PubMedCentralPubMedCrossRef 13. Volokhov DV, Duperrier S, Neverov AA, George J, Buchrieser C, Hitchins AD: The presence of the internalin gene in natural atypically haemolytic Listeria innocua strains suggests descent from L. monocytogenes . Appl Environ Microbiol 2007, 73:1928–1939.PubMedCentralPubMedCrossRef 14. Simpson PJ, Stanton C, Fitzgerald GF, Ross RP: Genomic diversity and relatedness of bifidobacteria isolated from a porcine cecum. J Bacteriol 2003, 185:2571–2581.PubMedCentralPubMedCrossRef 15. Ward TJ, Gorski L, Borucki MK, Mandrell RE, Hutchins J, Pupedis K: Intraspecific phylogeny and lineage group identification based on the prfA virulence gene cluster of Listeria monocytogenes . J Bacteriol 2004, 186:4994–5002.PubMedCentralPubMedCrossRef 16.

The band distribution of bacterial population in individual sampl

The band distribution of bacterial population in individual samples ranged from 20 to 26 (mean 22.40 ± 1.71 SD) in non-tumor where as 15 to 26 bands (mean 20.60 ± 3.10 SD) in tumor groups. The Mann–Whitney U test to compare the Shannon-Weaver indexes of diversity (H’) in non-tumor and tumor samples showed no significant differences (p > 0.05, two-tailed) in oral microbiota between two sample groups. The inter- group similarities were found to be 40% to 80% by cluster analysis (Figure 2). Most of the clinically distinct

samples (non-tumor and tumor) from the same patients clustered together with exception of one sample (184_N and 184_T) as seen in their intensity profiles. Figure 1 DGGE profile of microbial communities from two clinically distinct non-tumor and tumor

groups. N–Non-tumor; T–Tumor; Marker I & II: DGGE reference markers correspond to 16S rRNA gene fragments from quoted specific BYL719 manufacturer bacterial species [Marker I: 1. Fusobacterium nucleatum subsp. vincenti (ATCC 49256); 2. Fusobacterium nucleatum subsp. nucleatum (ATCC 25586); 3. Streptococcus sanguinis (ATCC 10556); 4. Streptococcus oralis (ATCC 35037); 5. Streptococcus salivarius (ATCC 7073); 6. Streptococcus mutans (UA 159); 7. Lactobacillus paracasei (ATCC 25598); 8. Porphyromonas gingivalis (ATCC 33277); 9. FDA approved Drug Library in vitro Actinomyces odontolyticus (ATCC 17929);10. Actinomyces Selleck MG132 naeslundii (ATCC 12104), Marker II: 1. F. nucleatum subsp. vincenti (ATCC 49256); 2. F. nucleatum subsp. nucleatum (ATCC 25586); 3. Bacteroides forsythus (ATCC 43037); 4. S. sanguinis (ATCC 10556); 5. S. oralis (ATCC 35037); 6. Veillonella parvula (ATCC 17745); 7. Prevotella intermedia (ATCC 25611); 8. Aggregatibacter actinomycemcomitans (ATCC 43717); 9. P. gingivalis (ATCC 33277); 10. A.odontolyticus (ATCC 17929); 11. A. naeslundii (ATCC 12104)]. Figure 2 Dendrogram representing the fingerprinting intensity profile

of two clinically distinct samples from non-tumor and tumor tissues. N–Non-tumor; T–Tumor. Similarity index (SI) was calculated based on the total number of high and low intensity bands per lane and position of band migration reflecting number of bands the two lanes have in common. The values signify similarities in bacterial composition between non-tumor and tumor groups (Table 1). The tumor samples (intra- group), 1457_T and 527_T showed total dissimilarity in their profiles despite sharing the same group. The band similarity correlation was highest in non-tumor and tumor tissue samples (inter- group), 142_N/142_T (77.27%) and 146_N/146_T (71.43%) from the same patient indicating that most of the microbiota were common at both the sites but there were changes in the bacterial composition. Chi-square test indicated significant differences in intra- and inter- groups bacterial profiles (X 2 = 10.76, p = 0.005).

49 −1 13 −1 17 −1 00 1 92 2 52 1 36 Cthe_2975 RNA polymerase sigm

49 −1.13 −1.17 −1.00 1.92 2.52 1.36 Cthe_2975 RNA polymerase sigma-I factor 1.24 1.47 −7.26 −2.59 −2.09 −1.94 1.15 1.45 4.32 1.96 Cthe_0403 RNA polymerase sigma-I factor −1.65

−1.92 −5.17 −3.64 1.89 1.76 −1.66 −1.08 −1.12 1.83 Bold values indicate significantly different expression levels as determined by ANOVA. For the PM vs. WT in 0% and 10% v/v Populus hydrolysate a positive/negative BGB324 concentration value represents a higher/lower level of expression in the PM compared to the WT. For the standard medium (0%) versus Populus hydrolysate media (10 or 17.5%) a positive/negative value represents a higher/lower expression in the hydrolysate media compared to standard medium. Values are indicated for samples collected during the mid-log (ML) and late-log (LL) growth phases. Categories of gene with increased Trichostatin A supplier expression in the PM The PM increases the gene expression in only two categories compared to the WT in standard and Populus hydrolysate media: energy production and conversion, and amino acid transport and metabolism (Figure 1). In addition to these, the PM also increases the expression of inorganic ion metabolism and transport genes compared to the WT in 10% v/v Populus hydrolysate medium. The increased expression in the energy production and conversion genes may allow for the increased growth phenotype observed in the PM strain. Increases in

glycolysis would lead to increases in reducing power (in the form of NADH) being available for downstream electron transport and ethanol production. The increase in ethanol production and increase in electron flux may generate sufficient NAD+ to ensure increased PLEKHB2 cellular metabolism [8]. The assemblage of genes encoding proteins involved in pyruvate metabolism and end-product synthesis dictate, in part, how carbon and electrons

flux is distributed between the catabolic, anabolic, and energy producing pathways of the cell [25]. C. thermocellum catabolizes glucose via the Embden-Meyerhof pathway using the “malate shunt” (Figure 2) [26–28]. Compared to the WT, the PM had a higher expression of 23 and 44 genes belonging to the energy production and conversion category in standard and Populus hydrolysate media, respectively. The PM upregulated 8 genes specific to the central metabolism and mixed-acid fermentation compared to the WT in standard medium (Figure 2 and Table 2). In 10% v/v Populus hydrolysate medium, the PM upregulated 10 genes along the central metabolism and mixed acid fermentation pathways compared to the WT. The PM has a mutation in the non-coding region upstream of the Cthe_0422-Cthe_0423 operon which encodes the rex (redox) repressor and the adhE alcohol dehydrogenase. This mutation may cause the observed increase in ethanol production [17,18]. A study of the effect of cellulose fermentation found that the central metabolism genes are typically upregulated during cellulose fermentation compared to cellobiose fermentation that the cells were grown on in this study [12,25].