A high index of suspicion, meticulous physical examination and close observation of the patient may assist in the early detection of such situations and facilitate proper and timely management in order to avoid future complications. Once airway management has been completed and all hemorrhage sites controlled, definitive management of bone and soft tissue injuries resulting from maxillofacial

trauma may be deferred until life- and/or organ-threatening injuries have been properly find more managed. The Complexity of the situation The maxillofacial trauma patient often presents a problem of difficult mask ventilation and difficult intubation. The trauma SHP099 usually disrupts the normal anatomy and causes oedema and bleeding in the oral cavity. The mask cannot be properly Momelotinib cost close-fitted to the face, to enable effective mask ventilation.

Furthermore, an injured airway may prevent efficient air transferring from the musk to the lungs. The challenge in performing the intubation arises mainly from a difficulty in visualizing the vocal cords with conventional direct laryngoscopy. The oral cavity, pharynx and larynx may be filled with blood, secretions, debris, soft tissue and bone fractures, all of which preclude good visualization of the vocal cords. Apart from the problem of anticipated difficult airway, several other factors may worsen the scenario: C-spine Injury A patient who sustained supra-clavicular trauma is considered to have a C-spine injury until proven otherwise. Complete C-spine clearance may take hours and sometimes days, and until then the patient’s neck must be supported by a collar and all neck movements should Phospholipase D1 be avoided. At the time of intubation the assistant performs “”in-line stabilization”", in order to support the head and neck

in place and prevent neck flexion throughout the procedure [8]. Recent data indicate, on one hand, that direct laryngoscopy and intubation are unlikely to cause clinically significant neck movements and, on the other hand, “”in-line stabilization”" may not always immobilize injured segments effectively. In addition, manual “”in-line stabilization”" degrades the laryngoscopic view which may, in turn, cause hypoxia and worsen the outcome in traumatic brain injury [9, 10]. Another approach suggested by Robitaille et al. is to use the GlideScope videolaryngoscopy for intubation rather than the commonly used Macintosh blade, thus minimizing neck movements [11]. Full stomach The maxillofacial trauma patient, as every trauma patient, is considered to have a “”full stomach”", since there was no time for stomach emptying prior to intubation. In addition, this patient often bleeds from the upper aerodigestive tract: blood is swallowed and accumulates in the stomach, and the risk of regurgitation and aspiration is high.

Poster No. 39 FGF-Mediated Suppression of RIG-I Contributes to the Low Responsiveness of Human Hepatocellular Carcinoma to IFN Treatment Yuanyuan Zheng 1 , Qiuyan Liu1, Ying Chen1, Yi Zhao1, Zhenzhen Zhan1, Xuetao Cao1 1 National Key Laboratory of Medical Immunology and Institute of Immunology, Second Military Medical University, Shanghai, China Retinoic acid-inducible gene I (RIG-I), as a sensor of viral RNA, plays important roles

in the induction of virus-mediated eFT-508 type I IFN production and antiviral responses. Recently, identification of negative regulator of RIG-I in the regulation of antiviral innate immune response has attracted much attention and many negative regulators of RIG-I have been discovered. However, the role of RIG-I in tumor development or treatment remain unclear. With tissue array, we find that the expression of RIG-I is reduced significantly in hepatocellular carcinoma (HCC) and some other tumors, such as bladder cancer, renal clear cell carcinoma, endometrial carcinoma and esophagus

cancer. Basis FGF, a member of the FGF family, is expressed in many kinds of cancer cells and can stimulate the proliferation of cancer cells of mesodermal, neuroectodermal, ectodermal and endodermal BI 10773 clinical trial origin. As a mitogenic factor, basic FGF has a close relation with cancer development. Interestingly, we demonstrate that basic FGF can inhibit the mRNA expression of RIG-I in a time-dependent manner in SMMC-7721 HCC cells which highly express FGFR1 and FGFR3. PD173034, the specific inhibitor of basic FGF, can reverse the inhibition of RIG-I expression by basic FGF. Furthermore, inhibitors of PI3K/Akt and ERK pathways (LY294002 or U0126) can also reverse the inhibition of RIG-I expression by basic FGF. Importantly, overexpression of RIG-I enhances the suppression of SMMC-7721 cell growth by interferon a (IFNa), which is attributed to more cell Buspirone HCl arrest at G2/M phase and the promotion of apoptosis of SMMC-7721 cells. These results demonstrate that FGF-mediated suppression

of RIG-I in HCC cells contributes to the low responsiveness of HCC to IFNa treatment. Poster No. 40 Emerging Role of the RAB25 GTPase in Head and Neck Cancer Metastasis Panomwat Amornphimoltham 1 , Kantima Leelahavanishkul1, J. selleck products Silvio Gutkind1, Roberto Weigert1 1 Oral and Phryngeal Cancer Branch, National Institutues of Dental and Craniofacial Research/ National Institutes of Health, Bethesda, MD, USA Invasion and metastasis of tumor cells from primary site into stroma and the metastatic organ is a key step in cancer progression with poor prognosis. The 5-year survival rate of head and neck cancer patients, the sixth most common cancer in the developed world, is approximately 50%, despite the recent advances in treatment modalities.

There is significant induction of euo mRNA at 20 μM mevastatin concentration. Figure 1 Immunofluorescent images of HepG2 cells infected with C. trachomatis in presence of mevastatin. HepG2 cells were set up, grown and infected with C. trachomatis in presence or absence of mevastatin as described in AZD5582 cost Methods. Immunofluorescence analysis was performed 48 hours after inoculation of the pathogen. A – non-infected cells; B — infected cells with no mevastatin; C — infected cells in presence of 1 μM mevastatin: D — infected cells in presence of 20 μM mevastatin; E — infected

cells in presence of 40 μM mevastatin. Scale bar = 10 μm. Figure 2 Expression of chlamydial 16S RNA and euo in infected hepatocytes grown at different concentration of mevastatin. HepG2 cells were set up, grown and infected with C. trachomatis in presence or absence of mevastatin as described in Methods. RNA was extracted

in 24 hours after inoculation ON-01910 purchase of the bacteria. Expression of chlamydial genes was normalized to copy number Mocetinostat purchase of eukaryotic β-actin. Inhibition of chlamydial growth in cultured cells in presence of mevastatin may take place due to abnormal internalization of chlamydial particles, since the entry of chlamydial particles into mammalian cells requires interaction of pathogens with lipid rafts of plasma membrane [24]. Therefore, we next investigated the internalization rate of chlamydial particles into HepG2 cells in presence of 40 μM mevastatin. As can be seen from Figure 3, HepG2 cells treated with 40 μM mevastatin have similar number of chlamydial particles attached to the plasma membrane when compared to untreated control cells. Mevastatin treatment did not

affect the number of internalized particles as well (results not shown). Figure 3 Attachment of chlamydial Anacetrapib particles to plasma membrane of hepatocytes in presence or absence of mevastatin. HepG2 cells were set up, grown and incubated with chlamydial particles (EB) in presence or absence of mevastatin as described in Methods. Attached particles were visualized with FITC-labeled antibody against chlamydial LPS. A — attachment of chlamydial particles in absence of 40 μM mevastatin: B — attachment of chlamydial particles in presence of 40 μM mevastatin. Scale bar = 10 μm. Discussion Although there is a small but growing body of evidence that C. trachomatis can be disseminated widely throughout the human body, the physiological consequences and overall medical relevance of extragenital propagation of C. trachomatis remains poorly understood. First of all, our results confirm initial observations [25] showing the ability of C. trachomatis to propagate in HepG2 hepatoma cell line. More importantly, we have demonstrated that propagation of C. trachomatis in hepatocytes follows full infectious cycle leading to the formation of infectious progeny in 48 and 72 hours of post-infection period. Propagation of the pathogen distinctively affects some specific functions of the liver cells. In particular, C.

Authors’ contributions XZ and JM participated in the study design, constructed lentiviral plasmid vector

,conducted the real-time PCR assays and drafted the manuscript; YJW and YL statisticsed the patient information and conducted immunohistochemical staining; HZL carried out the western bolt assay; QL and XJL carried out the proliferation and cell migration assay; PM conduced the trials in vivo. ; HYL conceived of the study, and participated in its design and coordination, and reviewed the manuscript. All authors read and approved the final manuscript.”
“Introduction Hepatocellular carcinoma (HCC) is the fifth most common cancer worldwide and the third leading cause of cancer-related death [1]. Although significant advances in surgical techniques and perioperative care over the last two decades, the long-term prognosis of HCC remains dismal largely due to the high frequency of metastasis or recurrence. Recently, more evidences suggest that LEE011 purchase HCC metastasis involves a complex cascade of signal events between tumor cells and host stroma microenvironment. selleck chemical These crosstalking might modulate or determine

the process of HCC invasion and metastasis. Thus, exclusive reliance on tumor cell itself for research cannot enable insight into the diverse pathological changes occurring in HCC metastasis. Generally, the microenvironment of HCC is composed of stromal cells (e.g., hepatic stellate cells, fibroblasts, invading inflammatory/immune cells, and endothelial cells) and non-cellular components (e.g., growth factors, proteolytic enzymes, Akt inhibitor ic50 inflammatory cytokines, and extensive extracellular matrix proteins). A lot of studies on HCC have validated the important roles of stromal cells in HCC progression [2]. Hepatic stellate

cells (HSCs) increase HCC growth and invasion both in vitro and in vivo. Conditioned media derived from HSCs induce HCC cell proliferation and migration. Moreover, on a three-dimensional spheroid co-culture system as well as an in vivo implantation of a mixture of HSCs and HCC cells, HSCs obviously accelerate HCC growth and diminish the extent of central necrosis [3, 4]. Activated HSCs also enhance HCC progression by other means such as regulating T cells that create Etomidate an immunosuppressive microenvironment and stimulating angiogenesis [5]. Through the release of different factors like cytokines, chemokines, or enzymes, tumor-associated macrophages (TAMs) can regulate tumor growth, angiogenesis, invasion, and metastasis [6]. Particularly, some secreted factors from TAMs also induce cancer cell motility, thereby enhancing tumor cell invasion capacity [7]. These data demonstrate that stromal cells can actively modulate the malignant characteristics of HCC cells and further determine the outcome of HCC. Given that tumors have abundant blood vessels for supplying oxygen and nutrition, endothelial cells (ECs) are ubiquitous within solid tumors.

For AvrPtoB, IpaH9.8, and SspH1, interference with signaling pathways is mediated by ubiquitination of host kinases, activities captured with the molecular function terms “”GO:0019901 protein kinase binding”" and “”GO:0004842

ubiquitin-protein ligase activity”" [22–24]. AvrPtoB Selleck Seliciclib ubiquitinates host kinases involved in resistance-gene mediated host immunity [24], while SspH1 ubiquitinates PKN1 [22, 25], a host kinase integral to innate immune response signaling pathways. The ability of IpaH9.8 to buy RG-7388 suppress innate immunity also appears linked to ubiquitination – in this case of MAP kinases [22]. Other effectors alter immune signaling pathways using alternative enzymatic activities. These include inactivation of MAP kinase signaling by “”GO:0034598 phosphothreonine lyase activity”", documented for both OspF [26] and HopAI1 [27], and targeting of MAP kinases by acetyltransferase-activity (GO:0016407) observed for YopP/J [28]. AvrPtoB, in addition to its ubiquitination-dependent suppression of resistance gene-mediated

host immunity, suppresses innate immunity through E3-ligase independent targeting of kinase signaling [29]. The specific molecular functions by which this suppression is accomplished have yet to be characterized. Putting Gene Ontology to work for you The Pto DC3000 and E. coli annotations have been see more deposited in the GO database where searches can be conducted for GO terms or particular gene products. At that site and through linked resources, users can search for gene products annotated to multiple, user-selected GO terms of interest or analyze microarray data for enrichment of genes annotated to particular terms. The value of the Gene Ontology project is directly proportional to the number and quality of the annotations being contributed, and though intensive efforts have been directed

toward annotation of virulence-related gene products in Pto DC3000 and E. coli, ongoing annotation Endonuclease of these and effectors deployed by a wider range of plant and animal pathogens would greatly enhance the insights that could be gained. Among the steps being taken to facilitate ongoing annotation are proposals that journals request suggested GO terms from manuscript authors akin to requests for keywords. Guidelines are also being developed to aid researchers in identification of appropriate terms for specific protein families. For example, a tutorial on GO term assignment for plant pathogenic effectors is presently available through the Pseudomonas-Plant Interaction website http://​www.​pseudomonas-syringae.​org.

The patients in the on-demand relaparotomy group did not have a significantly lower rate of death or major peritonitis-related

morbidity compared with the planned relaparotomy group but did have a substantial reduction in relaparotomies, health care P5091 ic50 utilization, and medical costs. In 2007 a randomised study by Robledo et al. [99] compared open with closed “”on demand”" management of severe peritonitis. The study however was interrupted after the inclusion of 40 patients because of a high rate of mortality for the open abdomen group (55 vs 30%). The “”open abdomen”" was managed with only a non-absorbable polypropylene mesh. Antimicrobial therapy in Intra-abdominal Infections Antimicrobial therapy plays an integral role in the management of intra-abdominal infections. The choice of an inadequate antimicrobial agent is a cause of therapeutic failure. Complicated intra-abdominal infections are predominantly related

to bowel perforation and contamination with its flora. The microbial etiology depends on the level of disruption of the gastrointestinal tract. Microbiology The upper gastrointestinal tract (stomach, duodenum, jejunum, and upper ileum) contains relatively few microorganisms, less than 103 to 105 bacteria/mL. Infections derived from the stomach, duodenum, and proximal small bowel can be caused by gram-positive and gram-negative aerobic and facultative organisms. The lower SCH727965 mouse gastrointestinal tract contains hundreds of bacterial species, and concentrations of 1011-13 bacteria/mL. Infections derived from distal ileum perforations can be caused by gram-negative facultative and aerobic organisms with variable density. Colon-derived intra-abdominal infections can be caused by facultative and obligate anaerobic organisms, gram-negative these facultative organism

(Enterobacteriaceae with E. coli at the first place), other gram-negative bacilli and Enterococci. Anaerobic bacteria are 1000 times more common than aerobes. With the exception of Bacteroides spp., most other anaerobes are the main barrier against colonization and infection by other pathogens. The medical antecedents of the patient can affect the normal flora. In particular, patients hospitalised may be colonized by altered flora including multidrug-resistant nosocomial pathogens or Candida spp. Microbiological specimens Once the diagnosis of complicated intra-abdominal infection is suspected, it is appropriate to begin empiric antimicrobial therapy before an exact diagnosis is established and before results of appropriate cultures are selleck chemicals available. The role of microbiologic workup of infected fluid has been debated in the last years. Since the causative pathogens can easily be predicted in community acquired infections, bacteriological diagnosis is not necessary.

In this way, the strain becomes compressive rather than tensile. A further investigation will study the point of strain conversion and the H-termination during cooling down with Fourier-transform infrared spectroscopy in a future work. To understand the strain reduction upon annealing, one should recall that pore size, pore distribution,

and porosity change upon annealing, as illustrated in the SEM insets learn more of Figure 3. Upon annealing, the total PSi internal surface area reduces [9], which leads to a reduction in the areal density of Si-H bonds on the pore walls. This produces a lower in-plane compressive stress on the side walls and, in turn, a lower out-of-plane expansion strain is present in the smaller pore area annealed porous layer than in the larger pore area as-etched porous layer. After the out-of-plane strain, the surface roughness of the annealed PSi monothis website layers was measured and analyzed using HRP. Figure 5 shows that the surface roughness of the seed layer increases with its thickness, as also observed in [3] and [6]. This result may be explained in light of previous observations that thick PSi layers tend to have less aligned and LY2874455 larger pores at the top which, in turn, results in a rougher seed surface. An epitaxial growth template with a rough surface is likely to generate crystal defects in the epitaxial

layer. Figure 5 RMS oxyclozanide values for surface roughness of annealed monolayers of PSi samples with different thicknesses 350, 750, 1,300 and 1,700 nm. The roughness increases as the thickness of the LPL increases. From the evolution of strain and roughness with layer thickness as observed with these low-porosity monolayers, a direct guideline would be to grow layers that are as thin as possible, in order to minimize both parameters. However, detachable epitaxial foils require formation of

porous stacks with a double layer, with a LPL on top of a HPL. The evolution of strain in the double-porosity layers is investigated in the next section. The case of PSi double layers The evolution of out-plane strain in double layers was investigated by adding a high-porosity layer under the low-porosity layers. In particular, the thickness of the LPL was varied as in the previous section, while the HPL, with a porosity of 55% ± 5%, was kept constant, as detailed in Table 1 (column “Impact of thickness”). Similarly to the as-etched PSi monolayers, the strains in as-etched double layers were tensile, as illustrated in Figure 6. However, contrarily to the monolayers, we can observe that, unexpectedly, the total out-of-plane strain decreases with the thickness of the LPL and saturates. Figure 6 Out-of-plane tensile strain values of the as-etched double layer of PSi. Strain decreases and saturates as the LPL thickness increases, the dashed line is a trend for the eye.

jejuni during slaughter can contaminate cooling water, knives and poultry meat in the processing plant [4]. During transmission of C. jejuni from animals, primarily poultry, to humans, this important zoonotic foodborne pathogen encounters various stresses, such as non-growth temperatures, starvation, hypo- and hyper-osmotic stress, and desiccation [5, 6].

Despite the well-known fact that Campylobacter is a fastidious bacterium, human campylobacteriosis cases have significantly increased presumably due to the ability of this pathogen to survive under harsh environmental conditions [7–10] in addition to its low infectious dose (400~800 bacteria) [11]. For example, high genetic diversity of Campylobacter spp. and the ability to transform into a viable-but-non-culturable BIBF 1120 chemical structure state may enhance its adaptability to unfavorable growth conditions [7, 8]. Additionally, biofilm formation and stringent response also contribute to the survival of Campylobacter under Selleck VX-680 stress conditions [9, 10]. However, the molecular mechanisms for stress resistance are still largely unknown in Campylobacter. In many bacterial species, alternative sigma factors play an important role in regulation of stress-defense genes

under hostile environmental conditions [12]. Because a sigma factor can TGF beta inhibitor coordinate gene transcription in response to environmental stimuli, many bacteria possess multiple alternative sigma factors, some of which are often dedicated to stress responses. For example, RpoS is a sigma factor important for adaptive responses in many Gram-negative pathogens, and RpoS mutations in Escherichia coli, Salmonella, Pseudomonas and Vibrio significantly impair bacterial ability to resist various stresses, such as starvation,

low pH, oxidative stress, hyperosmolarity, heat and cold [13–17]. In E. coli, RpoS is involved in resistance to high osmolarity in stationary-phase cells and survival in cold-shock by Aldehyde dehydrogenase regulating one set of RpoS-dependent genes, including otsA and otsB, which are necessary for synthesis of internal trehalose as an osmoprotectant and important for survival at low temperature [18, 19]. In addition, RpoS controls the acid resistance in E. coli by modulating gadC, a gene involved in the glutamate-dependent low pH-resistance, hdeAB, encoding pH-regulated periplasmic chaperons, and cfa, a gene for cycloporpane fatty acid synthesis [20]. As another stress-response sigma factor, RpoE regulates extracytoplasmic functions related to sensing and responding to bacterial periplasmic and extracellular environmental changes, which contributes to heat- and oxidative stress resistance in many Gram-negative bacteria, including E. coli, Pseudomonas and Salmonella [21, 22]. The RpoE mutation in Salmonella reduces bacterial survival and growth in macrophages by the loss of RpoE-dependent gene expression such as htrA, a gene required for oxidative stress resistance [23, 24].

The E. coli and H. influenzae YbaB proteins both exhibited preferences for certain tested DNA sequences, but neither showed the same high affinity for GTnAC as did the spirochetal ortholog. Both YbaB proteins also showed a marked preference for DNA derived from the B. burgdorferi erpAB promoter BAY 11-7082 research buy over poly(dI-dC). Such large differences in affinities for target and non-target sequences may account for the previous failure to detect DNA-binding by YbaBHi [3]. These results suggest that YbaBEc and YbaBHi have higher affinities for some DNA sequences than for others, but whether those preferences depend upon a specific nucleotide sequence(s), A+T content, and/or DNA topology remain to be determined. The three-dimensional

structure of dimeric YbaB resembles “”tweezers”", with α-helices 1 and 3 of each monomeric subunit protruding from the dimerization domains [3]. The spacing between the α-helical protrusions is approximately 15 Å at the base of the dimerization domain and approximately 22 Å at the distal ends of the α-helices [3], similar to the diameter of B-form duplex DNA (~20Å [3]). Site-directed mutagenesis Epigenetics inhibitor studies of the orthologous B. burgdorferi EbfC demonstrated that certain amino acid substitutions in either α-helix 1 or 3 of EbfC eliminate DNA-binding, without affecting dimerization [10]. It is noteworthy that many of the α-helix 1 and 3 residues of EbfC are

distinct from residues in both YbaBEc and YbaBHi (Fig. 1), consistent with the differences in DNA preferences between the E. coli and H. influenzae YbaB proteins and their spirochetal ortholog. YbaB/EbfC orthologs of other bacterial species likewise exhibit sequence variations in their α-helices 1 and 3, suggesting that they www.selleck.co.jp/products/cobimetinib-gdc-0973-rg7420.html may also possess unique DNA-binding properties. The function(s) of YbaB/EbfC proteins remains to be determined. Many bacterial ybaB/ebfC orthologs are located between dnaX and recR, a learn more synteny that has led to suggestions of roles in DNA replication or recombination [3, 5, 6, 15–18]. While the abilities of the examined orthologs to bind DNA may support those hypotheses, several lines

of evidence suggest that YbaB/EbfC proteins perform functions that are independent of DNA recombination or replication. Proteomic analyses of cultured H. influenzae detected production of YbaB without accompanying production of DNA repair proteins [19]. A ybaB recR double mutant of Streptomyces coelicolor exhibited recombination defects that could be complemented with recR alone [18]. The ybaB/ebfC orthologs of some bacterial species are not linked to recR or any other recombination-related gene and some, such as the B. burgdorferi, do not even encode RecR [8, 20]. Several bacteria, such as H. influenzae, have ybaB genes located distantly from their dnaX [2]. Moreover, some ybaB family genes can be transcribed independently of their upstream genes, using promoter elements within the 5′ gene [4, 6, 21–23].

NR = no expression ratio. ArcA as an activator Several of the genes involved in regulating EPZ015666 flagellar biosynthesis, motility, chemotaxis, learn more sugar transport, metabolism, and glycogen biosynthesis were found to be anaerobically activated by ArcA (Figure 3D-F and Additional file 1: Table S1). In particular, several of the middle (class 2) flagellar genes and late flagellar (class 3) genes had lower transcript levels in the arcA mutant than in the WT strain (Figure 3D-F). There was no significant difference in the transcript levels of the early flagellar genes (class 1) flhD and

flhC, whose gene products FlhD/FlhC are the master regulators of flagellar biosynthesis (Figure 3E). Additionally, several newly identified flagellar genes [43]

(i. e., mcpA, mcpC, and cheV) had lower expression levels in the arcA mutant than in the WT (Additional file 1: Table S1), while the expression of mcpB was not selleck screening library affected. Furthermore, genes coding for transcriptional repressor CytR, nitrite reductase, 2-dexoyribose-5-phosphate aldolase, thymidine phosphorylase, lysine/cadaverine transport protein, putrescine/ornithine antiporter, ornithine decarboxylase, ethanolamine operon, and propanediol operon as well as its transcriptional regulator PocR were activated by ArcA (Figure 3B and 3C, and Additional file 1: Table S1). The expression of SPI-1 associated genes was not affected by a mutation in arcA. However, two SPI-3 genes, slsA, encoding a putative inner membrane protein required for colonization of chickens and calves [1, 44], and STM3784, a putative sugar phosphotransferase, were activated by ArcA as their expression levels were significantly lower

in the mutant than in the WT (Figure 3A and Additional Rucaparib research buy file 1: Table S1). Phenotype of the arcA mutant Next, we correlated some of the microarray findings with the corresponding phenotypes of the WT and the arcA mutant strains. a. Flagellar biosynthesis and swarming motility The microarray data showed that, in anaerobiosis, the expression of the flagellar biosynthesis, motility, and chemotaxis genes was lower in the arcA mutant than in the WT. Therefore, we compared the swarming motility of the WT and the arcA mutant in soft agar under anaerobic conditions (Table 4). The data indicated that the arcA mutant was ~100% non-motile compared to the WT and that the inclusion of parcA complemented (~57%) this phenotype. We also compared the WT and the arcA mutant under anaerobic conditions for the presence of flagella by using SEM (Figure 4A and 4C, left panel) and TEM (Figure 4B and 4D, right panel). The data (Table 4 and Figure 4) clearly showed that the arcA mutant Lacked flagella and was non-motile. Table 4 Effect of the arcA mutation on swarming motility under anaerobic conditions   Diameter (cm) Genotype Anaerobic a % b WT 8.0 ± 0.1 100 arcA mutant 0.0 ± 0.0 0 Mutant/parcA 4.6 ± 0.