Furthermore, histological examination of both the skin and the small bowel specimens using special histochemical stains (PAS, Gomori Silvermethenamine) showed severe inflammation and massive areas of necrosis containing AS1842856 fungal spores and numerous budding hyphae (Figure 2). Figure 2 Histological section. A) Necrotic tissue from the cutaneous specimen, with fungal

hyphae. B-C) Hyphae in the small bowel specimen. In C some of them appear to cross Foretinib price the vessel wall. PAS stain (A) ×200; GMS stain (B) ×400, PAS stain (C) ×200. Some yeasts were present across vessel walls of the small bowel, suggesting systemic blood dissemination (Figure 2C). These findings were in keeping with culture results of intraoperative specimens and serial drainage fluids, showing fluconazole-resistant Candida albicans, susceptible to echinocandin according to CLSI cut off values [8]. Echinocandin (70 mg on the first day, i.e., day 103, followed by 50 mg/day) was administered parenterally for a total of 21 days. The patient’s clinical conditions improved, fever disappeared and she was subsequently discharged in a good clinical state. Discussion We have reported two cases of

abdominal surgery patients who developed Selumetinib manufacturer systemic candidiasis, and whose clinical symptoms improved following the initiation of therapy with 70/50 mg/day echinocandin. Oral thrush and esophageal candidiasis are the most common manifestations of Candida infection in the GI tract, with only occasional involvement of the colon and rectum. Despite the high concentration of Candida spp. in the lower GI tract, infection does not occur under normal circumstances, owing to innate defense mechanisms. In this manuscript, we have described abdominal lesions due to Candida albicans infection. In a previous case report, we described a vegetating gastric Candida albicans lesion in an immunocompetent

patient, endoscopically simulating a neoplasia [11]. This study reports two new cases of abdominal fungal infection in patients who had undergone abdominal surgery. Gastrointestinal candida lesions remain difficult to diagnose because of the prevalence of colonization without accompanying infection, non-specific symptoms, and variable presentation. In our two cases, despite blood cultures being negative for yeast, the histological analysis, performed with special histochemical stains, and culture Metformin manufacturer of specimens or drainage fluid allowed us to identify it. Although new, rapid and sensitive methods for diagnosing invasive fungal disease are available [12], histopathologic examination remains one of the major diagnostic tools in mycology because it permits rapid, presumptive identification of fungal infections [13, 14]. Newer fungal, invasive visceral candidiasis and multidrug-resistant bacteria involving hollow gastrointestinal viscera are emerging pathologies for abdominal surgery [11, 14, 15]. Minali et al. reported that stomach candidiasis was seen in 0.

The distributions of forming voltages and set and reset voltages are demonstrated in Figure  4a and b, respectively. A severe increase to over +10 V of forming voltage is selleck screening library observed for the samples with γ ray radiation, whereas a slight change of set and reset voltages can be observed. For the forming process, the scattering of Ag ions is reinforced by the γ ray radiation and more Ag ions have migrated into SU5402 in vivo the film bulk [11]. Simultaneously, radiation arouses defects

and trapped charges inside the film which needs a stronger electrical field to fulfill or recombine. Therefore, a higher forming voltage is needed to realize the first filament gathering and penetration. It is noticeable that the first operation to set the device Quisinostat cost to LRS is defined as forming process, also for the devices with a low initial resistance and recovered by a reset operation. As for the set process, the radiation-induced holes assist the formation of the Ag filament and result in a slight decrease of set voltage. While for the reset process, the filament rupture is related to the drift of Ag ions under the reset voltage-induced electrical field, therefore the role of the radiation-induced holes can be ignored [11]. Although the radiation leads to a scattering of

Ag ions into the film bulk, this scattering influence on the set and reset procedures is almost negligible. After forming operations, several filaments have been built inside the film bulk, and during the following set and reset operations, the rupture and the reconnection of the filaments only occurs within a relatively local region, near the electrode interface. Figure 4 Operation voltage distributions of the Ag/AlO x /Pt RRAM devices. Distribution of (a) the forming voltage and (b) the set and reset voltages with different doses of radiation. An obvious increase in forming voltage and a slight decrease in set voltage are observed. As the discussion described above, the effects of holes generated by the γ ray radiation

are important for the resistive switching of Ag/AlO x /Pt RRAM devices. In order to clarify the role of the radiation-induced holes, an elevated temperature measurement was carried out. The temperature dependence of resistance in LRS of the samples is studied, and the thermal coefficients of resistivity (α) are calculated and Farnesyltransferase shown in Figure  5. The α value of the devices without radiation is extracted to be 0.0041 K-1, which is quite close to the proposed value of 0.0038 K-1 for the high-purity silver at 293 K [23], meaning that the major constituent of conducting filaments in LRS is silver. Interestingly, the α values become smaller as the radiations dose increases, which are 0.0020 and 0.0017 K-1 for the device of 500 krad(Si) and 1 Mrad(Si) dose, respectively. The increase implies that the metal-like characteristic of the filaments changes as the radiation dose increases.

Moreover, patients with CNS TB and meningitis have extensive blood vessel involvement and significant endovasculitis with the intima (comprising brain endothelia) most severely affected [21]. Goldzieher et al. have further shown that M. tuberculosis can be found inside brain endothelia of patients with TB meningitis [22]. Seminal work by

Rich et al, later confirmed by MacGregor and colleagues, demonstrated that free M. tuberculosis can invade the CNS [7, 23]. More modern data utilizing CD18-/- leukocyte adhesion deficient mice suggest that free mycobacteria can traverse the BBB independent of leukocytes or macrophages [24]. These data emphasize the central role of brain endothelia in the pathogenesis of CNS TB and underscore GS-9973 clinical trial the importance of our observation that the pknD mutant displayed defective invasion and reduced survival in brain endothelia. While AZD6738 supplier endothelial cells are not professionally phagocytic, they are capable of mounting an antiSelleck Berzosertib bacterial response through the release of antimicrobial peptides. Activation of endothelial barriers can also trigger bacterial killing via

NO- or H2O2-dependent pathways [25, 26]. It is possible that disruption of pknD disables a bacterial response pathway necessary for survival in these unique conditions, resulting in the reduced intracellular growth we observed during infection of brain endothelial cells. Reduced invasion was not observed in other cells previously utilized to evaluate invasion and dissemination defects of M. tuberculosis mutants and clinical strains [19, 27]. However, one of the limitations of the current study is that other CNS cell types such as microglia and astrocytes, which could play Elongation factor 2 kinase a role in mycobacterial infection and killing in vivo, were not evaluated. M. tuberculosis pknD encodes a “”eukaryotic-like”" STPK, a family of bacterial signaling proteins. STPKs occur in numerous pathogenic bacteria, and M. tuberculosis encodes 11 putative STPKs (pknA-L). Good

et al have demonstrated that the M. tuberculosis PknD sensor is composed of a highly symmetric six-bladed β-propeller forming a cup with a functional binding surface [28]. The β-propeller is a widespread motif found mostly in eukaryotes, although it was first described in influenza virus neuraminidase [29]. Takagi et al have shown that nidogen, a β-propeller-containing protein in humans which is homologous to the sensor domain of M. tuberculosis PknD, is required for binding to laminin [30]. Similarly, Trypanosoma cruzi, a protozoan pathogen that causes meningoencephalitis in humans, has a PknD homolog (Tc85-11), also possessing a β-propeller, that selectively binds to laminin [31]. In accordance with bioinformatics predictions, M. tuberculosis PknD has been identified as an integral membrane protein in several proteomics studies [32, 33].

CT angiography can thereby pinpoint the location of the bleeding source, and direct further management [19, 20]. Figure 3 Diagnostic approach to gastrointestinal bleeding. Haemodynamically unstable check details patients with massive rectal haemorrhage should undergo emergency laparotomy [1]. Although the colon is the most likely source of extensive rectal bleeding in patients above 50 years of age, a high index of suspicion of a small intestinal site of bleeding should be maintained. It is mandatory to systematically inspect the small intestine, and owing to the mesenteric location of the diverticula, the intraoperative recognition can be facilitated by jejunal insufflations using

manual compression [1]. If no small intestine diverticula are found, a subtotal colectomy is recommended [1]. When jejunal diverticula are identified as the bleeding source, either preoperatively or intraoperatively, partial resection of the involved segment of jejunum with primary anastomosis is the procedure of choice. A special challenge

is in patients with multiple diverticula along the small intestine, where it is not possible to remove all of them. In such cases it is easy and safe to perform an intraoperative endoscopy through an enterotomy, which effectively can localize the bleeding source [21]. selleck inhibitor Another dilemma is that approximately 50% of patients with jejunal diverticula also have coexisting colonic diverticula. In such patients a preoperatively CT angiography can be helpful to pinpoint the bleeding source and thus avoid unnecessary colectomy. However, even when the preoperative studies implicate bleeding from colon, the finding of jejunal click here diverticula MS-275 chemical structure at laparotomy is justification for resection of the involved small intestine [22]. Failure to identify and remove jejunal diverticula may lead to continued bleeding after blind colectomy. In our case, as in many others with bleeding from jejunal diverticulosis, pathologic examination of the resected bowel segment did not localize the bleeding site. We consider the immediate and long-term cassation of bleeding achieved by resection of the diverticula as a satisfactory confirmation of diagnosis

of jejunal diverticular haemorrhage [23]. Conclusion Jejunoileal diverticulosis is an uncommon entity and a rare source of gastrointestinal haemorrhage. However, it should be considered in all patients with acute bleeding in the lower part of the gastrointestinal tract, especially in the elderly, because it may lead to life threatening complications and death. In case of massive ongoing rectal bleeding, CT angiography is an accurate, rapid, and non-invasive modality that may detect the bleeding site. If unstable or multiple jejunal diverticula, an intraoperative endoscopy can be performed safely via an enterotomy to localize the bleeding site. Surgical resection of the involved intestine and primary anastomosis is the treatment of choice.

g., production of selleck nitric oxide and reactive oxygen species), and immunological disease were most severely affected by dexamethasone (Fig. 3).

Dexamethasone and Pneumocystis infection were found to have opposite effects on certain genes. Of the 32 genes that were up-regulated by dexamethasone but down-regulated by Pneumocystis infection (Table 3), cadherin 17 (Cdh17) and glutathione-S-transferase alpha type2 (Gsta2) genes were most profoundly affected. Dexamethasone treatment increased Cdh17 expression by 7.15 fold, but Pneumocystis infection not only reversed this effect but also decreased its expression by 1.61 fold. Similarly, dexamethasone up-regulated Gsta2 by 4.77 fold, but Pneumocystis infection decreased it by 2.63 fold. Cadherin (calcium dependent adhesion molecule) plays a very important role in cell adhesion and assembly 4SC-202 molecular weight of the actin cytoskeleton [28]. Actin filaments are linked to α-catenin and to the cell membrane through vinculin which is linked to E-cadherin [29]. The decrease in cadherin

expression during PCP may be a reason why AMs are defective in phagocytosis, as this function requires the actin cytoskeleton. Glutathione S-transferases (GSTs) link reduced glutathione via a sulfhydryl group to electrophilic centers on a variety HM781-36B mw of substrates [30]. This activity detoxifies compounds such as peroxidized lipids [31] that are generated during oxidative stress. The reduction in GST expression during PCP may explain the reduction in AM number as a decrease in GST expression would increase the concentration of toxic molecules such as reactive oxygen species [32] which can trigger

apoptosis of AMs [33]. Equally important are genes that were down-regulated by dexamethasone but up-regulated by Pneumocystis infection. Among these genes (Spp1, Irf1, Cxcr4, Crp, Il1rn, Irf8, RT1-Aw2, Ier3, and Ccnl1) (Table 5), the secreted phosphoprotein 1 (Spp1) gene has the most dramatic reversal by Pneumocystic 4-Aminobutyrate aminotransferase infection followed by interferon regulatory factor 1 (Irf1). The SPP1 protein is also known as bone sialoprotein, early T-lymphocyte activation (ETA-1), and most commonly osteopontin (Opn). Opn is one of the most abundantly expressed proteins in various lung diseases; it mediates diverse cellular functions such as adhesion, migration, and survival of several cell types including macrophages, T cells and dentritic cells [34, 35]. OPN also functions as a Th1 cytokine, promotes cell-mediated immune responses, and plays a role in chronic inflammatory and autoimmune diseases and activation of immune cells [34]. Opn can be cleaved by thrombin to expose the sequence SVVYGLR which is a ligand of integrin receptors α4β1, α9β1, and α9β4 that are present on monocytes, macrophages, neutrophils, T cells, and mast cells [36, 37].

Photosynth Res 33:63–71PubMed Oguchi R, Hikosaka K, Hirose T (2003) Does the photosynthetic light-acclimation need change in leaf anatomy? Plant Cell Environ 26:505–512 Oja V, Laisk A (2012) Photosystem II antennae are not energetically connected: evidence based on flash-induced O2 evolution and chlorophyll fluorescence

in sunflower leaves. Photosynth this website Res 114:15–28PubMed Osmond CB (1994) What is photoinhibition? Some insights from the comparison of sun and shade plants. In: Baker NR, Bowyer JR (eds) Photoinhibition: molecular mechanisms to the field. Bios Scientific, Oxford, pp 189–258 Oukarroum A, El Madidi S, Schansker G, Strasser RJ (2007) Probing the responses of barley cultivars (Hordeum vulgare L.) by chlorophyll a fluorescence OLKJIP under drought stress and re-watering. Environ Exp Bot 60:438–446 Oxborough K, Baker NR (1997) Resolving chlorophyll a fluorescence images of photosynthetic efficiency into photochemical and non-photochemical components—calculation of qP and Fv′/Fm′ without measuring Fo. Photosynth Res 54:135–142 Paillotin G (1976) Movement of excitations in the photosynthesis domain of photosystem II. J Theor Biol 58:237–252 Papageorgiou G, Govindjee (eds) (2004) Chlorophyll a fluorescence: a signature of photosynthesis. Kluwer (now Springer), Dordrecht Powles SB (1984) Photoinhibition of photosynthesis induced by visible light. Annu Rev Plant Physiol 35:15–44

Quick W, Horton P (1984) Studies check details on the induction of chlorophyll fluorescence in barley protoplasts. II Resolution of fluorescence quenching by redox state and the transthylakoid pH gradient. Proc R Soc Lond B 220:371–382 Quick WP, Stitt M (1989) An CYT387 cell line explanation of factors contributing to non-photochemical quenching of fluorescence in barley leaves. Biochim Biophys Acta 977:287–296 Redillas MC, Kim YS, Jeong JS, Strasser RJ, Kim JK (2011) The use of JIP test to evaluate drought-tolerance of transgenic rice overexpressing OsNAC10. Plant Biotechnol Rep 5:169–176 Repkova

J, Brestic M, Zivcak M (2008) Bioindication of barley leaves vulnerability in conditions of water deficit. Cereal Res Commun 36:1747–1750 Rosenqvist E (2001) Light acclimation maintains the redox state of the PSII electron acceptor QA within a narrow range over a broad range of light intensities. Photosynth Res 70:299–310PubMed Thiamet G Schansker G, Srivastava A, Govindjee, Strasser RJ (2003) Characterization of the 820-nm transmission signal paralleling the chlorophyll a fluorescence rise (OJIP) in pea leaves. Funct Plant Biol 30:785–796 Schansker G, Tóth SZ, Strasser RJ (2005) Methylviologen and dibromothymoquinone treat-ments of pea leaves reveal the role of photosystem I in the chlorophyll a fluorescence rise OJIP. Biochim Biophys Acta 1706:250–261PubMed Schansker G, Toth S, Kovacs L, Holzwarth AR, Garab G (2011) Evidence for a fluorescence yield change driven by a lightinduced conformational change within photosystem II during the fast chlorophyll a fluorescence rise.

Looking forward While we have discussed the successes for algae in the U.S. agricultural framework and the pitfalls that still exist, we can also identify areas of progress. Individual states have taken initiative to pave the way in recognizing algae cultivation as agriculture. In 2012 two states, Arizona and Ohio, specifically amended their laws to define algaculture as part of agriculture. While these changes had different specific effects in each state, they were both carried out with the purpose of increasing investment in algaculture and attracting the industry to those states. In Ohio, the recognition of algae farming as agriculture allows land used for algae cultivation to BAY 11-7082 cell line be eligible for the same land use valuation

as agriculture, thus allowing lower property taxes for algae farms. It also limits the authority of zoning laws to restrict algaculture on lands. The Ohio legislation was proposed with widespread click here support from many factions including the Farm Bureau, the Poultry Association and the Soybean Association (OH-H.R. 2012). In

Arizona, state trust lands can now be leased for algaculture, and algae farmland is eligible for lower property taxes afforded to traditional farmland (AZ-HR 2012a, selleck chemicals b). In 2013, Iowa also passed a similar bill defining land used for algal cultivation as agricultural (IA-H.R. 2013). Arizona’s bills have allowed for the development of a national test bed for algal biomass production, led by Arizona State University. This multi-regional private and public partnership, funded by the DOE, focuses on developing algae cultivation on large, economically relevant scales and involves coordination between facilities in Arizona, Ohio, California, Hawaii, and Georgia. see more Other public–private partnerships include the California Center for Algal Biotechnology, which coordinates and promotes research, commercialization and public education projects. Conclusions Large-scale cultivation of algae, or algaculture, has existed for over half a century. More recently, algaculture for food and

fuel purposes has begun the transition from R&D and pilot-scale operations to commercial-scale systems. It is crucial during this period that institutional frameworks (i.e., policies) support and promote development, and commercialization. While the U.S. government has supported the R&D stage of algaculture for biofuels over the last few decades, it is imperative that policies anticipate and stimulate the evolution of the industry to the next level. Large-scale cultivation of algae merges the fundamental aspects of traditional agriculture and aquaculture. Despite this overlap, algaculture has not yet been afforded an official position within agriculture or the benefits associated with it. Recognition of algaculture as part of agriculture under the USDA at national, regional, and local levels will expand agricultural support and assistance programs to algae cultivation, thus encouraging progression of the industry. The U.S.

Vascular Cx43 may therefore represent a novel target for anti-angiogenic or vascular normalization strategies. Supported in part by NIH CA138727. Poster No. 159 Investigating

a Role for CCN3 in the Promotion of selleck kinase inhibitor Breast Cancer Metastasis to Bone Veronique Ouellet 1,2 , Jenna Fong3, Svetlana Komorova2,3,4, Bernard Perbal5, Danh Tran-Tanh6, Eitan Amir7, Mark Clemons7, Peter Siegel1,2,8 1 Goodman Cancer Centre, McGill University, Montreal, Quebec, Canada, 2 Department of Medecine, McGill University, Montreal, Quebec, Canada, 3 Department of Dentistry, McGill University, Montreal, Quebec, Canada, 4 Department of Anatomy and Cell Biology, McGill University, Montreal, Quebec, Canada, 5 Research and Development, L’Oreal, Clark, New Jersey, USA, 6 Department of Pathology, The Princess Margaret Hospital, Toronto, Ontario, Canada, 7 Department of Orthopaedic Surgery, The Princess Margaret Hospital, Toronto, Ontario, Canada, 8 Department of Biochemistry, McGill University, Montreal, Quebec, Canada Breast cancer is the most frequent and the second most lethal cancer affecting women in Canada. The skeleton is a common site for breast 3-deazaneplanocin A mw cancer metastasis; however, the reasons for this

are not fully understood. We have used mouse models to isolate 4 T1 breast cancer cell populations that aggressively metastasize to bone and have compared them to cells that are weakly bone metastatic. Through gene expression profiling, we have identified ccn3 (nov), which is expressed at higher levels in the aggressively bone metastatic cells versus those that weakly metastasize to bone. We have verified that our bone metastatic breast cancer cells overexpress ccn3 mRNA and

that elevated levels of CCN3 protein are detected in the conditioned media of the bone metastatic 4 T1 sub-populations. To determine the relevance of CCN3 expression in human breast cancer, we have interrogated ccn3 expression in publically available gene expression datasets and have observed a correlation between ccn3 expression and the luminal BYL719 in vitro sub-type. These results are interesting in light Glutathione peroxidase of the fact that breast cancers that metastasize to the bone are most likely to be of the luminal subtype. Finally, we have performed immunohistochemical staining of CCN3 in bone metastases derived from patients with breast cancer and have found that CCN3 is expressed in every lesion (20/20). Together, these data implicate CCN3 as an interesting target associated with breast cancer bone metastasis. Given the osteolytic nature of the bone metastases that develop in our 4 T1 breast cancer model, we wished to test the hypothesis that CCN3 plays a causal role in promoting the formation of osteolytic lesions through the inhibition of osteoblast differentiation. Using primary cultures of mouse bone marrow cells, we confirmed that a recombinant CCN3 protein impaired osteoblast differentiation.

Furthermore, SWNTs can act as a quantum dot between metal electrodes and hence show Coulomb blockade (CB) tunneling characteristics at sufficiently low temperatures [44–47]. Incidentally, both TLL and CB theories predict the same scaling laws: the resistance R is proportional to T -α when eV < < k B T (low-bias regime) and to V -α when eV > > k B T (high-bias regime), where V, α, and e, are the EX 527 clinical trial voltage drop across the sample, a single scaling

coefficient, and the charge of an electron, respectively [46]. In order to extract the values of buy QNZ R in the two different regimes, current–voltage (IV) curves for both samples are measured at various temperatures as shown in Figure 5a,b. At high-bias voltages and low-bias Compound C chemical structure voltage at high temperatures, the IV curves are basically linear with the current I in both samples. However, at low bias and low temperatures, the IVs are not

linear, especially in sample SWNT2. The origin of this curvature is discussed below. Figure 5 Current–voltage (IV) curves. For samples (a) SWNT1 and (b) SWNT2 measured at several temperatures from 300 to 2 K. Solid lines are guides to the eyes. First, for sample SWNT1, the low bias R is extracted from the IV curves at I = 1 nA and plotted in a log-log graph versus temperature as shown in Figure 6a. The data fits well a power law above 30 K, with α ≈ 0.1. Note that k B T = 2.59 meV > > eV = 0.29 meV at 30 K. This is in agreement with the regime of validity of the theory. Furthermore, the value of α ≈ 0.1 is in the same order as the reported values in the literature for SWNTs [41, 46, 47]. Next, R, in the high-bias regime, Selleck PR 171 is extracted from the IV curves at T = 2, 5, and 10 K and plotted in a log-log graph versus voltage as shown in Figure 6b. The low temperatures were chosen in order to be as close as possible

to the condition eV > > k B T for this regime. For voltages V higher than about 10 mV, the curve fits well a power law, with α ≈ 0.1. This is in very good agreement with the extracted value from R versus T in the other regime. Furthermore, knowing that k B T ≈ 0.9 meV at T = 10 K, the range of voltages where the power-law fit is found to hold (i.e., above 10 meV), indeed satisfies reasonably well the condition eV > > k B T. The inset of Figure 6b shows that from 20 K and above, the resistance is essentially independent of the applied voltage, i.e., the IV curves are linear, which is exactly what was observed in Figure 5a. Hence, the behavior of SWNT1 is consistent with both LLD and CB theories with a scaling exponent α ≈ 0.1. First, it is noted that the extracted contact resistance, R c  = 8 kΩ, is higher than the quantum resistance R Q , which satisfies a necessary condition for the occurrence of the CB [48]. Another theoretical condition for achieving CB is to have the charging energy E c of the SWNT higher than the thermal energy k B T, with E c   ≈ 2.

The OD600 values were determined after 12 h. Data represent the means ± standard deviations of three independent experiments. To further investigate the influence of manganese ions on the mntE – mutant, different concentrations of manganese ions were added to TGY medium, and the growth of the mntE – mutant was measured (Figure 3C). The results showed that in comparison with R1, the growth of the mntE -

mutant was clearly delayed in the presence of low concentrations of manganese ions. When the manganese concentration increased, the growth defect phenotype became more pronounced. This phenotype is similar to that observed in Rosch’s study in which the growth of S. pneumoniae having a disrupted selleck chemicals llc calcium efflux system was more severely inhibited at higher calcium concentrations [18]. The mntE- mutant shows high intracellular IWR-1 molecular weight manganese concentrations To confirm that

the mntE – mutant had lost its ability to export manganese ions, the intracellular manganese ion levels of wild-type R1 and the mntE – mutant were measured by inductively coupled plasma-mass spectrometry (ICP-MS). As expected, when grown on TGY medium supplemented with manganese ions, the manganese ion level in the mntE – mutant was almost four-fold higher than that in wild-type R1. However, there was no significant difference in the intracellular Fe ion learn more concentrations of R1 and the mutant (Figure 4A). Similar results were obtained when the mntE – mutant and wild-type R1 were grown on TGY medium (Figure 4B). This result indicates that Dr1236 is a manganese ion exporter. Figure 4 Analysis of the intracellular ion content of wild-type R1 and mntE – cultured in medium supplemented with

or without cations. (A) R1 (white bars) and mntE – (grey bars) were cultured in TGY medium supplemented with 50 μM manganese, 10 μM ferric chloride, 100 mM magnesium, or 100 mM calcium chloride to determine the effects of these specific cations. (B) R1 (white bars) and mntE – (grey bars) were cultured in TGY medium without added cations. Cells (OD600 = 0.8) were harvested, and Liothyronine Sodium the extracellular cations were removed by washing in EDTA. The cation concentration was determined by ICP-MS. The data represent the means ± standard deviations of three independent experiments. The mntE- mutant shows higher resistance to γ-radiation, UV, and oxidative Recently, there has been a debate on whether the high intracellular Mn/Fe ratio of D. radiodurans contributes to the extreme oxidative resistance of this microorganism. Daly et al proposed that the high Mn/Fe ratio can effectively suppress protein carbonylation and increase radiation resistance [7, 8]. In contrast, Sukhi et al and Shashidhar et al argued that D. radiodurans exhibits the same radiation resistance even when the intracellular Mn/Fe ratio changed substantially [19, 20].