Currently only two studies have reported HMB’s acute effects on skeletal muscle damage and recovery. Wilson et al. [17] examined the acute and timing effects of an oral 3 g bolus of HMB-Ca supplement on 16 untrained males using a unilateral, isokinetic leg extension based training protocol. These researchers found that HMB-Ca consumed 60 minutes prior to exercise prevented a significant rise in LDH, and tended to decrease soreness of the quadriceps relative

to either the HMB-Ca supplement consumed following exercise, or a placebo supplement given prior to exercise. Collectively these findings lead us to suggest the following: HMB supplementation appears to speed recovery in untrained buy Tubastatin A and trained individuals if the exercise stimulus is high intensity, and/or high volume in H 89 ic50 nature. For untrained individuals this would Selleckchem PLX4032 likely occur with the introduction of most exercise regimens; however, in a trained population the exercise stimulus will likely need to center on free weights and compound movements. In regards to optimizing HMB supplementation, it appears that HMB has both acute and chronic effects. HMB’s acute effects likely depend upon supplementation pre-exercise. If taking HMB-Ca, the recommendation would be to consume 3 g, at least 60 minutes prior to

intense exercise. If consumed with glucose it may need to be taken as long as two hours prior to training. HMB in the HMB-FA form may have an overall faster and greater effect based upon the rise in plasma levels. Thus, athletes could consume the supplement in HMB-FA form 30–60 minutes prior to exercise.

Finally, in order to optimize HMB’s chronic effects, the recommendation would be to consume 3 g daily, divided into three equal servings for a minimum of two weeks prior to a potentially damaging skeletal muscle event. The effects of HMB supplementation on skeletal muscle hypertrophy in healthy untrained and trained adults HMB’s effects on skeletal muscle mass, strength, and hypertrophy have been studied in exercising humans for nearly two decades [7, 9]. Similar to its reported effects on skeletal muscle damage, a wide range of subject populations (untrained vs. resistance trained; male vs. female) and training protocols (Table 2) have been examined. Training protocols triclocarban have varied in duration (10 days to 12 weeks) [13, 19], periodization scheme [13, 42]), and training modalities (machines and free weights [22] vs. free weights only [42]) (Table 2). To confound the situation further, some researchers have designed and monitored the resistance-training protocol [7, 13, 20], while others have left it up to subjects to train on their own [15, 22]. In other cases, subjects have participated in unspecified training protocols reportedly provided by various team coaches or training camps [19, 26]. In addition, studies have provided a variety HMB doses ranging from 1.

CrossRefPubMed 47. Taylor J, Wilkins MP, Payne JM: Relation of rabbit gut reactions to enteropathogenic Escherichia coli. Br J Exp Pathol 1961, 42:43–52.PubMed 48. Taylor J, Bettelheim Sapitinib KA: The action of chloroform-killed suspensions of enteropathogenic Escherichia

coli on ligated rabbit-gut segments. J Gen Microbiol 1966, 42:309–313.PubMed 49. Robins-Browne RM, Yam WC, O’Gorman LE, Bettelheim KA: Examination of archetypal strains of enteropathogenic Escherichia coli for properties associated with bacterial virulence. J Med Microbiol 1993, 38:222–226.CrossRefPubMed 50. Camguilhem R, Milon A: Biotypes and O serogroups of Escherichia coli involved in intestinal infection of weaned rabbits: clues to diagnosis of pathogenic strains. J Clin Microbiol 1989, 27:743–747.PubMed 51. Peeters

JE, Geeroms R, Orskov F: Biotype, serotype, and pathogeniCity of attaching and effacing enteropathogenic Escherichia coli strains isolated from diarrheic commercial rabbits. Infect Immun 1988, 56:1442–1448.PubMed 52. Perna NT, Plunkett G, Burland V, Mau B, Glasner JD, Rose DJ, Mayhew GF, Evans PS, Gregor J, Kirkpatrick HA, et al.: Genome sequence of enterohaemorrhagic Escherichia coli O157:H7. Nature 2001, 409:529–533.CrossRefPubMed 53. Vial P, Robins-Browne R, Lior H, Selleckchem FHPI Prado V, Kaper JB, Nataro JP, Maneval D, Elsayed A, Levine MM: Characterization of enteroadherent-aggregative Escherichia coli , a putative agent of diarrheal disease. J Infect Dis 1988, 158:70–79.PubMed 54. Doughty S, Sloan J, Bennett-Wood V, click here Robertson M, Robins-Browne

RM, Hartland EL: Identification of a novel fimbrial gene cluster related to long polar fimbriae in locus of enterocyte effacement-negative strains of enterohemorrhagic Escherichia coli. Infect Immun 2002, 70:6761–6769.CrossRefPubMed 55. Pillien F, Chalareng C, Boury M, Tasca C, De Rycke J, Milon A: Role of adhesive factor/rabbit 2 in experimental enteropathogenic Escherichia coli O103 diarrhea of weaned rabbit. Vet Microbiol 1996, 50:105–115.CrossRefPubMed 56. Cantey JR, Blake RK: Diarrhea due to Escherichia coli in the rabbit: a novel mechanism. J Infect Dis 1977, 135:454–462.PubMed 57. Hull SI, Hull RA, Minshew BH, Falkow S: Genetics of hemolysin of Escherichia coli. J Bacteriol 1982, 151:1006–1012.PubMed 58. Ausubel FM, Brent Adenosine R, Kingston RE, Moore DD, Seidman JG, Smith JA, Struhl K: Current protocols in molecular biology New York, NY: John Wiley & Sons, Inc 2003. 59. Kumar S, Tamura K, Jakobsen IB, Nei M: MEGA2: Molecular Evolutionary Genetics Analysis Software. Tempe, Arizona, USA, Arizona State University 2001. 60. Ramachandran V, Brett K, Hornitzky MA, Dowton M, Bettelheim KA, Walker MJ, Djordjevic SP: Distribution of intimin subtypes among Escherichia coli isolates from ruminant and human sources. J Clin Microbiol 2003, 41:5022–5032.CrossRefPubMed 61.

Bacterial invasion and intracellular viability Analysis of the capability of mutants to enter avian macrophages was carried out using an invasion assay in the avian macrophage HD-11 cell line. Results showed no significant differences between mutant strains and the parent strains E058 and U17, with the invasion ratios varying from 0.24–0.26 (P>0.05). To determine whether the iron uptake systems are required for intracellular survival, we compared the CFU of the wild-types and isogenic mutants recovered at 2, 4, 6, 12, and 24 hours post infection (h.p.i.). We observed similar intracellular bacterial

proliferation rates, with rates of 62–65% at 2 h.p.i., which then decreased to a rate of approximately 50% at 4 h.p.i.. Rates fell sharply to approximately 10% at 6 h.p.i.. The numbers of recovered CFU at 12 and 24 h.p.i. were below detectable levels. Volasertib mouse Since

iron acquisition systems are assumed to be functionally redundant, this may permit intracellular survival in the absence of one or several systems. Further, there may be TonB-independent transport systems that could compensate for the mutations in the intracellular environment. Histopathological lesions caused by iron acquisition Selumetinib chemical structure defective mutants in chickens Histopathological lesions in chickens challenged see more with virulent wild-type strains or iron acquisition defective mutants were compared. The lesions in the tested organs were graded according to the lesion severity and check details character (Table  1). The pathological characteristics of the tested visceral organs from chickens challenged with wild-type strains were as follows. In the heart sections, unequal-sized focal necrotic lesions were present in the disintegrated muscle fibers, and fibrous exudates appeared in the epicardium (Figure 3A and Figure 3F). The

liver sections showed that inflammatory cell infiltrations were present in the hepatic lobule, and numerous small fat granule vacuoles were observed in the cytoplasm (Figure 4A and Figure 4F). The lung sections revealed numerous inflammatory exudates in the bronchial cavity (data not show). However, no obvious pathological lesions were observed in the heart or liver sections of birds challenged with any of the mutant strains, except for the Δ chuT mutants (Figure 3 and Figure 4). The ΔchuT mutants caused lesions in both the heart and liver of the challenged birds that were equivalent to the wild-type strains. This was in accordance with the results obtained in chicken colonization and persistence assays, from which the chuT mutation did not affect the virulence of the wild-type strains (Figure 1).

For colony formation assay, the 2′-O-Methyl

modified duplexes of both miR-320c and NC were used. 2′-O-Methyl modified miR-320c inhibitor (named as miR-320c-Inh) and NC inhibitor (named as Inh-NC) were used for observing the reversed effect of over-expression of miR-320c. The small interference RNA targeting human CDK6 mRNA (named as siCDK6) was synthesized as described previously [22], which targeted nucleotides 1424–1442 according to Genbank accession NM_001145306.1. All RNA duplexes were chemically synthesized by GenePharma Corporation (Shanghai, China). All the applied sequences Selleck LY2835219 were listed in Table 1. Table 1 The oligonucleotides used in this study Name a Sequence (5′- > 3′) miR-320c

mimics (sense) AAAAGCUGGGUUGAGAGGGU NC (sense) ACUACUGAGUGACAGUAGA miR-320c inhibitor ACCCUCUCAACCCAGCUUUU microRNA inhibitor NC CAGUACUUUUGUGUAGUACAA siCDK6 (sense) GDC0449 CUGGAAAGGUGCAAAGAAAdTdT miR-320c F AAAAGCTGGGTTGAGAGGGT U6 F TGCGGGTGCTCGCTTCGGCAGC CDK6 F GGATAAAGTTCCAGAGCCTGGAG CDK6 R GCGATGCACTACTCGGTGTGAA GAPDH F AAGGTGAAGGTCGGAGTCA GAPDH R GGAAGATGGTGATGGGATTT CDK6-Wt F cAATCAATGCAAGAGTGATTGCAGCTTTATGTTCATTTGTTTGTTTGTTg CDK6-Wt R tcgacAACAAACAAACAAATGAACATAAAGCTGCAATCACTCTTGCATTGATTgagct CDK6-Mut F cAATCAATGCAAGAGTGATTGgtcgaaatTGTTCATTTGTTTGTTTGTTg CDK6-Mut R tcgacAACAAACAAACAAATGAACAatttcgacCAATCACTCTTGCATTGATTgagct aF, forward primer; R, reverse primer. Tissue samples Paired bladder cancer tissues and para-carcinoma bladder mucosal tissues were acquired from patients receiving radical cystectomy. The samples were gained between Jan 2011 and June 2011 from the First Affiliated Hospital, School of Medicine, Zhejiang University (Hangzhou, P.R. China) learn more with informed consent and Ethics Committee’s approval. The clinical data of the patients were listed in Table 2. All tissue samples were stored in liquid nitrogen before use. Table 2 Clinical data of the patients Patient no. Sex Age TNM stage Histological grade 1 M 62 T2N0M0 III 2 M 60 T1N0M0 I 3 M 53 T1N0M0 III 4 M 86 T1N0M0

III 5 M 55 T1N0M0 II 6 F 74 T2N0M0 III 7 M 56 T2N0M0 III 8 F 76 T3N0M0 III 9 M 65 T2N0M0 II 10 F 69 T2N0M0 II 11 M 72 T3N0M0 III 12 M 78 T1N0M0 II 13 M 76 T3N0M0 III Cell culture and transfection The human bladder cancer cell lines UM-UC-3, T24, and Selleckchem LEE011 non-tumor urothelial cell line SV-HUC-1 (Shanghai Institute of Cell Biology, Chinese Academy of Sciences) were cultured in RPMI1640 medium (Gibco) containing 10% heat-inactivated fetal bovine serum (Gibco), 50U/ml penicillin and 50 μg/ml streptomycin under a humid atmosphere including 5% CO2 at 37°C. Cells were plated to 60–70% confluency in medium without antibiotics 1 day before transfection. Lipofectamine 2000 Reagent (Invitrogen, Carlsbad, CA, USA) was selected for transfection under the guide of the instruction.

J Clin Oncol 2009,27(9):1368–1374.PubMed 122. Sirohi B, A’Hern R, Coombes G, Bliss JM, Hickish T, Perren T, Crawford M, O’Brien M, Iveson T, Ebbs S, Skene A, Laing R, Smith IE: A randomised comparative trial of infusional ECisF versus conventional FEC as adjuvant chemotherapy in early breast cancer: the TRAFIC trial. Ann Oncol 2010,21(8):1623–1629.PubMed 123. Tada K, Yoshimoto M, Nishimura S, Takahashi this website K, Makita M, Iwase T, Takahashi S, Ito Y, Hatake K, Ueno M, JSH-23 supplier Nakagawa K, Kasumi F: Comparison of two-year

and five-year tamoxifen use in Japanese post-menopausal women. Eur J Surg Oncol 2004,30(10):1077–1083.PubMed 124. Adjuvant Breast Cancer Trials Collaborative Group: Polychemotherapy for early breast cancer: results from the international adjuvant breast cancer chemotherapy randomized trial. J Natl Cancer Inst 2007,99(7):506–515. 125. Adjuvant Breast Cancer Trials Collaborative Group: Ovarian ablation or suppression in premenopausal early breast cancer: results from the international

adjuvant breast cancer ovarian ablation or suppression randomized trial. J Natl Cancer Inst 2007,99(7):516–525. 126. Martin M, Villar A, Sole-Calvo A, Gonzalez R, Massuti B, Lizon Angiogenesis inhibitor J, Camps C, Carrato A, Casado A, Candel MT, Albanell J, Aranda J, Munarriz B, Campbell J, Diaz-Rubio E, GEICAM Group (Spanish GNA12 Breast Cancer Research Group), Spain: Doxorubicin in combination with fluorouracil and cyclophosphamide (i.v. FAC regimen, day 1, 21) versus methotrexate in combination with fluorouracil and cyclophosphamide (i.v. CMF regimen, day 1, 21) as adjuvant chemotherapy for operable breast

cancer: a study by the GEICAM group. Ann Oncol 2003,14(6):833–842.PubMed 127. Linden HM, Haskell CM, Green SJ, Osborne CK, Sledge GW, Shapiro CL, Ingle JN, Lew D, Hutchins LF, Livingston RB, Martino S: Sequenced Compared With Simultaneous Anthracycline and Cyclophosphamide in High-Risk Stage I and II Breast Cancer: Final Analysis From INT-0137 (S9313). J Clin Oncol 2007,25(6):656–661.PubMed 128. Recommended breast cancer surveillance guidelines: American Society of Clinical Oncology. J Clin Oncol 1997,15(5):2149–2156. 129. Oltra A, Santaballa A, Munarriz B, Pastor M, Montalar J: Cost-benefit analysis of a follow-up program in patients with breast cancer: a randomized prospective study. Breast J 2007,13(6):571–574.PubMed 130. van Hezewijk M, van den Akker ME, van de Velde CJ, Scholten AN, Hille ET: Costs of different follow-up strategies in early breast cancer: a review of the literature. Breast 2012,21(6):693–700.PubMed 131.

In rats with peritonitis, Montravers et al. showed that adjunction of Enterococcus faecalis was associated with increased mortality as well as higher levels of TNFα and IL-6 in peritoneal fluid [32, 33]. Evidence regarding a specific role of some pathogens on the pattern of the sepsis response is rather small, preventing any definitive conclusion from these results. However it is well known that patients with severe sepsis or septic shock may benefit from aggressive

antimicrobial treatment in order to curb the spread of the multiple organ dysfunction syndrome caused by an ongoing peritoneal trigger. For these patients, a de-escalated approach may be the most appropriate strategy. Increasing rates of resistance and a more comprehensive understanding of the sepsis process have prompted many experts to advocate the use of broad-spectrum antimicrobial regimens in the initial

https://www.selleckchem.com/products/MS-275.html stages of treatment for sepsis [34, 35]. Subsequent modification (de-escalation) of the initial regimen becomes possible later, when culture results are available and clinical status can be better assessed, 48–72 hours after initiation of empiric therapy. When treating abdominal sepsis, clinicians must be aware that drug pharmacokinetics may differ significantly between patients due to the variable pathophysiology of sepsis, and must also take into account the pathophysiological learn more and immunological status of the patient [36]. The “dilution effect”, also called the ‘third spacing’ phenomenon, must be considered when administering hydrophilic agents such as β-lactams, aminoglycosides, and glycopeptides, which selectively distribute to the extracellular

space. Low plasma antimicrobial levels can contribute to lower than expected antimicrobial concentrations in peritoneal fluid with potentially reduced antimicrobial delivery to the target tissues. In fact, the target plasma concentration (Ct) that should be achieved with the loading dose (LD) depends solely on the volume of distribution (Vd) of the drug (LD = Ct × Vd). If the Vd is enlarged the Ct will results in a lower than expected level with the standard LD [36]. Higher than standard loading doses of β-lactams, aminoglycosides, or glycopeptides should be administered to ensure optimal drug exposure to the PRN1371 infection site GNA12 in patients with severe sepsis or septic shock [36]. Lastly it should be kept in mind that the loading dose of lipophilic antibiotics (Macrolides, Fluoroquinolones, Tetracyclines, Chloramphenicol, Rifampicin, Linezolid) which are not influenced by the “diluition effect”, should not be influenced by the severe sepsis or septic shock status [36]. Once appropriate initial loading is achieved, it is mandatory to reassess the antimicrobial regimen daily, because the pathophysiological changes that may occur, may significantly affect drug disposition in the critically ill patients.

The replication locus of the theta-type SCP2 comprises repI and repII genes and an adjacent non-coding sequence to which RepI protein binds [7, 13]. pFP1 and pFP11 contain basic replication loci

of rep and Selleck Pictilisib iteron types (direct repeats and/or inverted repeats), to which Rep proteins bind [8]. Conjugal transfer of Streptomyces RC plasmid (e.g. pIJ101) needs a tra gene along with a clt (cis-acting locus of transfer) site [14]. Streptomyces tra genes encode a DNA translocase resembling the chromosomal DNA translocase FtsK of E. coli or SpoIIIE of B. subtilis[3], with double-stranded DNA probably entering the recipient [15]. The TraB of pSVH1 binds to the clt sequence as multimers on the mobilized plasmid and translocates unprocessed DNA at the hyphal tip to a recipient cell [16]. Conjugal transfer of Streptomyces theta-type plasmids (e.g. SCP2 and pZL12) requires a major tra gene and two adjacent genes [17, 18]. In contrast to most bacteria, Streptomyces

species often harbor linear plasmids [19, 20]. Unlike the terminal protein-capped linear replicons of adenoviruses that replicate by a mechanism of strand displacement [21], Streptomyces linear plasmids start replication from a centrally located ori locus [22] and replication PI3K inhibitor proceeds bi-directionally toward the telomeres [23]. At least some Streptomyces linear plasmids (e.g. pSCL1) can propagate in circular mode when the telomeres are deleted [22], while some theta-type circular plasmids (e.g. SCP2 and pFP11) can also propagate in linear mode when the telomeres from a linear plasmid are attached [8]. Results Identification of a

widely distributed Streptomyces species Y27 and its indigenous plasmid pWTY27 among endophytic Streptomyces strains During the course of investigating naturally circular plasmids, we detected 27 plasmids among ~300 newly isolated actinomycete strains from plant samples of Gingko, Taxus and Artemisia annua L in China. Interestingly, 14 of them (Table 1) displayed similar sizes of ca.14-kb DNA bands on agarose gel. These plasmids were Reverse transcriptase this website digested with NcoI and all showed five bands (~8, 2.2, 1.7, 1.3 and 1 kb) on gel electrophoresis (Additional file 1: Figure S1), suggesting that they were an identical plasmid (designated pWTY27). Table 1 Strains and plasmids used in this study Strain and plasmid Genotype or description Source or reference Strains     Streptomyces strains (Y27, Y32, Y33, Y34, Y41, Y42 and G2-1) Isolated from Gingko harboring pWTY27 This work Streptomyces strains(W15, W24, W37 and W41) Isolated from Artemisia annua L harboring pWTY27 This work Streptomyces strains (Z20, Z54 and Z70) Isolated from Taxus harboring pWTY27 This work S. lividans ZX7 pro-2 str-6 rec-46 dnd SLP2- SLP3- 34 S.

rhizomorpha also produce rhizomorphs, but they are not in the same clade (Fig. 7); our PD173074 order observation suggests that presence of rhizomorphs has evolved multiple times in the genus. Subclade D includes P. straminea, P. piceicola Y.C. Dai and P. tibetica, and is characterized by resupinate basidiocarps, branched, indextrinoid to slightly dextrinoid skeletal hyphae and truncate, dextrinoid

basidiospores. Subclade E includes P. aridula and P. tephropora, and is characterized by resupinate basidiocarps, branched skeletal hyphae, and truncate, dextrinoid basidiospores. Subclade F includes P. corticola (Corner) Decock, P. maackiae (Bondartsev & Ljub.) Parmasto and P. tenuis, and it is characterized by resupinate basidiocarps with yellow pore surface and branched skeletal hyphae, and

truncate, dextrinoid basidiospores; morphologically, a yellow pore surface is a key character to unify this group. Subclade G includes P. pyricola Y.C. Dai & B.K. Cui and P. truncatospora (Lloyd) Ryvarden, and is characterized by frequently branched, Dorsomorphin price dextrinoid skeletal hyphae, and truncate, indextrinoid to dextrinoid basidiospores. Clade II includes Perenniporia detrita (Berk.) Ryvarden, P. ochroleuca (Berk.) LXH254 price Ryvarden and P. ohiensis (Berk.) Ryvarden, and it is characterized by smaller, pileate basidiocarps, indextrinoid to weakly dextrinoid skeletal hyphae, and larger, truncate, strongly dextrinoid basidiospores. Pilát (1953) established the genus Truncospora typified by T. ochroleuca (Berk.) Pilát to accommodate the species P. ochroleuca, but many mycologists considered Truncospora as a synonym of Perenniporia (Ryvarden 1972, 1991; Ryvarden and Johansen 1980; Gilbertson and Ryvarden 1987; Ryvarden and Gilbertson Aurora Kinase 1994; Dai et al. 2002). Decock and

Ryvarden (1999) concluded that P. detrita, P. ochroleuca and P. ohiensis formed a morphologically homogeneous alliance, which could be recognized at the genus level, and the name Truncospora would be available. Phylogenetic analysis based on DNA sequences data by Robledo et al. (2009) showed that these three taxa formed a monophyletic clade distinct from Perenniporia s.s., and should be recognized at genus level (Decock 2011). In our study (Fig. 7), Perenniporia ochroleuca complex forms a monophyletic entity, and it was distinct from Perenniporia s.s., which may indicate that these three species could be recognized as a separate genus of Truncospora (MycoBank: MB 18685). Clade III is formed by species in Perenniporiella Decock & Ryvarden. Perenniporiella was segregated from Perenniporia by Decock and Ryvarden (2003), characterized by pileate basidiocarps, a dimitic hyphal system, and non-truncate, weakly dextrinoid basidiospores. Preliminary phylogenetic relationship of Perenniporiella and Perenniporia was analyzed inferred from partial nuclear ribosomal LSU and ITS DNA sequences data (Robledo et al.

Optical transitions from the lower triplet and the upper singlet states are forbidden and allowed respectively, due to spin selection rules [1, selleck chemicals 2, 39, 40, 53]. However, the lifetime

of the triplet state becomes weakly allowed due to spin-orbit interaction [39, 40, 53]. Hence, the triplet lifetime is expected to be considerably longer than the singlet lifetime. At low temperatures (where kT < < Δ, and Δ is the singlet-triplet splitting energy; see inset to Figure 3b), only the triplet level is populated and therefore, the PL decay time is dominated by the triplet lifetime and is relatively long (the low-temperature plateau regions in Figure 3a). As the temperature increases (above approximately 30 K), the upper singlet

level becomes thermally populated and the overall lifetime shortens according to the following expression: (2) where τ R PS-341 price stands for the radiative decay time and τ L and τ U are the lower triplet and the upper singlet lifetimes respectively (g = 3 is the levels degeneracy ratio) [1, 39, 40, 53]. At high temperatures, the decay time is dominated by the much faster upper singlet lifetime. Figure 2 PL decay curves. The PL decay curves of H-PSi measured Dibutyryl-cAMP mw at a photon energy of 2.03 eV (610 nm) and at various temperatures. The solid lines present the best fit to a stretched exponential function (Equation 1). Inset shows the PL spectrum of H-PSi measured at room

temperature. Figure 3 PL lifetime and integrated PL. (a) Arrhenius Bacterial neuraminidase plot of the PL lifetime (on a semi-logarithmic scale) as a function of 1/T, at a photon energy of 2.03 eV (610 nm) for H-PSi (red circles) and O-PSi (black squares). The solid lines represent the best fit to the singlet-triplet model of Eq.2. (b) Arrhenius plot of the integrated PL. Inset shows the schematics of the excitonic two-level model with the upper excitonic singlet-triplet state and the ground (no exciton) state. The arrows represent the allowed (from the singlet) and the forbidden (from the triplet) optical transitions. From Figure 3a we found that within the experimental errors, the upper singlet decay times of H- and O- PSi (at photon energy of 2.03 eV) are essentially the same (1.0 ± 0.2 μs and 1.3 ± 0.2 μs for H-PSi and O-PSi, respectively). However, at low temperatures the H-PSi decay time is faster than that of the O-PSi (200 ± 50 μs relative to 480 ± 50 μs, respectively). To further explore the differences between H- and O- PSi decay times, the singlet and the triplet lifetimes as well as the energy splitting were extracted over the measurement’s range of photon energies and are plotted in Figure 4. As expected, the upper singlet lifetime (τ U) is significantly shorter (by about one to two orders of magnitude) than the lower triplet lifetime (τ L) over this range of photon energies.

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