However, in previous studies inhibition of HSP90 by GA was shown to diminish NF-κB activity in tumor cells due to impaired expression of the NK-κB signaling regulators IKK [15], NIK [16], and RIP1 [17]. Limited activity of either regulator may contribute to attenuated RelB

expression in stimulated MO-DCs cotreated with GA. In T cells GA may inhibit the expression of the tyrosine kinase lck, and impair its stimulation-induced phosphorylation as evidenced in a human T cell line (Jurkat) [52, 53]. Due to this early block in T cell activation, IL-2 production of stimulated T cells was largely abrogated. Most recently, GA was demonstrated to affect as well the expression of several T cell receptor-associated molecules, namely TCRαß, CD4 and CD28 [54]. In accordance, GA prevented the proliferation of lymphocytes treated with stimulatory this website antibodies [53] and of T cells stimulated by either MO-DCs or mitogen [54]. In line, we observed largely abrogated proliferation of CD4+ T cells stimulated DAPT solubility dmso by unstimulated or stimulated MO-DCs or by application of stimulatory antibodies. Conclusions Our study has shown that GA-mediated inhibition of HSP90 in unstimulated MO-DCs may result in partial activation of the cells by yet unknown mechanisms. On the other hand, GA treatment

impaired MO-DC stimulation and largely abrogated both polyclonal and DC-mediated T cell proliferation. Chemotherapeutics that act to inhibit HSP90 may therefore exert rather inhibitory effects on the patients’ immune system, and most likely are not preferable for combination Plasmin with immunotherapy that targets the DC/T cell axis to mount potent anti-tumor responses. Acknowledgements We thank Claudia Eider and Dr. Dirk Prawitt (both Center for Pediatrics and Adolescent Medicine, University Medical Center

of the Johannes Gutenberg-University, Mainz, Germany) for providing us with the cell line IGROV1. This study was supported by grants of the University Medical Center Mainz (MAIFOR program), and of the Deutsche Forschungsgemeinschaft (grant number RE 617/1-1). Stefanie Trojandt did partial fulfillment of the requirements of the doctoral thesis. Electronic supplementary material Additional file 1: Table S1: GA affects surface marker expression by MO-DCs in an activation state-dependent manner. (DOC 37 KB) Additional file 2: Figure S1: GA slightly reduces the endocytotic activity of unstimulated MO-DCs. (TIFF 2 MB) Additional file 3: Figure S2: MO-DCs acquire potent T cell stimulatory capacity in response to stimulation. (TIFF 760 KB) References 1. da Silva VC, Ramos CH: The network interaction of the human cytosolic 90 kDa heat shock protein Hsp90: a target for cancer therapeutics. J Proteomics 2012, 75:2790–2802.PubMedCrossRef 2. Echeverría PC, Bernthaler A, Dupuis P, Mayer B, Picard D: An interaction network predicted from public data as a discovery tool: application to the Hsp90 molecular chaperone machine.

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26. Hanefeld M, Pfutzner A, Forst T, Kleine I, Fuchs W. Double-blind, randomized, multicentre, and active comparator controlled investigation of the effect of pioglitazone, metformin, and the combination of both on cardiovascular risk in patients with type 2 diabetes receiving stable basal insulin therapy: the PIOCOMB study. Cardiovasc Diabetol. 2011;10:65.PubMedCentralPubMedCrossRef 27. Snell-Bergeon JK, Wadwa RP. Hypoglycemia, diabetes, and cardiovascular disease. find more Diabetes Technol Ther. 2012;14(Suppl 1):S51–8.PubMed 28. Fujita Y, Tamada D, Kozawa J, Kobayashi Y, Sasaki S, Kitamura T, Yasuda T, Maeda N, Otsuki M, Okita K, Iwahashi H, Kaneto H, Funahashi T, Imagawa A, Shimomura I. Successful treatment of reactive hypoglycemia secondary to late dumping syndrome using miglitol. Intern Med. 2012;51:2581–5.PubMedCrossRef Ivacaftor in vivo 29. Heinz G, Komjati M, Korn A, Waldhausl W. Reduction of postprandial blood glucose by the α-glucosidase inhibitor Miglitol (BAY m 1099) in type II diabetes. Eur J Clin Pharmacol. 1989;37:33–6.PubMed 30. Kingma PJ, Menheere PP, Sels JP, Nieuwenhuijzen Kruseman AC. α-Glucosidase inhibition by miglitol in NIDDM patients. Diabetes Care. 1992;15:478–83.PubMedCrossRef 31. Schnack C, Prager RJ, Winkler J, Klauser RM, Schneider BG, Schernthaner G. Effects of 8-week α-glucosidase inhibition on metabolic control, C-peptide secretion,

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MAJOR study. Diabetes Technol Ther. 2011;13:303–8.PubMedCrossRef 35. Furuta M, Tomisaka R, Yamana A, Morita S, Ueyama M, Imanishi K, Ooishi RAS p21 protein activator 1 C, Hara Y, Ooishi H, Sanke T. Evaluation of seasonal changes in hemoglobin A1c in diabetic patients. Rinsho Byori. 2012;60:599–604.PubMed”
“Key Points Attention-deficit hyperactivity disorder (ADHD) medications may be subject to abuse, misuse, and diversion. We found that overlapping prescriptions from two or more prescribers dispensed by three or more pharmacies defines ADHD medication shopping. 1 Introduction Medications for the treatment of attention-deficit hyperactivity disorder (ADHD) are subject to misuse, abuse, and diversion [1–3]. The non-medical use of ADHD medications in high-school-age children in the US is estimated at around 9 %, and in college-age individuals goes from 5 to 35 % [1].

Among them, plants of the genus Phyllanthus (Euphorbiaceae) are widely distributed in tropical forests throughout the world and have long been used in folk medicine to treat kidney and urinary tract infections [15]. Based on this knowledge, Ratnayake et al. [16] at the NCI screened extracts of the Tanzanian plant Phyllanthus engleri and have reported the isolation of two novel bioactive sesquiterpenes, named englerin A (EA) and englerin B. Initial learn more studies by the NCI demonstrated that EA possessed very potent growth inhibitory activity (GI50 = 10–87 nM) against

most RCC with a selectivity that is approximately 1,000-fold higher compared to other cancers. Although several synthetic routes toward the synthesis of EA have been established [16–21], other than EA’s selective toxicity to RCC, recently confirmed by us [21], very little is known about its biological actions and mechanism(s) of action. Only recently, one study reported that

EA induced necrosis in RCC [22]. The most recent report concluded that EA bound and activated protein kinase C-θ (PKCθ) to inhibit insulin signaling while, concurrently, activating HSF1, a known inducer of glucose dependence [23]. This dual signaling, that promotes glucose addiction while inhibiting glucose uptake by the cells, was proposed to be the mechanism for the selective cytotoxicity of EA. Although the data presented is compelling, whether in fact this mechanism accounts for the cytotoxicity of EA is not yet clear. Based on its cytotoxicity profile against the NCI60 cell panel, EA is Selleck 5-Fluoracil clearly a very unique agent and there is much to be learned about the actions of EA Tangeritin in RCC and the mechanisms and targets involved in these actions. In this study, using the highly EA-sensitive A498 human renal carcinoma cells as our model system, we report the results of a thorough and systematic investigation to uncover the mechanisms of growth inhibition and cell death induced by EA and reveal for the first time that

EA induces multiple mechanisms of cell death as well as cell cycle arrest while inducing autophagy. Material and methods Cell lines The A498 human kidney carcinoma cell line was purchased from ATCC and maintained in RPMI medium supplemented with 10% FBS and 100 units/ml penicillin/streptomycin (complete medium). Reagents Englerin A was purchased from Cerilliant Corporation. (Round Rock, Texas). Rapamycin was purchased from Enzo Life Sciences (Farmingdale, NY) as part of the Cyto-ID® Autophagy Detection Kit. VP16 was purchased from Sigma Aldrich (St. Louis, MO). MEM 100X non-essential amino acids (NEAA) was purchased from Gibco Life Technologies (Grand Island, NY). Antibody against caspase-3 was a gift from Dr. Robert Naviaux and anti LC3B was purchased from Cell Signaling Technology (Danvers, MA).

Cancer Res 2003, 63: 812–816.PubMed 10. Lee KM, Park SK, Hamajima N, Tajima K, Yoo KY, Shin A, Noh DY, check details Ahn SH, Hirvonen A, Kang D: Genetic polymorphisms of TGF-beta1 & TNF-beta and breast cancer risk. Breast Cancer Res Treat 2005, 90: 149–155.CrossRefPubMed 11. Nikolova PN, Pawelec GP, Mihailova SM, Ivanova MI, Myhailova AP, Baltadjieva DN, Marinova DI, Ivanova SS, Naumova EJ: Association of cytokine gene polymorphisms

with malignant melanoma in Caucasian population. Cancer Immunol Immunother 2007, 56: 371–379.CrossRefPubMed 12. Howell WM, Bateman AC, Turner SJ, Collins A, Theaker JM: Influence of vascular endothelial growth factor single nucleotide polymorphisms on tumour development in cutaneous malignant melanoma. Genes Immun 2002, 3: 229–232.CrossRefPubMed 13. Lin CC, Wu HC, Tsai FJ, Chen HY, Chen WC: Vascular endothelial growth factor gene-460 C/T polymorphism is a biomarker for prostate cancer. Urology 2003, 62: 374–377.CrossRefPubMed 14. Jakowlew

SB: Transforming growth factor-beta in cancer and metastasis. Cancer Metastasis Rev 2006, 25: 435–457.CrossRefPubMed 15. Bierie B, Moses HL: Tumour microenvironment: Midostaurin TGFbeta: the molecular Jekyll and Hyde of cancer. Nat Rev Cancer 2006, 6: 506–520.CrossRefPubMed 16. Yoo YA, Kang MH, Kim JS, Oh SC: Sonic hedgehog signaling promotes motility and invasiveness of gastric cancer cells through TGF-beta-mediated activation of the ALK5-Smad 3 pathway. Carcinogenesis 2008, 29: 480–490.CrossRefPubMed 17. Yoshinaga K, Obata H, Jurukovski V, Mazzieri R, Chen Y, Zilberberg L, Huso D, Melamed J, Prijatelj P, Todorovic V, Dabovic B, Rifkin DB: Perturbation of transforming growth factor (TGF)-beta1 association with latent TGF-beta binding protein yields inflammation Resveratrol and tumors. Proc Natl Acad Sci USA 2008, 105: 18758–18763.CrossRefPubMed 18. Komuro A, Yashiro M, Iwata C, Morishita Y, Johansson E, Matsumoto Y, Watanabe A, Aburatani H, Miyoshi H, Kiyono K, Shirai YT, Suzuki HI, Hirakawa K, Kano MR, Miyazono K:

Diffuse-type gastric carcinoma: progression, angiogenesis, and transforming growth factor beta signaling. J Natl Cancer Inst 2009, 101: 592–604.CrossRefPubMed 19. Tsirlis TD, Papastratis G, Masselou K, Tsigris C, Papachristodoulou A, Kostakis A, Nikiteas NI: Circulating lymphangiogenic growth factors in gastrointestinal solid tumors, could they be of any clinical significance? World J Gastroenterol 2008, 14: 2691–2701.CrossRefPubMed 20. Suthanthiran M, Li B, Song JO, Ding R, Sharma VK, Schwartz JE, August P: Transforming growth factor-beta 1 hyperexpression in African-American hypertensives: A novel mediator of hypertension and/or target organ damage. Proc Natl Acad Sci USA 2000, 97: 3479–3484.CrossRefPubMed 21.

Drs. Marras, Tyagi, and Kramer used these probes to distinguish alleles that differ in as little as a single nucleotide

polymorphism (SNPs) [55, 56]. The basis of this extraordinary specificity is that hairpin-shaped probes can assume two different stable states, by: (i) forming double-stranded hybrids with their LY294002 manufacturer target sequence, or (ii) retaining their partially double-stranded structure when not bound to a target. Any mismatch between the probe sequence of the molecular beacon and the target sequence destabilizes the probe-target hybrid, leading to return of the molecular beacon in its stable hairpin structure [57, 58]. Unlike hairpin-shaped probes, linear probes such a TaqMan probes have only one conformation, either on or off the target. This decreases

difference between the melting temperature of a perfectly matched target sequence and a single-nucleotide mismatched target sequence makes discrimination between two scenarios more difficult to discern [58–60]. Furthermore, Taqman probes are digested by the endonuclease activity of the Taq polymerase in each PCR cycle, such that optimization of both annealing and digestion of the probe becomes buy Daporinad more challenging in the development of multiplex assays. Our success in utilizing the extraordinary specificity of molecular beacon probes to detect the recA gene of B. burgdorferi, and to quantitate the number of spirochetes present in infected mouse tissue [61] offered us an incentive to develop the assay for diagnosis of Lyme disease in humans. We have now optimized the assay to work in the presence of human DNA for it to become useful as diagnostic test for human Lyme disease. We describe here expansion of a simplified, highly sensitive multiplex

real-time PCR assay by incorporating specific molecular beacons that can distinguish B. burgdorferi, A. phagocytophilum and B. microti simultaneously. Application of this assay will make a significant difference in achieving the rapid and accurate diagnosis of Lyme disease, anaplasmosis and babesiosis in a cost-effective Ketotifen manner. Methods Microbial strains and human cell line For standardization of conditions for real-time PCR diagnostic assay for Lyme disease, N40 strain clone D10/E9 of B. burgdorferi (sensu stricto), VS461 strain of B. afzelii and PBi strain of B. garinii were grown in BSKII medium supplemented with 6% rabbit serum at 33°C. Dr. Edouard Vannier of Tufts Medical Center at Boston, and Dr. Errol Fikrig of Yale University School of Medicine generously provided the genomic DNA from B. microti strain RM/NS and A. phagocytophilum strain HZ, respectively. Human embryonic kidney 293 cells were cultured in a 1:1 mix of DMEM (low glucose) and Ham’s F12 medium (Life Technologies, NY) supplemented with 10% FBS to isolate human DNA used in the assays. Isolation of B.

The data indicate that FA1090(M1) possessed a small insertion of 7 nucleotides about midway through the coding sequence, producing a frame shift mutation in nfsB. This genetic data supported the hypothesis that the nitrofurantoin resistant phenotype is due to the loss of nitroreductase activity. Conclusive evidence that this gene was responsible for nitrofurantoin resistance was obtained by deleting the coding

sequence for this gene from FA1090 and then demonstrating that FA1090NfsB-BsmIS lacked nitroreductase CT99021 molecular weight activity (data not shown). Identification of the genetic basis of spontaneous nitrofurantoin resistant mutants We isolated numerous independent spontaneous nitrofurantoin resistant mutants and determined the DNA sequence of the ABT-737 mw nfsB gene in these strains. Most of these mutants (90%) possessed the insertion of an adenine in a run of 5 adenines near the beginning of the gene, suggesting a bias for base insertion during

DNA replication at this position. This gene contains three other polynucleotide runs of five nucleotides distal to the start codon; 2 poly adenines and one polythymine. Interestingly, even though we were able to isolate base insertions at each of these three clusters, none of the clusters showed the elevated propensity for generating spontaneous mutations. To eliminate the bias introduced by the 5 bp polyadenine run at the 5′ end of the all gene, this DNA sequence was altered to remove the poly-A tract, while preserving the corresponding amino acid sequence. The plasmid, pEC3 was constructed as described in figure 4. Plasmid DNA was isolated from E. coli and DNA used to transform N. gonorrhoeae. Spectinomycin resistant transformants were identified, and DNA sequence analysis of a PCR amplicon derived

from the constructed strain indicated that the derivative of FA1090, FA1090-NfsB(mod) contained the desired sequence modification. Nitroreductase assays of this strain indicated that it possessed wild-type NfsB activity (data not shown). Figure 4 Schematic illustrating the strategy used to modify the nfsB coding region. Each numbered arrow corresponds to the procedures summarized below: 1: PCR using primers NfsBsmI-3F and NfsBsmI-2R to introduce a BsmI recognition sequence and to alter a poly-A tract. 2: Treatment with S1 nuclease to create blunt ends, polynucleotide kinase to phosphorylate 5′ ends, and T4 DNA ligase. E. coli were transformed using this construct (pEC2). Plasmid DNA was isolated by alkaline lysis. 3: Treatment with BsmI to generate pEC1. Digestion product was ligated with T4 DNA ligase. The construct was transformed into E. coli. 4: pEC1 was amplified with primers dwnstrm-F and dwnstrm-R.

Also a review by Rösler (1994) reports the same amount of increase in age-corrected HTLs at 4 kHz, after the first 10 years of exposure. When comparing the age-corrected PTA3,4,6

values of the study population and the ISO predicted NIPTS as a function of exposure time, the greater inter-individual variation in the distribution of NIHL in exposed construction workers is remarkable. This suggests a high variation in factors influencing the susceptibility to hearing loss in each exposure year interval of the study group, such as HPD use, prior employment, non-occupational noise exposure, hearing disorders, and variability in noise intensity. However, the median values of both the noise-exposed workers and the ISO predictions have a similar slope, at least for exposure times between 10 and 40 years. An interesting aspect is the relationship during the first 10 years of noise exposure. Construction workers employed selleck inhibitor for less than 10 years show greater hearing losses than expected Ku-0059436 order based on the interpolation of ISO-1999. In addition, observed hearing loss increases over the first 10 years of exposure at the same rate as in

the following 10–40 years of exposure duration, where a pattern of strongly increasing thresholds would have been expected (ISO 1990; Rösler 1994; Prince 2002). To investigate the role of job history in this group with short exposure duration, this relationship is determined only for construction workers younger than 30 years of age that reported no prior employment. This selection of 2,190 employees shows the same pattern of median age-corrected PTA3,4,6 values that is about 10 dB higher than predicted by ISO. A number of previous studies also found a discrepancy between ISO predictions and measured hearing loss during the first years of exposure.

Acetophenone Analyses based on serial audiograms of railway workers showed that hearing thresholds exceed model predictions in the very beginning of noise exposure, showing age-corrected hearing loss at job entrance of 9 dB averaged over 2 and 4 kHz (Henderson and Saunders 1998). Another study, monitoring a cohort of newly enrolled construction apprentices, showed HTLs of 12.2 dB HL at 4 kHz at baseline (Seixas et al. 2004) without any change in audiometric hearing thresholds over the first 3 years of employment (Seixas et al. 2005). The reported hearing threshold levels at job entrance in these studies are all higher than 0 dB HL and correspond to the median age-corrected PTA3,4,6 of 10.9 dB HL found here. The ISO-1999 model depends on the interpolation of predicted hearing thresholds after 10 years of exposure and the assumed hearing thresholds of 0 dB HL at the beginning of employment. Our findings suggest that this may not correctly represent the true development of NIHL over this period of exposure.

CrossRefPubMed 5. Robins-Browne RM, Hartland EL:Escherichia coli as a cause of diarrhea. J Gastroenterol Hepatol 2002, 17:467–475.CrossRefPubMed 6. 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 7. Robins-Browne RM, Bordun A-M, Tauschek

M, Bennett-Wood VR, Russell J, Oppedisano F, Lister NA, Bettelheim KA, Fairley CK, Sinclair MI, Hellard ME:Escherichia coli and community-acquired gastroenteritis, Melbourne, Australia. Emerg Infect Dis 2004, 10:1797–1805.PubMed 8. Sethabutr O, Venkatesan M, Yam S, buy Cabozantinib Pang LW, Smoak BL, Sang WK, Echeverria P, Taylor DN, Isenbarger DW: Detection of PCR products of the ipaH gene from Shigella and enteroinvasive Escherichia coli by enzyme-linked immunosorbent assay. Diagn Microbiol Infect Dis 2000, 37:11–16.CrossRefPubMed ZD1839 mw 9. Gross RJ, Rowe B: Serotype of Escherichia coli. The virulence of Escherichia coli: reviews and methods (Edited by: Sussman M). Academic Press Inc: London 1985.

10. Clinical and Laboratory Standards Institute: Performance standards for antimicrobial susceptibility testing: fifteenth informational supplement. Clinical Laboratory Standards Institute, Wayne, PA 2005. 11. Rotimi VO, Jamal W, Pal T, Sovenned A, Albert MJ: Emergence of CTX-M-15 type extended-spectrum β -lactamase-producing Salmonella spp. in Kuwait and the United Arab Emirates. J Med Microbiol 2008, 57:881–886.CrossRefPubMed 12. World Health Organisation: Programme for control of diarrhoeal diseases (CDD/83.3 Rev 1). Manual for laboratory investigations of acute enteric infections World Health Organisation, Geneva 1987, 27. 13. Levine MM, Edelman R: Enteropathogenic Escherichia coli of classic serotypes associated with infant diarrhea: epidemiology and pathogenesis. Epidemiol Rev 1984, 6:31–51.PubMed 14. Rao MR, Abu-Elyazeed R, Savarino SJ, Naficy AB, Wierzba

TF, Abdel-Messih I, Shaheen H, Frenck RW Jr, Svennerholm A-M, Clemens JD: High disease burden of diarrhea due to enterotoxigenic Escherichia coli among rural Egyptian infants and young children. J Clin Microbiol from 2003, 41:4862–64.CrossRefPubMed 15. Aslani MM, Ahrabi SS, Alikhani YM, Jafari F, Zali RM, Mani M: Molecular detection and antimicrobial resistance of diarrheagenic Escherichia coli strains isolated from diarrheal cases. Saudi Med J 2008, 29:388–392.PubMed 16. Al-Gallas N, Bahri O, Bouratbeen A, Ben Haasen A, Ben Aissa R: Etiology of acute diarrhea in children and adults in Tunis, Tunisia, with emphasis on diarrheagenic Escherichia coli : prevalence, phenotyping, and molecular epidemiology. Am J Trop Med Hyg 2007, 77:571–582.PubMed 17. Porat N, Levy A, Fraser D, Deckelbaum RJ, Dagan R: Prevalence of intestinal infections caused by diarrheagenic Escherichia coli in Bedouin infants and young children in Southern Israel. Pediatr Infect Dis J 1998, 17:482–488.

2001; Leakey et al. 2004). Few studies, in which both responses were simultaneously analyzed in plants growing in the field (Logan et al. 1997; Watling et al. 1997b; Adams et al. 1999), showed adjustment of the partitioning of absorbed light energy between photochemistry and photoprotection of photosystem

II (PSII) in response to dynamically changing PAR over a day, somewhat increased accumulation of the xanthophyll-cycle pigments (violaxanthin, V; antheraxanthin, A; zeaxanthin, Z), and retention of A and Z in leaves after exposure to strong sunflecks. The light-induced de-epoxidation of V to A and Z in the xanthophyll cycle is known to be involved in photoprotective thermal energy dissipation (Demmig-Adams 1990; Niyogi et al. 1998) and protection of thylakoid membranes against lipid peroxidation (Havaux and Niyogi 1999; Havaux et al. 2007). Thus, upregulation of these photoprotective mechanisms seems to be crucial for acclimation of LL-grown INK 128 clinical trial plants to fluctuating light environment with sunflecks. Compared to diurnal changes in photosynthesis and photoprotection under fluctuating light environment or physiological and biochemical properties

of leaves acclimated https://www.selleckchem.com/products/Fulvestrant.html to sunfleck conditions, much less is known about the acclimatory processes which bring about such alterations in leaf properties. How quickly can the capacities of photoprotection and carbon gain change in leaves during acclimation to sunfleck conditions? Are the acclimatory processes Phospholipase D1 for photosynthesis and photoprotection similarly or differently affected by duration, frequency and intensity of sunflecks? In order to address these questions, we exposed LL-grown plants of the model species Arabidopsis thaliana (hereafter Arabidopsis), a common laboratory accession Columbia-0 (Col-0), to well-defined sunfleck conditions in a controlled climate chamber and monitored acclimatory

changes in PSII activities, starch accumulation, and leaf growth for 7 days. Owing to the availability of large genetic resources and extensive knowledge accumulating at all levels from genes to whole plant, Arabidopsis has become an important model system in plant biology. Unlike forest understorey plants, however, Arabidopsis usually occupies open or disturbed habitats and is a poor competitor in dense vegetations (Koornneef et al. 2004). This may imply limited capacities of Arabidopsis plants to grow under LL + sunflecks environments, possibly due to low carbon gain and/or insufficient photoprotection in such conditions. Effects of sunfleck duration, frequency, and intensity on the acclimatory responses were examined by applying short sunflecks (SSF, lasting 20 s) at two different intensities (650 or 1,250 μmol photons m−2 s−1) and two different intervals (every 6 or 12 min) or long sunflecks (LSF, lasting 40 min) at 650 μmol photons m−2 s−1 once a day. The sunfleck treatments were performed under PAR of the LL growth condition (50 μmol photons m−2 s−1).