Importantly, the definition of treatment failure (virological, immunological

or clinical) was the strongest predictor of resistance. Immunological and clinical treatment failure were categorised as inclusion criteria because access to plasma HIV-1 RNA and CD4 quantification was irregular during the study period. The finding that immunological and clinical criteria were poor predictors of treatment failure attributable to resistance is important and has relevance for other resource-poor settings where access to VL testing may be limited. Our results are in agreement with recent Torin 1 research buy data which also show that CD4 cell counts and clinical criteria do not accurately identify patients with virological treatment failure [17–19]. In this study, we estimated that the overall prevalence of resistance-associated mutations was 81% among the investigated Honduran patients,

who were selected on the basis of signs and symptoms of treatment failure. This finding agrees well with results from the United Kingdom (80% resistance) [10], United States (76% resistance) [11], and France (88% resistance) [12], in spite of the fact that the cART conditions in these countries are very different from those in Honduras. It is somewhat surprising that 19% of the 138 studied patients did not appear to harbour a resistant virus even though they had been selected as experiencing treatment failure. The absence of resistance in 19% of the patients indicates that adherence in these patients may have been PD-0332991 chemical structure too low to drive the development of resistance. However, and as discussed above, the significant association of resistance

with type of failure (virological, immunological or clinical) also demonstrates that it is difficult Etofibrate to monitor HIV therapy without regular access to plasma HIV-1 quantification. Thus, patients with adequate adherence and low plasma HIV RNA levels may incorrectly have been perceived to have immunological or clinical treatment failure. We observed that the presence of genotypic resistance was positively correlated with years on therapy and the number of ART regimens used. When this study was carried out, access in Honduras to boosted PIs was very limited. The broad resistance to NRTIs, NNRTIs and unboosted PIs indicates that many of our study subjects were in need of salvage therapy with boosted PIs as well as entry and integrase inhibitors [3]. Improved access to these drugs is urgently needed for these and other heavily treatment-experienced Honduran patients. M184V and K103N were the most prevalent NRTI and NNRTI mutations in our study, at 62% and 30%, respectively. M184V causes high-level (>100-fold) resistance to lamivudine/emtricitabine and emerges rapidly in patients who receive lamivudine monotherapy [20]. It is also the first mutation to develop in patients receiving partially suppressive triple combination therapy including lamivudine [21–23].

The database is a depository of complete information on: the chemical structure of peptides; target species; target object of cell; peptide antimicrobial/haemolytic/cytotoxic activities; and experimental conditions UK-371804 in vitro at which activities were estimated. The dbaasp search page allows the user to search peptides according to their structural characteristics, complexity type (monomer,

dimer and two-peptide), source, synthesis type (ribosomal, nonribosomal and synthetic) and target species. The database prediction algorithm provides a tool for rational design of new antimicrobial peptides. dbaasp is accessible at http://www.biomedicine.org.ge/dbaasp/. “
“There is limited information on whether parasites

act as vectors to transmit bacteria in fish. In this trial, we used Ichthyophthirius multifiliis and fluorescent Edwardsiella ictaluri as a model to study the interaction between parasite, bacterium, and fish. The percentage (23–39%) of theronts fluorescing after exposure to E. ictaluri was significantly higher than control theronts (~ 6%) using flow cytometry. Theronts exposed to E. ictaluri at 4 × 107 CFU mL−1 showed a higher percentage (~ 60%) of fluorescent theronts compared to those (42%) exposed to 4 × 103 CFU mL−1 at 4 h. All tomonts (100%) carried the bacterium after exposure to E. ictaluri. Tanespimycin mw Edwardsiella ictaluri survived and replicated during tomont division. Confocal microscopy demonstrated that E. ictaluri was associated with the tomont surface. Among theronts released from tomonts exposed to E. ictaluri, 31–66% were observed with attached E. ictaluri. Sixty percent of fish exposed to theronts treated with 5 × 107E. ictaluri mL−1 were positive for E. ictaluri at 4 h as determined by qPCR or fluorescent microscopy. Fluorescent E. ictaluri were observed on trophonts in skin and gill wet mounts of dead fish. This study demonstrated that Ich could vector E. ictaluri to channel catfish. In aquaculture systems, fish rarely encounter

a single pathogen. Most often, fish are concomitantly infected by multiple disease agents (Shoemaker et al., 2008). Parasitism has been demonstrated to enhance bacterial invasion where parasitic injuries serve as portals of entry Axenfeld syndrome (Buchmann & Lindenstrøm, 2002; Busch et al., 2003; Bandilla et al., 2006). Ahne (1985) reported that parasites Argulus foliaceus and Piscicola geometra served as mechanical vectors for spring viremia of carp virus (SVCV). Vijayan et al. (2005) reported that polychaete worms acted as vectors of white spot syndrome virus in the transmission of white spot disease to the shrimp Penaeus monodon. Cusack & Cone (1985) detected bacterial colonies on the surface of Gyrodactylus by scanning electron microscopy. However, they did not determine whether the bacteria were pathogenic to fish, and thus, the exact role of the bacteria was not clear.

Carey Special Immunology Unit at University Hospitals Case Medical Pexidartinib clinical trial Center in Cleveland, OH. All individuals provided written informed consent to participate in the HIV Metabolic Research Center trials and also to have their blood stored for use in future HIV-related metabolic research. This study was approved by the University Hospital Case Medical Center Institutional Review Board with a waiver for further informed consent. All data collected, demographics, HIV and cardiovascular characteristics, laboratory values and stored samples were obtained on the date on which FMD was performed. The primary outcome

of this study was endothelial function determined using FMD of the brachial artery. Secondary outcomes of interest included markers of inflammation [interleukin-6 (IL-6), soluble tumour necrosis factor receptors I and II (sTNFR-I and -II), high-sensitivity C-reactive protein (hs-CRP), soluble intercellular adhesion molecule-1 (sICAM-1) and soluble

vascular cell adhesion molecule-1 (sVCAM-1)], coagulation (D-dimer and fibrinogen), oxidative stress (F2-isoprostanes), lipoprotein levels and insulin resistance estimated using the homeostasis model assessment of insulin resistance (HOMA-IR). Endothelial function was evaluated by measuring FMD of the brachial artery with ultrasound [15] as previously described [16]. Participants were instructed to come Forskolin in vivo fasting, to not take anti-hypertensive medications and not to use tobacco or caffeine-containing products for 12 h before the study. All studies were performed by a single technologist (CW) using a Phillips iU22 Ultrasound and an L10-7 MHz linear array transducer (Phillips Healthcare, Bothell, WA, USA) and a 5-min occlusion time. Images were read using Brachial Artery Analyzer software (Medical Imaging Applications LLC, Coralville, IA, USA), a semi-automated, border-interfacing program. For FMD determination, brachial artery diameters before and after confirmed reactive hyperaemia were measured in triplicate and averaged from a 1-cm segment of the artery. FMD is expressed

as a percentage change from baseline brachial artery diameter to brachial artery diameter after reactive hyperaemia. Plasma from each participant Selleckchem Cobimetinib was previously stored at −70°C immediately after processing. Stored samples were then batched and tested for the markers of inflammation, coagulation and oxidative stress outlined above. IL-6, sTNFR-I and -II, sICAM-1 and sVCAM-1 were determined by quantitative sandwich enzyme-linked immunosorbent assays (ELISAs) (R&D Systems, Minneapolis, MN, USA). Interassay variability was 2.02–15.36%, 3.66–5.77%, 2.13–3.79%, 3.43–7.37% and 4.76–8.77%, respectively. hs-CRP and fibrinogen were determined using particle enhanced immunonephelometric assays on a BNII nephelometer (Siemens, Indianapolis, IN, USA). Interassay variability was 3.01–6.46% and 3.42–7.59%, respectively.

However, where there is a risk of frequent prolonged treatment interruptions, EFV-based regimens may be associated with more frequent selection for drug resistance compared with PI/r. Clinicians are poor at both predicting future adherence to ART in naïve

subjects [11] and at detecting non-adherence during ART [12, 13]. However, in a case where a clinician or patient has concerns about a patient’s future adherence, should this influence the choice of first-line therapy? The consequences of low adherence depend on drug pharmacokinetics, potency, fitness of resistant strains and genetic barrier to resistance [14]. Hence, both the level and pattern of non-adherence must be considered. Large RCTs of first-line therapy may not be able to inform this choice as subjects likely to be non-adherent are often excluded from such trials. On the other hand, observational studies often select patients already established on ART [15, 16] RG7422 chemical structure where the observed effects of non-adherence on treatment outcome are likely to differ from those in patients starting ART de novo. This selection bias may exclude those who have Atezolizumab manufacturer either experienced early virological failure, disease progression (or even death) or have defaulted from care. In addition, most studies either pre-date the use of boosted-PI regimens in first-line therapy [15, 17] or include large numbers of patients on unboosted

PI regimens. Three different outcomes may be considered: virological suppression, selection of drug resistance, and effect of pattern of non-adherence. There are no data from RCTs that directly address this question. Among subjects reporting <95% adherence in a RCT comparing LPV/r with once-daily DRV/r, virological failure was more likely in the LPV/r arm [18]. Among patients who were virologically suppressed initially, adherence <95% was associated with an increased risk of failure

[16], and very low adherence (<50%) results in virological rebound irrespective of regimen [5, 16, 19]. However, virological suppression has been observed with only moderate adherence (50–75%) Carbohydrate among patients on NNRTIs [5, 16, 19] and virological failure has been reported to be significantly more likely among all patients on unboosted PI-based regimens where adherence was <95% [16]. However, this finding may have been confounded by the once-daily dosing in the EFV group. A further study [20] examined only patients with undetectable viraemia and found no difference in rates of virological rebound for patients on PI/r vs. NNRTIs. The effect of level of non-adherence on selection of drug resistance varies by class. This was first described for unboosted PI regimens where moderate-to-high adherence was associated with increased risk of resistance [21]. The incidence of resistance in studies of boosted-PI regimens is low [18, 22-26] but is observed with adherence just below 80–95% [15, 27].

Participants performed tasks investigating the ability to visually discriminate changes in the form or action of body parts affected by somatosensory and motor disconnection. SCI patients showed a

specific, cross-modal deficit in the visual recognition of the disconnected lower body parts. This deficit affected both body action and body form perception, hinting at a pervasive influence of ongoing Panobinostat in vitro body signals on the brain network dedicated to visual body processing. Testing SCI patients who did or did not practise sports allowed us to test the influence of motor practice on visual body recognition. We found better upper body action recognition in sport-practising SCI patients, indicating that motor practice is useful for maintaining visual representation of actions after deafferentation and deefferentation. This may be a potential resource to be exploited for rehabilitation. “
“During brain maturation, neurons form specific connections with each other to establish functional neuronal circuits.

The processes underlying the development of connectivity, such as the selection of synaptic partners and the fine-tuning of neuronal networks, act with single-synapse precision. Calcium is an intracellular secondary messenger that operates with remarkable spatio-temporal Ku0059436 specificity and regulates functional and structural adaptations at the level of individual synapses. Although Cyclin-dependent kinase 3 the structure, molecular composition and function of an emerging synapse changes dramatically during its development, the single-synapse specificity of calcium signaling

is maintained at every step of synapse formation: when the first contacts between axons and dendrites form, during the onset of synaptic function and later, when spine synapses emerge. Here, we describe the mechanisms that help developing neurons to confine calcium signaling to individual synapses, and discuss how these local calcium dynamics facilitate the development of accurate neuronal connections at each step of synapse maturation. “
“Changes in the strength of synapses in the hippocampus that occur with long-term potentiation (LTP) or long-term depression (LTD) are thought to underlie the cellular basis of learning and memory. Memory formation is known to be regulated by spacing intervals between training episodes. Using paired whole-cell recordings to record from synapses connecting two CA3 pyramidal neurons, we now show that stimulation frequency and spacing between LTP and LTD induction protocols alter the expression of synaptic plasticity. These effects were found to be dependent on protein phosphatase 1 (PP1), an essential protein serine/threonine phosphatase involved in synaptic plasticity, learning and memory. We also show for the first time that PP1 not only regulates the expression of synaptic plasticity, but also has the ability to depress synaptic transmission at basal activity levels.

Participants performed tasks investigating the ability to visually discriminate changes in the form or action of body parts affected by somatosensory and motor disconnection. SCI patients showed a

specific, cross-modal deficit in the visual recognition of the disconnected lower body parts. This deficit affected both body action and body form perception, hinting at a pervasive influence of ongoing AZD9291 solubility dmso body signals on the brain network dedicated to visual body processing. Testing SCI patients who did or did not practise sports allowed us to test the influence of motor practice on visual body recognition. We found better upper body action recognition in sport-practising SCI patients, indicating that motor practice is useful for maintaining visual representation of actions after deafferentation and deefferentation. This may be a potential resource to be exploited for rehabilitation. “
“During brain maturation, neurons form specific connections with each other to establish functional neuronal circuits.

The processes underlying the development of connectivity, such as the selection of synaptic partners and the fine-tuning of neuronal networks, act with single-synapse precision. Calcium is an intracellular secondary messenger that operates with remarkable spatio-temporal www.selleckchem.com/products/Everolimus(RAD001).html specificity and regulates functional and structural adaptations at the level of individual synapses. Although Tyrosine-protein kinase BLK the structure, molecular composition and function of an emerging synapse changes dramatically during its development, the single-synapse specificity of calcium signaling

is maintained at every step of synapse formation: when the first contacts between axons and dendrites form, during the onset of synaptic function and later, when spine synapses emerge. Here, we describe the mechanisms that help developing neurons to confine calcium signaling to individual synapses, and discuss how these local calcium dynamics facilitate the development of accurate neuronal connections at each step of synapse maturation. “
“Changes in the strength of synapses in the hippocampus that occur with long-term potentiation (LTP) or long-term depression (LTD) are thought to underlie the cellular basis of learning and memory. Memory formation is known to be regulated by spacing intervals between training episodes. Using paired whole-cell recordings to record from synapses connecting two CA3 pyramidal neurons, we now show that stimulation frequency and spacing between LTP and LTD induction protocols alter the expression of synaptic plasticity. These effects were found to be dependent on protein phosphatase 1 (PP1), an essential protein serine/threonine phosphatase involved in synaptic plasticity, learning and memory. We also show for the first time that PP1 not only regulates the expression of synaptic plasticity, but also has the ability to depress synaptic transmission at basal activity levels.

For example, Silmitasertib purchase MinCEc causes enlargement of chloroplasts in higher plants (Tavva et al., 2006), a MinD homologue from Arabidopsis thaliana complements the minicell phenotype of E. coliΔminDE mutant (Zhang et al., 2009), MinD and MinE from Neisseria gonorrhoeae can oscillate in E. coli (Ramirez-Arcos et al., 2002) and gonococcal MinCD is able to elongate N. gonorrhoeae and E. coli cells (Szeto et al., 2001). So far there has

been no reference to the functional exchange of Min systems between Gram-negative and Gram-positive bacteria. The results presented in this study extend previous findings about the heterologous functioning of Min proteins and shows for the first time that the E. coli Min system can partially substitute the Min system when introduced into B. subtilis cells. The authors thank Emília Chovancová find more for technical assistance, all members of the laboratory for consultations and help, David H. Edwards for strain 1920,

David Rudner for pED962 plasmid, Daniel B. Kearns for strain DS3185 and Juraj Labaj for help with graphics. This work was supported by Grants 2/7007/27 from Slovak Academy of Sciences, by grants from the Slovak Research and Development Agency under contract No. APVT-51-0278 and No. LPP-0218-06, by grant from the European Science Foundation ESF-EC-0106, and by grant 066732/Z/01/Z from The Wellcome Trust. “
“Validation of bactericidal profiles owing to a deficiency of target bacterial molecule provides opportunities to discover antimicrobial drug candidates. In this study, we constructed genetic-engineered Escherichia coli strains, in which the target gene expression is conditionally regulated by a tryptophan promoter, while the target protein expression is regulated by N-end rule-based proteolysis. Among 10 genes, whose correspondent proteins are target candidates of antibiotics for community acquired respiratory tract infection, it was clearly

demonstrated that the suppression of DnaB,GlmU, or DnaX results in a bactericidal profile, while the suppression of FabB,PyrG,DnaG,Der,PyrH,Era, or IspA leads to a bacteriostatic profile. This study is the first to predict the antibacterial inhibition profiles of Der,DnaG,DnaX,Era,GlmU,IspA,PyrG, ifenprodil and PyrH, and confirms previous findings for DnaB and FabB. The results suggested that the system constructed in this study is a novel and useful tool to validate whether the target bacterial molecule has appropriate properties as a target of antimicrobial agents. The ability to induce bactericidality is one of the crucial profiles for an antimicrobial drug, as eliminating pathogens in hosts is difficult with bacteriostatic drugs alone. In fact, the frequency of recurrences of the primary infection in community acquired respiratory tract infections (RTIs) is higher especially in immunocompromised patients, when treated with bacteriostatic as opposed to bactericidal antibiotics (Douidar & Snodgrass, 1989; von Rosenstiel & Adam, 1994).

The ability of elevated levels of the AP endonuclease Nfo to increase the wet heat resistance of nfo exoAα−β− spores supports previous suggestions that AP sites are major damaging lesions generated in DNA by wet heat treatment of α−β− spores, and further that AP endonucleases may be important in repairing this damage (Salas-Pacheco et al., 2005). In contrast, overexpression of Nfo in wild-type spores (strain PERM869)

had no effect on these spores’ wet heat resistance (Fig. 2c). Although the nfo exoAα−β− spores with overexpressed Nfo were resistant to wet heat, extended FDA-approved Drug Library cell line wet heat treatment did result in spore killing (Fig. 2b). This killing is most likely due to damage to some essential protein(s) (Coleman et al., 2007), as there was no increase in auxotrophic and asporogenous mutants among the survivors of extended wet heat treatment of the spores with high Nfo levels (Table 2). In contrast, AZD8055 in vivo wet heat treatment of nfo exoAα−β− spores generated a high level of mutants in survivors (Table

2). Nfo overexpression also increased the dry heat resistance of exoA nfoα−β− spores (Fig. 2d). While ∼95% dry spores were killed in 7 min at 90 °C, there was essentially no killing of the exoA nfoα−β− spores with overexpressed Nfo under these conditions. In addition, ∼99% of dry wild-type spores were killed after 120 min at 120 °C, while <10% of dry nfo exoAα−β− spores with overexpressed Nfo were killed under these same conditions (Fig. 2e). Moreover, as shown in Fig. 2f, Nfo overexpression also caused a slight, but significant,

increase in the dry heat resistance of wild-type spores. The increased dry heat resistance of exoA nfoα−β− and wild-type spores with elevated Nfo levels is consistent with dry heat killing of both α−β− and wild-type spores by DNA damage, but more importantly, is consistent with much of this damage being AP lesions. However, the much higher dry heat resistance of exoA nfo PsspB-nfoα−β− spores than wild-type spores with high Nfo levels suggests that dry heat generates DNA damage in addition to AP sites selleck inhibitor in wild-type spores (see Discussion). To investigate whether overexpression of nfo would increase the resistance of nfo exoAα−β− spores to other DNA-damaging treatments, we determined the resistance of spores of various strains to UV-C radiation, a treatment that kills spores almost exclusively by generating photoproducts in DNA (Setlow, 1987, 2006). As expected (Salas-Pacheco et al., 2005), the nfo exoAα−β− spores (and also α−β− spores; Mason & Setlow, 1987) were much more sensitive to UV-C radiation (LD90=30±5 J m−2) than wild-type spores (LD90=274±8 J m−2) (Fig. 3). However, Nfo overexpression did not increase the UV-C resistance of the nfo exoAα−β− spores because they showed an LD90 value of 28±6 J m−2 (Fig. 3).

The Km for the substrate 1-H2NA remained unaltered

in the presence of NADPH or NADH (Table 5). The enzyme showed similar Km for NADPH and NADH (Table 5). The saturation plot for FAD was hyperbolic and Km was determined to be 4.7 μM (Table 5). Alcaligenes sp. strain PPH degrades phenanthrene, hydroxybenzoates (o-, m- and p-) and o-phthalate (Deveryshetty et al., 2007). Based on metabolic analysis, the proposed pathway for phenanthrene degradation is: phenanthrene 1-H2NA 1,2-DHN salicylaldehyde salicylic acid catechol. The steps involved in the metabolism of 1-H2NA to salicylic acid are similar to that involved in naphthalene degradation and hence referred to as the ‘naphthalene Natural Product Library clinical trial route’. The generated catechol enters the central carbon cycle via the meta ring-cleavage pathway. Organisms capable of degrading phenanthrene via the ‘naphthalene route’ have the ability to degrade naphthalene (Davies & Evans, 1964; Evans et al., 1965; Menn et al., 1993; Sanseverino et al., 1993; Kiyohara et al., 1994; Takizawa et al., 1994; Yang et al., 1994). Interestingly, strain PPH failed to metabolize naphthalene as the carbon source; this could be due to lack of naphthalene dioxygenase or the presence of highly specific phenanthrene dioxygenase in this strain. Compared to salicylate,

phenanthrene-grown cells showed higher specific activity of 1-hydroxy-2-naphthoic acid hydroxylase (Table 2). As observed for several aromatic degradative pathways (Grund et al., 1990; Gescher et al., 2002; Phale et al., 2007; Swetha et al., Forskolin datasheet 2007; Deveryshetty & Phale, 2009), enzymes of phenanthrene

degradation in strain PPH were also found to be inducible in nature. The upper-pathway enzymes of naphthalene degradation (naphthalene to salicylic acid) have been proposed to be involved in the conversion of phenanthrene to 1-H2NA and anthracene to 2-hydroxy-1-naphthoic acid (Menn et al., 1993). Further, 1-H2NA was metabolized to 1,2-DHN by salicylate-1-hydroxylase and reported to have broad substrate specificity (Balashova et al., 2001). In Alcaligenes sp. strain PPH, enzyme induction pattern and heat stability studies suggested the existence of two different enzymes, 1-hydroxy-2-naphthoic acid hydroxylase Rebamipide and salicylate-1-hydroxylase, responsible for the conversion of 1-H2NA to 1,2-DHN and salicylic acid to catechol, respectively. The enzyme responsible for the hydroxylation of 1-H2NA has not been reported so far. This is the first study reporting the existence of 1-hydroxy-2-naphthoic acid hydroxylase. The property of heat stability helped to resolve 1-hydroxy-2-naphthoic acid hydroxylase from salicylate hydroxylase and was exploited to partially purify the protein (Table 3). The enzyme was yellow in color and showed characteristic flavoprotein absorption spectrum (Fig. 2), as observed for several other hydroxylases (Yamamoto et al., 1965; Hesp & Calvin, 1969; White-Stevens & Kamin, 1972).

(2010) on cell growth and metabolite concentration profiles. Izumi et al. (1994) reported that R. erythopolis D-1 desulfurized DBT to 2-hydroxybiphenyl (HBP) successfully. They used 500 mL of Selleckchem PARP inhibitor a glucose-based biosynthetic medium with 0.125 mM DBT as the sole sulfur source at 30 °C to examine the desulfurization activity of growing cells.

They measured pH, cell growth, DBT concentration, and HBP concentration at various times during their experiment. In another study, Davoodi-Dehaghani et al. (2010) isolated R. erythropolis SHT87. They used growing cells at 30 °C in a 50 mL solution of glycerol containing a synthetic medium with 0.25 mM of DBT as the sole sulfur source. They also measured cell growth, DBT concentration, and HBP concentration at different times over 120 h. The experimental data from the above two independent studies provided a sound basis for validating our proposed model. We used their cell growth data and DBT/HBP concentration profiles from the exponential GSK126 purchase phase to compute specific cell growth rates (1 h−1) and DBT (HBP) uptake (secretion) rates (mmol g−1 dcw h−1). Our reconstructed model consists of 87 intracellular metabolic reactions, 66 transport reactions, and 196 metabolites related to either sulfur or

central metabolism. The sulfur metabolism includes the 4S pathway; the CoA biosynthetic pathway; metabolism of inorganic sulfur, cysteine, and methionine; and biosynthesis of cysteine, methionine, mycothiol, biotin, and thiamine. The central metabolism includes gluconeogenesis, citric acid cycle, pentose phosphate pathway, and Embden Meyerhoff Glycogen branching enzyme Paranas pathway for glycolysis. Figure 1 shows a complete picture of the pathways and reactions in our model, with full details in the Supporting information. We simulated the experiments

of Izumi et al. (1994) and Davoodi-Dehaghani et al. (2010) and compared our predicted cell growth rates with their measured data. As the 4S pathway is aerobic, we assumed unlimited oxygen flux in all of our validation studies and analyses. Sulfur was a limiting substrate in the experiments of Izumi et al. (1994) and Davoodi-Dehaghani et al. (2010). We inferred this from the fact that the stationary phase in their experiments was triggered, when DBT concentration went to zero and HBP concentration reached its maximum. Therefore, we allowed unlimited glucose flux for simulating the experiment of Izumi et al. (1994) and unlimited glycerol flux for Davoodi-Dehaghani et al. (2010). Then, we fixed the DBT uptake and HBP production rates (mmol g−1 dcw h−1) to be at some values computed from their data, and predicted specific cell growth rates at those values. Figure 2 shows that our growth predictions are in close agreement with the two experimental data. The accuracy of our predictions is confirmed by the argument that the limiting sulfur solely determines the growth.