The conversion of L-malate to L-lactate and carbon dioxide during

The conversion of L-malate to L-lactate and carbon dioxide during malolactic fermentation facilitates the maintenance of the ATP pool of the cell and supports the production of more alkaline metabolites.

Therefore MLF directly contributes to the competitive fitness of S. mutans in the complex, multispecies environment of the dental plaque. Recently, Sheng and Marquis showed that cells of S. mutans UA159 possess MLF activity but no information about its regulation was available [17]. According to the information of MLF from L. lactis it was likely that the LTTR mleR adjacent to the MLF genes might be involved in their regulation. Low pH is required for induction of MLF A knockout of mleR significantly decreased MLF activity of S. mutans cells and thus confirmed its participation in AZD6738 solubility dmso the regulation of MLF. Applying promoter luciferase reporter constructs we BIBW2992 chemical structure showed that the regulation of the mle genes is much more

complex than just being induced in the presence of MleR. The luciferase fusion data and the acid killing profiles showed that the mle genes are activated within 30 minutes by acidic pH values, independently of MleR and malate. Therefore, the transcription of the mle genes is driven from acid inducible promoters and MLF is part of the early acid tolerance response. The EMSA experiments showed a clear interaction of MleR with malate, even under alkaline conditions. However, under Selleck BMS202 neutral pH conditions no effect of malate on the transcription (using the luciferase reporters) was noticeable, suggesting that uptake of malate occurs only under low pH conditions. Indeed, Poolman et al. [12] showed that in the presence of a pH gradient, membrane vesicles of L. lactis are able to take up L-malate with one proton or the monoanionic

form of L-malate (MH-). They conclude that a pH gradient stimulates indirectly a malate/lactate antiport, by affecting the L-lactate gradient or promotes directly electrogenic malate uptake, respectively. Resminostat They showed that with decreasing pH, the pH gradient adjusted to the membrane potential or even exceeded it, which resulted in an increased uptake of added malate. Assuming a similar mechanism in S. mutans explains why malate under neutral pH conditions did not cause an induction of the mle genes. Since the uptake of malate is reduced in a neutral pH environment, the intracellular amount of malate is not sufficient to stimulate MleR and subsequent avoided a positive regulation. MleR fully induces the MLF only at low pH, with malate acting as a coinducer. A similar mechanism was recently disclosed by Liu et al. for the agmatine deiminase system [23]. They showed that its induction by AguR requires both low pH and agmatine. Using a linker scanning mutagenesis approach they were able to isolate mutant forms of AguR that lost their ability to activate transcription in response to pH, agmatine or both signals, respectively.

PSR carried out the BCVI studies, participated in the sequence al

PSR carried out the BCVI studies, participated in the sequence alignment and drafted the manuscript. FB participated in the sequence alignment, analysis and interpretation of datas. Selinexor JA participated in the design of the study and performed the statistical analysis. GG participated in the study of the imagem and award of the angiotomography.

BD participated in the coordination and study of blunt trauma. All authors read and approved the final manuscript.”
“Background Blunt abdominal trauma may cause both crush and shearing effects on healthy abdominal wall and viscera [1]. Acute onset indirect inguinal hernia with testicular dislocation after blunt trauma is rarely reported [2], but, to our knowledge, a case resulting in complete obliteration of the inguinal canal with direct herniation of the abdominal viscera has not been documented. The inguinal Dactolisib supplier canal extends from the anterior superior iliac spine to the pubic tubercle. A defect in the posterior wall results in a direct hernia. In our case, all boundaries of the inguinal canal including the floor, posterior, inferior, medial walls and deep and superficial rings were obliterated causing traumatic herniation of the terminal ileum and caecum beneath an attenuated external oblique aponeurosis. We describe the timely reconstruction of the abdominal wall in the inguinal region and the importance of the restoration of normal anatomy with definitive

repair after resolution of swelling and haematoma. Case Presentation A 24 year old man was admitted to hospital following a road traffic accident after his motorcycle collided with a lorry. The speed of collision was 35 mph and abdominal injuries were sustained as a result of impact against the motorcycle

handle bars. On arrival to the Emergency Department the patient was haemodynamically stable and fully conscious. Primary survey revealed a soft abdomen with tenderness, swelling and bruising in right groin and scrotum. There was no previous history of groin hernia. Secondary survey, plain X ray and CT scan Selleckchem Entospletinib confirmed a fracture dislocation of the right shoulder, open fracture of right radius and ulna, multiple Rho right lung contusions and a new right inguinal hernia. Internal fixation of the upper limb injuries was performed. Reconstruction of the abdominal wall was deferred, in the absence of obvious visceral damage, until resolution of groin swelling and bruising (Fig. 1). Figure 1 Acute onset right groin hernia with bruising and swelling. 12 days after admission, repair of the inguinal hernia was performed. At surgery, the external oblique aponeurosis overlying the inguinal canal was contused inferiorly, and the inguinal ligament was found to be sheared off the full length of its attachment from the anterior superior iliac spine to the pubic tubercle, with all boundaries of the canal obliterated (Fig. 2 &3).

Colony circular, dense, compact #

Colony circular, dense, compact PF-01367338 manufacturer with well-defined margin, numerous yellow crystals formed in the agar. Aerial hyphae abundant, often with subglobose thickenings to 6–11 μm terminally or along their length; forming a thick white to yellowish cottony mat, ascending to the lid of the Petri dish. Autolytic activity and coilings absent. Reverse yellow, orange, 4–5AB4–5, to orange-brown or yellow-brown, 5CD7–8. No distinct odour noted. Conidiation noted after 3 days; conidia produced in small numbers in wet to dry heads on scant solitary, cylindrical or subulate

phialides on aerial hyphae. Conidia (5–)6–15(–21) × (3.0–)4.0–6.7(–9.3) μm, l/w (1.1–)1.3–2.7(–3.9) (n = 30), variable in shape, ellipsoidal, oval, subglobose, oblong, broadly fusoid, or clavate, hyaline, smooth, eguttulate or rarely with few small guttules; scar indistinct or truncate; often adhering in small clusters. At 15°C colony coarsely zonate, with crystals and white cottony mat; no conidiation seen. On SNA after 72 h 4 mm at 15°C, 10 mm at 25°C; mycelium covering the plate after 13 days at 25°C. Colony circular, dense, with well-defined or irregular margin, becoming hairy by numerous, loosely disposed, long, dichotomously branched aerial hyphae ascending to the lid of the Petri dish along the Alvocidib colony margin, with some thickenings 6–9(–15) μm. Autolytic excretions locally frequent, coilings absent. No diffusing pigment, no distinct odour noted. No chlamydospores seen. Conidiation

noted after 10 days. Conidia (examined after 14–28 days) produced in small numbers in minute wet to dry heads on solitary phialides or simple conidiophores on long aerial hyphae in mostly marginal, whitish, arachnoid to cottony areas. Conidiophores 2–5(–6.5) μm wide, of a main axis to 150 μm long, with few unpaired, often right-angled branches or phialides, apically with one, more rarely 2–3(–4) divergent phialides. Phialides (11–)22–43(–55) × (2.3–)3.0–4.0(–5.0)

μm, l/w (2.7–)6.5–13(–17), (1.7–)2.2–3.0(–3.5) μm wide at the base (n = 40), cylindrical or subulate, sometimes lanceolate or fusoid, mostly straight, equilateral, sometimes with a clamp-like widening on their base. Conidia (5–)6–16(–29) × (3.0–)4.0–6.5(–8.0) μm, l/w (1.2–)1.3–3.0(–5.0) (n = 70), hyaline, extremely variable in shape, mostly oblong to cylindrical, also ellipsoidal, subglobose, Ibrutinib price oval, pyriform, sometimes curved, smooth, eguttulate, scar indistinct or truncate; often adhering in clusters. Habitat: on forest Baf-A1 cell line litter in mixed forests dominated by conifers such as Picea abies. Distribution: North Europe, northern areas of Finland and Sweden. Holotype: Finland, Oulun Pohjanmaa. Haukipudas, Kello, Kalimeenkylä, Kalimeenoja, 1.5 km upstream of Saarela, in a spruce forest at the Suo-oja brook, 24 Aug. 1967, T. Ulvinen (OULU F 49597, isotype OULU F 49596; not examined). Material examined: Finland, Oulun Pohjanmaa, Kiiminki. Pikkuhalmeenmaa, Jolosmäki. In calcareous spruce forest. Grid 27°E 7228:445, elev. 45 m, on soil/leaf litter, 15 Aug.

Results showed that DDIT3 was up-regulated by PTL, and DDIT3 knoc

Results showed that DDIT3 was up-regulated by PTL, and DDIT3 knockdown resulted in reduced expression of TNFRSF10B and PMAIP1 which leading to weaker apoptosis compared with control. DDIT3 is an important molecule Selleck Crenigacestat in ER stress pathway. We next analyzed whether PTL could induce ER stress. ERN1, HSPA5, p-EIF2A and ATF4, which are all key proteins involved in ER stress, were all up-regulated by PTL in both concentration- and time-manner. ATF4 Knockdown also led to DDIT3 reduction and weaker apoptosis. All these results indicated that PTL can induce apoptosis in lung cancer cells via activation of ER stress

response (Figure 8). PTL is reported to induce ROS which can trigger ER stress response [44]. It was found that the NAC could protect cell form PTL induced apoptosis, which is the scavenging agent of ROS [7]. But whether PTL triggers ER stress through ROS in our system find more requires future study. Figure 8 Summary of parthenolide-induced signaling pathway in NSCLC cell lines. Briefly, PTL induces ER stress response and eventually results in up-regulation of DDIT3 which could increase the expression of TNFRSF10B Compound Library and PMAIP1 by binding to their promoter sites as a transcription factor. As the critical members of extrinsic and intrinsic apoptotic

pathway respectively, TNFRSF10B and PMAIP1 consequently activate these two pathways

to induce apoptosis in human lung cancer cells. What interested us most is how PTL selectively kills cancer stem cell. The cells in which CDH1 expression is inhibited can present properties of cancer stem cells [32, 40]. We found that the expression of stem cell maker SOX2 and POU5F1/Oct-4 were up-regulated in A549/shCDH1 cells. So, we used A549/shCDH1 cells to explore the apoptosis induced by PTL in cancer stem cells. Major proteins related in PTL-induced signal pathway were detected. We observed that the level of TNFRSF10B was increased, and CFLAR was decreased more clearly in A549/shCDH1 cells compared with A549/Ctrl cells after PTL treatment, Quinapyramine which could explain the enhanced cleavage of CASP8. Furthermore, MCL1 level was much lower, and PMAIP1 level was much higher in A549/shCDH1 cells than that in control cells after PTL exposure. Although the basal levels of p-EIF2A in the two cell lines were almost equal, it was up-regulated more clearly in A549/shCDH1 cells than that in control cells after PTL treatment. In addition, ATF4 and DDIT3 were both up-regulated in A549/shCDH1 cells more dramatically than that in control cells after exposure with PTL. Afterwards, we knocked down DDIT3 in the two cell lines side by side and found that PMAIP1 was down-regulated, and apoptosis was receded.


Interestingly, TNF-alpha inhibitor we observed that the missense mutation in algU can

reduce, but not completely abolish, the activity of AlgU as an activator for alginate production. This data may explain why mutant algU alleles have reduced P mucE activity (Figure 2). Furthermore, since AlgU is an auto-regulated protein [25], this may explain why the P mucE activity induced by mutant AlgU is lower than that of wild type AlgU. A slightly higher activity of P mucE noted in CF149(+algU) than in PAO1VE1 (Figure 3A) could be due to a combined effect of dual mutation of algU and mucA in CF149. In strains of FRD2 and CF14, the retention of the AlgW cleavage site is not sufficient to restore mucoidy. This is because of the partial function of AlgU, which can be seen with alginate production and AlgU-dependent P algD promoter activity (Figure 6). Altogether, these MGCD0103 nmr results suggest that mucoidy in clinical isolates can be modulated by a combination of two factors, the size of the MucA protein and the genotype of the algU allele in a particular strain. MucA size determines its cellular localization and its ability to sequester AlgU, and the algU allele determines whether AlgU is fully or partially active. The

iTRAQ results showed that the expression of two proteins was significantly increased and the expression of nine proteins was decreased in the mucE over-expressed strain VE2 (Additional file 1: find more Table S3). Of these Amylase 11 proteins, nine of them are AlgU dependent, for including flagellin type B. Garrett et al. previously reported that AlgU can negatively regulate flagellin type B and repress flagella expression [33]. However, no AlgU consensus promoter sequences were found within the upstream of the 11 regulated genes through bioinformatics analysis, indicating that these may be indirect effect. In addition, two proteins (elongation

factor Tu and transcriptional regulator MvaT) were significantly decreased when compared to PAO1 proteome, but remained unchanged when comparison was made between VE2 and VE2ΔalgU, suggesting the reduction of these two proteins was independent of AlgU in the MucE over-expressed strain. MvaT is a global regulator of virulence in P. aeruginosa[34], and elongation factor Tu is important for growth and translation. Elongation factor Tu has also been shown to act as a chaperone in E. coli, consistent with induction of proteins involved in responding to heat or other protein damaging stresses [35]. Recently, elongation factor Tu has been shown to have a unique post-translational modification that has roles in colonization of the respiratory tract [36, 37]. The differential expression of Tu due to mucE overexpression suggests there may be signaling networks dependent upon mucE that we have not yet been identified.

Methods Fungal strains and culture conditions P chrysogenum NRRL

Methods Fungal strains and culture conditions P. chrysogenum NRRL 1951, the natural isolate obtained from an infected cantaloupe [43] was used as wild-type strain. P. chrysogenum Wis54-1255, which contains a single copy of the penicillin gene cluster [6], was used as parental strain. P. chrysogenum npe10-AB·C [11], a derivative of the npe10 pyrG- strain (Δpen) [9, 10] complemented with the pcbAB and pcbC genes was used in the molecular analysis of IAT. P. chrysogenum DS54465 strain, a derivative of DS17690 [28] wherein the P. chrysogenum KU70 homologue has been deleted (Marco A. van den Berg, unpublished results), were used in the ial

gene deletion experiments. Fungal spores were collected from plates in Power medium [44] grown for 5 days at 28°C. P. chrysogenum liquid cultures were initiated by inoculating fresh spores in complex medium CIM (20 g/l corn steep solids, 10 g/l yeast extract, Cilengitide 58 mM sucrose, 50 mM calcium

carbonate, pH 5.7) or defined DP medium [44] without phenylacetate. After incubation at 25°C for 20 h in an orbital shaker (250 rpm), aliquots were inoculated in complex penicillin production CP medium (4 g/l potassium phenylacetate, 20 g/l pharmamedia, 50 g/l lactose, 0.03 M ammonium sulphate, 0.05 M calcium carbonate, pH 6.6) or in defined DP medium with or without phenylacetate (4 g/l). Spores of the ial null mutant were used to inoculate shake flasks with synthetic media supporting β-lactam production [45]. To verify the validity

of the findings, two different penicillin side chain precursors were added to the media, phenyl acetic acid and adipate, at 0.3 and 0.5 g/l respectively. Cultivation was for 168 hours at 25°C and 280 rpm. As controls both parent strains, DS17690 and DS54465, were used. Plasmid constructs To completely block the Vactosertib research buy transcription of the ial gene, 1500 base pairs of the promoter and the ORF were PCR amplified (for oligonucleotides see the Appendix) and fused to the amdS selection marker, obtained from pHELY-A1 [46] by of PCR amplification (Fig. 2). To block eventual read trough from any unconventional transcription start sites in the amdS gene, the trp terminator was PCR amplified from plasmid pAMPF21 [47] and inserted between the amdS gene and the ial ORF (Fig. 2). Plasmid p43gdh-ial was constructed to overexpress the ial gene in P. chrysogenum starting from plasmid pIBRC43BglII, a derivative of pIBRC43 [48] that contains the NcoI restriction site mutated to BglII. The ial gene was amplified from genomic P. chrysogenum Wis54-1255 DNA using the primers DElikeF and DElikeR (see the Appendix) and was cloned in the BglII-StuI sites of plasmid pIBRC43BglII, between the A. awamori gdh gene promoter (a very efficient promoter in ascomycetes) and the Saccharomyces cerevisiae cyc1 transcriptional terminator.



Baf-A1 ic50 maximum misorientation angle ψ of the crystal lattice, which characterizes the degree of structure fragmentation, was found from azimuthal tailing of diffraction reflections compared to single-crystalline samples. The sizes of fragments were measured by electron microscopy (microscope PREM-200, Moscow, USSR). Results and discussion γ-α-γ transformations X-ray studies of alloy 1 have shown that all the austenitic reflections present in the single-crystalline samples are washed out in the azimuthal direction after reverse α-γ transformation. On the pole figure (homostereographic projection), the centers of all initial and reversed austenitic reflections coincided at the region of measurement accuracy (1° to 2°). Azimuthal tailing of reflections monotonously increased with the increase of the quantity of transformation cycles (Figure  1A,B,C,D). At the same time, the angle ψ of martensite was always less than that of austenite (Figure  2A,B). Debye lines on the Selleckchem VX-680 X-ray pattern filled up in the azimuthal direction. Hence, the rotational X-ray pattern of single-crystalline samples after 35 to 50 γ-α-γ transformations was the same as that of a textured selleck screening library polycrystalline sample. After 80 to 120 γ-α-γ cycles, the diffraction pattern displays practically continuous lines of austenite. It indicates

a practically full recrystallization of austenite and a transformation of the initial single crystalline into a polycrystalline sample. Different azimuthal tailing of the γ and α phase reflections qualify the different degrees of crystal lattice fragmentation of the austenite and the martensite phase, respectively. Figure 1 X-ray patterns of alloy 1 single crystal in the austenitic

state (f.c.c.), FeK α radiation. Initial state (A) and after 1 (B), 10 (C), and 80 (D) γ-α-γ transformations. Figure 2 Misorientation angle ψ of austenite (1) and martensite (2) in alloys 1 (A) and 2 (B). N, number of thermocycles. Electron microscopic investigation has shown that in the process of thermocycling, subgrain boundaries were created in reversed austenite. These boundaries were formed by dislocations generated by repeated γ-α and α-γ transformations. medroxyprogesterone At a certain stage, subgrain boundaries form the observed fragments in the initial austenite grains. After 10 to 20 cycles, the decomposition of the reflections into three to five components was observed (Figure  1B) parallel with the progress of azimuthal tailing of reflections on the electron diffraction pattern that provide evidence for the formation of additional subgrain boundaries at this stage. In reversed austenite, the fragment size decreased with increasing number of transformation cycles. After 30 cycles, the major fraction of fragments was in the range 0.2 to 0.8 μm. After 80 to 100 cycles, the size of fragments reached the nanoscale level (about 100 nm).

For Ecol Manage 257:2217–2225 Konrad P (1936) Notes critiques sur

For Ecol Manage 257:2217–2225 Konrad P (1936) Notes critiques sur quelques champignons du Jura. Quat série Bill Trimestr Soc Mycol Fr 52:35–53

Konrad P, Maublanc A (1937) Icones selectae fungorum, vol 6. Paul Lechevalier, Paris Konrad P, Maublanc A (1953) Les Agaricales 2: Russulacées, Hygrophoracées, Gompkidiacées, Paxillacées, Boletacées. Encyclopédie Mycologique, XX. P. Lechevalier, Paris, pp 202 Kost G (1986) Morphologie, anatomie und systematic carotinoidhaltiger blätterpilze. Ber Deutsch Bot Ges 99:43–58 Kotlaba F, Pouzar Z (1966) Haasiella, a new agaric PARP inhibitor genus and H. splendidissima sp. nov. Ceská Mykol 20:135–140 Kovalenko A (1988) New combinations within the Hygrophoraceae Lotsy. Mikol Fitopatol 22:207–209 Kovalenko A (1989) Definitorium fungorum URSS. Ordo Hygrophorales. Nauka 37, Leningrad Kovalenko A (1999) The STI571 arctic-subarctic and alpine-subalpine component of the Hygrophoraceae in Russia. Kew Bull 54:695–704 Kovalenko A (2012) In: Knudsen H, Vesterholt J (eds) Funga Nordica. Agaricoid, boletoid cyphelloid and gasteroid genera. Nordsvamp, Copenhagen, pp 282–293 Krieglsteiner GJ, Enderle M (1987) Über neue, seltene, kritische makromyzeten in der Bundesrepulik Deutschland (Mitteleuropa) IX. Z Mykol 53:3–38 Kranner I, Lutzoni F (1999) Evolutionary consequences of transition to a lichen GSI-IX ic50 symbiotic state and physiological adaptation to oxidative

damage associated with poikilohydry. In: Lerner HR (ed) Plant response to environmental stresses: from phytohormones to genome reorganization. Urease Marcel Dekker, New York, pp 591–628 Kropp BR, Trappe JM (1982) Ectomycorrhizal fungi of Tsuga heterophylla. Mycologia

74:479–488 Kühner R (1926) Contribution à l’Étude des Hyménomycètes et spécialement des agaricacées. Botaniste 17:53 Kühner R (1947) Quelques agarics rares, critiques, ou noveaux de la région de Besancon. Ann Scient Franche-Comté 2:26–42 Kühner R (1949) Hygrophorus picea sp. nov. Champignon meconnu des sapinieres de Montagne. Voisin de eburneus. Bull Mens Soc Linn de Lyon 18:179–182 Kühner R (1976) Agaricales de la zone alpine. Genre Hygrocybe (Fries) Kummer. Bull Soc Myc Fr 92:455–515 Kühner R (1977a) Agaricales de la zone alpine. Hygrophoracées. Genre Camarophyllus (Fries) Kummer. Bull Soc Myc Fr 93:121–144 Kühner R (1977b) Vers un system phylogénetique des Camarophyllus (Fr.) et Hygrocybe (Fr.) (Agaricales–Hygrophoraceae). Rev Mycol 41:73–90 Kühner R (1980) Les Hymenomycetes agaricoides. Bull mens Soc Linn Lyon 49:1–1027 Kühner R, Romagnesi H (1953) Flore Analytique de Champignons Supérieurs. Masson et cie, Paris Kummer P (1871) Der Führer in die Pilzkunde. C. Luppe, Zerbst Kunth CS (1822) Synop Plant 1:1–491 Lamarche J, Hamelin R (2007) No evidence of an impact on the rhizosphere diazotroph community by the expression of Bacillus thuringiensis Cry1Ab toxin by Bt white spruce. Appl Env Microbiol 73:6577. doi:10.​1128/​AEM.

Similarly, restriction digest analysis using Sfi1 showed that all

Similarly, restriction digest analysis using Sfi1 showed that all strains were clonal (data INK1197 manufacturer not shown). The fact that all our strains showed identical pattern in antibiotic susceptibility patterns, pathogeniCity genes, and the diversity of mobile genetic elements strongly suggest that this population of O1 strains that have

caused outbreaks since 1994 to as recent as 2007 are clonally related. The absence of the st gene (which is common among non-01 and non-0139 strains) [19] and the absence of the classical biotype-specific tcpA and hylA genes in these strains further indicates that genetic exchanges between this population and other V. cholerae serotypes that might be in circulation

in Kenya have been highly restricted. In a previous study by Jiang et al. [54] it was noted that a number of O1 strains from Kenya failed to cluster with those isolated from other parts of the world when using Amplified Fragment Length Polymorphism (AFLP) genotyping technique. Similarly, the study by Pugliese et al. [7] showed that strains that carried the SXT-element alone or in combination with an incC plasmid belonged to a unique RAPD cluster IV. In the same study [7], strains without this ICE were shown to belong to other cluster types shared A-1155463 manufacturer by isolates from Ethiopia and Somali. It is also interesting to note that none of the isolates from 1998-1999 study shared a RAPD cluster with strains isolated in India and Bahrain isolated in 1948 and 1978. Such observations have led to a theory that some toxigenic V. cholerae strains circulating in different countries may not have originated from a single clone in Asia as is popularly believed, Glutathione peroxidase but

may have been derived locally from genetic exchange between the Asian O1 strains and the O1 or non-O1 strains from local environments [54]. Figure 2 PFGE of Not1 digested genomic DNA of V . Inaba strains isolated from various regions of Kenya between 1994 and 2007. Genomic DNA from representative strains was digested with Not1 restriction enzyme and loaded as follows; M: molecular weight see more marker (S. Braenderup), Kw: Kwale, Sy: Siaya, Mn: Malindi, Mk: Makindu, Nr: Nairobi, Kb: Kibwezi, Mo: Mombasa, Bu: Busia, Kf: Kilifi, Ka: Kakuma, Da: Daadab, Ma; Mandera. The year when each of the isolate included in this experiment are also indicated. Conclusions We observed that antibiotic susceptibility and genomic content of the strains bearing the SXT/R391-like ICE that have been in circulation in Kenya between 1994 and 2007 has not changed significantly and there are indications that these strains have undergone minimum genotypic changes during this entire period. In the absence of older isolates for molecular characterization, it is not possible to determine whether other clones of V.

BMC Fam Pract 7:7PubMedCrossRef 72 Sale JE, Beaton D, Posen J, E

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